AAPD Reference Manual “ the manual ”
American Academy of Pediatric Dentistry 2010-11 Definitions, Oral Health Policies, and Clinical Guidelines
American Academy of Pediatric Dentistry 2010-11 Definitions, Oral Health Policies, and Clinical Guidelines (aka “Reference”, “the Manual”) Introduction 2 4 5 7 10
Overview Vision Statement/Mission Statement Core Values Strategic Plan AAPD Research Agenda
Definitions Reaffirmed Dental Home
12 13 14 15 16 17
Reaffirmed Dental Neglect Dental Disability Early Childhood Caries Medically Necessary Care Special Health Care Needs
Oral Health Policies Medically Necessary Care Oral Health Care Programs for Infants, Children, and Adolescents Reaffirmed Dental Home Child Identification Programs Mandatory School-entrance Oral Health Examinations New
School Absences for Dental Appointments Emergency Oral Care for Infants, Children, and Adolescents Use of Fluoride
Revised
Use of Xylitol in Caries Prevention Interim Therapeutic Restorations (ITR) Early Childhood Caries (ECC): Classifications, Consequences, and Preventive Strategies Early Childhood Caries (ECC): Unique Challenges and Treatment Options Dietary Recommendations for Infants, Children, and Adolescents Vending Machines in Schools
Revised
Tobacco Use Intraoral and Perioral Piercing
Revised
Prevention of Sports-related Orofacial Injuries Use of Dental Bleaching for Child and Adolescent Patients Minimizing Occupational Health Hazards Associated With Nitrous Oxide Use of Deep Sedation and General Anesthesia in the Pediatric Dental Office
Revised
Hospitalization and Operating Room Access for Dental Care of Infants, Children, Adolescents and Persons With Special Health Care Needs
Revised
Hospital Staff Membership Model Dental Benefits for Infants, Children, Adolescents, and Individuals with Special Health Care Needs Third-party Reimbursement of Medical Fees Related to Sedation/General Anesthesia for Delivery of Oral Health Services Third-party Reimbursement for Oral Health Care Services Related to Congenital Orofacial Anomalies Third-party Reimbursement of Fees Related to Dental Sealants Role of Pediatric Dentists as Both Primary and Specialty Care Providers Patient Safety Ethical Responsibility to Treat or Refer
New
Second Opinion for Pediatric Oral Health Care
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19 24 25 27 29 31 33 34 36 39 41 45 48 50 52 56 58 62 65 67 69 71 73 76 78 80 81 82 85 86
88 90 91
Patient's Bill of Rights and Responsibilities Stem Cells Infection Control
Clinical Guidelines Reaffirmed Oral and Dental Aspects of Child Abuse and Neglect Periodicity of Examination, Preventive Dental Services, Anticipatory Guidance, and Oral Treatment for Children Revised
Caries-risk Assessment and Management for Infants, Children, and Adolescents - (Chart) Perinatal Oral Health Care Infant Oral Health Care
Revised
Adolescent Oral Health Care Oral Health Care for the Pregnant Adolescent Management of Dental Patients With Special Health Care Needs Role of Dental Prophylaxis in Pediatric Dentistry Fluoride Therapy Behavior Guidance for the Pediatric Dental Patient Use of Local Anesthesia for Pediatric Dental Patients Use of Nitrous Oxide for Pediatric Dental Patients Monitoring and Management of Pediatric Patients During and After Sedation for Diagnostic and Therapeutic Procedures Use of Anesthesia Personnel in the Administration of Office-based Deep Sedation/General Anesthesia to the Pediatric Dental Patient Pediatric Restorative Dentistry Pulp Therapy for Primary and Immature Permanent Teeth
Revised
Management of Acute Dental Trauma Management of the Developing Dentition and Occlusion in Pediatric Dentistry Oral Health Care/Dental Management of Heritable Dental Developmental Anomalies
Revised
Acquired Temporomandibular Disorders in Infants, Children, and Adolescents
Revised
Pediatric Oral Surgery Use of Antibiotic Therapy for Pediatric Dental Patients Antibiotic Prophylaxis for Patients at Risk for Infection Dental Management of Pediatric Patients Receiving Chemotherapy, Hematopoietic Cell Transplantation, and/or Radiation
137 93 101 109 114 119 127 132 141 143 147 156 163 167 184 187 194 202 213 226 232 238 246 249 253 260 268
Recordkeeping Informed Consent
Endorsements Prescribing Dental Radiographs for Infants, Children, Adolescents, and Persons With Special Health Care Needs Management of Patients With Cleft Lip/Palate and Other Craniofacial Anomalies Periodontal Diseases of Children and Adolescents Periodontal Therapy Treatment of Plaque-induced Gingivitis, Chronic Periodontitis, and Other Clinical Conditions
272 277 279 285 290
Resource Section Dental Growth and Development Revised
Growth Charts Body Mass Index (BMI) Charts Food Pyramid Recommended Childhood and Adolescent Immunization Schedules
Revised
Speech and Language Milestones Post-surgery Instructions for Extractions/Oral Surgery Preparing for Your Child's Sedation Visit Sedation Record Record Transfer
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301 302 306 308 310 311 320 316 318 321
New
Release for School Absences
New
Decision Trees for Management of an Avulsed Permanent Tooth Common Laboratory Values
Management of Medical Emergencies
324 325
Cardiopulmonary Resuscitation
326
Delineation of Privileges
327 334
Common Pediatric Medications
New
New
Analysis and Policy Recommendations Concerning Mid-level Dental Providers
Copyright © 2002-2010 American Academy of Pediatric Dentistry. All Rights Reserved. Website Designed by AmericanEagle.com, Inc. http://www.aapd.org/media/policies.asp
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Overview Definitions and scope of pediatric dentistry Pediatric dentistry is an age-defined specialty that provides both primary and comprehensive preventive and therapeutic oral health care for infants and children through adolescence, including those with special health care needs.1 To become a pediatric dental specialist, a dentist must satisfactorily complete a minimum of 24 months in an advanced education program accredited by the Commission on Dental Accreditation of the American Dental Association (ADA). Such programs “must be designed to provide special knowledge and skills beyond the DDS or DMD training...”1 The curriculum of an advanced program provides the dentist with necessary didactic background and clinical experiences to provide comprehensive primary oral health care and the services of a specialist. Pediatric dentists provide care, conduct research, and teach in a variety of clinical and institutional settings, including private practice and public health. They work in coordination with other health care providers and members of social disciplines for the benefit of children. The primary focus of most dental specialties is a particular area of dental, oral, or maxillofacial expertise. Pediatric dentistry encompasses a variety of disciplines, techniques, procedures, and skills that share a common basis with other specialties, but are modified and adapted to the unique requirements of infants, children, adolescents, and those with special health care needs. By being an age-specific specialty, pediatric dentistry encompasses disciplines such as behavior guidance, care of the medically and developmentally compromised and disabled patient, supervision of orofacial growth and development, caries prevention, sedation, pharmacological management, and hospital dentistry, as well as other traditional fields of dentistry. These skills are applied to the needs of children throughout their ever-changing stages of development and to treating conditions and diseases unique to growing individuals. The American Academy of Pediatric Dentistry (AAPD), founded in 1947, is the membership organization representing the specialty of pediatric dentistry. The membership provides care to millions of our nation’s infants, children, adolescents, and persons with special health care needs. They are the primary contributors to professional education programs and publications on pediatric oral health. The AAPD, in accordance with its vision and mission, advocates optimal oral health and health care for all children and persons with special health care needs. Its advocacy activities take place within the broader health care community and with the public at local, regional, and national levels. The Reference Manual is one of the components of the AAPD’s advocacy activities.
Intent of the AAPD Reference Manual The AAPD Reference Manual is intended to encourage a diverse audience to provide the highest possible level of care to 2
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children. This audience includes, but is not limited to: 1. pediatric dentists; 2. general dental practitioners and other dental specialists; 3. physicians and other health care providers; 4. government agencies and health care policy makers; 5. individuals interested in the oral health of children. The AAPD Reference Manual is divided into 5 sections: (1) definitions; (2) oral health policies; (3) clinical guidelines; (4) endorsements; and (5) resources. Oral health policies are statements relating to AAPD positions on various public health issues. Clinical guidelines are practice recommendations designed to assist the dental provider in making decisions concerning direct patient care. Adherence to the guidelines increases the probability of a favorable practice outcome and decreases the likelihood of an unfavorable practice outcome. Practice recommendations that have been developed by the AAPD appear in the “Clinical Guidelines” section. “Endorsements” includes clinical guidelines relevant to the practice of pediatric dentistry that have been developed by another organization with recognized expertise and adopted by the AAPD. “Resources” contains supplemental information to be used as a quick reference when more detailed information is not readily accessible, as well as clinical forms offered to facilitate excellence in practice. Proper utilization of this Reference Manual necessitates recognizing the distinction between “standards” and “guidelines”. Although there are certain instances within the guidelines where a specific action is mandatory, the AAPD Reference Manual is not intended nor should it be construed to be either a standard of care or a scope of practice document. The AAPD Reference Manual contains practice guidelines which are intended to be recommendations for care that could be modified to fit individual patient needs based on the patient, the practitioner, the health care setting, and other factors.
Definitions For the purpose of this document, the following definitions shall apply. They are based on definitions established by the ADA, the Institute of Medicine, and the Joint Commission on Accreditation of Health Care Organizations. Standards: Any definite rule, principle, or measure established by authority. Standards are intended to be applied rigidly and carry the expectation that they are applied in all cases and any deviation from them would be difficult to justify. A standard of care indicates that measurable criteria are present and these criteria shall be used to arrive at a given level of outcome. Standards say what must be done. The courts define legal standards of care. Guidelines: Systematically developed recommendations designed to assist the practitioner, patient, and caregiver in making decisions relating to specific clinical situations.
american academy of pediatric dentistry
Guidelines are intended to be more flexible than standards. Guidelines should be followed in most cases, but they recognize that treatment can and should be tailored to fit individual needs, depending on the patient, practitioner, setting, and other factors. Deviations from guidelines could be fairly common and could be justified by differences in individual circumstances. Guidelines are designed to produce optimal outcomes, not minimal standards of practice. Guidelines originate in an organization with recognized professional expertise and stature. Although they may be unsolicited, they usually are developed following a stated request or perceived need for clinical advice or instruction. Guidelines are kept current by regular review and modification by the developing body. Must or shall: Indicates an imperative need and/or duty; an essential or indispensable item; mandatory. Should: Indicates the recommended need and/or duty; highly desirable. May or could: Indicates freedom or liberty to follow a suggested alternative. Parent: Unless otherwise indicated, the term “parent” as used in these oral health policies and clinical guidelines has a broad meaning encompassing a natural/biological father or mother of a child with full parental legal rights, a custodial parent who in the case of divorce has been awarded legal custody of a child, a person appointed by a court to be the legal guardian of a minor child, or a foster parent (a noncustodial parent caring for a child without parental support or protection who was placed by local welfare services or a court order).
Policy and guideline development The oral health policies and clinical guidelines of the AAPD are developed under the direction of the Board of Trustees (BOT), utilizing the resources and expertise of its membership operating through the Council on Clinical Affairs (CCA). CCA is comprised of individuals representing the 6 geographical (trustee) districts of the AAPD, along with additional consultants confirmed by the BOT. Council members and consultants derive no financial compensation from the AAPD for their participation and are asked to disclose potential conflicts of interest. Proposals to develop or modify policies and guidelines may originate from 4 sources: 1. the officers or trustees acting at any meeting of the BOT; 2. a council, committee, or task force in its report to the BOT; 3. any member of the AAPD who submits a written re quest to the BOT as per the AAPD Administrative Policy and Procedure Manual, Section 9 (the full text of this manual is available on the Members’ Only page of the AAPD Web site at: “http://www.aapd.org/ members/resources/pdf/PolicyProcedure.pdf ”); 4. officers, trustees, council and committee chairs, or other participants at the AAPD’s Annual Strategic Planning Session.
Regardless of the source, proposals are considered carefully, and those deemed sufficiently meritorious by a majority vote of the BOT are referred to the CCA for development or review/revision. Once a charge (directive from the BOT) for development or review/revision of an oral health policy or clinical guideline is sent to the CCA, it is assigned to 1 or more members of the CCA for completion. CCA members are instructed to follow the specified format for a policy or guideline. Oral health policies and clinical guidelines utilize 2 sources of evidence: the scientific literature and experts in the field. CCA, in collaboration with the Council on Scientific Affairs, performs a comprehensive literature review for each document. When scientific data do not appear conclusive, experts may be consulted. The CCA meets on an interim basis to discuss proposed oral health policies and clinical guidelines. Each new or reviewed/revised policy and guideline is discussed, amended if necessary, and confirmed by the entire council. Once developed by the CCA, the proposed policy or guideline is submitted for the consideration of the BOT. While the Board may request revision, in which case it is returned to the council for modification, once accepted by majority vote of the Board, it is referred for Reference Committee hearing at the upcoming Annual Session. The Reference Committee hearing is an open forum for the membership to provide comment or suggestion for alteration of the document. CCA carefully considers all remarks presented at the Reference Committee hearing prior to submitting its final document for ratification by a majority vote of the membership present and voting at the General Assembly. If accepted by the General Assembly, either as proposed or as amended by that body, the document then becomes the official AAPD oral health policy or clinical guideline for publication in the AAPD’s Reference Manual and on the AAPD’s Web site (www.aapd.org-click on Policies and Guidelines on the left sidebar).
Review and revision of existing policies and guidelines Each AAPD oral health policy and clinical guideline is reviewed for accuracy, relevance, and currency by the CCA no less than once every 5 years and more often if directed by the BOT. AAPD members may submit (through a Web site survey) suggestions and/or resources for consideration during CCA’s review of existing documents. After completing a new literature review, the council may recommend retention of the document without change (ie, reaffirm), propose revision, or recommend elimination of a policy or guideline. Policies and guidelines of other organizations that have been endorsed by the AAPD are reviewed annually to determine currency as well as appropriateness for the AAPD’s continued endorsement.
Reference 1. American Dental Association Commission on Dental Accreditation. Accreditation standards for advanced specialty education programs in pediatric dentistry. Chicago, Ill; 2000.
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American Academy of Pediatric Dentistry Vision Statement / Mission Statement Adopted 2003
Revised 2008
Vision statement
Mission statement
The vision of the American Academy of Pediatric Dentistry (AAPD) is optimal health and care for infants and children through adolescence, including those with special health care needs. The Academy is the leader in representing the oral health interests of children. The pediatric dentist is a recognized primary oral health care provider and a resource for specialty referral.
The mission of the American Academy of Pediatric Dentistry is to advocate policies, guidelines, and programs that promote optimal oral health and oral health care for infants and children through adolescence, including those with special health care needs. The Academy serves and represents its membership in the areas of professional development and governmental and legislative activities. It is a liaison to other health care groups and the public.
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American Academy of Pediatric Dentistry Core Values Adopted 2003
Revised 2009
American Academy of Pediatric Dentistry values (AAPD) 1. Health and health care equity. A. AAPD values oral health as an inseparable part of the overall health and welfare of the infant, child, and adolescent. B. AAPD values universal access to comprehensive oral health care that meets each child’s unique needs and promotes optimal oral health. C. AAPD values effectiveness and efficiency in providing oral health services to infants, children, and adolescents and supports efforts that improve access through effective and efficient delivery systems. D. AAPD values improvements in access to oral health care that reduce or eliminate financial, logistic, and cultural barriers to care. E. AAPD values oral health care for children that is safe, comprehensive, accessible, affordable, high quality, continuous, and respectful of individual children and their families. F. AAPD values volunteerism and charitable care that improves children’s health but rejects these approaches as significant solutions to reducing disparities in oral health care for infants, children, and adolescents covered by public insurance programs. 2. An effective dental workforce. A. AAPD values a workforce that can meet the needs of infants, children, and adolescents by being adequate in size, distribution, diversity, and competency. B. AAPD values the unique skills and knowledge that pediatric dentists bring to children’s oral health care. C. AAPD values the role of other dental specialists and general dentists in caring for children. D. AAPD values programs that improve the capacity of general dentists, hygienists, and assistants to improve children’s oral health by providing appropriate care and effectively referring to pediatric dentists when unable to meet the comprehensive needs of individual infants, children, and adolescents. E. The AAPD values the educators who mentor those who treat children, including pediatric dentists, general
dentists, dental hygienists, and auxiliary personnel, by teaching the skills and promoting the professional behaviors that serve children’s interests. 3. Effective public programs. A. AAPD values government’s role in assuring comprehensive dental care for vulnerable children and values the legal requirements of Early and Periodic Screening, Diagnosis and Treatment (EPSDT), which ensure access for covered children that is equivalent to access for noncovered children in the same geographic area. B. AAPD values public health programs proven to prevent or minimize disease in infants, children, and adolescents. 4. Oral health promotion. A. AAPD values health promotion and disease prevention, including effective anticipatory guidance beginning with comprehensive dental care in a dental home starting at age 1. B. AAPD values the critical role of the dental home in promoting optimal oral health for all children. C. AAPD values health promotion and disease prevention as integral components of perinatal care. 5. Child and adolescent welfare. A. AAPD values health, health equity, and the quality of life that results from health attainment, including oral health attainment. B. AAPD values society’s recognition of oral disease as a significant health problem for infants, children, and adolescents that needs to be addressed in all pediatric health policies. C. AAPD values society’s recognition of oral diseases that affect children’s function, development, and quality of life as significant health problems. 6. Science, education, research, and evidence-based care. A. AAPD values the scientific basis of its profession and the need to continue improving that base through research, experimentation, and the promotion of evidence-based care.
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B. AAPD values the critical role of clinical judgment to promote primary and comprehensive preventive and therapeutic oral health care for which evidence is incomplete or unavailable. C. AAPD values professional education programs and their faculties, community service, scientific contributions to pediatric dentistry, and the preparation of skilled practitioners. D. AAPD values the dissemination of valid information about children’s oral health to the professions and the public. 7. Children with special health care needs. A. AAPD values the unique qualities of each person and the need to ensure maximal health attainment for all regardless of their developmental or other special health needs. B. AAPD values dentists’ unique roles and responsibilities in diagnosing oral conditions and in coordinating, managing, and directing the oral health care of infants, children, and adolescents.
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8. Families and communities. A. AAPD values the roles of families and communities in promoting infant, child, and adolescent health and welfare and attaining maximal oral health. B. AAPD values the diversity of children, their families, and their communities and respects the contribution of culture to the attainment of oral health and use of dental services. 9. Membership. AAPD values its members–their involvement with the Academy, their commitment to children and youth, their professional endeavors, and their support of policies that improve the health and welfare of children and youth.
american academy of pediatric dentistry
American Academy of Pediatric Dentistry 2009-12 Strategic Plan Revised 2009
Goal 1—Optimal Health for All Children and Persons with Special Health Care Needs Objective 1.1: An oral disease-free population. Strategy 1.1.1 Promote universal acceptance of antici patory guidance and preventive oral health care in a dental home beginning no later than age 1. Strategy 1.1.2 Support water fluoridation efforts and appropriate use of other topical and sys temic fluoride vehicles. Strategy 1.1.3 Increase public and governmental aware ness and education regarding pediatric oral health strategies. Strategy 1.1.4 Encourage and support research in oral disease prevention and evidence-based care. Strategy 1.1.5 Employ risk assessment and tailored interventions. Objective 1.2: Access to appropriate oral health care for all children and persons with special health care needs. Strategy 1.2.1 Recognize and address barriers to access and quality care. Strategy 1.2.2 Assure adequate and appropriate financ ing in public sector programs. Strategy 1.2.3 Recognize and support appropriate pro vision of care by safety net providers. Strategy 1.2.4 Increase the availability of reimbursement for medically necessary care (general anesthesia and sedation).
Goal 2—Valued and Worthwhile Membership Services Objective 2.1: An informed membership. Strategy 2.1.1 Provide valuable continuing education. Strategy 2.1.2 Communicate through Pediatric Dentistry Today and other appropriate venues Aca demy activities and programs on behalf of the membership. Strategy 2.1.3 Produce respected scientific publications Strategy 2.1.4 Maximize utilization of information technology.
Objective 2.2: A membership adept at adapting to changes in delivery of care and technological advances. Strategy 2.2.1 Provide contemporary guidance in prac tice administration, communication, and marketing skills in pediatric dentistry. Strategy 2.2.2 Assist in disseminating information con cerning member career transitions and business opportunities, including those designed for the new pediatric dentist. Strategy 2.2.3 Involve the Academy in the dissemination of information regarding new products and techniques. Objective 2.3: Maximized membership dues value. Strategy 2.3.1 Support the personal issues of Academy members. Strategy 2.3.2 Provide office brochures and other valu able materials. Strategy 2.3.3 Monitor and evaluate membership bene fits on a continuing basis. Objective 2.4: Effective response to crucial pediatric dental issues. Strategy 2.4.1 Identify and anticipate emergent mem bership issues. Strategy 2.4.2 Develop and maintain a protocol and mechanism for responding to the public, media, and membership on anticipated and unanticipated critical issues. Strategy 2.4.3 Develop and maintain a network of trained spokespersons. Objective 2.5: Strong pediatric dental organization representation. Strategy 2.5.1 Development of international mem bership. Strategy 2.5.2 Sustain recruitment and retention efforts, including programs and policies directed to the new pediatric dentist and dental faculty.
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Goal 3—Recognized Authority in Pediatric Oral Health Objective 3.1: Optimal care, including translation of science into clinical practice. Strategy 3.1.1 Develop optimal care through our oral health policies, clinical guidelines, and other venues. Strategy 3.1.2 Promote optimal care through our oral health policies, clinical guidelines, and other venues. Strategy 3.1.3 Maintain optimal care through our oral health policies, clinical guidelines, and other venues. Objective 3.2: Expert resource on children’s oral health recognition. Strategy 3.2.1 Build and maintain coalitions with other healthcare organizations. Strategy 3.2.2 Anticipate and respond effectively to changes in the clinical and scientific environment. Strategy 3.2.3 Identify and support areas of clinical and scientific research important to pediatric oral health. Strategy 3.2.4 Communicate to the profession and the public issues about pediatric oral health. Strategy 3.2.5 Encourage and support volunteer leader ship by pediatric dentists in all organiza tions involved in oral health or child welfare. Objective 3.3: Effective advocate of public policy. Strategy 3.3.1 Coordinate all elements of advocacy resources, including the congressional liaison, child advocate, political action committee (PAC), Children’s Dental Health Project (CDHP), volunteer advo cates, and lobbyists. Strategy 3.3.2 Identify public policy issues, conduct policy research and development, and develop implementation strategies. Strategy 3.3.3 Develop an effective advocacy network.
Goal 4—Satisfy Worforce Issues Objective 4.1: Enlarged and appropriately distributed pediatric dental workforce. Strategy 4.1.1 Encourage effective geographic distribu tion of pediatric dentists. Strategy 4.1.2 Expansion of pediatric dental residency and fellowship programs. Strategy 4.1.3 Innovate and support programs to assure a well-qualified applicant pool for pedia tric dental training.
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Objective 4.2: Greater engagement of the general dentist and dental specialists in the treatment of children. Strategy 4.2.1 Improve pre-doctoral education and experience in pediatric dentistry. Strategy 4.2.2 Development of continuing education programs. Strategy 4.2.3 Promote the value of the Affiliate mem bership category. Objective 4.3: Appropriate and optimized utilization of allied dental health professionals. Strategy 4.3.1 Development of continuing education programs. Strategy 4.3.2 Identify appropriate roles for allied den tal health professionals which include dental assistants, expanded function dental assistants (EFDA), and hygienists. Objective 4.4: Appropriate and effective utilization of nondental healthcare providers. Strategy 4.4.1 Development of continuing education programs. Strategy 4.4.2 Identify appropriate roles for physicians and non-dental health care providers.
Goal 5—Meet Dental Education Needs Objective 5.1: Academic faculties of excellent caliber and sufficient number. Strategy 5.1.1 Educate AAPD membership on academic crisis issues. Strategy 5.1.2 Foster a fundraising campaign for aca demic support. Strategy 5.1.3 Foster improved business practices in teaching clinics. Strategy 5.1.4 Foster academic career loan forgiveness programs. Strategy 5.1.5 Foster creative use of private clinics and practitioner mentors in residency programs. Strategy 5.1.6 Foster effective modeling, mentoring, and education for potential academicians. Strategy 5.1.7 Foster development of shared basic in formation distance learning modules. Strategy 5.1.8 Increase the transition of “master clinicians” into teaching, including full time positions. Strategy 5.1.9 Foster dissemination of “best practice” models. Objective 5.2: Physical plants of educational institutions adequate to support educational objectives. Strategy 5.2.1 Aid and support facility development programs. Strategy 5.2.2 Support legislation to secure capital fund ing for pediatric dentistry education facilities.
american academy of pediatric dentistry
Objective 5.3: Increased standardization of pre- and postdoctoral training experiences. Strategy 5.3.1 Implement consistent standards in pre and post- doctoral programs.
Objective 5.4: Appropriate accreditation standards for the pre- and post- doctoral level. Strategy 5.4.1 Support Academy initiatives on pre- and post- doctoral curriculum standardization.
Goal 6—Efficient and Effective Organization Objective 6.1: The structure of the Academy serves and represents its membership. Strategy 6.1.1 Increase communication between mem bership and leadership. Strategy 6.1.2 Review the mechanism of accountability of the headquarters office to leadership. Objective 6.2: Adequate funding for Academy operations, programs, and initiatives. Strategy 6.2.1 Offset expenses by appropriately maximiz ing corporate and other outside support of Academy projects and endeavors. Strategy 6.2.2 Assure an appropriate dues structure and other sources of income. Objective 6.3: Efficient headquarters office operations. Strategy 6.3.1 Assure a technologically-advanced com munication to the membership. Strategy 6.3.2 Provide an appropriately-sized and ad equately-equipped facility for business operations. Strategy 6.3.3 Support a qualified and well-motivated staff in appropriate numbers and respon sibilities to accomplish Academy business operations.
Objective 6.4: Effective volunteer leadership. Strategy 6.4.1 Assure appropriate leadership training. Strategy 6.4.2 Assure objective assessment of the volunteer leadership. Strategy 6.4.3 Assure a fair and equitable process to identify and select individuals at al l volunteer leadership levels. Objective 6.5: Effective tripartite organizational structure. Strategy 6.5.1 Clarify and enhance the role of District Trustee in Academy operations. Strategy 6.5.2 Promote efforts to strengthen effectiveness and number of district organizations and state units. Strategy 6.5.3 Explore opportunities for increased mem bership participation in Academy deci sion making. Objective 6.6: Effective relationship between the Academy and its Foundation. Strategy 6.6.1 Healthy Smiles, Healthy Children: The Foundation of the American Academy of Pediatric Dentistry will function as the tax-exempt charitable research, education, and service arm of the Academy. Strategy 6.6.2 Reflecting the AAPD Research Agenda and to further developments in the spe cialty, Healthy Smiles, Healthy Children: The Foundation of the American Acad emy of Pediatric Dentistry will sponsor research grants and awards, along with professional and public education opportunities. Objective 6.7: Effective relationship between the Academy and the American Board of Pediatric Dentistry (ABPD). Strategy 6.7.1 Sponsor and support a strong and vital American Board of Pediatric Dentistry.
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American Academy of Pediatric Dentistry Research Agenda Adopted 2005
Reaffirmed 2007
The American Academy of Pediatric Dentistry (AAPD) recognizes that the clinical practice of pediatric dentistry has to be driven by science and evidence-based dentistry (EBD). Where possible, our clinical guidelines in pediatric dentistry should be supported by the best available evidence. No longer is it acceptable for our clinical guidelines to be based on expert opinions solely. Where the evidence or science is lacking, research needs to be conducted to answer the relevant questions that arise in our clinical practice. The AAPD Research Agenda is a strategic list of scientific and clinical questions and topics that are specific to the clinical practice of pediatric dentistry. These questions will benefit from scientific review and set the agenda for the AAPD, as well as the AAPD Foundation research grants. The AAPD Council on Scientific Affairs (CSA) is charged with proposing a mechanism by which the AAPD Research Agenda is to be developed and maintained. Other dental organizations have embraced evidence-based research. The National Institute of Dental and Craniofacial Research (NIDCR) has a Strategic Plan that outlines research opportunities to support its mission to improve oral, dental, and craniofacial health through research, research training, and the dissemination of health information by performing and supporting basic and clinical research. While interested in supporting clinical research, the NIDCR supports research that offers the most significant scientific promise. The American Dental Association (ADA) is committed to bringing EBD concepts and practices to the dental profession. The ADA Research Agenda was developed to promote research in areas of dental practice and to designate priorities for conducting and funding evidence-based studies. The ADA Research Agenda reflects important clinical questions that are relevant to the entire profession of dentistry.
Methodology, Results, and Recommendations The 14 members of the 2004-05 AAPD CSA submitted 41 research topics/questions/issues that were thought to be the most pertinent to pediatric dentistry. These topics were evaluated for duplication, consolidated, and returned to the CSA members for ranking in terms of importance. After 2 rounds of elimination, the CSA members identified the 5 research topics that were deemed to be the most important for pediatric dentistry and would benefit the most from scientific review. These topics are listed below in descending order of priority: 1. Transmission, etiology, risk assessment, early detection, prevention, and management of caries. introduction 10
2. Caries management using antimicrobials, fluorides, and remineralizing agents. 3. Disparities and barriers to accessing dental care. 4. Development of a national databank on pediatric den tal issues. 5. Efficacy of infant oral health (ie, first dental visit by age 12 months). Additional topics of relevance are as follows: 1. Pulp biology and efficacious and biocompatible pulp treatment. 2. Safe and effective sedative agents for pain and anxiety control. 3. Specific (immunity) and non-specific host factors in the etiology and prevention of dental caries. 4. Interface between medicine and dentistry in address ing access to care. 5. Biologic and behavioral factors in the natural history of caries. 6. Parenting styles. 7. Non-pharmacologic behavior guidance approaches. 8. Efficacy and biocompatibility of restorative materials. 9. Pediatric dentist’s role in monitoring, preventing, and managing obesity. 10. Etiology, detection, prevention, and management of pre-pubertal and juvenile periodontal disease. As to be expected from a group of individuals who practice in different regions of the United States and who possess a wide array of scientific expertise and interests, CSA members did not share a consensus in terms of how the research topics ought to be ranked. Some CSA members found it difficult to rank the research topics. Some members felt that the AAPD Research Agenda should reflect the unique aspects of pediatric dentistry practice that have limited appeal to other dental disciplines. Others felt that while some topics have been left off the “top 10,” they are important to include in the overall Research Agenda. Nevertheless, the “top 5” topics received composite ranking scores that were significantly higher than the rest and they were ranked more frequently. The Council on Clinical Affairs was consulted. The Cariesrisk Assessment Tool (CAT) was specifically recommended to be included in the list of research topics of relevance. Although CAT could be included under the broad topic of “Transmission, etiology, risk assessment, early detection, prevention, and management of caries,” it was singled out as needing research. CSA recommends that council reevaluate and update the AAPD Research Agenda on an annual basis.
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Definition of Dental Home Originating Council
Council on Clinical Affairs Adopted 2006
Reaffirmed 2010
The dental home is the ongoing relationship between the dentist and the patient, inclusive of all aspects of oral health care delivered in a comprehensive, continuously accessible, coordinated,
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and family-centered way. Establishment of a dental home begins no later than 12 months of age and includes referral to dental specialists when appropriate.
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Definition of Dental Neglect Originating Committee
Child Abuse Committee Review Council
Council on Clinical Affairs
Adopted 1983
Revised 1987, 1992
Reaffirmed 1996, 2001, 2006, 2010
Dental caries, periodontal diseases, and other oral conditions, if left untreated, can lead to pain, infection, and loss of function. These undesirable outcomes can adversely affect learning, communication, nutrition, and other activities necessary for normal growth and development.
Dental neglect is willful failure of parent or guardian to seek and follow through with treatment necessary to ensure a level of oral heath essential for adequate function and freedom from pain and infection.
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Definition of Dental Disability Originating Committee
Child Abuse Committee Review Council
Council on Clinical Affairs
Adopted 1983
Revised 1992, 2000, 2008
Reaffirmed 1996, 2003
Dental caries, periodontal disease, dentoalveolar trauma, and other oral conditions left untreated can limit substantially a child’s development and an individual’s participation in life activities. An individual should be considered to have a dental disability if pain, infection, or lack of stable and functional dentition:
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1. restricts nutritional intake adequate for growth and energy needs; 2. delays or otherwise alters growth and development; 3. inhibits participation in life activities; or 4. diminishes quality of life.
american Academy of Pediatric Dentistry
Definition of Early Childhood Caries (ECC) Originating Council Council on Clinical Affairs
Review Council Council on Clinical Affairs
Adopted 2003
Revised 2007, 2008
Caries is a biofilm (plaque)-induced acid demineralization of enamel or dentin, mediated by saliva. The disease of early childhood caries (ECC) is the presence of 1 or more decayed (noncavitated or cavitated lesions), missing (due to caries), or filled tooth surfaces in any primary tooth in a child 71 months of age or younger. In children younger than 3 years
of age, any sign of smooth-surface caries is indicative of severe early childhood caries (S-ECC). From ages 3 through 5, 1 or more cavitated, missing (due to caries), or filled smooth surfaces in primary maxillary anterior teeth or a decayed, missing, or filled score of ≥4 (age 3), ≥5 (age 4), or ≥6 (age 5) surfaces constitutes S-ECC.
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Definition of Medically Necessary Care Originating Committee Clinical Affairs Committee
Review Council Council on Clinical Affairs
Adopted 1997
Revised 2001, 2003, 2007
Medically necessary care (MNC) is the reasonable and appropriate diagnostic, preventive, and treatment services (including supplies, appliances, and devices) and follow-up care as determined by qualified, appropriate health care providers in treating any condition, disease, injury, or congenital or developmental malformation. MNC includes all supportive health care services that, in the judgment of the attending dentist, are necessary for the provision of optimal quality therapeutic and preventive oral care. These services include, but are not
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limited to, sedation, general anesthesia, and utilization of surgical facilities. MNC must take into account the patient’s age, developmental status, and psychosocial well-being, in addition to the setting appropriate to the needs of the child and family. Dental care is medically necessary to prevent and eliminate orofacial disease, infection, and pain, to restore the form and function of the dentition, and to correct facial disfiguration or dysfunction.
american Academy of Pediatric Dentistry
Definition of Special Health Care Needs Originating Council
Council on Clinical Affairs Review Council Council on Clinical Affairs
Adopted 2004
Revised 2008
Special health care needs include any physical, developmental, mental, sensory, behavioral, cognitive, or emotional impairment or limiting condition that requires medical management, health care intervention, and/or use of specialized services or programs. The condition may be developmental or acquired and may cause limitations in performing daily
self-maintenance activities or substantial limitations in a major life activity. Health care for individuals with special needs requires specialized knowledge, increased awareness and attention, adaptation, and accommodative measures beyond what are considered routine.
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american academy of pediatric Dentistry
Policy on Medically Necessary Care Originating Council
Council on Clinical Affairs Adopted 2007
Purpose The American Academy of Pediatric Dentistry (AAPD) recognizes that dental care is medically necessary for the purpose of preventing and eliminating orofacial disease, infection, and pain, restoring the form and function of the dentition, and correcting facial disfiguration or dysfunction.
Methods This policy is based upon a review of the current dental and medical literature related to the concept of medically necessary care. A MEDLINE search was performed using the terms “medically necessary care”, “systemic disease and oral disease”, “dentistry as medically necessary care”, “periodontal disease and cardiovascular disease”, “maternal oral disease and pregnancy”, and “oral disease and respiratory illness”.
Background The AAPD defines medically necessary care (MNC) as the reasonable and appropriate diagnostic, preventive, and treatment services (including supplies, appliances, and devices) and follow-up care as determined by qualified, appropriate health care providers in treating any condition, disease, injury, or congenital or developmental malformation. MNC includes all supportive health care services that, in the judgment of the attending dentist, are necessary for the provision of optimal quality therapeutic and preventive oral care. These services include, but are not limited to, sedation, general anesthesia, and utilization of surgical facilities. MNC must take into account the patient’s age, developmental status, and psychosocial well-being, in addition to the setting appropriate to the needs of the child and family.1 MNC is based upon current preventive and therapeutic practice guidelines formulated by professional organizations with recognized clinical expertise. Such recommendations ideally are evidence based but, in the absence of conclusive evidence, may rely on expert opinion and clinical observations. Expected benefits of care should outweigh potential risks. MNC increases the probability of good health and well-being and decreases the likelihood of an unfavorable outcome. Value of services is an important consideration, and all stakeholders should recognize that cost-effective care is not necessarily the least expensive treatment.2 Dental care is medically necessary to prevent and eliminate orofacial disease, infection, and pain, to restore the
form and function of the dentition, and to correct facial disfiguration or dysfunction. Following the US Surgeon General’s report3 emphasizing that oral health is integral to general health, the US Department of Health and Human Services recommended changing perceptions of the public, policy makers, and healthcare providers so that oral health becomes an accepted component of general health.4 Oral diseases can have a direct and devastating impact on overall health, especially for those with certain systemic health problems or conditions. Caries is the most common chronic disease of childhood.3 Approximately 60% of children experience caries in their primary teeth by age 5.5 Between 1988-1994 and 1999-2004, prevalence of caries in primary teeth increased for youths aged 2 to 11 years, with a significant increase noted for those in the 2-5 year age range.6 By 17 years of age, 78% of children in the US have experienced caries.4 As much as 90% of all caries in school-aged children occurs in pits and fissures. Caries, periodontal diseases, and other oral conditions, if left untreated, can lead to pain, infection, and loss of function. These undesirable outcomes can adversely affect learning, communication, nutrition, and other activities necessary for normal growth and development.7 Rampant caries is one of the factors causing insufficient development in children who have no other medical problems.8 Children with early childhood caries (ECC) may be severely underweight because of the associated pain and disinclination to eat. Nutritional deficiencies during childhood can impact cognitive development.9 Other oral conditions also can impact general health and well-being. Gingivitis is nearly universal in children and adolescents, and children can develop severe forms of periodontitis.10 There exists a relationship between periodontal disease and cardiovascular disease11,12 and periodontal disease and adverse pregnancy outcomes.13,14 An association between oral health and respiratory diseases has been recognized.15,16 Oral health, oral microflora, and bacterial pneumonia, especially in populations at high risk for respiratory disease, have been linked. The mouth can harbor respiratory pathogens that susbequently are aspirated, resulting in airway infections.16 Problems of esthetics, form, and function can affect the developing psyche of children, with life-long consequences in social, educational, and occupational environments.17 Self-image, self-esteem, and selfconfidence are unavoidable issues in society, and an acceptable orofacial presentation is a necessary component of these psychological concepts.18
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Congenital orofacial anomalies (eg, ectodermal dysplasia, cleft defects) that result in malformed or missing teeth can have significant negative functional, esthetic, and psychological effects on individuals and their families.19,20 Patients with craniofacial anomalies often require oral health care as a direct result of their craniofacial condition. These services are an integral part of the rehabilitative process.19 Young children benefit from esthetic and functional restorative techniques and readily adapt to appliances that replace missing teeth and improve function, appearance, and self-image. During the period of facial and oral growth, appliances require frequent adjustment and have to be remade as the individual grows. Professional care is necessary to maintain oral health,3 and risk assessment is an integral element of contemporary preventive care for infants, children, adolescents, and persons with special health care needs.21 The goal of caries risk assessment is to prevent disease by identifying and minimizing causative factors (eg, microbial burden, dietary habits, dental morphology) and optimizing protective factors (eg, fluoride exposure, personal oral hygiene, sealants).22 Ideally, risk assessment and implementation of preventive strategies would occur before the disease process has been initiated. Infants and young children have unique caries-risk factors such as ongoing establishment of oral flora and host defense systems, susceptibility of newly erupted teeth, and development of dietary habits and childhood food preferences. Children are most likely to develop caries if mutans streptococci is acquired at an early age.23 High-risk dietary practices appear to be established early, probably by 12 months of age, and are maintained throughout early childhood.24 Adolescence can be a time of heightened caries activity and periodontal disease due to an increased intake of cariogenic substances and inattention to oral hygiene procedures.25,26 An analysis of caries risk includes determination of protective factors, such as fluoride exposure. More than one-third of the US population does not benefit from community water fluoridation.3 Fluoride contributes to the prevention, inhibition, and reversal of caries.27 Therefore, early determination of a child’s systemic and topical fluoride exposure is important. Children experiencing caries as infants and toddlers have a much greater probability of subsequent caries in both the primary and permanent dentitions.9 An individualized preventive plan based on the Caries-risk Assessment Tool (CAT)21 is the key component of caries prevention. Because any risk assessment tool may fail to identify all infants at risk for developing ECC, early establishment of the dental home is the ideal approach for disease prevention.28 Early diagnosis and timely intervention, including appropriate referrals, can prevent the need for more extensive and expensive care often required when problems have gone unrecognized and/or untreated.29 When very young children have not been the beneficiaries of adequate preventive care and subsequently develop ECC, therapeutic intervention should be provided by a practitioner with the training, experience, and expertise to manage both the child and the disease process. Because of the aggressive nature
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of ECC, treatment should be definitive yet specific for each individual patient. Conventional restorative approaches may not arrest the disease.30 Areas of decalcification and hypoplasia can develop cavitation rapidly. The placement of stainless steel crowns may be necessary to inhibit the caries process. Stainless steel crowns decrease the number of tooth surfaces at risk for new or secondary caries and are less likely than other restorations to require retreatment.31,32 Low levels of compliance with follow-up care and a high recidivism rate of children requiring additional treatment also can influence a practitioner’s decisions for management of ECC.33 Sealants are particularly effective in preventing pit and fissure caries and providing cost savings if placed on patients during periods of greatest risk.34 Children with multiple risk factors and tooth morphology predisposed to plaque retention (ie, developmental defects, pits and fissures) benefit from having such teeth sealed prophylactically. A child who receives sealants is 72% less likely to receive restorative services over the next 3 years than children who do not.35 Although sealant retention rates initially are high, sealant loss does occur.36 It is in the patient’s interest to receive periodic evaluation of sealants. With follow-up care, the success rate of sealants may be 80 to 90%, even after a decade.36 The extent of the disease process, as well as the patient’s developmental level and comprehension skills, affect the practitioner’s behavior guidance approaches. To perform treatment effectively and efficiently while instilling a positive dental attitude, the practitioner caring for a pediatric patient may employ advanced behavior guidance techniques such as protective stabilization and/or sedation or general anesthesia.36 The patient’s age, dental needs, disabilities, medical conditions, and/or acute situational anxiety may preclude the patient’s being treated safely in a traditional outpatient setting.37 For some infants, children, adolescents, and persons with special health care needs, treatment under sedation/general anesthesia in a hospital, outpatient facility, or dental office or clinic represents the only appropriate method to deliver necessary oral health care.37 The success of restorations may be influenced by the child’s response to the chosen behavior guidance technique. Although general anesthesia may provide optimal conditions to perform restorative procedures, it can add significantly to the cost of care. General anesthesia, under certain circumstances, may offer a cost-saving alternative to sedation for children with ECC.9,38 Reimbursement issues defined by the concept of MNC have been a complicated topic for dentistry. Pediatric dental patients may be denied access to oral health care when insurance companies refuse to provide reimbursement for sedation/general anesthesia and related facility services. Most denials cite the procedure as “not medically necessary”. This determination appears to be based on arbitrary and inconsistent criteria.39-44 For instance, medical policies often provide reimbursement for sedation/general anesthesia or facility fees related to myringotomy for a 3-year-old child, but deny these benefits when related to treatment of dental disease and/or infection for the same patient. American Dental Association Resolution
american academy of pediatric Dentistry
1989-546 states that insurance companies should not deny benefits that would otherwise be payable “solely on the basis of the professional degree and licensure of the dentist or physician providing treatment, if that treatment is provided by a legally qualified dentist or physician operating within the scope of his or her training and licensure.”44 Patients with craniofacial anomalies often are denied third party coverage for initial appliance construction and, more frequently, replacement of appliances as the child grows. The distinction between congenital anomalies involving the orofacial complex and those involving other parts of the body is often arbitrary and unfair. For instance, health care policies may provide reimbursement for the prosthesis required for a congenitally missing extremity and its replacement as the individual grows, but deny benefits for the initial prosthesis and necessary periodic replacement for congenitally missing teeth. Third-party payors frequently will refuse to pay for oral health care services even when they clearly are associated with the complete rehabilitation of the craniofacial condition.45 Although sealants are safe and effective, their use continues to be low.46 Initial insurance coverage for sealants often is denied, and insurance coverage for repair and/or replacement may be limited.47,48 Although some third party carriers restrict reimbursement for sealants to patients of certain ages, it is important to consider that timing of dental eruption can vary widely. Furthermore, caries risk may increase at any time during a patient’s life due to changes in habits (eg, dietary, home care), oral microflora, or physical condition, and previously unsealed teeth subsequently might benefit from sealant application.36
Policy statement Dental care is medically necessary to prevent and eliminate orofacial disease, infection, and pain, to restore the form and function of the dentition, and to correct facial disfiguration or dysfunction. MNC is based upon current preventive and therapeutic practice guidelines formulated by professional organizations with recognized clinical expertise. Expected benefits of MNC outweigh potential risks of treatment or no treatment. Early detection and management of oral conditions can improve a child’s oral health, general health and well-being, school readiness, and self-esteem. Early recognition, prevention, and intervention could result in savings of health care dollars for individuals, community health care programs, and third party payors. Because a child’s risk for developing dental disease can change over time, continual professional reevaluation and preventive maintenance are essential for good oral health. Value of services is an important consideration, and all stakeholders should recognize that cost-effective care is not necessarily the least expensive treatment.
The AAPD: 1. recommends oral health care be included in the design and provision of individual and community-based health care programs to achieve comprehensive health care.
2. encourages establishment of a dental home for all children by 12 months of age in order to institute an individualized preventive oral health program based upon each patient’s unique caries risk assessment. 3. recommends that health care providers who diagnose oral disease either provide therapy or refer the patient to an appropriately trained individual for treatment. Immediate intervention is necessary to prevent further dental destruction, as well as more widespread health problems. 4. recognizes evaluation and care provided for an infant, child, or adolescent by a cleft lip/palate, orofacial, or craniofacial deformities team as the optimal way to coordinate and deliver complex services. 5. believes that the dentist providing the oral health care for the patient determines the medical indication and justification for treatment. The dental care provider must assess the patient’s developmental level and comprehension skills, as well as the extent of the disease process, to determine the need for advanced behavior guidance techniques such as sedation or general anesthesia. Furthermore, the AAPD encourages third party payors to: 1. recognize that malformed and missing teeth and resultant anomalies of facial development seen in orofacial anomalies are congenital defects, just as the congenital absence of other body parts, requiring care over the lifetime of the patient; 2. include oral health care services related to these facial and dental anomalies as benefits of health insurance without discrimination between the medical and dental nature of the congenital defect. These services, optimally provided by the craniofacial team, include, but are not limited to, initial appliance construction, periodic examinations, and replacement of appliances; 3. end arbitrary and unfair refusal of compensation for oral health care services related to orofacial and dental anomalies; 4. recognize the oral health benefits of dental sealants and not base coverage for sealants on a patient’s age; 5. ensure that all children have access to the full range of oral health delivery systems. If sedation or general anesthesia and related facility fees are payable benefits of a health care plan, these same benefits shall apply for the delivery of oral health services; and 6. regularly consult the AAPD with respect to the development of benefit plans that best serve the oral health interests of infants, children, adolescents, and persons with special health care needs, especially those with craniofacial anomalies.
References 1. American Academy of Pediatric Dentistry. Definition of medically necessary care. Pediatr Dent 2007;29(suppl):14. 2. American Academy of Pediatrics. Policy statement: Model contractural language for medical necessity for children. Pediatrics 2005;116(1):261-2.
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3. US Dept of Health and Human Services. Oral health in America: A report of the Surgeon General. Rockville, Md: US Dept of Health and Human Services, National Institute of Dental and Craniofacial Research, National Institutes of Health; 2000. 4. US Dept of Health and Human Services. National call to action to promote oral health. Rockville, Md: US Dept of Health and Human Services, Public Health Service, National Institute of Health, National Institute of Dental and Craniofacial Research; NIH Publication No. 03-5303, Spring 2003. 5. Crall JJ. Development and integration of oral health services for preschool-age children. Pediatr Dent 2005;27 (4):323-30. 6. D ye BA, Tan S, Smith V, et al. Trends in oral health status: United States, 1988-1994 and 1999-2004. National Center for Health Statistics. Vital Health Stat 11 (248). Hyattsville, Md; 2007. 7. A merican Academy of Pediatric Dentistry. Definition of dental neglect. Pediatr Dent 2007;29(suppl):11. 8. Acs G, Lodolini G, Kaminsky S, Cisneros GJ. Effect of nursing caries on body weight in a pediatric population. Pediatr Dent 1992;14(5):302-5. 9. American Academy of Pediatric Dentistry. Policy on early childhood caries (ECC): Classifications, consequences, and preventive strategies. Pediatr Dent 2007;29(suppl):39-41. 10. American Academy of Periodontology. Periodontal Diseases of Children and Adolescents. J Periodontol 2003; 74(11):1696-704. 11. Geismar K, Stoltze K, Sigurd B, Gyntelberg F, Holmstrup P. Periodontal disease and coronary heart disease. J Periodontol 2006;77(9):1547-54. 12. Demmer RT, Desvarieux M. Periodontal infections and cardiovascular disease: The heart of the matter. J Am Dent Assoc 2006;137(suppl):14-20. 13. Bobetsis YA, Barros SP, Offenbacher S. Exploring the relationship between periodontal disease and pregnancy complications. J Am Dent Assoc 2006;137(suppl):7-13. 14. Muerman JH, Furuholm J, Kaaja R, Rintamaki H, Tikkanen U. Oral health in women with pregnancy and delivery complications. Clin Oral Investig 2006;10(2):96-101. 15. Azarpazhooh A, Leake JL. Systematic review of the association between respiratory diseases and oral health. J Periodontol 2006;77(9):1465-82. 16. Scannapieco FA. Pneumonia in nonambulatory patients: The role of oral bacteria and oral hygiene. J Am Dent Assoc 2006;137(suppl):21-5. 17. Shaw WC. The influence of children’s dentofacial appearance on their social attractiveness as judged by peers and lay adults. Am J Orthod 1981;79(4):399-415. 18. Shaw WC, Rees G, Dawe M, Charles CR. The influence of dentofacial appearance on the social attractiveness of young adults. Am J Orthod 1985;87(1):21-6.
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19. American Cleft Palate-Craniofacial Association. Parameters for evaluation and treatment of patients with cleft lip/ palate or other craniofacial anomalies. Revised ed. Chapel Hill, NC: American Cleft Palate-Craniofacial Association; April 2000. 20. National Foundation for Ectodermal Dysplasias. Parameters of oral health care for individuals affected by ectodermal dysplasias. National Foundation for Ectodermal Dysplasias. Mascoutah, Ill; 2003:9. 21. American Academy of Pediatric Dentistry. Policy on use of a caries-risk assessment tool (CAT) for infants, children, and adolescents. Pediatr Dent 2007;29(suppl):29-33. 22. Fontana M, Zero DT. Assessing patients’ caries risk. J Am Dent Assoc 2006;37(9):1231-9. 23. Harris R, Nicoll AD, Adair PM, Pine CM. Risk factors for dental caries in young children: A systematic review of the literature. Community Dent Health 2004;21(suppl 1): 71-85. 24. Douglass JM. Response to Tinanoff and Palmer: Dietary determinants of dental caries and dietary recommendations for preschool children. J Public Health Dent 2000; 60(3):207-9. 25. American Psychological Association. Developing adolescents: A reference for professionals. Washington DC: American Psychological Association; 2002. 26. Macgregor ID, Regis D, Balding J. Self-concept and dental health behaviors in adolescents. J Clin Periodontol 1997; 24(5):335-9. 27. CDC. Recommendations for using fluoride to prevent and control dental caries in the United States. MMWR Recomm Rep 2001;50(RR14):1-42. 28. American Academy of Pediatric Dentistry. Guideline on infant oral health care. Pediatr Dent 2007;29(suppl):81-4. 29. Lee LJ, Bouwens TJ, Savage MF, Vann WF Jr. Examining the cost-effectiveness of early dental visits. Pediatr Dent 2006;28(2):102-5, discussion 192-8. 30. Randall RC, Vrijhoef MMA, Wilson NHF. Efficacy of preformed metal crowns vs amalgam restorations in primary molars: A systematic review. J Am Dent Assoc 2000; 131(3):337-43. 31. Foster T, Perinpanayagam H, Pfaffenbach A, Certo M. Recurrence of early childhood caries after comprehensive treatment with general anesthesia and follow-up. J Dent Child 2006;73(1):25-30. 32. Eidelman E, Faibis S, Peretz B. A comparison of restorations for children with early childhood caries treated under general anesthesia or conscious sedation. Pediatr Dent 2000;22(1):33-7. 33. Almeida AG, Roseman MM, Sheff M, Huntington N, Hughes CV. Future caries susceptibility in children with early childhood caries following treatment under general anesthesia. Pediatr Dent 2000;22(4):302-6.
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34. Weintraub JA. Pit and fissure sealants in high-caries risk individuals. J Dent Educ 2001;65(10):1084-90. 35. A nderson M. Risk assessment and epidemiology of dental caries: Review of the literature. Pediatr Dent 2002; 24(5):377-85. 36. Feigal RJ. The use of pit and fissure sealants. Pediatr Dent 2002;24(5):415-22. 37. American Academy of Pediatric Dentistry. Guideline on behavior guidance for the pediatric dental patient. Pediatr Dent 2007;29(suppl):115-24. 38. Lee JY, Vann WF, Roberts MW. A cost analysis of treating pediatric dental patients using general anesthesia vs conscious sedation. Pediatr Dent 2000;22(1):27-32. 39. Patton LL, White BA, Field MJ. State of the evidence base for medically necessary oral health care. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2001;92(3):272-5. 40. Flick WG, Claybold S. Who should determine the medical necessity of dental sedation and general anesthesia? A clinical commentary supported by Illinois patient and practitioner surveys. Anesth Prog 1998;45(2):57-61. 41. Conway TE. What is currently available in terms of medically necessary oral care? Spec Care Dentist 1995;15(5); 187-91.
42. White BA. The costs and consequences of neglected medically necessary oral care [Review]. Spec Care Dentist 1995;15(5):180-6. 43. Cameron CA, Litch CS, Liggert M, Heimburg S. National alliance for oral health consensus conference on medically necessary oral health care: Legal issues. Spec Care Dentist 1995;15(5):192-200. 44. American Dental Association. Transactions of the ADA: Benefits for services by qualified practitioners. Chicago, Ill; 1989:546. 45. Strauss RP. The organization and delivery of craniofacial services: The state of the art. Cleft Palate Craniofac J 1999; 36(3):189-95. 46. US Dept of Health and Human Services. Healthy people 2010. Rockville, Md: US Dept of Health and Human Services, National Institutes of Health; 2000. 47. American Dental Association. Statement on preventive coverage in dental benefits plans. Chicago, Ill; 1992:602; 1994:656. 48. American Dental Association Council on Access, Prevention, and Interprofessional Relations, American Dental Association Council on Scientific Affairs. Dental sealants. J Am Dent Assoc 1997;128(4):485-8.
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Policy on Oral Health Care Programs for Infants, Children, and Adolescents Originating Committee Dental Care Programs Committee
Review Council Council on Clinical Affairs
Adopted 1972
Revised 1976, 1992, 1995, 2002, 2006
Reaffirmed 1999
Purpose The American Academy of Pediatric Dentistry (AAPD) recognizes the importance of prevention, diagnosis, and treatment necessary to restore and maintain the oral health of infants, children, and adolescents. Comprehensive health care cannot be achieved unless oral care is included in all health service programs.
Methods This policy revision is based upon a review of current publications and Web sites of health care organizations. A MEDLINE search was performed using the terms “oral health policy”, “infant oral health policy”, “child oral health policy”, and “adolescent oral health policy”.
Background The US Department of Health and Human Services (DHHS) documents there exists a perception that oral health is separate from general health and, therefore, less important. By raising oral health awareness, the prevention, early detection, and management of dental, oral, and craniofacial tissues can become integrated into health care, community-based programs, and social services.1 DHHS recognizes that oral health can have a significant impact on overall health and well-being. Major themes of the US Surgeon General’s report on “Oral Health in America”1 include: 1. “Oral health means much more than healthy teeth.” 2. “Oral health is integral to general health.” Accordingly, the DHHS report “National Call to Action to Promote Oral Health”2 recommends: 1. Changing perceptions of the public, policymakers, and health providers regarding oral health and disease so that oral health becomes an accepted component of general health.
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2. Removing known barriers between people and oral health services. 3. Accelerating the building of the scientific and evidence base, as well as the application of research findings, to improve oral health. 4. Ensuring the adequacy of public and private health personnel and resources to meet the oral health needs of all Americans and enable the integration of oral health effectively with general health. The focus is on having a responsive, competent, diverse, and flexible workforce. 5. Expanding public-private partnerships and building upon common goals to improve the oral health of those who suffer disproportionately from oral diseases.
Policy statement The AAPD recommends oral health care be included in the design and provision of individual and community-based health care programs to achieve comprehensive health care. This can be achieved through the recommendations of the DHHS report “National Call to Action to Promote Oral Health.”2
References 1. US Dept of Health and Human Services. Oral Health in America: A Report of the Surgeon General. Rockville, Md: US Dept of Health and Human Services, National Institute of Dental and Craniofacial Research, National Institutes of Health; 2000. 2. US Dept of Health and Human Services. National Call to Action to Promote Oral Health. Rockville, Md: US Dept of Health and Human Services, Public Health Service, National Institute of Health, National Institute of Dental and Craniofacial Research; NIH Publication No. 035303, Spring 2003.
american academy of pediatric Dentistry
Policy on the Dental Home Originating Council Council on Clinical Affairs
Review Council Council on Clinical Affairs
Adopted 2001
Revised 2004
Reaffirmed 2010
Purpose The American Academy of Pediatric Dentistry (AAPD) supports the concept of a dental home for all infants, children, adolescents, and persons with special health care needs. The dental home is inclusive of all aspects of oral health that result from the interaction of the patient, parents, nondental professionals, and dental professionals. Establishment of the dental home is initiated by the identification and interaction of these individuals, resulting in a heightened awareness of all issues impacting the patient’s oral health. This concept is derived from the American Academy of Pediatrics’ (AAP) definition of a medical home which states pediatric primary health care is best delivered where comprehensive, continuously-accessible, family-centered, coordinated, compassionate, and culturallyeffective care is available and delivered or supervised by qualified child health specialists.1-4
Methods This policy is based on a review of the current dental and medical literature related to the establishment of a dental home. A MEDLINE search was conducted using the terms “dental home”, “medical home in pediatrics”, and “infant oral health care”. Expert opinions and best current practices were relied upon when clinical evidence was not available.
Background The AAP issued a policy statement defining the medical home in 1992.5 Since that time, it has been shown that health care provided to patients in a medical home environment is more effective and less costly in comparison to emergency care facilities or hospitals.4-6 Strong clinical evidence exists for the efficacy of early professional dental care complemented with caries-risk assessment, anticipatory guidance, and periodic supervision. The establishment of a dental home may follow the medical home model as a cost-effective and higher quality health care alternative to emergency care situations.
Children who have a dental home are more likely to receive appropriate preventive and routine oral health care. Referral by the primary care physician or health provider has been recommended, based on risk assessment, as early as 6 months of age, 6 months after the first tooth erupts, and no later than 12 months of age.7-9 Furthermore, subsequent periodicity of reappointment is based upon risk assessment. This provides time-critical opportunities to implement preventive health practices and reduce the child’s risk of preventable dental/oral disease.10
Policy statement 1. The AAPD encourages parents and other care provi 2.
ders to help every child establish a dental home by 12 months of age. The AAPD recognizes a dental home should provide:11 a. comprehensive oral health care including acute care and preventive services in accordance with AAPD periodicity schedules12; b. comprehensive assessment for oral diseases and conditions; c. individualized preventive dental health program based upon a caries-risk assessment 13 and a periodontal disease risk assessment14; d. anticipatory guidance about growth and development issues (ie, teething, digit or pacifier habits); e. plan for acute dental trauma; f. information about proper care of the child’s teeth and gingivae. This would include the prevention, diagnosis, and treatment of disease of the supporting and surrounding tissues and the maintenance of health, function, and esthetics of those structures and tissues; g. dietary counseling; h. referrals to dental specialists when care cannot di rectly be provided within the dental home;
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i. education regarding future referral to a dentist know ledgeable and comfortable with adult oral health issues for continuing oral health care; referral at an age determined by patient, parent, and pediatric dentist. 3. The AAPD advocates interaction with early intervention programs, schools, early childhood education and child care programs, members of the medical and dental communities, and other public and private community agencies to ensure awareness of age-specific oral health issues.15
References 1. American Academy of Pediatrics Committee on Children with Disabilities. Care coordination: Integrating health and related systems of care for children with special health care needs. Pediatrics 1999;104(4Pt1):978-81. 2. American Academy of Pediatrics. Committee on Pediatric Workforce. Culturally effective pediatric care: Education and training issues. Pediatrics 1999;103(1):167-70. 3. American Academy of Pediatrics Committee on Pediatric Workforce. Pediatric primary health care. AAP News November 1993;11:7. Reaffirmed June 2001. 4. American Academy of Pediatrics. The medical home. Pediatrics 2002;110(1Pt1):184-6. 5. American Academy of Pediatrics Ad Hoc Task Force on the Definition of the Medical Home. The medical home. Pediatrics 1992;90(5):774. 6. Kempe A, Beaty B, Englund BP, Roark RJ, Hester N, Steiner JF. Quality of care and use of the medical home in a state-funded capitated primary care plan for low-income children. Pediatrics 2000;105(5):1020-8. 7. Nowak AJ, Casamassimo PS. The dental home: A primary oral health concept. J Am Dent Assoc 2002;133 (1):93-8.
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8. Nowak AJ. Rationale for the timing of the first oral evaluation. Pediatr Dent 1997;19(1):8-11. 9. American Academy of Pediatrics Section on Pediatric Dentistry. Oral health risk assessment timing and establishment of the dental home. Pediatrics 2003;111(5): 1113-6. 10. US Dept of Health and Human Services. Healthy People 2010: Understanding and improving health. 2 nd ed. Washington, DC. US Government Printing Office; November 2000. 11. Poland C. Pediatric oral health. In: Burns CE, Brady MA, Dann AM, Starr N, eds. Pediatric Primary Care: A Handbook for Nurse Practitioners. 2nd ed. Philadelphia, Pa: WB Saunders Co; 2000. 12. American Academy of Pediatric Dentistry. Guideline on periodicity of examination, preventive dental services, anticipatory guidance, and oral treatment for children. Pediatr Dent 2009;31(special issue):118-25. 13. A merican Academy of Pediatric Dentistry. Guideline on caries-risk assessment and management for infants, children, and adolescents. Pediatr Dent 2010;32(special issue):101-8. 14. American Academy of Periodontology. Periodontal diseases of children and adolescents. J Periodontol 2003; 74(11):1696-704. 15. American Academy of Pediatric Dentistry. Dental home resource center. Available at: “http://www.aapd.org/ dentalhome/”. Accessed June 24, 2010.
AMERICAN ACADEMY OF PEDIATRIC DENTISTRY
Policy on Child Identification Programs Originating Council Council on Clinical Affairs
Review Council Council on Clinical Affairs
Adopted 2003
Revised 2008
Purpose The American Academy of Pediatric Dentistry (AAPD), recognizing the role that dental records play in forensic identification, encourages dental practitioners and administrators of child identification programs to implement simple practices that can aid in identification of unknown infants, children, and adolescents. The AAPD recommends that parents establish a dental home, where clinical data is gathered, stored, and updated routinely and can be made available to assist in identification of missing and/or abducted persons.
Methods This policy revision is based on a review of the current dental, medical, and public literature, and interviews with forensic odontologists, pathologists, and law enforcement agencies. A MEDLINE search was conducted using the terms “child”, “forensic”, “dental”, and “identification”. An electronic search using “child identification” also was conducted. Manuals on forensics1,2 utilized by the American Academy of Forensic Science and the American Society of Forensic Odontology demonstrate the vital role of dentistry in identification of missing and unknown persons.
Background More than 800,000 children in America are reported missing each year.3 Since the passage of the Missing Children Act in 1982 and the creation of the National Crime Information Center, the dental profession has provided much of the information used to compare missing persons with the unidentified living and dead.4 Numerous cases have been published in which law enforcement agencies called upon dentistry to provide information that proved vital to the identification process.5-7 Dental records used for identification purposes have included dental radiographs, facial photographs, study casts, dental histories documenting teeth present and distinguishing features of oral structures, restorative history documenting restored surfaces and materials used, and bite registrations.8 Nondental sources of distinguishing information currently include fingerprints, photographs, physical descriptions, and DNA from blood, saliva, and other tissue.9 Some of these
nondental sources have practical limitations. Few children have fingerprint records. DNA sampling, while being state of the art, can be protracted and costly. Dentistry can provide data without many of these limitations. Many programs have been developed and sponsored by community groups that use various child identification methods. Examples are: 1. Child Identification Program (CHIP), sponsored by the Masons. This program gathers saliva samples for DNA fingerprinting, videos, toothprints, and fingerprints.10 2. The National Child Identification Program, sponsored by the American Football Coaches Association with the Optimist International and Clear Channel Int. They use an identification card which includes fingerprints, a physical description, photographs, and the physician’s office address/telephone number.3 3. New England Kids Identification System (KIDS) sponsored by the Massachusetts Free Masons and the Massachusetts Dental Society, which incorporated dental bite impression and cheek swabs to gather DNA material into the CHIP events.10,11
Policy statement The AAPD recognizes the importance of dentistry’s role in the provision of data for identification of missing and/or deceased children and encourages dental professionals to assist in identifying such individuals through dental records and other mechanisms. The AAPD also encourages community identification programs to include a dental component documenting the child’s dental home12 and encouraging consistent dental visits. A dental home should be established for every child by 12 months of age.13 A detailed dental record, updated at recall appointments, economically establishes an excellent database of confidential, state-of-the-art child identification information that can be retrieved easily, stored safely, and updated properly. The dental record may contain a thorough description of the oral cavity documenting all anomalies, a record of restorative care delivered including materials used, appropriate dental radiographs,14 photographs, study casts, and bite registration.
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References 1. Bowers CM, Bell GL, eds. Dental identification. Manual of Forensic Odontology. 3 rd ed. Saratoga Springs, NY: American Society of Forensic Odontology; 1997:9-73. 2. Stimson PG, Mertz CA, eds. Scientific methods of investigation. Forensic Dentistry. New York, NY: Robert Stern, CRC Press; 1997:1-29. 3. National Child Identification Program Web site. Available at: “http://www.childidprogram.com”. Accessed March 21, 2008. 4. Sperber N. Identification of children and adults through federal and state identification systems: Recognition of human bite marks. Forensic Sci Int 1986;3(2-3):87-93. 5. Berthold M. Police seek ID in Illinois. ADA News 2002: 33:27. 6. Goodman NR, Himmerberger LK. Identifying skeletal remains found in a sewer. J Am Dent Assoc 2002;133 (11):1508-13. 7. Dental ID beats DNA. Available at: “http://www.newscientist.com/article.ns?Id+mg18725163.900”. Accessed July 30, 2007. 8. Adams BJ. Establishing personal identification based on specific patterns of missing, filled and unrestored teeth. J Forensic Sci 2003;48(3):487-96.
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9. Bowers CM, Johansen RJ. Digital analysis of bite marks and human identification. ASFO News 2001; Spring:1: 15-9. 10. Massachusetts Free Masons Child Identification Program Web site. Available at: “http://www.mychip.org”. Accessed July 31, 2007. 11. Tesini DA, Harte DB, Crowley K. Dentistry’s role in identification of missing and unknown children: Update on the dental bite impression technique. J Mass Dent Soc 1999;48(2):29-34, 50. 12. American Academy of Pediatric Dentistry. Policy on the dental home. Pediatr Dent 2007;29(suppl):22-3. 13. American Academy of Pediatric Dentistry. Guideline on infant oral health. Pediatr Dent 2007:29(suppl):81-4. 14. American Dental Association, US Dept of Health and Human Services. The Selection of Patients for X-Ray Examination: Dental Radiographic Examinations. Rockville, Md: Food and Drug Administration, 2004; HHS Publication Number 88-8273. Available at: “http:// www.ada.org/prof/resources/topics/radiography.asp”. Accessed August 8, 2008.
AMERICAN ACADEMY OF PEDIATRIC DENTISTRY
Policy on Mandatory School-entrance Oral Health Examinations Originating Council Council on Clinical Affairs
Review Council Council on Clinical Affairs
Adopted 2003
Revised 2008
Purpose The American Academy of Pediatric Dentistry (AAPD) encourages policy makers, public health and education officials, and the dental community to recognize that poor oral health can affect a child’s ability to learn. An oral examination prior to matriculation into school could improve school readiness by providing a timely opportunity for diagnosis and treatment of oral conditions.
Methods This policy is based on a review of current dental and medical literature, including the US Surgeon General’s report “Oral Health in America”,1 as well as policies and guidelines established by stakeholders in the health and education of our nation’s children. Data is not available to determine the effectiveness of various approaches by states that currently encourage schoolentry dental examinations.
Background Professional care is necessary to maintain oral health.1 The AAPD “emphasizes the importance of initiating professional oral health intervention in infancy and continuing through adolescence and beyond. The periodicity of professional oral health intervention and services is based on a patient’s individual needs and risk indicators.”2 The American Academy of Pediatrics recommends that, beginning at age 3, a child’s comprehensive health assessment should include attention to problems that might influence school achievement.3 General health examinations prior to school entrance are mandated by many states. Integration of general health and oral health care programs is lacking.1 Only 6 states and Washington, DC require a dental examination prior to school matriculation. In the United States, many children have not received a professional oral health assessment prior to entering kindergarten.1 While laws may not guarantee that every child will be examined by a dentist, they do increase the likelihood of this happening. Caries is the most common chronic disease of childhood.1 Caries and gingivitis can be prevented and eradicated, but not
everyone is aware of the measures necessary to do so. More than one third of the population of the United States does not benefit from community water fluoridation.1,4 Because the use of fluoride contributes to the prevention, inhibition, and reversal of caries,5,6 early determination of a child’s systemic and topical fluoride exposure is important. A dental home provides the necessary diagnostic, preventive, and therapeutic practices, as well as ongoing risk assessment and education, to improve and maintain the oral health of infants, children, and adolescents.7,8 To maximize effectiveness, the dental home should be established within 6 months of eruption of a child’s first tooth and no later than his/her first birthday.9 The public’s lack of awareness of the importance of oral health is a major barrier to dental care.1 Oral health is integral to general health. Oral conditions can interfere with eating and adequate nutritional intake, speaking, self-esteem, and daily activities.10 Children with early childhood caries may be severely underweight because of associated pain and the disinclination to eat. Nutritional deficiencies during childhood can impact cognitive development.10,11 Rampant caries is one of the factors causing insufficient development in children who have no other medical problems.12 Unrecognized disease and postponed care result in exacerbated problems, which lead to more extensive and costly treatment needs. Early recognition and intervention could result in savings of health care dollars for individuals, community health care programs, and third-party payors. The National Association of State Boards of Education recognizes “health and success in school are interrelated. Schools cannot achieve their primary mission of education if students and staff are not healthy and fit physically, mentally, and socially.”13 Children with dental pain may be irritable, withdrawn, or unable to concentrate. Pain can affect test performance as well as school attendance.10 In 1996, students aged 5 to 17 missed an average of 3.1 days/100 students due to acute dental problems.10 When these problems are treated and children no longer are experiencing pain, their learning and school attendance improve.10
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According to the US Surgeon General, “a national public health plan for oral health does not exist.”14 Profiles on state and local populations, although rarely available, are necessary for planning oral health care programs. Descriptions of requirements for oral health examinations (oral health indicators), implementation/enforcement of regulations, and administrative disposition of collected data vary both among and within states that encourage dental examinations prior to school matriculation.
Policy statement Early detection and management of oral conditions can improve a child’s oral health, general health and well-being, and school readiness. Recognizing the relationship between oral health and education, the AAPD supports legislation mandating a comprehensive oral health examination by a qualified dentist for every student prior to matriculation into school. The examination should be performed in sufficient detail to provide meaningful information to a consulting dentist and/or public health officials. This would include documentation of oral health history, soft tissue health/pathologic conditions, oral hygiene level, variations from a normal eruption/exfoliation pattern, dental dysmorphology or discoloration, caries (including white-spot lesions), and existing restorations. The examination also should provide an educational experience for both the child and the parent. The child/parent should be made aware of age-related caries-risk and caries-protective factors, as well as the benefits of a dental home. Because a child’s risk for developing dental disease changes and oral diseases are cumulative and progressive, the AAPD also supports such legislation to include subsequent comprehensive oral examinations at periodic intervals throughout the educational process. In addition, the AAPD encourages state and local public health and education officials, along with other stakeholders, such as health care providers and dental/medical organizations, to document oral health needs, work toward improved oral health and school readiness for all children, and address related issues such as barriers to oral health care. The AAPD recognizes that, without appropriate follow-up care, requiring oral health examinations is insufficient to ensure school readiness. Thus, the AAPD encourages local leaders to establish a referral system to help parents obtain needed oral health care for their children. The AAPD opposes regulations that would prevent a child from attending school due to noncompliance with mandated examinations.
References 1. US Dept of Health and Human Services. Oral health in America: A report of the Surgeon General. Rockville, Md: US Dept of Health and Human Services, National Institute of Dental and Craniofacial Research, National Institutes of Health; 2000.
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2. American Academy of Pediatric Dentistry. Guideline on periodicity of examination, preventive dental services, anticipatory guidance, and oral treatment for children. Pediatr Dent 2007;29(suppl):102-8. 3. American Academy of Pediatrics. School health assessment. Pediatrics 2000;105(4Pt1):875-7. 4. National Center for Fluoridation Policy and Research. University of Buffalo School of Dental Medicine. Available at: “http://www.fluoride.oralhealth.org”. Accessed December 23, 2007. 5. CDC. Recommendations for using fluoride to prevent and control dental caries in the United States. MMWR Recomm Rep 2001;50(RR14):1-42. 6. Burt B, Eklund S. Dentistry, Dental Practice, and the Community. Philadelphia, Pa: WB Saunders Company; 1999. 7. American Academy of Pediatric Dentistry. Policy on the dental home. Pediatr Dent 2007;29(suppl):22-3. 8. Poland C. Pediatric oral health. In: Burns CE, Brady MA, Dann AM, Starr N, eds. Pediatric Primary Care: A Handbook for Nurse Practitioners. 2nd ed. Philadelphia, Pa: WB Saunders Co; 2000. 9. American Academy of Pediatric Dentistry. Guideline on infant oral health care. Pediatr Dent 2007;29(suppl):81-4. 10. National Center for Education in Maternal and Child Health and Georgetown University. Fact sheet: Oral health and learning. Arlington, Va: NCEMCH; 2001. 11. Center on Hunger, Poverty, and Nutrition Policy. Statement on the link between nutrition and cognitive development in children. Medford, Ma: Tufts University, Center on Hunger, Poverty, and Nutrition Policy; 1998, 4th ed. 12. Acs G, Lodolini G, Kaminsky S, Cisneros GJ. Effect of nursing caries on body weight in a pediatric population. Pediatr Dent 1992;14(5):302-5. 13. Bogden JF, Vega-Matos CA. Fit, healthy, and ready to learn: A school health policy guide, part 1: Physical activity, healthy eating, and tobacco-use prevention. Alexandria, Va: National Association of State Boards of Education; 2000. 14. US Dept of Health and Human Services. Oral health in America: A report of the Surgeon General–Executive summary. Rockville, Md: US Dept of Health and Human Services, National Institute of Dental and Craniofacial Research, National Institutes of Health; 2000:12.
AMERICAN ACADEMY OF PEDIATRIC DENTISTRY
Policy on School Absences for Dental Appointments Originating Council Council on Clinical Affairs
Adopted 2010
Purpose The American Academy of Pediatric Dentistry (AAPD) recognizes dental care as medically necessary and that poor oral health can negatively affect a child’s ability to learn. This policy is intended to assist public health and school education administrators in developing enlightened policies on school absence for dental appointments. It also is intended to assist parents in making informed decisions.
Methods This policy is based on a review of current dental, medical, educational, and public health literature and state statutes and regulations related to student absence for dental appointments. An electronic search was conducted using the search parameters: Terms: “school absences for dental appointments”, “excused school absences”, and “department of education”; Fields: all fields; Limits: within the last 10 years; humans; English. 841 articles matched these criteria. Papers for review were chosen from this list and from references within selected articles. When data did not appear sufficient or were inconclusive, recommendations were based on expert and/or consensus opinion by experienced researchers and clinicians. It is beyond the scope of this document to review every state statute and regulation on absences from school for dental appointments.
Background Oral health is integral to general health. Oral conditions can interfere with eating and adequate nutritional intake, speaking, self-esteem, and daily activities.1 Dental care is medically necessary to prevent and eliminate orofacial disease, infection, and pain. It is also important to restore the form and function of the dentition and correct facial disfiguration or dysfunction.2 The public’s lack of awareness of the importance of oral health is a major barrier to dental care.3 Unrecognized disease and postponed care result in exacerbated problems, which lead to more extensive and costly treatment needs.2 The National Association of State Boards of Education recognizes “health and success in schools are interrelated. Schools cannot achieve their primary mission of education if students and staff are not healthy and fit physically, mentally, and socially”.4 Children with dental pain may be irritable, withdrawn, or unable to concentrate. Pain can affect
test performance as well as school attendance.3 Left untreated, the pain and infection caused by tooth decay can lead to problems in eating, speaking, and learning.5 In 1996, students aged 5 to 17 years missed an average of 3.1 days/100 students due to acute dental problems.1 When these problems are treated and children no longer are experiencing pain, their learning and school attendance improve.1 According to the US Surgeon General, “a national public health plan for oral health does not exist”.3 This corresponds with the fact that there is no national policy on excused absences from school for dental appointments. Some states (eg, California, Texas) have very specific laws excusing students for dental appointments.6,7 Other state laws are more general and recognize absences due to doctor’s appointments or illness.8,9
Policy statement Dental care is medically necessary and oral health is integral to general health. Undiagnosed and untreated oral conditions may interfere with a child’s ability to eat, sleep, or function well at home or at school due to discomfort or pain. The unesthetic nature of caries and dental malocclusion may compromise a child’s self-esteem and social development. Schools’ policies that prevent or discourage legitimate school absence for the purpose of delivery of vital health care services may cause harm to their students. Children who have dental conditions corrected improve their learning and attendance in school. State laws and local school district policies are not uniform on absences from school for dental appointments. A uniform policy that recognizes the negative effect of chronic truancy on academic performance would be useful. Such policies should not restrict necessary health care delivery. The AAPD: 1. Supports state law or school policy that allows the absence for legitimate healthcare delivery, including that of oral health services. 2. Encourages parents, school administrators, and dentists to work together to ensure that children receive dental care while minimizing school absences.
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References 1. National Center for Education in Maternal and Child Health and Georgetown University. Fact sheet: Oral health and learning. Arlington, Va: NCEMCH; 2001. Available at: “http://www.collierhealthdept.org/pdf/dental/oral healthlearning.pdf\”. Accessed October 21, 2009. 2. American Academy of Pediatric Dentistry. Policy on medically necessary care. Pediatr Dent 2009;31(special issue):16-20. 3. US Dept of Health and Human Services. Oral Health in America: A Report of the Surgeon General. Rockville, Md: US Dept of Health and Human Services, National Institute of Dental and Craniofacial Research, National Institutes of Health; 2000:12. 4. Bogden JF, Vega-Matos CA. Fit, healthy, and ready to learn: A school health policy guide, part 1: Physical activity, healthy eating, and tobacco-use prevention. Alexandria, Va: National Association of State Boards of Education; 2000.
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5. US General Accounting Office. Oral Health; Dental Disease is a Chronic Problem Among Low-income and Vulnerable Populations. Washington, DC; US General Accounting Office. 2000. 6. California Education Code. Available at: “http://Law. Onecle.com/california/education/48205.html”. Accessed March 8, 2010. 7. Texas Education Code. Available at: “http://law.onecle. com/Texas/education/25.087.00.html”. Accessed March 8, 2010. 8. Georgia Department of Education. Available at: “http:// www.doeK12.ga.us/_documents/doe/legalservices/1605-1-.10pdf ”. Accessed March 8, 2010. 9. Michigan Department of Education. Available at: “http: //www.Michigan.gov/documents/mde/compulsory_ attendance_257944_7.pdf ”. Accessed March 8, 2010.
AMERICAN ACADEMY OF PEDIATRIC DENTISTRY
Policy on Emergency Oral Care for Infants, Children, and Adolescents Originating Committee
Policy and Review Committee Review Council Council on Clinical Affairs
Adopted 1976
Revised 1993, 2000, 2003
Reaffirmed 1996, 2007
The American Dental Association’s Principles of Ethics and Code of Professional Conduct states that emergency care is an essential duty of every dentist.1 A dentist who accepts an infant, child, or adolescent as a patient of record shall make reasonable arrangements for emergency oral/dental care, along with providing instructions to the parent for accessing emergency care. When consulted in an emergency by patients not of record, the dentist should make reasonable arrangements for emergency care.
Reference 1. American Dental Association. Principles of Ethics and Code of Professional Conduct. Available at: “http://www. ada.org/prof/prac/law/code/index.asp”. Accessed February 28, 2007.
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Policy on Use of Fluoride Originating Committee
Liaison with Other Groups Committee Review Council Council on Clinical Affairs
Adopted 1967
Revised 1978, 1995, 2000, 2001, 2003, 2007, 2008
Reaffirmed 1977
Purpose The American Academy of Pediatric Dentistry (AAPD), affirming that fluoride is a safe and effective adjunct in reducing the risk of caries and reversing enamel demineralization, encourages public health officials, health care providers, and parents/ caregivers to optimize fluoride exposure.
Methods A MEDLINE search was conducted using the terms “fluoride”, “fluoridation”, “acidulated phosphate fluoride”, “fluoride varnish”, “fluoride therapy”, and “topical fluoride”. Expert opinions and best current practices also were relied upon for this guideline.
Background The adjustment of the fluoride level in community water supplies to optimal concentration is the most beneficial and inexpensive method of reducing the occurrence of caries.1 Epidemiologic data within the last half-century indicate reductions in caries of 55 to 60% and recent data still shows caries reduction of approximately 25%, without significant enamel fluorosis, when domestic water supplies are fluoridated at an optimal level.2 Evidence accumulated from long-term use of fluorides has demonstrated that the cost of oral health care for children can be reduced by as much as 50%.3 These savings in health dollars accrue to private individuals, group purchasers, and government care programs. An even higher caries reduction can be obtained if the proper use of fluorides is combined with other dietary, oral hygiene, and preventive measures4,5 as prescribed by a dentist familiar with the child’s oral health and family history. A large body of literature supports the incorporation of optimal fluoride levels in drinking water supplies. When fluoridation of drinking water is impossible, effective systemic fluoridation can be achieved through the intake of daily fluoride supplements. Before supplements are prescribed, it is essential to review dietary sources of fluoride (eg, all drinking water sources, consumed beverages, prepared food, toothpaste) to determine
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the patient’s true exposure to fluoride.1,6-9 Fluoride content of ready to use infant formulas in the US and Canada ranges from 0.1 to 0.3 mg/L10, which provides only a modest source of fluoride. Non-milk based formulas have higher fluoride content because the calcium that is added to formula contains fluoride. The more important issue, however, is the fluoride content of concentrated or powdered formula when reconstituted with fluoridated water. Considering the potential for mild fluorosis, caution is advised for infants consuming formula that is reconstituted with optimally-fluoridated water. Significant cariostatic benefits can be achieved by the use of fluoride-containing preparations such as toothpastes, gels, and rinses, especially in areas without water fluoridation.11 Monitoring children’s use of topical fluoride-containing products, including toothpaste, may prevent ingestion of excessive amounts of fluoride.12 A number of clinical trials have confirmed the anticaries effect of professional topical fluoride treatments, including 5% neutral sodium fluoride varnish.13,14 Fluoride varnishes can prevent or reverse enamel demineralization.15 In children with moderate to high caries risk, fluoride varnishes14,16 and fluoridereleasing restorative and bonding materials have been shown to be beneficial and are best utilized as part of a comprehensive preventive program in the dental home.17-19
Policy statement 1. The AAPD endorses and encourages the adjustment of fluoride content of domestic community water supplies to optimal levels where feasible. 2. When fluoride levels in community water supplies are suboptimal, and after consideration of sources of dietary fluoride, the AAPD endorses the supplementation of a child’s diet with fluoride according to the guidelines jointly recommended by the AAPD8, the American Academy of Pediatrics20, and the American Dental Association (ADA)21 and endorsed by the Centers for Disease Control and Prevention.1
american academy of pediatric dentistry
3. The AAPD encourages dental professionals to inform medical peers of the potential of enamel fluorosis when excess fluoride is ingested prior to enamel maturation. 4. The AAPD encourages continued research on the causes of enamel fluorosis. 5. The AAPD does not support the use of prenatal fluoride supplements.19 6. The AAPD recommends an individualized patient cariesrisk assessment before prescribing the use of supplemental fluoride-containing products.8,22 7. The AAPD encourages the continued research on safe and effective fluoride products, including fluoride-releasing restorative materials. 8. The AAPD supports the delegation of fluoride application to auxiliary dental personnel, or other trained allied health professionals, by prescription or order of a qualified dentist, after a comprehensive oral examination has been performed. 9. The AAPD endorses ADA 2002 House of Delegates Resolution 67H to encourage labeling of bottled water with the fluoride concentration and company contact information. 23 The resolution also supports including information with each home water treatment system on the system’s effects on fluoride levels. 10. The AAPD encourages all beverage and infant formula manufacturers to include fluoride concentration with the nutritional content on food labels. 11. The AAPD encourages dentists and other health care providers to educate parents that both infant formula and the water used to reconstitute the formula may contain fluoride. Dentists and other health care providers, therefore, should assist parents in determining the infant’s fluoride exposure.
References 1. CDC. Recommendations for using fluoride to prevent and control dental caries in the United States. MMWR Recomm Rep 2001;50(RR14):1-42. 2. CDC. Achievements in public health, 1900-1999: Fluoridation of drinking water to prevent dental caries. MMWR 1999;48(12):933-40. 3. Griffen SO, Jones K, Tomar, SL. An economic evaluation of community water fluoridation. J Pub Health Dent 2001;61(2):78-86. 4. Featherstone JD. The science and practice of caries prevention. J Am Dent Assoc 2000;131(7):887-99. 5. Burrell KH, Chan JT. Systemic and topical fluorides. In: Ciancio SG, ed. ADA Guide to Dental Therapeutics. 2nd ed. Chicago, Ill: ADA Publishing; 2000:230-41. 6. Levy SM, Kohout FJ, Kiritsy MC, Heillman JR, Wefel JS. Infants’ fluoride ingestion from water, supplements, and dentifrice. J Am Dent Assoc 1995;126(12):1625-32.
7. Bowen WH. Fluorosis, is it a problem? J Am Dent Assoc 2002;133(10):1405-7. 8. American Academy of Pediatric Dentistry. Guideline on fluoride therapy. Pediatr Dent 2008;30(suppl):121-4. 9. Adair SM. Evidence-based use of fluoride in contemporary pediatric dental practice. Pediatr Dent 2006:28(2): 133-42. 10. Foman SJ, Ekstrand J. Fluoride intake. In Fejerskov O, Ekstrand J, Burt BA eds. Fluoride in Dentistry, 2 nd ed. Copenhagen: Munksgaard; 1996:40-52. 11. Forsyth Dental Center – Report on the Remineralization Symposium 22-24, June 1999. Emerging issues and future directions in remineralization. J Clin Dent 1999;10 (special issue):55-93. 12. Warren JJ, Levy SM. A review of fluoride dentifrice related to dental fluorosis. Pediatr Dent 1999;21(4):265-71. 13. B eltran-Aguilar E, Goldstein J. Fluoride varnishes: A review of their clinical use, cariostatic mechanisms, efficacy, and safety. J Am Dent Assoc 2000;131:589-96. 14. Weintraub JA, Ramos-Gomez F, Jue B, et al. Fluoride varnish efficacy in preventing early childhood caries. J Dent Res 2006;85(2):172-6. 15. Castellano JB, Donly KJ. Potential remineralization of demineralized enamel after application of fluoride varnish. Am J Dent 2004;17(6):462-4. 16. Hicks J, García-Godoy F, Donly K, Flaitz C. Fluoridereleasing restorative materials and secondary caries. Dent Clin North Am 2002;46(2):247-76, vi. 17. Nowak AJ, Casamassimo PS. The dental home: A primary care oral health concept. J Am Dent Assoc 2002;133(1): 93-8. 18. American Academy of Pediatric Dentistry. Policy on the dental home. Pediatr Dent 2006;28(suppl):17-8. 19. L everett DH, Adair SM, Vaughan BM, Proskin HM, Moss ME. Randomized clinical trial of the effect of prenatal fluoride supplements in preventing dental caries. Caries Res 1997;31(3):174-9. 20. American Academy of Pediatrics Committee on Nutrition. Fluoride supplementation for children: Interim policy recommendations. Pediatrics 1995;95(5):777. 21. Meskin LH, ed. Caries diagnosis and risk assessment: A review of preventive strategies and management. J Am Dent Assoc 1995;126(suppl):1-24. 22. American Academy of Pediatric Dentistry. Policy on use of a caries-risk assessment tool (CAT) for infants, children, and adolescents. Pediatr Dent 2006;28(suppl):24-8. 23. A merican Dental Association. House of Delegates Resolution 67H: Chicago, Ill; 2002.
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Policy on the Use of Xylitol in Caries Prevention Originating Council
Council on Clinical Affairs Adopted 2006
Review Council Council on Clinical Affairs
Revised 2010
Purpose The American Academy of Pediatric Dentistry (AAPD) recognizes the benefits of caries preventive strategies involving sugar substitutes, particularly xylitol, on the oral health of infants, children, adolescents, and persons with special health care needs. This policy is intended to assist oral health care professionals make informed decisions about the use of xylitol-based products in caries prevention.
Methods This policy is an update of the previous policy, adopted in 2006. The update is based upon a review of current dental and medical literature related to the use of xylitol in caries prevention. A MEDLINE literature search was conducted using PubMed with the following parameters: Terms: “xylitol” AND “caries prevention”; Field: all fields; Limits: within the last 10 years; humans, English; birth through 18. Two hundred forty articles matched these criteria; 25 papers were reviewed at this revision. When data did not appear sufficient or were inconclusive, recommendations were based upon expert and/or consensus opinion by experienced researchers and clinicians.
Background Xylitol is a five-carbon sugar alcohol derived primarily from forest and agricultural materials. It has been used since the early 1960’s in infusion therapy for post-operative, burn, and shock patients; in the diet of diabetic patients; and, most recently, as a sweetener in products aimed at improved oral health.1 Dental benefits of xylitol first were recognized in Finland in 1970, using animal models.2 The first chewing gum developed with the aim of reducing caries and improving oral health was released in Finland in 1975 and in the United States shortly after. The first xylitol studies in humans, known as the Turku Sugar Studies,3,4 demonstrated the relationship between dental plaque and xylitol, as well as the safety of xylitol for human consumption. These early studies showed the decayed, missing, and filled (dmf) incidence in teeth in a sucrose chewing-gum group was 2.92 compared to 1.04 in the xylitol gum group. The most comprehensive study with xylitol gum,
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conducted in 1995, compared the effect on caries incidence for xylitol, sorbitol, and sucrose consumption.5 The group that received 100% xylitol gum 5 times/day had significantly lower levels of sucrose and free sialic acid in whole saliva than at baseline and significantly lower plaque index scores.5 The xylitol group also exhibited the lowest levels of salivary lactobacilli at endpoint, and this group did not experience the age-related increase in Mutans streptococci (MS) as did the other groups.5 Xylitol studies show varying results in the reduction of the incidence of caries or MS levels.5-13 Studies suggest xylitol intake that consistently produces positive results ranged from 4-10 grams per day divided into 3 to 7 consumption periods.5-12 Higher amounts did not result in greater reduction in incidence of caries and may lead to diminishing anticariogenic results.5-13 Similarly, consumption frequency of less than 3 times per day at optimal xylitol amount showed no effect.14-16 Abdominal distress and osmotic diarrhea have been reported following the ingestion of xylitol.17-18 Diarrhea has been reported in patients who have consumed 3-60 grams of xylitol per day.19-23 Xylitol reduces plaque formation and bacterial adherence (ie, is antimicrobial), inhibits enamel demineralization (ie, reduces acid production), and has a direct inhibitory effect on MS. Prolonged use of xylitol appears to select for a “xylitolresistant” mutant of the MS cells.24 These mutants appear to shed more easily into saliva than the parent strains,23 resulting in a reduction of MS in plaque26 and possibly hampering their transmission/colonization from mother to child. Long-lasting effects have been demonstrated up to 5 years after 2 years of using xylitol chewing gum.27-28 Use of xylitol gum by mothers (2-3 times per day starting 3 months after delivery and until the child was 2 years old) reduced the MS levels in children up to 6 years of age and was significantly better than applying fluoride varnish or chlorhexidine varnish at 6, 12, and 18 months after delivery. At 5 years of age, the xylitol group had 70% reduction in caries (dmf ) as compared with the varnish and chlorhexidine groups. Fluoride varnish alone had little effect on total salivary levels of MS.27 Some studies suggest the chewing process may enhance the caries inhibitory effect of xylitol chewing gum.28-31
american academy of pediatric dentistry
Xylitol currently is available in many forms (eg, gums, mints, chewable tablets, lozenges, toothpastes, mouthwashes, cough mixtures, nutraceutical products).32-33 Xylitol chewing gum has been shown to be effective as a preventive agent. The effectiveness of other xylitol products is being studied at this time.
Policy statement The AAPD: 1. supports the use of xylitol as part of a preventive strategy aimed specifically at long term caries pathogen suppression and caries (dmf ) reduction in higher risk populations. 2. recommends that, as further research and evidence-based knowledge is available, protocols be established to further clarify the impact of delivery vehicles, the frequency of exposure, and the optimal dosage to reduce caries and improve the oral health of children. 3. encourages xylitol-containing products be labeled clearly with regard to their xylitol content to enable dentists and consumers to ensure therapeutic levels of exposure.31
References 1. Mäkinen KK. Biochemical principles of the use of xylitol
in medicine and nutrition with special consideration of dental aspects. Experientia Suppl 1978;30:1-160. 2. Muhlemann HR, Regolati B, Marthaler TM. The effect on rat fissure caries of xylitol and sorbitol. Helv Odontol Acta 1970;14(1):48-50. 3. Scheinin A, Mäkinen KK, Tammisalo E, Rekola M. Turku sugar studies. XVIII. Incidence of dental caries in relation to 1-year consumption of xylitol chewing gum. Acta Odontol Scand 1975;33(5):269-78. 4. Scheinin A, Mäkinen KK, Ylitalo K. Turku sugar studies. V. Final report on the effect of sucrose, fructose and xylitol diets on caries incidence in man. Acta Odontol Scand 1976;34(4):179-216. 5. Mäkinen KK, Benett CA, Hujoel PP, et al. Xylitol chewing gums and caries rates: A 40-month cohort study. J Dent Res 1995;74(12):1904-13. 6. Mäkinen KK, Hujoel PP, Bennett CA, et al. A descriptive report of the effects of a 16-month xylitol chewing-gum programme subsequent to a 40-month sucrose gum programme. Caries Res 1998;32(2):107-12. 7. Milgrom P, Ly KA, Roberts M, Rothen M, Mueller G, Yamaguchi DK. Mutans Streptococci dose response to Xylitol chewing gum. J Dent Res 2006;85(2):177-81. 8. Hujoel PP, Mäkinen KK, Bennett CA, et al. The optimum time to initiate habitual xylitol gum-chewing for obtaining long-term caries prevention. J Dent Res 1999; 78(3):797-803. 9. Mäkinen KK. The rocky road of xylitol to its clinical application. J Dent Res 2000;79(6):1352-5.
10. Mäkinen KK, Chiego DJ Jr, Allen P, et al. Physical, chemical, and histologic changes in dentin caries lesions of primary teeth induced by regular use of polyol chewing gums. Acta Odontol Scand 1998;56(3):148-56. 11. Mäkinen KK, Mäkinen PL, Pape HR, et al. Conclusion and review of the Michigan Xylitol Programme (19861995) for the prevention of dental caries. Int Dent J 1996;46(1):22-34. 12. Deshpande A, Jadad AR. The impact of polyol-containing chewing gums on dental caries: A systematic review of original randomized controlled trials and observational studies. J Am Dent Assoc 2008;139(12):1602-14. 13. Stecksén-Blicks C, Holgerson PL, Twetman S. Effect of xylitol and xylitol-fluoride lozenges on approximal caries development in high caries-risk children. Int J Paediatr Dent 2008;18(3):170-7. 14. Isokangas P. Xylitol chewing gum in caries prevention. A longitudinal study on Finnish school children. Proc Finn Dent Soc 1987;83(suppl 1):1-117. 15. Rekola M. Correlation between caries incidence and frequency of chewing gum sweetened with sucrose or xylitol. Proc Finn Dent Soc 1989;85(1):21-4. 16. Thaweboon S, Thaweboon B, Soo-Ampon S. The effect of xylitol chewing gum on mutans streptococci in saliva and dental plaque. Southeast Asian J Trop Med Public Health 2004;35(4):1024-7. 17. Scheie AA, Fijerskov O. Xylitol in caries prevention: What is evidence for clinical efficacy? Oral Dis 1998;4(4): 268-78. 18. Mäkinen KK. Dietary prevention of dental caries by xylitol – Clinical effectiveness and safety. J Appl Nutr 1992;44:16-28. 19. Akerblom HK, Koivukangas T, Puuka R, Mononen M. The tolerance of increasing amounts of dietary xylitol in children. Int J Vitam Nutr Res Suppl 1982;22:53-66. 20. Giertsen E, Emberland H, Scheie AA. Effects of mouth rinses with xylitol and fluoride on dental plaque and saliva. Caries Res 1999;33(1):23-31. 21. Salminen EK, Salminen SJ, Porkka L, Kwasowski P, Marks V, Koivistoinen PE. Xylitol vs glucose: Effect on the rate of gastric emptying and motilin, insulin, and gastric inhibitory polypeptide release. Am J Clin Nutr 1989; 49(6):1228-32. 22. Uhari M, Kontiokari T, Koskela M, Niemela M. Xylitol chewing gum in prevention of acute otitis media: Double blind randomized trial. Brit Med J 1996;313(7066): 1180-4. 23. Waler SM, Rolla G. [Xylitol, mechanisms of action and uses]. Nor Tannelaegeforen Tid 1990;100(4):140-3. 24. Trahan L, Mouton C. Selection for Streptococcus mutans with an altered xylitol transport capacity in chronic xylitol consumers. J Dent Res 1987;66(5):982-8.
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25. Trahan L, Söderling E, Dréan MF, Chevrier MC, Isokangas P. Effect of xylitol consumption on the plaquesaliva distribution of mutans streptococci and the occurrence and long-term survival of xylitol-resistant strains. J Dent Res 1992;71(11):1785-91. Erratum in: J Dent Res 1993;72(1):87-8. 26. Söderling E, Trahan L, Tammiala-Salonen T, Hakkinen L. Effects of xylitol, xylitol-sorbitol, and placebo chewing gums on the plaque of habitual xylitol consumers. Eur J Oral Sci 1997;105(2):170-7. 27. Söderling E, Isokangas P, Pienihakkinen K, Tenovuo J, Alanen P. Influence of maternal xylitol consumption on mother-child transmission of mutans streptococci: 6 year follow-up. Caries Res 2001;35(3):173-7. 28. Mäkinen KK, Alanen P, Isokangas P, et al. Thirty-nine month xylitol chewing gum programme in initially 8year-old school children: A feasibility study focusing on mutans streptococci and lactobacilli. Int Dent J 2008; 58(1):41-50.
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29. Machiulskiene V, Nyvad B, Baelum V. Caries preventive effect of sugar-substituted chewing gum. Community Dent Oral Epidemiol 2001;29(4):278-88. 30. Scheie AA, Fejerskov O, Danielsen B. The effects of xylitol-containing chewing gums on dental plaque and acidogenic potential. J Dent Res 1998;77(7):1547-52. 31. Van Loveren C. Sugar alcohols: What is the evidence for caries-preventive and caries-therapeutic effects? Caries Res 2004;38(3):286-93. 32. Ly KA, Milgrom P, Rothen M. Xylitol, sweeteners, and dental caries. Pediatr Dent 2006;28(2):154-63. Discussion 92-8. 33. Lynch H, Milgrom P. Xylitol and dental caries: An overview for clinicians. J Calif Dent Assoc 2003;31:205-9.
american academy of pediatric dentistry
Policy on Interim Therapeutic Restorations (ITR) Originating Council
Council on Clinical Affairs Review Council
Council on Clinical Affairs Adopted 2001
Revised 2004, 2008
Purpose The American Academy of Pediatric Dentistry (AAPD) recognizes that unique clinical circumstances can result in challenges in restorative care for infants, children, adolescents, and persons with special health care needs. When circumstances do not permit traditional cavity preparation and/or placement of traditional dental restorations or when caries control is necessary prior to placement of definitive restorations, interim therapeutic restorations (ITR)1 may be beneficial and are best utilized as part of comprehensive care in the dental home.2,3 This policy will differentiate ITR from atraumatic/alternative techniques (ART)4 and describe the circumstances for its use.
Methods This policy is based upon a review of current dental literature. A MEDLINE search was performed using key words “dental caries”, “atraumatic restorative treatment”, and “glass ionomer cement”.
Background Atraumatic/alternative restorative technique (ART) has been endorsed by the World Health Organization as a means of restoring and preventing caries in populations with little access to traditional dental care.4 In many countries, practitioners provide treatment in non-traditional settings that restrict restorative care to placement of provisional restorations. Because circumstances do not allow for follow-up care, ART mistakenly has been interpreted as a definitive restoration. ITR utilizes similar techniques but has different therapeutic goals. Interim therapeutic restoration more accurately describes the procedure used in contemporary dental practice in the US. ITR may be used to restore and prevent further decalcification and caries in young patients, uncooperative patients, or patients with special health care needs or when traditional cavity preparation and/or placement of traditional dental restorations are not feasible and need to be postponed.5,6 Additionally, ITR may be used for step-wise excavation in children with multiple open carious lesions prior to definitive restoration of the teeth.7
The use of ITR has been shown to reduce the levels of cariogenic oral bacteria (eg, mutans streptococci, lactobacilli) in the oral cavity.8-10 The ITR procedure involves removal of caries using hand or slow speed rotary instruments with caution not to expose the pulp. Leakage of the restoration can be minimized with maximum caries removal from the periphery of the lesion. Following preparation, the tooth is restored with an adhesive restorative material such as self-setting or resin-modified glass ionomer cement.11 ITR has the greatest success when applied to single surface or small 2 surface restorations.12,13 Inadequate cavity preparation with subsequent lack of retention and insufficient bulk can lead to failure.12 Follow-up care with topical fluorides and oral hygiene instruction may improve the treatment outcome in high caries-risk dental populations.
Policy statement The AAPD recognizes ITR as a beneficial provisional technique in contemporary pediatric restorative dentistry. ITR may be used to restore and prevent dental caries in young patients, uncooperative patients, patients with special health care needs, and situations in which traditional cavity preparation and/or placement of traditional dental restorations are not feasible. ITR may be used for caries control in children with multiple carious lesions prior to definitive restoration of the teeth.
References 1. American Academy of Pediatric Dentistry. Guideline on pediatric restorative dentistry. Pediatr Dent 2008:30 (suppl):163-9. 2. Nowak AJ, Casamassimo PS. The dental home. J Am Dent Assoc 2002;133(1):93-8 3. American Academy of Pediatric Dentistry. Policy on the dental home. Pediatr Dent 2007;29(suppl):22-3. 4. Yip HK, Smales RJ, Ngo HC, Tay FR, Chu F. Selection of restorative materials for the atraumatic restorative treatment (ART) approach: A review. Spec Care Dent 2001;21 (6):216-21.
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5. Louw AJ, Sarvan I, Chikte UME, Honkala E. One-year evaluation of atraumatic restorative treatment and minimum intervention techniques on primary teeth. South African Dent J 2002;57(9):366-71. 6. Lo ECM, Holmgren CJ. Provision of atraumatic restorative treatment (ART) restorations to Chinese preschool children: A 30-month evaluation. International J Paediatr Dent 2001;11(1):3-10. 7. Mandari GJ, Frencken JE, van’t Hof MA. Six-year success rates of occlusal amalgam and glass-ionomer restorations placed using three minimal intervention approaches. Caries Res 2003;37(4):246-53. 8. Castro A, Feigal RF. Microleakage of a new improved glass ionomer restorative material in primary and permanent teeth. Pediatr Dent 2002;24(1):23-8.
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9. Grossman ES, Mickenautsch S. Microscope observations of ART excavated cavities and restorations. South African Dent J 2002;57(9):359-63. 10. Croll TP, Nicholson JW. Glass ionomer cements in pediatric dentistry: Review of the literature. Pediatr Dent 2002;24(5):423-9. 11. Berg JH. Glass ionomer cements. Pediatr Dent 2002;24 (5):430-7. 12. Castro A, Feigal RF. Microleakage of a new improved glass ionomer material in primary and permanent teeth. Pediatr Dent 2002;24(1):23-7.
american academy of pediatric dentistry
Policy on Early Childhood Caries (ECC): Classifications, Consequences, and Preventive Strategies Originating Group A collaborative effort of the American Academy of Pediatric Dentistry and the American Academy of Pediatrics
Review Council Council on Clinical Affairs
Adopted 1978
Revised 1993, 1996, 2001, 2003, 2007, 2008
Purpose The American Academy of Pediatric Dentistry (AAPD) recognizes early childhood caries (ECC; formerly termed “nursing bottle caries”, “baby bottle tooth decay”) as a significant public health problem.1 The AAPD encourages oral health care providers and caregivers to implement preventive practices that can decrease a child’s risks of developing this devastating disease.
Methods This policy revision is based on a review of the current pediatric dental, medical, and public health literature related to ECC, including proceedings of the 2005 Symposium on the Prevention of Oral Diseases in Children and Adolescents, Chicago, Ill.1 A MEDLINE search was conducted using the terms “early childhood caries”, “nursing caries”, and “baby bottle caries”. Preventive recommendations were based primarily upon review of published studies and proceedings. In cases where the data did not appear sufficient or were inconclusive, recommendations were based upon expert and consensus opinion.
Background In 1978, the AAPD released “Nursing Bottle Caries”, a joint statement with the American Academy of Pediatrics, to address a severe form of caries associated with bottle usage.2 Initial policy recommendations were limited to feeding habits, concluding that nursing bottle caries could be avoided if bottle feedings were discontinued soon after the first birthday. An early policy revision added ad libitum breastfeeding as a causative factor. Over the next 2 decades, however, recognizing that this distinctive clinical presentation was not consistently associated with poor feeding practices and that caries was an infectious disease, AAPD adopted the term “early childhood caries” to reflect better its multifactoral etiology. Caries is a common, complex, chronic disease resulting from an imbalance of multiple risk factors and protective factors over time.3 Fundamentally, caries is biofilm (plaque)-induced acid demineralization of enamel or dentin, mediated by saliva.
Given time, the interaction of cariogenic microorganisms and fermentable carbohydrates (sucrose) may induce demineralization, which can progress to loss of tooth structure/cavitation.4 The disease of ECC has been defined as “the presence of 1 or more decayed (noncavitated or cavitated lesions), missing (due to caries), or filled tooth surfaces” in any primary tooth in a child 71 months of age or younger.5,6 In children younger than 3 years of age, any sign of smooth-surface caries is indicative of severe early childhood caries (S-ECC). From ages 3 through 5, 1 or more cavitated, missing (due to caries), or filled smooth surfaces in primary maxillary anterior teeth or a decayed, missing, or filled score of ≥4 (age 3), ≥5 (age 4), or ≥6 (age 5) surfaces constitutes S-ECC.7 Caries is a transmissible infectious disease; understanding the acquisition of cariogenic microbes is necessary to improving preventive strategies. Vertical transmission is the passing of microbes from caregiver to child, and the major reservoir from which infants acquire cariogenic bacteria [eg, mutans streptococci (MS)] is their mother’s saliva.4,8 The success of the transmission and resultant colonization of maternal MS may be related to several factors, including magnitude of the inoculum,9 frequency of small dose inoculations,10 and a minimum infective dose.11 Infants whose mothers have high levels of MS, a result of untreated caries, are at greater risk of acquiring the organism earlier than children whose mothers have low levels.9 Suppressing maternal reservoirs of MS via dental rehabilitation and antimicrobial treatments can prevent or delay infant inoculation.12,13 Ideally, these interventions would be initiated in the prenatal period.14 Horizontal transmission (eg, between members of a family or group such as daycare) of MS also occurs.8 Eliminating saliva-sharing activities (ie, sharing utensils, orally cleansing a pacifier) may help decrease an infant’s or toddler’s acquisition of cariogenic microbes. Recent studies have shown that MS can colonize the mouths of predentate infants.8 Oral cleanings following feedings, if not previously implemented, need to begin with eruption of the first primary tooth.14 Newly-erupted teeth, because of immature
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enamel, and teeth with enamel hypoplasia may be at higher risk of developing caries. Current best practice includes recommending twice-daily use of a fluoridated toothpaste for dentate children in optimally fluoridated and fluoride-deficient communities.15 Therapeutic use of fluoride for children needs to focus on regimens that maximize topical contact, preferably in lower-dose, higher-frequency approaches.15 Twice-daily use has benefits greater than once-daily brushing.15 A ‘smear’ of fluoridated toothpaste (see Figure 1) for children less than 2 years of age may decrease risk of fluorosis.16 A ‘pea-size’ amount of toothpaste is appropriate for children aged 2 through 5 years.16-18 Parents should dispense the toothpaste onto a soft, age-appropriate sized toothbrush and perform or assist with toothbrushing of preschool-aged children. To maximize the beneficial effect of fluoride in the toothpaste, rinsing after brushing should be kept to a minimum or eliminated altogether.16,19
Figure 1. Comparison of a smear (left) with a pea-sized (right) amount of toothpaste.
In addition to the establishment of oral flora, infants and young children have other unique caries-risk factors including development of dietary habits and childhood food preferences. High-risk dietary practices appear to be established early, probably by 12 months of age, and are maintained throughout early childhood.20,21 The role of carbohydrates in caries initiation is unequivocal. Frequent bottle feeding at night, breastfeeding ad libitum, and extended and repetitive use of a no-spill training cup are associated with, but not consistently implicated in, ECC.22 While ECC may not arise from breast milk alone, breast feeding in combination with other carbohydrates has been found in vitro to be highly cariogenic.23 Frequent consumption of between-meal snacks and beverages containing fermentable carbohydrates (eg, juice, milk, formula, soda) increases the risk of caries due to prolonged contact between sugars in the consumed food or liquid and cariogenic bacteria on the susceptible teeth.24 The American Academy of Pediatrics has recommended children 1-6 years of age consume no more than 4-6 ounces of fruit juice per day, from a cup (ie, not a bottle or covered cup) and as part of a meal or snack.25 Children are at varying levels of risk for developing caries throughout life. Evidence increasingly suggests that to be successful at preventing dental disease, dentists must begin preventive interventions within the first year of life.26 Consequences
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of ECC include a higher risk of new carious lesions in both the primary and permanent dentitons,27-32 hospitalizations and emergency room visits,33-36 increased treatment costs and time,37,38 insufficient physical development (especially in height/ weight),39,40 loss of school days and increased days with restricted activity,41-43 diminished ability to learn,41,44-47 and diminished oral health-related quality of life.48-51
Policy statement The AAPD recognizes caries as a common, complex, chronic disease resulting from an imbalance of multiple risk factors and protective factors over time. To decrease the risk of developing ECC, a potentially devastating infectious disease, the AAPD encourages professional and at-home preventive measures including age-appropriate feeding practices that do not contribute to a child’s caries risk. These include: 1. Reducing the mother’s/primary caregiver’s/sibling(s) MS levels (ideally during the prenatal period) to decrease transmission of cariogenic bacteria. 2. Minimizing saliva-sharing activities (eg, sharing utensils) between an infant or toddler and his family/cohorts. 3. Implementing oral hygiene measures no later than the time of eruption of the first primary tooth. • If an infant falls asleep while feeding, the teeth should be cleaned before placing the child in bed. • Toothbrushing of all dentate children should be per formed twice daily with a fluoridated toothpaste and a soft, age-appropriate sized toothbrush. Parents should use a ‘smear’ of toothpaste to brush the teeth of a child less than 2 years of age. For the 2-5 year old, parents should dispense a ‘pea-size’ amount of toothpaste and perform or assist with their child’s toothbrushing. • Flossing should be initiated when adjacent tooth surfaces can not be cleansed by a toothbrush. 4. Establishing a dental home within 6 months of eruption of the first tooth and no later than 12 months of age to conduct a caries risk assessment and provide parental education including anticipatory guidance for prevention of oral diseases. 5. Avoiding caries-promoting feeding behaviors. In particular: • Infants should not be put to sleep with a bottle con taining fermentable carbohydrates. • Ad libitum breast-feeding should be avoided after the first primary tooth begins to erupt and other dietary carbohydrates are introduced. • Parents should be encouraged to have infants drink from a cup as they approach their first birthday. Infants should be weaned from the bottle at 12 to 14 months of age. • Repetitive consumption of any liquid containing fer mentable carbohydrates from a bottle or no-spill training cup should be avoided. • Between-meal snacks and prolonged exposures to foods and juice or other beverages containing fermentable carbohydrates should be avoided.
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References 1. American Academy of Pediatric Dentistry. Symposium on the prevention of oral disease in children and adolescents. Chicago, Ill; November 11-12, 2005: Conference papers. Pediatr Dent 2006;28(2);96-198. 2. American Academy of Pedodontics and American Academy of Pediatrics. Nursing bottle caries. January, 1978. Chicago, Ill. 3. Crall JJ. Rethinking prevention. Pediatr Dent 2006;28(2): 96-101. 4. Loescshe WJ. Dental caries: A treatable infection. Grand Haven, Mich; Automated Diagnostic Documentation, Inc.; 1993. 5. Kaste LM, Drury TF, Horowitz AM, Beltran E. An evaluation of NHANES III estimates of early childhood caries. J Public Health Dent 1999;59(3):198-200. 6. Drury TF, Horowitz AM, Ismail AI, et al. Diagnosing and reporting early childhood caries for research purposes. J Public Health Dent 1999;59(3):192-7. 7. Ismail AI, Sohn W. A systematic review of clinical diagnostic criteria of early childhood caries. J Public Health Dent 1999;59(3):171-91. 8. Berkowitz RJ. Mutans streptococci: Acquisition and transmission. Pediatr Dent 2006;28(2):106-9. 9. Berkowitz RJ, Turner J, Green P. Maternal salivary levels of Streptococcus mutans and primary oral infection in infants. Arch Oral Biol 1981;26(2):147-9. 10. Loesche WJ. Role of Streptococcus mutans in human dental decay. Microbiol Rev 1986;50(4):353-80. 11. Van Houte J, Green DB. Relationship between the concentration of bacteria in saliva and colonization of teeth in humans. Infect Immun 1974;9(4):624-30. 12. Köhler B, Bratthall D, Krasse B. Preventive measures in mothers influence the establishment of the bacterium Streptococcus mutans in their infants. Arch Oral Biol 1983; 28(3):225-31. 13. Isokangas P, Söderling E, Pienihäkkinen K, Alanen P. Occurrence of dental decay in children after maternal consumption of xylitol chewing gum, a follow-up from 0 to 5 years of age. J Dent Res 2000;79(11):1885-9. 14. American Academy of Pediatric Dentistry. Guideline on infant oral health care. Pediatr Dent 2008;30(suppl):90-3. 15. Adair SM. Evidence-based use of fluoride in contemporary pediatric dental practice. Pediatr Dent 2006;28(2): 133-42. 16. Scottish Intercollegiate Guideline Network. Prevention and Management of Dental Decay in the Pre-school Child. A National Guideline #83. November 2005;1-44. Available at: “http://www.sign.ac.uk/pdf/qrg83.pdf ”. Accessed March 30, 2008. 17. Pang DT, Vann WF Jr. The use of fluoride-containing toothpastes in young children: The scientific evidence for recommending a small quantity. Pediatr Dent 1992;14: 384-7.
18. Ramos-Gomez FJ, Crall JJ, Gansky SA, Slayton RL, Featherstone JDB. Caries risk assessment appropriate for the age 1 visit (infants and toddlers). J Calif Dent Assoc 2007;35(10):687-702. 19. Sjögren K, Birkhed D: Factors related to fluoride retention after toothbrushing and possible connection to caries activity. Caries Res 1993;27(6):474-7. 20. Douglass JM. Response to Tinanoff and Palmer: Dietary determinants of dental caries and dietary recommendations for preschool children. J Public Health Dent 2000; 60(3):207-9. 21. Kranz S, Smiciklas-Wright H, Francis LA. Diet quality, added sugar, and dietary fiber intake in American preschoolers. Pediatr Dent 2006;28(2)164-71. 22. Reisine S, Douglass JM. Psychosocial and behavioral issues in early childhood caries. Comm Dent Oral Epidem 1998;26(suppl 1):32-44. 23. Erickson PR, Mazhari E. Investigation of the role of human breast milk in caries development. Pediatr Dent 1999;21(2):86-90. 24. Marino R, Bonze K, Scholl T, Anhalt H. Nursing bottle caries: Characteristics of children at risk. Clin Pediatr 1989;28(3):129-31. 25. American Academy of Pediatrics Committee on Nutrition. Policy statement: The use and misuse of fruit juices in pediatrics. Pediatrics 2001;107(5):1210-3. Reaffirmed October, 2006. 26. Lee JY, Bouwens TJ, Savage MF, Vann WF. Examining the cost-effectiveness of early dental visits. Pediatr Dent 2006;28(2):102-105, discussion 192-8. 27. Grindefjord M, Dahllöf G, Modéer T. Caries development in children from 2.5 to 3.5 years of age: A longitudinal study. Caries Res 1995;29(6):449-54. 28. O’Sullivan DM, Tinanoff N. The association of early childhood caries patterns with caries incidence in preschool children. J Public Health Dent 1996;56(2):81-3. 29. Johnsen DC, Gerstenmaier JH, DiSantis TA, Berkowitz RJ. Susceptibility of nursing-caries children to future approximal molar decay. Pediatr Dent 1986;8(3):168-70. 30. Al-Shalan TA, Erickson PR, Hardie NA. Primary incisor decay before age 4 as a risk factor for future dental caries. Pediatr Dent 1997;19(1):37-41. 31. Gray MM, Marchment MD, Anderson RJ. The relationship between caries experience in deciduous molars at 5 years and in first permanent molars of the same child at 7 years. Community Dent Health 1991;8(1):3-7. 32. Heller KE, Eklund SA, Pittman J, Ismail AA. Associations between dental treatment in the primary and permanent dentitions using insurance claims data. Pediatr Dent 2000;22(6):469-74. 33. Sheller B, Williams BJ, Lombardi SM. Diagnosis and treatment of dental caries-related emergencies in a children’s hospital. Pediatr Dent 1997;19(8):470-5.
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34. Majewski RF, Snyder CW, Bernat JE. Dental emergencies presenting to a children’s hospital. J Dent Child 1988:55(5):339-42. 35. Fleming P, Gregg TA, Saunders ID. Analysis of an emergency dental service provided at a children’s hospital. Int J Paediatr Dent 1991;1(1):25-30. 36. Schwartz S. A one-year statistical analysis of dental emergencies in a pediatric hospital. J Can Dent Assoc 1994; 60(11):959-62, 966-8. 37. Griffin SO, Gooch BF, Beltran E, Sutherland JN, Barsley R. Dental services, costs, and factors associated with hospitalization for Medicaid-eligible children, Louisiana 1996-97. J Public Health Dent 2000;60(3):21-7. 38. Ramos-Gomez FJ, Huang GF, Masouredis CM, Braham RL. Prevalence and treatment costs of infant caries in Northern California. ASDC J Dent Child 1996;63(2): 108-12. 39. Acs G, Lodolini G, Kaminsky S, Cisneros GJ. Effect of nursing caries on body weight in a pediatric population. Pediatr Dent 1992;14(5):302-5. 40. Ayhan H, Suskan E, Yildirim S. The effect of nursing or rampant caries on height, body weight, and head circumference. J Clin Pediatr Dent 1996;20(3):209-12. 41. Reisine ST. Dental health and public policy: The social impact of disease. Am J Public Health 1985;75(1):27-30. 42. Gift HC, Reisine ST, Larach DC. The social impact of dental problems and visits. Am J Public Health 1992;82 (12):1663-8. 43. Hollister MC, Weintraub JA. The association of oral status with systemic health, quality of life, and economic productivity. J Dent Educ 1993;57(12):901-12.
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44. Peterson J, Niessen L, Nana Lopez G. Texas public school nurses’ assessment of children’s oral health status. J Sch Health 1999;69(2):69-72. 45. Schechter N. The impact of acute and chronic dental pain on child development. J Southeast Soc Pediatr Dent 2000;6:16. 46. Ramage S. The impact of dental disease on school performance. J Southeast Soc Pediatr Dent 2000;6:26. 47. National Center for Education in Maternal and Child Health and Georgetown University. Fact sheet: Oral health and learning. Arlington, Va: NCEMCH; 2001. 48. Low W, Tan S, Schwartz S. The effect of severe caries on the quality of life in young children. Pediatr Dent 1999;21 (6):325-6. 49. Acs G, Pretzer S, Foley M, Ng MW. Perceived outcomes and parental satisfaction following dental rehabilitation under general anesthesia. Pediatr Dent 2001;23(5): 419-23. 50. Thomas CW, Primosch RE. Changes in incremental weight and well-being of children with rampant caries following complete dental rehabilitation. Pediatr Dent 2002;24(2):109-13. 51. Filstrup SL, Inglehart MR, Briskie D, daFonseca M, Lawrence L, Wandera A. The effects on early childhood caries (ECC) and restorative treatment of children’s oral health-related quality of life (OHRQOL)–The parents’/ guardians’ and the child’s perspective [master’s thesis]. Ann Arbor, Mich: The University of Michigan; 2001.
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Policy on Early Childhood Caries (ECC): Unique Challenges and Treatment Options Originating Council Council on Clinical Affairs
Review Council Council on Clinical Affairs
Adopted 2000
Revised 2003, 2007, 2008
Purpose The American Academy of Pediatric Dentistry (AAPD), to promote appropriate, quality oral health care for infants and children with early childhood caries (ECC), must educate the health community and society about the unique challenges and treatment options of this disease. This policy will not attempt to duplicate information found in the AAPD’s Guideline on Infant Oral Health Care.1
Methods The proceedings of the Conference on Early Childhood Caries held in Bethesda, Maryland in October, 1997 were reviewed. A MEDLINE search was conducted using the terms “early childhood caries”, “nursing caries”, and “bottle caries”. Recommendations were based primarily upon review of those proceedings and published studies. In cases where the data did not appear sufficient or were inconclusive, recommendations were based upon expert and consensus opinion.
Background Caries is biofilm (plaque)-induced acid demineralization of enamel or dentin, mediated by saliva. The disease of ECC is defined as “the presence of 1 or more decayed (noncavitated or cavitated lesions), missing (due to caries), or filled tooth surfaces” in any primary tooth in a child 71 months of age or younger.2 In children younger than 3 years of age, any sign of smoothsurface caries is indicative of severe early childhood caries (SECC). From ages 3 through 5, 1 or more cavitated, missing (due to caries), or filled smooth surfaces in primary maxillary anterior teeth, or a decayed, missing, or filled score of >4 (age 3), >5 (age 4), or >6 (age 5) surfaces constitutes S-ECC.2 While the collective oral health of children has improved over the past several decades, between 1988-1994 and 19992004, prevalence of caries in primary teeth increased for youths aged 2 to 11 years.3 For 2 to 5 year olds, the prevalence increased from approximately 24% to 28%.3 ECC, a serious
public health problem, is prevalent in low socioeconomic groups, but also is found in the general population.3,4 ECC can be a particularly virulent form of caries, beginning soon after dental eruption, developing on smooth surfaces, progressing rapidly, and having a lasting detrimental impact on the dentition. Children experiencing caries as infants or toddlers have a much greater probability of subsequent caries in both the primary and permanent dentitions.5-8 Not only does ECC affect teeth, but consequences of this disease may lead to more widespread health issues.9,10 Infants with ECC grow at a slower pace than caries-free infants. Some young children with ECC may be severely underweight because of associated pain and the disinclination to eat. ECC also may be associated with iron deficiency.10 Prevention of ECC begins with intervention in the prenatal and perinatal periods.11 Women should be advised to optimize nutrition during the third trimester and the infant’s first year, when enamel is undergoing maturation. Enamel hypoplasia is common in children with low birthweight or systemic illness in the neonatal period.12,13 There is considerable presumptive evidence that malnutrition/undernutrition during the perinatal period causes hypoplasia.14 A consistent association exists between clinical hypoplasia and ECC.12,15 Cariogenic bacteria (specifically mutans streptococci) may be transmitted to the child; decreasing the mother’s/primary caregiver’s/ sibling(s)’ mutans streptococci levels may decrease the child’s risk of developing ECC.9,16-19 Motivational interviewing may help direct parents to improve home oral health habits.20,21 Frequent bottle feeding at night, ad libitum breast-feeding, and extended and repetitive use of a no-spill training cup are associated with, but not consistently implicated in, ECC.22 While ECC may not arise from breastmilk alone, breast-feeding in combination with other carbohydrates has been found to be highly cariogenic.23 The severity of ECC is associated with poor feeding habits.24 Because poor feeding practices alone will not cause caries, previously used terms such as “baby bottle tooth decay”, “bottle
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mouth”, and “nursing decay” are misleading. ECC is a term that better reflects the multifactorial etiologic process. When very young children have not been the beneficiaries of adequate preventive care and, subsequently, develop ECC, therapeutic intervention should be provided by a practitioner with the training, experience, and expertise to manage both the child and the disease process. Because of the aggressive nature of ECC, treatment should be specific for each individual patient. Areas of decalcification and hypoplasia can rapidly develop cavitation. The use of anticariogenic agents may reduce the risk of development and progression of caries. Interim therapeutic restorations (ITR), using materials such as glass ionomers that release fluoride, are efficacious in both preventive and therapeutic approaches.25,26 Stainless steel crowns are indicated to decrease the number of tooth surfaces at risk for new or secondary caries and are less likely than other restorations to require retreatment.27,28 Low levels of compliance with follow-up care and a high rate of children requiring additional treatment also can influence a practitioner’s decisions for a more definitive restorative management of ECC.29 The extent of the disease process as well as the patient’s developmental level and comprehension skills affect the practitioner’s behavior guidance approaches. To perform treatment effectively and efficiently while instilling a positive dental attitude, the practitioner caring for a child with ECC often must employ advanced behavior guidance techniques. These may include protective stabilization and/or sedation or general anesthesia. The success of restorations may be influenced by the child’s level of cooperation during treatment. General anesthesia may provide optimal conditions to perform restorative procedures. General anesthesia, under certain circumstances, may offer a cost-saving alternative to sedation for children with ECC.30
Policy statement The AAPD recognizes the unique and virulent nature of ECC. Health care providers who diagnose ECC should either provide therapy or refer the patient to an appropriately trained individual for treatment. Immediate intervention is medically necessary to prevent further destruction, as well as more widespread health problems. Because children who experience ECC are at greater risk for subsequent caries development, preventive and therapeutic measures such as optimizing home care, ITR, more frequent visits with regimented applications of topical fluoride, and full crown coverage often are necessary. The dental care provider must assess the patient’s developmental level and comprehension skills, as well as the extent of the disease process, to determine the need for advanced behavior guidance techniques such as protective stabilization, sedation, or general anesthesia.
References 1. American Academy of Pediatric Dentistry. Guideline on infant oral health care. Pediatr Dent 2006;28(suppl): 69-72.
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2. Drury TF, Horowitz AM, Ismail AI, Haertens MP, Rozier RG, Selwitz RH. Diagnosing and reporting early childhood caries for research purposes. J Public Health Dent 1999;59(3):192-7. 3. Dye BA, Tan S, Smith V, et al. Trends in oral health status: United States, 1988-1994 and 1999-2004. National Center for Health Statistics. Vital Health Stat 11(248). Hyattsville, Md; 2007. 4. Tang JM, Altman DS, Robertson DC, O’Sullivan DM, Douglass JM, Tinanoff N. Dental caries prevalence and treatment levels in Arizona preschool children. Public Health Rep 1997;112(4):319-29. 5. Proceedings of the Conference on Early Childhood Caries, Bethesda, Md; October 1997. Community Dent Oral Epidemiol 1998;26(suppl):1-119. 6. Helfenstein V, Steiner M, Marthaler TM. Caries prediction on the basis of past caries including precavity lesions. Caries Res 1991;25(5):372-6. 7. Peretz B, Ram D, Azo E, Efrat Y. Preschool caries as an indicator of future caries: A longitudinal study. Pediatr Dent 2003;25(2):114-8. 8. Foster T, Perinpanayagam H, Pfaffenbach A, Certo M. Recurrence of early childhood caries after comprehensive treatment with general anesthesia and follow up. J Dent Child 2006;73(1):25-30. 9. Acs G, Lodolini G, Kaminshy S, Cisneros GJ. Effect of nursing caries on body weight in pediatric populations. Pediatr Dent 1992;14(5):302-5. 10. Clarke M, Locker D, Berall G, Pencharz P, Kenny DJ, Judd P. Malnourishment in a population of young children with severe early childhood caries. Pediatr Dent 2006; 28(3):254-9. 11. Ismail AI. Prevention of early childhood caries. Community Dent Oral Epidemiol 1998;26(suppl):49-61. 12. Seow WK, Humphrys C, Tudehope DI. Increased prevalence of developmental dental defects in low-birthweight children: A controlled study. Pediatr Dent 1987;9(3):221-5. 13. Davies GN. Early childhood caries: A synopsis. Community Dent Oral Epidemiol 1998;26(suppl):106-16. 14. S eow WK. Biological mechanisms of early childhood caries. Community Dent Oral Epidemiol 1998;26 (suppl):8-27. 15. Horowitz HS. Research issues in early childhood caries. Community Dent Oral Epidemiol 1998;26(suppl):67-81. 16. C aufield PW, Cutter GR, Dasanayake AP. Initial acquisition of mutans streptococci by infants: Evidence for a discrete window of infectivity. J Dent Res 1993;72(1): 37-45. 17. Li Y, Caufield PW. The fidelity of initial acquisition of mutans streptococci by infants from their mothers. J Dent Res 1995;74(2):681-5. 18. Köhler B, Bratthal D, Krasse B. Preventive measures in mothers influence the establishment of the bacterium Streptococcus mutans in their infants. Arch Oral Biol 1983; 28(3):225-31.
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19. Berkowitz RJ. Mutans streptococci: Acquisition and transmission. Pediatr Dent 2006;28(2):106-9. 20. Weinstein P, Harrison R, Benton T. Motivating mothers to prevent caries: Confirming the beneficial effect of counseling. J Am Dent Assoc 2006;137(6):789-93. 21. Weinstein P. Provider versus patient-centered approaches to health promotion with parents of young children: What works/does not work and why. Pediatr Dent 2006; 28(2):172-6. 22. Tinanoff N. Introduction to early childhood caries conference: Initial description and current understanding. Communitry Dent Oral Epidemiol 1998;26(suppl):5-7. 23. Erickson PR, Mazhari E. Investigation of the role of human breast milk in caries development. Pediatr Dent 1992;21(2):86-90. 24. Hallett KB, O’Rourke PK. Pattern and severity of early childhood caries. Community Dent Oral Epidemiol 2006; 34(1):25-35. 25. van’t Hof MA, Frencken JE, van Palenstein Helderman WH, Holmgren CJ. The atraumatic restorative treatment (ART) approach for managing dental caries: A metaanalysis. Int Dent J 2006;56(6):345-51.
26. American Academy of Pediatric Dentistry. Guideline on Restorative Dentistry. Pediatr Dent 2008;30(suppl):163-9. 27. Randall RC, Vrijhoef MM, Wilson NH. Efficacy of preformed metal crowns vs amalgam restorations in primary molars: A systematic review. J Am Dent Assoc 2000;131 (3):337-43. 28. Eidelman E, Faibis S, Peretz B. A comparison of restorations for children with early childhood caries treated under general anesthesia or conscious sedation. Pediatr Dent 2000;22(1):33-7. 29. Almeida AG, Roseman MM, Sheff M, Huntington N, Hughes CV. Future caries susceptibility in children with early childhood caries following treatment under general anesthesia. Pediatr Dent 2000;22(4):302-6. 30. Lee JY, Vann WF, Roberts MW. A cost analysis of treating pediatric dental patients using general anesthesia vs conscious sedation. Pediatr Dent 2000;22(1):27-32.
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Policy on Dietary Recommendations for Infants, Children, and Adolescents Originating Committee Clinical Affairs Committee
Review Council Council on Clinical Affairs
Adopted 1993
Revised 1999, 2002, 2005, 2006, 2008
Purpose The American Academy of Pediatric Dentistry (AAPD) recognizes its role in promoting well-balanced, low caries-risk, and nutrient-dense diets for infants, children, adolescents, and persons with special health care needs.
Methods The revision of this policy is based on a review of current dental and medical literature related to diet and nutrition for infants, children, and adolescents. A MEDLINE search was performed using the terms “body mass index”, “breast-feeding”, “caries”, “diabetes”, “hypertension”, “physical activity”, “nutrition”, and “obesity”. Expert opinions and best current practices also were relied upon for this policy.
Background Establishment of a dental home by 12 months of age allows the institution of appropriate caries-preventive strategies, including dietary recommendations and appropriate oral hygiene instruction, as the primary teeth begin to erupt.1 Dietary choices affect oral health as well as general health and well-being. Epidemiological research shows that human milk and breast-feeding of infants provide general health, nutritional, developmental, psychological, social, economic, and environmental advantages while significantly decreasing risk for a large number of acute and chronic diseases.2 Human breast milk is uniquely superior in providing the best possible nutrition to infants and, by itself, has been shown to be noncariogenic.3 While early childhood caries (ECC) may not arise from breastfeeding alone, an in vitro study has shown that breast-feeding in combination with other carbohydrates is highly cariogenic.3 Frequent bottle-feeding at night, ad libitum breast-feeding, and extended and repetitive use of a no-spill training cup are associated with, but not consistently implicated in, ECC. ECC can be a particularly virulent form of caries, beginning soon after tooth eruption, developing on smooth surfaces, progressing
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rapidly, and having a lasting detrimental impact on the dentition.4 Consequences of this disease may lead to more widespread health issues.5 Caries and its sequelae are among the most prevalent health problems facing American infants, children, and adolescents. Frequent ingestion of sugars and other carbohydrates (eg, fruit juices, acidic beverages) and prolonged contact of these substances with teeth are particular risk factors in the development of caries. Along with increasing caries risk, increased consumption of sugar-sweetened beverages and snack foods also has been linked to obesity.6 Childhood overweight and obesity have reached epidemic proportions worldwide, and the prevalence among US youth has quadrupled in children ages 6 to 11 and nearly doubled in adolescents ages 12 to 19 in the past 25 years.7 Health risks associated with childhood overweight and obesity are strong indicators for predisposition to adult morbidity and mortality and include type 2 diabetes, cardiovascular disease (hypertension, hypercholesterolemia, and dyslipidemia), and psychological stress (depression and low self-esteem), as well as respiratory (obstructive sleep apnea and asthma), orthopedic (fractures), and hepatic (steatohepatitis) problems.8 To help the public make choices for a healthy diet, the US Department of Agriculture (USDA) and the Department of Health and Human Services (DHHS) published Dietary Guidelines for Americans.9 These guidelines include: 1. eating a variety of foods; 2. balancing foods eaten with physical activity to maintain a healthy body mass index; 3. maintaining a caloric intake adequate to support normal growth and development and to reach or maintain a healthy weight; 4. choosing a diet with plenty of vegetables, fruits, and whole grains and low in fat, saturated (especially trans-saturated) fat, and cholesterol; 5. using sugars and salt (sodium) in moderation.9
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Food companies can encourage food and beverage selections that contribute to healthier lifestyles by increasing the prominence, simplicity, and uniformity of nutritional information on food packaging labels.
Policy statement The AAPD, in its efforts to promote optimal health for infants, children, and adolescents, supports the position of the American Dietetic Association (AmDA) that all children should have access to food and nutrition programs that ensure the availability of a safe and adequate food supply that promotes optimal physical, cognitive, and social growth and development.10 The AAPD recommends: 1. breast-feeding of infants to ensure the best possible health and developmental and psychosocial outcomes, with cessation of ad libitum breast-feeding as the first primary tooth begins to erupt and other dietary carbohydrates are introduced; 2. educating the public about the association between frequent consumption of carbohydrates and caries; 3. educating the public about other health risks associated with excess consumption of simple carbohydrates, fat, saturated fat, and sodium.
Furthermore, the AAPD encourages: 1. pediatric dentists and other health care providers who treat children to provide dietary and nutrition counseling (commensurate with their training and experience) in conjunction with other preventive services for their patients; 2. food and beverage manufacturers to make nutritional content on food labels more prominent and consumerfriendly and consumers to monitor the presence and relative amounts of carbohydrates and saturated fats as listed on food labels; 3. school health education programs and food services to promote nutrition programs that provide well-balanced and nutrient-dense foods of low caries-risk, in conjunction with encouraging increased levels of physical activity; 4. research, education, and appropriate legislation to promote diverse and balanced diets. Additional information on nutrition recommendations may be obtained from Web sites for the USDA11, USDA and DHHS9, and AmDA12.
References 1. American Academy of Pediatric Dentistry. Policy on the dental home. Pediatr Dent 2007;29(suppl);22-3. 2. American Academy of Pediatrics. Policy statement: Breastfeeding and the use of human milk. Pediatrics 2005;115 (2):496-506. 3. Erickson PR, Mazhari E. Investigation of the role of human breast milk in caries development. Pediatr Dent 1999;21(2):86-90. 4. American Academy of Pediatric Dentistry. Guideline on infant oral health care. Pediatr Dent 2007;29(suppl):81-4. 5. Acs G, Lodolini G, Kaminshy S, Cisneros GJ. Effect of nursing caries on body weight in pediatric populations. Pediatr Dent 1992;14(5):302-5. 6. Ludwig DS, Peterson KE, Gormaker SL. Relation between consumption of sugar-sweetened drinks and childhood obesity: A prospective, observational analysis. Lancet 2001;357(9255):505-8. 7. Hedley AA, Ogden CL, Johnson CL, Carroll MD, Curtin LR, Flegal KM. Overweight and obesity among US children, adolescents, and adults, 1999-2002. JAMA 2004; 291(23):2847-50. 8. American Academy of Pediatrics Committee on Nutrition. Policy statement on prevention of pediatric obesity and overweight. Pediatrics 2003;112(2):424-30. 9. US Dept of Agriculture, US Dept of Health and Human Services. Dietary Guidelines for Americans. 6 th ed. Washington, DC: US Dept of Agriculture and US Dept of Health and Human Services; 2005. Available at: “http:// www.health.gov/dietary guidelines/dga2005/document/”. Accessed December 23, 2007. 10. Stang J, Bayerl CT. Position of the American Dietetic Association: Child and adolescent food and nutrition programs. J Am Diet Assoc 2003;103(7):887-93. 11. US Dept of Agriculture. Available at: “http://www.my pyramid.gov”. Accessed December 23, 2007. 12. American Dietetic Association. Available at: “http://www. eatright.org”. Accessed December 23, 2007.
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Policy on Vending Machines in Schools Originating Council Council on Clinical Affairs
Review Council Council on Clinical Affairs
Adopted 2002
Revised 2005, 2009
Purpose The American Academy of Pediatric Dentistry (AAPD) recognizes that targeted marketing and easy access to sweetened foods and beverages (acidulated carbonated and noncarbonated) by children and adolescents may increase the amount and frequency of their consumption, which, in turn, may contribute to an increase in caries risk and a negative influence on overall nutrition and health.
Methods The revision of this policy included a new systematic literature search of the MEDLINE/Pubmed database using the following parameters: Terms: “schools”, “vending machines”, AND “dental”; Fields: all fields; Limits: within the last 10 years, humans, English, and clinical trials. The update also included a review of the American Academy of Pediatrics’ policy on soft drinks in schools1 and the US Department of Agriculture’s policy on school meals.2 Fifty articles matched these criteria. Papers for review were chosen from these articles and from references within selected articles. When data did not appear sufficient or were inconclusive, recommendations were based upon expert and/or consensus opinion by experienced researchers and clinicians.
Background There has been a reduction in untreated caries among certain demographic groups of children and adolescents in recent years.3 Frequent consumption of refined carbohydrates, however, can be a significant factor in the child and adolescent diet that contributes to the initiation and progression of caries.4 Vending machines provide ready access to highly-refined carbohydrates, especially soft drinks.* The acids present in carbonated beverages can have a greater deleterious effect (ie, erosion) on enamel than the acids generated by oral flora from the sugars present in sweetened drinks.5 Analysis of NHANES III data indicated that 13% of children aged 2 through 10 had diets high in consumption of carbonated softdrinks, and these children had a significantly higher dental
caries experience in the primary dentition than did children with other fluid consumption patterns.6 Many soft drinks also contain significant amounts of caffeine which, if consumed regularly, may lead to increased, even habitual, usage.7 There is growing concern that vending machine items with limited nutritional value are “competitive foods”, resulting in snack options that are considered to be of poor nutritional quality.8 A significant increase in caries scores has been reported for children who attended schools that had vending machines.9 An effort is underway to increase the healthy choices available in vending machines by replacing sugarsweetened drinks with bottled water, candy bars with nutrition bars, and potato chips with dried fruits and nuts.10 Increased consumption of refined carbohydrates by children and adolescents may have a negative impact on their overall nutrition by displacing foods with higher nutrient density.11 Nutrient density refers to the amount of nutrients in a food compared to the calories. Foods low in calories and high in nutrients are nutrient rich (dense). Foods high in calories and low in nutrients are of poor nutritional quality. As teenage girls have increased their consumption of soft drinks, their consumption of milk has decreased by 40%, which may contribute to a decrease in bone density, subsequent increase in fractures, and future risk of osteoporosis.12,13 Increased ingestion of sugar-sweetened drinks also has been linked to the increased incidence of childhood obesity.14 Many beverage and snack food products are targeted specifically and aggressively at the child and adolescent market. Vending machines containing these products are readily accessible to children and adolescents in schools. In exchange for money to the individual school or districts, “pouring rights contracts” give beverage companies exclusive rights to sell their products at school events and place vending machines on school property, along with other measures that increase student exposure to the beverages.15 Presently, several states have legislation and others are considering legislation to limit pouring rights contracts to healthier options.16,17
* For the purposes of this statement, the term soft-drinks refers to such beverages as sodas, fruit juices, and sports drinks.
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Policy statement The AAPD: 1. encourages collaboration with other dental and medical organizations, governmental agencies, education officials, parent and consumer groups, and corporations to increase public awareness of the negative effects of frequent and/or inappropriate intake of sweetened drinks (carbonated and noncarbonated) and low nutrient dense snack foods on infant, child, and adolescent oral health, nutrition, and general health; 2. opposes any arrangements that may decrease access to healthy nutritional choices for children and adolescents; 3. encourages school officials and parent groups to consider the importance of maintaining healthy choices in vending machines in schools and encourages the promotion of food and beverages of high nutritional value; bottled water and other more healthy choices should be available instead of soft drinks; 4. promotes educating and informing the public about the importance of good oral hygiene and nutritional habits as they pertain to consumption of items available in vending machines.
References 1. American Academy of Pediatrics. Policy statement: Soft drinks in schools. Pediatrics 2004;113(1Pt+1):152-4. 2. US Dept of Agriculture. Food and Nutrition Service. Available at: “http://www.fns.usda.gov/fncs”. Accessed December 7, 2008. 3. Brown LJ, Wall TP, Lazar V. Trends in total caries experience: Permanent and primary teeth. J Am Dent Assoc 2000;131(2):223-31. 4. Ismail IA, Burt BA, Eklund SA. The cariogenicity of soft drinks in the United States. J Am Dent Assoc 1984;109 (2):241-5. 5. Joint Report of the American Dental Association Council on Access, Prevention, and Interprofessional Relations and Council on Scientific Affairs to the House of Delegates. Response to Resolution 73H-2000. Chicago, Ill: ADA; October 2001.
6. Sohn W, Burt BA, Sowers MR. Carbonated soft drinks and dental caries in the primary dentition. J Dent Research 2006;85(3):262-6. 7. Majewski R. Dental caries in adolescents associated with caffeinated carbonated beverages. Pediatr Dent 2001;23 (3):198-203. 8. US Government Accountability office. Report to Congressional Requests: School Meal Programs Competitive Foods are Widely Available and Generate Substantial Revenues for Schools. August 2005. Available at: “http:// www.gao.gov/new.items/d05563.pdf ”. Accessed December 7, 2008. 9. Maliderou M, Reeves S, Nobel C. The effect of social demographic factors, snack consumption, and vending machine use on oral health of children living in London. British Dental J 2006;201(7):441-4. 10. US Dept of Agriculture. Food and Nutrition Service, Office of Analysis, Nutrition and Evaluation. National School Lunch Program Competitive Food Policies by State. Available at: “http://schoolmeals.nal.usda.gov/ Recipes/menuplan/menuplan.html”. Accessed December 7, 2008. 11. Freeman R, Sheiham A. Understanding decision-making processes for sugar consumption in adolescence. Community Dent Oral Epidemiol 1997;25(3):228-32. 12. Wyshak G. Teenaged girls, carbonated beverage consumption, and bone fractures. Arch Pediatr Adolesc Med 2000;154(6):610-3. 13. Ludwig DS, Peterson KE, Gortmaker SL. Relation between consumption of sugar-sweetened drinks and childhood obesity: A prospective, observational analysis. Lancet 2001;357(9255):505-8. 14. Fox K. Soft drinks under scrutiny. ADA News November 20; 2000:22. 15. Maihofer M. “Pouring wrongs”: MDA discourages pop deals. J Mich Dent Assoc 2000;82(2):10. 16. Berthold M. Michigan opposes school-soda deals. ADA News November 20, 2000:8. 17. National Council of State Legislatures. Available at: “http: //www.ncsl.org/programs/health/vending.htm”. Accessed December 7, 2008.
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Policy on Tobacco Use Originating Council Council on Clinical Affairs
Review Council Council on Clinical Affairs
Adopted 2000
Revised 2003, 2006, 2010
Purpose The American Academy of Pediatric Dentistry (AAPD), in order to reduce pain, disability, and death caused by nicotine addiction, recommends routine screening for tobacco use, treating tobacco dependence, preventing tobacco use among children and adolescents, and educating the public on the enormous health and societal costs of tobacco.
Methods This policy revision is based upon a review of current dental, medical, and public health literature related to tobacco use. An electronic search was conducted using the following parameters: Terms: “tobacco”, “teen tobacco use”, “tobacco use in children”, “smoking”, “smokeless tobacco”, “smokeless tobacco and oral disease”, “pregnancy and tobacco”, “secondhand smoke”, and “caries and smoking”; Field: all fields; Limits: within the last 10 years; humans, English; clinical trials; birth through age 19. Three hundred sixteen articles matched these criteria. Web sites for the American Lung Association, American Cancer Society, Centers for Disease Control and Prevention, Environmental Protection Agency, Campaign for Tobacco Free Kids, and US Department of Health and Human Services were reviewed. When data did not appear sufficient or were inconclusive, recommendations were based upon expert and/ or consensus opinion by experienced researchers and clinicians.
Background Tobacco is a risk factor for 6 of the 8 leading causes of deaths in the world and kills up to one-half of its users.1 In the US, the Surgeon General’s report states that smoking is the single greatest avoidable cause of death.2 This report concludes that even in nonsmokers, secondhand smoke exposure causes disease and death. The Centers for Disease Control and Prevention (CDC) has conducted a National Youth Tobacco Survey (NYTS) for the years 1999, 2000, 2002, 2004 and 2006 as part of the Healthy People 2010 objectives on tobacco use.3 While middle school students showed a decrease in the use of cigarettes, cigars, and bidis (unfiltered cigarettes from India)4, they did
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not show a change in the use of smokeless tobacco, pipes, or kreteks (unfiltered cigarettes from India)4 between 2004 and 2006.4,5 Unfortunately during this same period, no significant change was seen in the tobacco use of high school students.4,5 Tobacco use among high school students is 20.0% or 3.5 million, while 19.8% of adults smoke.5,6 Smokeless tobacco use is seen in 13.4% of male high school students and 2.3% of females.5,6 Each day approximately 3,600 youth between 12-17 years of age try smoking with 1,100 a day becoming regular daily users.6,7 Signficant health consequences for tobacco use include 440,000 deaths per year from smoking and an additional 50,000 deaths per year from secondhand smoke.5,6 Other catastrophic sequelae are cardiovascular disease; reproductive effects; pulmonary disease; cancers of the cervix, kidney, pancreas, stomach, lung, larynx, bladder and esophagus; leukemia; cataracts; abdominal aortic aneurysm; bronchitis; and other lung diseases including pneumonia.7,8 Secondhand exposure to tobacco smoke imposes significant risks as well. Cardiovascular disease and lung cancer are increased by 25-30% in nonsmokers who inhale secondhand smoke.9 Infants and children who are exposed to smoke are at risk for sudden infant death syndrome (SIDS), acute respiratory infections, middle ear infections, bronchitis, pneumonia, asthma10, allergies11,12, and infections during infancy.13 Caries in the primary dentition also is related to secondhand smoke exposure.14-16 Enamel hypoplasia in both the primary and permanent dentition also is seen in children exposed to cigarette smoke.17 A new term, “thirdhand” smoke, has been proposed to describe the particulate residual toxins that are deposited in layers all over the home after a cigarette has been extinguished.18 These volatile compounds are deposited and “off gas” into the air over months.19,20 Since children inhabit these low-lying contaminated areas and because the dust ingestion rate in infants is more than twice that of an adult, they are even more susceptible to thirdhand smoke. Studies have shown that these children have associated cognitive defects in addition to the other associated risks of secondhand smoke exposure.21
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Tobacco use can result in oral disease. Oral cancer,9 periodontitis,22-25 compromised wound healing, a reduction in the ability to smell and taste, smoker’s palate and melanosis, coated tongue, staining of teeth and restorations, implant failure, and leukoplakia26,27 are all seen in tobacco users. Smokeless tobacco is a risk factor for periodontal conditions28-30 and oral cancer.31 Initiation of tobacco use begins before age 19 for 90% of adult smokers.32 In fact, most studies show that people who do not use tobacco as a teen never use it.32 Aggressive marketing of tobacco products by manufacturers,33,34 smoking by parents,35 peer influence, a functional belief in the benefits and normalcy of tobacco,36 availability and price of tobacco products, low socioeconomic status, low academic achievement, lower self image, and a lack of behavioral skills to resist tobacco offers all contribute to the initiation of tobacco use during childhood and adolescence.37 Teens who use tobacco are more likely to use alcohol and other drugs and engage in high risk sexual behaviors.38 The monetary costs of this addiction and resultant morbidity and mortality is staggering. Annually, cigarette smoking costs the US $193 billion, based on lost productivity (more than $97 billion) and health care expenditures (more than $96 billion).7 Health care cost from the exposure to secondhand smoke is about $10 billion annually.7 Contrast this with tobacco industry expenditures on advertising and political influence of $13.11 billion in 2005.7 Current trends indicate that tobacco use will cause more than 8 million deaths a year by 2030.39 It is incumbent on the healthcare community to reduce the burden of tobacco-related morbidity and mortality by supporting preventive measures, educating the public about the risks of tobacco, and screening for tobacco use and nicotine dependence.
Policy statement The AAPD opposes the use of all forms of tobacco including cigarettes, pipes, cigars, bidis, kreteks, and smokeless tobacco and alternative nicotine delivery systems (ANDS), such as tobacco lozenges, nicotine water, nicotine lollipops, or “heated tobacco” cigarette substitutes. The AAPD supports national, state, and local legislation that eliminates tobacco advertising and promotions that appeal to or influence children, adolescents, or special groups. The AAPD supports prevention efforts through merchant education and enforcement of state and local laws prohibiting tobacco sales to minors. As environmental tobacco smoke (ETS) is a “known human carcinogen” and there is no evidence to date of a “safe” exposure level to ETS (secondhand or passive smoke),40 the AAPD also supports the enactment and enforcement of state and local clean indoor air and/or smoke-free policies or ordinances prohibiting smoking in public places. Furthermore, the AAPD encourages its members to: 1. promote and establish policies that ensure dental offices, clinics, and/or health care facilities, including property grounds, are tobacco free;
2. support tobacco-free school laws and policies as advocated by the American Dental Association;41,42 3. serve as role models by not using tobacco and urging staff members who use tobacco to stop; 4. routinely examine patients for oral signs of and changes associated with tobacco use; 5. determine and document tobacco use by patients and smoking status of their parents, guardians, and caregivers; 6. educate patients, parents, and guardians on the serious health consequences of tobacco use and exposure to ETS in the home; 7. provide both prevention and cessation services using evidence-based interventions identified as “best practice” for treating tobacco use and nicotine addiction; 8. work to ensure all third-party payors include “best practice” tobacco cessation counseling and pharmacotherapeutic treatments as benefits in health packages; 9. work with school boards to increase tobacco-free environments for all school facilities, property, vehicles, and school events; 10. work on the national level and within their state and community to organize and support anti-tobacco campaigns and to prevent the initiation of tobacco use among children and adolescents, eliminate cigarette sales from vending machines, and increase excise tax on tobacco products to reduce demand; 11. work with legislators, community leaders, and health care organizations to ban tobacco advertising, promotion, and sponsorships; 12. organize and support efforts to pass national, state, and local legislation prohibiting smoking in businesses such as day-care centers where children routinely visit and other establishments where adolescents frequently are employed; 13. establish and support education/training activities and prevention/cessation services throughout the community; 14. recognize the US Public Health Service Clinical Practice Guideline “Treating Tobacco Use and Dependence”43 as a valuable resource. References 1. World Health Organization. Tobacco key facts. Available at: “http://www.who.int/topics/tobacco/facts/en/index. html”. Accessed June 29, 2010. 2. US Dept of Health and Human Services. The health consequences of smoking: A report of the Surgeon General. US Dept of Health and Human Services, CDC, National Center of Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2004. Available at: “http://www.surgeongeneral.gov/library/smokingconse quences/”. Accessed June 29, 2010. 3. US Dept of Health and Human Services. Healthy people 2010: Tobacco use and healthy people 2010 objectivesTobacco priority area. Washington, DC. Available at: “http://www.healthypeople.gov/document/HTML/ Volume2/27Tobacco.htm”. Accessed June 29, 2010.
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4. CDC. 2006 National Youth Tobaccao Survey and Key Prevalence Indicators. Available at: “http://www.cdc. gov/tobacco/data_statistics/fact_sheets/tobacco_industry/ bidis_kreteks/”. Accessed November 8, 2009. 5. CDC. Smoking and tobacco use: Surveys: 2006 National Youth Tobacco Survey and key prevalence indicators. Available at: “http://www.cdc.gov/tobacco/data_statis tics/surveys/nyts/pdfs/indicators.pdf ”. Accessed June 29, 2010. 6. CDC. Smoking and tobacco use: Youth and tobacco use: Current estimates. Available at: “http://www.cdc.gov/ tobacco/data_statistics/fact_sheets/youth_data/tobacco_use/ index.htm#estimates”. Accessed June 29, 2010. 7. Campaign for Tobacco-Free Kids. Toll of tobacco in the United States of America. Tobacco use in the USA. Campaign for Tobacco-Free Kids, December 8, 2008. Available at: “http://www.tobaccofreekids.org/research/fact sheets”. Accessed August 6, 2009. 8. CDC. Smoking and tobacco use. Health effects of cigarette smoking. Updated December 1, 2009. Available at: “http://www.cdc.gov/tobacco/data_statistics/fact_sheets/ health_effects/effects_cig_smoking/index.htm”. Accessed June 29, 2010. 9. US Dept. of Health and Human Services. The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon Gerneral. US Dept of Health and Human Services, CDC, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, Atlanta, Ga. 2006. Available at: “http://www.surgeongeneral.gov/library/secondhand smoke/report/chapter1.pdf ”. Accessed June 29, 2010. 10. Dietert RR, Zelikoff JT. Early-life environment, developmental immunotoxicology, and the risk of pediatric allergic disease including asthma. Birth Defects Res B Dev Reprod Toxicol 2008;83(6):547-60. 11. Goodwin RD, Cowles RA. Household smoking and childhood asthma in the United States: A state-level analysis. J Asthma 2008;45(7):607-10. 12. Lannerö E, Wickman M, van Hage M, Bergström A, Pershagen G, Nordvall L. Exposure to environmental tobacco smoke and sensitisation in children. Thorax 2008; 63(2):172-6. 13. Ladomenou F, Kafatos A, Galanakis E. Environmental tobacco smoke exposure as a risk factor for infections in infancy. Acta Paediatr 2009;98(7):1137-41. 14. Leroy R, Hoppenbrouwers K, Jara A, Declerck D. Parental smoking behavior and caries experience in preschool children. Community Dent Oral Epidemiol 2008;36(3): 249-57. 15. Hanioka T, Nakamura E, Ojima M, Tanaka K, Aoyama H. Dental caries in 3-year-old children and smoking status of parents. Paediatr Perinat Epidemiol 2008;22(6):546-50.
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16. Aligne CA, Moss ME, Auinger P, Weitzman M. Association of pediatric dental caries with passive smoking. JAMA 2003;289(10):1258-64. 17. Ford D, Seow WK, Kazoullis S, Holcombe T, Newman B. A controlled study of risk factors for enamel hypoplasia in the permanent dentition. Pediatr Dent 2009;31(5):382-8. 18. Winickoff JP, Friebely J, Tanski SE, et al. Beliefs about the health effects of “thirdhand” smoke and home smoking bans. Pediatrics 2009;123(1):e74-9. 19. Matt GE, Quintana PJ, Hovell MF, et al. Households contaminated by environmental tobacco smoke: Sources of infant exposures. Tob Control 2004;13(1):29-37. 20. Singer BC, Hodgson AT, Guevarra KS, Hawley EL, Nazaroff WW. Gas-phase organics in environmental tobacco smoke. 1. Effects of smoking rate, ventilation, and furnishing level on emission factors. Environ Sci Technol 2002;36(5):846-53. 21. Yolton K, Dietrich K, Auinger P, Lanphear BP, Hornung R. Exposure to environmental tobacco smoke and cognitive abilities among US children and adolescents. Environ Health Perspect 2005;113(1):98-103. 22. Johnson GK, Hill M. Cigarette smoking and the periodontal patient. J Periodontol 2004;75(2):196-209. 23. Bergström J, Eliasson S, Dock J. A 10-year prospective study of tobacco smoking and periodontal health. J Periodontol 2000;71(8):1338-47. 24. Albandar JM, Streckfus CF, Adesanya MR, Winn DM. Cigar, pipe, and cigarette smoking as risk factors for periodontal disease and tooth loss. J Periodontol 2000;71(2):1874-81. 25. Johnson GK, Slach NA. Impact of tobacco use on periodontal status. J Dent Educ 2001;65(4):313-21. 26. Vellappally S, Fiala Z, Smejkalová J, Jacob V, Somanathan R. Smoking related systemic and oral diseases. Acta Medica 2007;50(3):161-6. 27. Reibel J. Tobacco and oral diseases. Update on the evidence, with recommendations. Med Princ Pract 2003; 12(Suppl 1):22-32. 28. Montén U, Wennström JL, Ramberg P. Periodontal conditions in male adolescents using smokeless tobacco (moist snuff ). J Clin Periodontol 2006;33(12):863-8. 29. Kallischnigg G, Weitkunat R, Lee PN. Systematic review of the relation between smokeless tobacco and nonneoplastic oral diseases in Europe and the United States. BMC Oral Health 2008;8(PMCID:PMC2390522. Published online May 1. doi:10.1186/1472-6831-8-13): 13-33. 30. Bergström J, Keilani H, Lundholm C, Rådestad U. Smokeless tobacco (snuff ) use and periodontal bone loss. J Clin Periodontol 2006;33(8):549-54. 31. Rodu B, Jansson C. Smokeless tobacco and oral cancer: A review of the risks and determinants. Crit Rev Oral Biol Med 2004;15(5):252-63.
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32. American Cancer Society. Child and Teen Tobacco Use. Available at: “http://www.cancer.org/docroot/PED/ content/PED_10_2X_Child_and_Teen_Tobacco_Use. asp?sitearea=PED”. Accessed June 29, 2010. 33. CDC. Cigarette brand preference among middle and high school students who are established smokers – United States, 2004 and 2006. MMWR Morb Mortal Wkly Rep 2009;58(5):112-5. 34. Lavoto C, Linn G, Stead LF, Best A. Impact of tobacco advertising and promotion on increasing adolescent smoking behaviours. Cochrane Database Syst Rev 2003; (4):CD003439. 35. Gilman SE, Rende R, Boergers J, et al. Parental smoking and adolescent smoking initiation: an intergenerational perspective on tobacco control. Pediatrics 2009;123(2): e274-81. 36. Song AV, Morrell HE, Cornell JL, et al. Perceptions of smoking-related risks and benefits as predictors of adolescent smoking initiation. Am J Public Health 2009; 99(3):487-92. 37. US Dept of Health and Human Services. Reducing Tobacco Use: A Report of the Surgeon General. US Dept of Health and Human Services, CDC, Coordinating Center for Health Promotion, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, Atlanta, Ga: 2000. Available at: “http:// www.cdc.gov/mmwr/preview/mmwrhtml/rr4916a1.htm”. Accessed June 29, 2010. 38. CDC. Best Practices for Comprehensive Tobacco Programs2007. US Dept. of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office
on Smoking and Health; Atlanta, Ga: October 2007. Available at: “http://www.cdc.gov/tobacco/tobacco_ control_programs/stateandcommunity/best_practices/ pdfs/2007/BestPractices_Complete.pdf ”. Accessed June 29, 2010. Errata notices available at: “http://www.cdc. gov/tobacco/tobacco_control_programs/stateandcommunity/best_practices/errata/index.htm” http://www.cdc.gov/ tobacco/tobacco_control_programs/stateandcommunity/ best_practices/errata/index.htm”. Accessed June 29, 2010. 39. World Health Organization. WHO report on the global tobacco epidemic, 2009. Available at: “http://whqlibdoc. who.int/publications/2009/9789241563918_eng_full. pdf\”. Accessed July 4, 2010. 40. US Dept of Health and Human Services. The health consequences of involuntary exposure to tobacco smoke: A report of the Surgeon General. US Dept of Health and Human Services, 2007. Available at: “http://www.surgeongeneral. gov/library/secondhandsmoke/factsheets/factsheet7.html”. Accessed November 8, 2009. 41. Crozier S. Resolution directs ADA to support tobaccofree school policies. American Dental Association News, November 10, 2009. Available at: “http://www.ada/org/ news/528.aspx”. Accessed July 4, 2010. 42. American Dental Association. Tobacco Control. Available at: “http://www.ada.org/2788.aspx”. Accessed July 4, 2010. 43. US Dept of Health and Human Services. Treating Tobacco Use and Dependence: Clinical Practice Guidelines. 2008 Update. Available at: “http://www.ncbi.nlm.nih. gov/bookshelf/br.fcgi?book=hsahcpr&part=A28163”. Accessed June 29, 2010.
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Policy on Intraoral and Perioral Piercing Originating Council Council on Clinical Affairs
Review Council Council on Clinical Affairs
Adopted 2000
Revised 2003
Reaffirmed 2007
Purpose The American Academy of Pediatric Dentistry (AAPD) recognizes the importance of educating the public and health professionals on the health implications of oral and perioral piercings.
Methods This policy was based on a MEDLINE search using keywords “body piercing” and “oral piercing” and relevant articles from the dental and medical literature.
Background The use of intraoral jewelry and piercings of oral and perioral tissues have been gaining popularity among adolescents and young adults. Oral piercings involving the tongue, lips, cheeks, and uvula have been associated with pathological conditions including pain, infection, scar formation, tooth fractures, metal hyper-sensitivity reactions, localized periodontal disease, speech impediment, and nerve damage.1-13 Life-threatening complications associated with oral piercings have been reported, including bleeding, edema, and airway obstruction.14-16 Unregulated piercing parlors and techniques have been identified by the National Institutes of Health as a possible vector for disease transmission (eg, hepatitis, tetanus, tuberculosis) and as a cause of bacterial endocarditis in susceptible patients.1
Policy statement The AAPD strongly opposes the practice of piercing intraoral and perioral tissues and use of jewelry on intraoral and perioral tissues due to the potential for pathological conditions and sequelae associated with these practices.
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References 1. National Institutes of Health. Management of hepatitis C and infectious disease. NIH Consensus Conference Statement 105. Section 5, paragraph 2; March 24-26, 1997. 2. American Dental Association. ADA statement on intraoral/perioral piercings and tongue splitting. Available at: “http://www.ada.org/prof/resources/positions/statements/ piercing.asp”. Accessed February 28, 2007. 3. Boardman R, Smith RA. Dental implications of oral piercing. J Calif Dent Assoc 1997;25:200-7. 4. Botchway C, Kuc I. Tongue piercing and associated tooth fracture. J Can Dent Assoc 1998;64(11):803-5. 5. Kretchmer MC, Moriarty JD. Metal piercing through the tongue and localized loss of attachment: A case report. J Periodontol 2001;72(6):831-3. 6. DeMoor RJ, DeWitte AM, Debuyne MA. Tongue piercing and associated oral and dental complications. Endod Dent Traumatol 2000;16(5):232-7. 7. Price SS, Lewis MW. Body piercing involving oral sites. J Am Dent Assoc 1997;128(7):1017-20. 8. Campbell A, Moore A, Williams E, Stephens J, Tatakis DN. Tongue piercing: Impact of time and barbell stem length on lingual gingival recession and tooth chipping. J Periodontol 2002;73(3):289-97. 9. Sardella A, Pedrinazzi M, Bez C, Lodi G, Carrassi A. Labial piercing resulting in gingival recession. A case series. J Clin Periodontol 2002;29(10):961-3. 10. Dibart S, DeFeo P, Surabian G, Hart A, Capri D, Su MF. Oral piercing and gingival recession: Review of the literature and a case report. Quintessence Int 2002;33(2): 110-2. 11. Ng KH, Siar CH, Ganesapillai T. Sarcoid-like foreign body reaction in body piercing: A report of two cases. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1997; 84(1):28-31.
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12. Kuczkowski KM, Benumof JL. Tongue piercing and obstetric anesthesia: Is there cause for concern? J Clin Anesth 2002;14(6):447-8. 13. Berenguer G, Forrest A, Horning GM, Towle HJ, Karpinia K. Localized periodontitis as a long-term effect of oral piercing: A case report. Compend Contin Educ Dent 2006;27(1):24-7.
14. Neiberger E. A large hypertrophic-keloid lesion associated with tongue piercing: A case report. Gen Dent 2006;54(1):46-7. 15. Perkins CS, Meisner J, Harrison JM. A complication of tongue piercing. Br Dent J 1997;182(4):147-8. 16. Brennan M, O’Connell P, O’Sullivan M. Multiple dental fractures following tongue barbell placement: A case report. Dent Traumatol 2006;22(1):41-3.
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Policy on Prevention of Sports-related Orofacial Injuries Originating Committee Clinical Affairs Committee
Review Council Council on Clinical Affairs
Adopted 1991
Revised 1995, 1999, 2002, 2006, 2010
Purpose The American Academy of Pediatric Dentistry (AAPD) recognizes the prevalence of sports-related orofacial injuries in our nation’s youth and the need for prevention. This policy is intended to educate dental professionals, health care providers, and educational and athletic personnel on the prevention of sports-related orofacial injuries.
Methods This policy is an update of the previous document, revised in 2006. The update included an electronic search using the following parameters: Terms: “sports injuries”, “injury prevention”, “dental injuries”, “orofacial injuries”, and “mouthguard”; Field: all fields; Limits: within the last 10 years; humans; English; clinical trials and literature reviews. The reviewers agreed upon the inclusion of 48 articles that met the defined criteria. When data did not appear sufficient or were inconclusive, recommendations were based upon expert and/or consensus opinion by experienced researchers and clinicians.
Background The tremendous popularity of organized youth sports and the high level of competitiveness have resulted in a significant number of dental and facial injuries.1,2 Over the past decade, approximately 46 million youths in the United States were involved in “some form of sports”.3 It is estimated that 30 million children in the US participate in organized sport programs.4 All sporting activities have an associated risk of orofacial injuries due to falls, collisions, contact with hard surfaces, and contact from sports-related equipment. Sports accidents reportedly account for 10-39% of all dental injuries in children.5 Children are most susceptible to sports-related oral injury between the ages of 7 and 11 years.5-8 The administrators of youth, high school, and college football, lacrosse, and ice hockey have demonstrated that dental and facial injuries can be reduced significantly by introducing mandatory protective equipment. Popular sports such as baseball, basketball, soccer,
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softball, wrestling, volleyball, and gymnastics lag far behind in injury protection for girls and boys. Youths participating in leisure activities such as skateboarding, inline or roller skating, and bicycling also benefit from appropriate protective equipment.6,9-11 Studies of dental and orofacial athletic injuries are reported throughout the medical and dental literature.12,13 A review of literature published over the past 20 years showed that the injury rate varied greatly depending on the size of the sample, the sample’s geographic location, the ages of the participants, and the specific sports involved in the study.12,13 Although the statistics vary, many studies reported that dental and orofacial injuries occurred regularly and concluded that participation in sports carries a considerable risk of injury.5,12-15 Consequences of orofacial trauma for children and their families are substantial because of potential for pain, psychological effects, and economic implications. Children with untreated trauma to permanent teeth exhibit greater impacts on their daily living than those without any traumatic injury.16,17 The yearly costs of all injuries, including orofacial injuries, sustained by young athletes have been estimated to be as high as 1.8 billion dollars.4 The National Youth Sports Safety Foundation in 2005 estimated the cost to treat an avulsed permanent tooth and provide followup care is between $5000 and $20,000 over a lifetime.18 Traumatic dental injuries have additional indirect costs that include children’s hours lost from school and parents’ hours lost from work, consequences that disproportionately burden lower income, minority, and noninsured children.19-22 The majority of sport-related dental and orofacial injuries affect the upper lip, maxilla, and maxillary incisors, with 5090% of dental injuries involving the maxillary incisors.5,12,13,23 Use of a mouthguard can protect the upper incisors. However, studies have shown that even with a mouthguard in place, up to 25% of dentoalveolar injuries still can occur.24 Identifying patients who participate in sports and recreational activities allows the healthcare provider to recommend
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and implement preventive protocols for individuals at risk for orofacial injuries. In 2000, a predictive index was developed to identify the risk factors involved in various sports. This index is based upon a defined set of risk factors that predict the chance of injury including demographic information (age, gender, dental occlusion), protective equipment (type/usage), velocity and intensity of the sport, level of activity and exposure time, level of coaching and type of sports organization, whether the player is a focus of attention in a contact or noncontact sport, history of previous sports-related injury, and the situation (eg, practice vs game).15,25 Behavioral risk factors (eg, hyperactivity) also have been associated significantly with injuries affecting the face and/or teeth.26 The frequency of dental trauma is significantly higher for children with increased overjet and inadequate lip coverage.27,28 A dental professional may be able to modify these risk factors. Initiating preventive orthodontic treatment in early- to middlemixed dentition of patients with an overjet >3 mm has the potential to reduce the severity of traumatic injuries to permanent incisors.27 Although some sports-related traumatic injuries are unavoidable, most can be prevented.15,18,29,30 Helmets, facemasks, and mouthguards have been shown to reduce both the frequency and severity of dental and orofacial trauma.15 However, few sports have regulations that require their use. The National Federation of State High School Associations mandate mouthguards for only 4 sports: football, ice hockey, lacrosse, and field hockey.30 Several states have attempted to increase the number of sports which mandate mouthguard use, with various degrees of success and acceptance. Four New England states have been successful in increasing the number of sports requiring mouthguard use to include sports such as soccer, wrestling, and basketball.30,31 Initially used by professional boxers, the mouthguard has been used as a protective device since the early 1900’s.13,32 The mouthguard, also referred to as a gumshield or mouth protector, is defined as a “resilient device or appliance placed inside the mouth to reduce oral injuries, particularly to teeth and surrounding structures.”5 The mouthguard was constructed to “protect the lips and intraoral tissues from bruising and laceration, to protect the teeth from crown fractures, root fractures, luxations, and avulsions, to protect the jaw from fracture and dislocations, and to provide support for edentulous space.”33 The mouthguard works by “absorbing the energy imparted at the site of impact and by dissipating the remaining energy.”34 The American Society for Testing and Materials (ASTM) classifies mouthguards by 3 categories35: 1. Type I – Custom-fabricated mouthguards are produced on a dental model of the patient’s mouth by either the vacuum-forming or heat-pressure lamination technique.5,15 The ASTM recommends that for maxixmum protection, cushioning, and retention, the mouthguard should cover all teeth in one arch, customarily the maxillary arch, less the third molar.35 A mandibular mouthguard is recommended for individuals with a Class III malocclusion.
The custom-fabricated type is superior in retention, protection, and comfort. 5,15,34,36,37 When this type is not available, the mouth-formed mouthguard is preferable to the stock or preformed mouthguard.32,38,39 2. Type II – Mouth-formed, also known as “boil-and-bite”, mouthguards are made from a thermoplastic material adapted to the mouth by finger, tongue, and biting pressure after immersing the appliance in hot water.5 Available commercially at department and sporting-good stores, these are the most commonly used among athletes but vary greatly in protection, retention, comfort, and cost.8,15 3. Type III – Stock mouthguards are purchased over-thecounter. They are designed for use without any modification and must be held in place by clenching the teeth together to provide a protective benefit.5,15 Clenching a stock mouthguard in place can interfere with breathing and speaking and, for this reason, stock mouthguards are considered by many to be less protective.5,8,33,40 Despite these shortcomings, the stock mouthguard could be the only option possible for patients with particular clinical presentations (eg, use of orthodontic brackets and appliances, periods of rapidly changing occlusion during mixed dentition). The Academy for Sports Dentistry (ASD) “recommends the use of a properly fitted mouthguard. It encourages the use of a custom fabricated mouthguard made over a dental cast and delivered under the supervision of a dentist. The ASD strongly supports and encourages a mandate for use of a properly fitted mouthguard in all collision and contact sports.”41 During fabrication of the mouthguard, it is recommended to establish proper anterior occlusion of the maxillary and mandibular arches as this will prevent or reduce injury by better absorbing and distributing the force of impact.41 The practitioner also should consider the patient’s vertical dimension of occlusion, personal comfort, and breathing ability.39 By providng cushioning between the maxilla and mandible, mouthguards also may reduce the incidence or severity of condylar displacement injuries as well as the potential for concussions.8,42 Due to the continual shifting of teeth in orthodontic therapy, the exfoliation of primary teeth, and the eruption of permanent teeth, a custom-fabricated mouthguard may not fit the young athlete soon after the impression is obtained.43 Several block-out methods used in both the dental operatory and laboratory may incorporate space to accommodate for future tooth movement and dental development.43 By anticipating required space changes, a custom fabricated mouthguard may be made to endure several sports seasons.43 Parents play an important role in the acquisition of a mouthguard for young athletes. In a 2004 national fee survey, custom mouthguards ranged from $60 to $285.44 In a study to determine the acceptance of the 3 types of mouthguards by 7- and 8-year old children playing soccer, only 24% of parents surveyed were willing to pay $25 for a custom mouthguard.45 Therefore, cost may be a barrier.44
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Attitudes of officials, coaches, parents, and players about wearing mouthguards influence their usage.46 Although coaches are perceived as the individuals with the greatest impact on whether or not players wear mouthguards, parents view themselves as equally responsible for maintaining mouthguard use.46,47 However, surveys of parents regarding the indications for mouthguard usage reveal a lack of complete understanding of the benefits of mouthguard use.46 Players’ perceptions of mouthguard use and comfort largely determine their compliance and enthusiasm.34,45 Therefore, the dental profession needs to influence and educate all stakeholders about the risk of sports-related orofacial injuries and available preventive strategies.32,44,48 Routine dental visits can be an opportunity to initiate patient/parent education and make appropriate recommendations for use of a properly-fitted athletic mouthguard.15
Policy statement The AAPD recommends: 1. dentists play an active role in educating the public in the use of protective equipment for the prevention of orofacial injuries during sporting and recreational activities; 2. continuation of preventive practices instituted in youth, high school and college football, lacrosse, field hockey, and ice hockey; 3. for youth participating in organized baseball and softball activities, an ASTM-certified face protector be required (according to the playing rules of the sport); 4. mandating the use of properly-fitted mouthguards in other organized sporting activities that carry risk of orofacial injury; 5. prior to initiating practices for a sporting season, coaches/ administrators of organized sports consult a dentist with expertise in orofacial injuries for recommendations for immediate management of sports-related injuries (eg, avulsed teeth); 6. continuation of research in development of a comfortable, efficacious, and cost-effective sports mouthguard to facilitate more widespread use of this proven protective device; 7. dentists of all specialties, including pediatric and general dentists, provide education to parents and patients regarding prevention of orofacial injuries as part of the anticipatory guidance discussed during dental visits; 8. dentists should prescribe, fabricate, or provide an appropriate referral for mouthguard protection for patients at increased risk for orofacial trauma; 9. that third party payors realized the benefits of mouthguards for the prevention and protection from orofacial sports-related injuries and, furthermore, encourages them to improve access to these services; 10. the ASD and the International Association of Dental Traumatology be consulted as valuable resources for the professions and public.
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References 1. Castaldi CR. Sports-related oral and facial injuries in the young athlete: A new challenge for the pediatric dentist. Pediatr Dent 1986;8(4):311-6. 2. Castaldi CR. Athletic mouthguards: History and present status. Sports Med Digest 1988;10:1-2. 3. Barron M, Powell J. Fundamentals of injury prevention in youth sports. J Pediatr Dent Care 2005;11(2):10-2. 4. Adirim T, Cheng T. Overview of injuries in the young athlete. Sports Med 2003;33(1):75-81. 5. Newsome P, Tran D, Cooke M. The role of the mouthguard in the prevention of sports-related dental injuries: A review. Int J Paediatr Dent 2001;11(6):396-404. 6. Tesini DA, Soporowski NJ. Epidemiology of orofacial sportsrelated injuries. Dent Clin North Am 2000;44(1):1-18. 7. Rodd HD, Chesham DJ. Sports-related oral injury and mouthguard use among Sheffield school children. Community Dent Health 1997;14(1):25-30. 8. American Dental Association Council on Access, Prevention, and Interprofessional Relations and Council on Scientific Affairs. Using mouthguards to reduce the incidence and severity of sports-related oral injuries. J Am Dent Assoc 2006;137(12):1712-20. 9. Ranalli DN. Prevention of sports-related dental traumatic injuries. Dent Clin North Am 2000;44(1):35-51. 10. Finnoff JT, Laskowski ER, Altman KC, Diehl NW. Barriers to bicycle helmet use. Pediatrics 2001;108(1):4-10. 11. Fasciglione D, Persic R, Pohl Y, Fillippi A. Dental injuries in inline skating – Level of information and prevention. Dent Traumatol 2007;23(3);143-8. 12. Kumamoto D, Maeda Y. Global trends and epidemiology of sports injuries. J Pediatr Dent Care 2005;11(2):15-25. 13. Kumamoto D, Maeda Y. A literature review of sportsrelated orofacial trauma. Gen Dent 2004;52(3);270-80. 14. Gassner R, Tuli T, Hachl O, Rudisch A, Ulmer H. Craniomaxillofacial trauma: A 10 year review of 9,543 cases with 21,067 injuries. J Craniomaxillofac Surg 2003;31:51-61. 15. Ranalli DN. Sports dentistry in general practice. Gen Dent 2000;48(2):158-64. 16. Cortes M, Marcenes W, Sheiham A. Impact of traumatic injuries to the permanent teeth on the oral health-related quality of life in 12-14-year old children. Community Dent and Oral Epidemiol 2002;30(3):193-8. 17. Berger TD, Kenny DJ, Casas MJ, Barrett EJ, Lawrence HP. Effects of severe dentoalveolar trauma on the qualityof-life of children and parents. Dent Traumatol 2009; 25(5);462-9. 18. National Youth Sports Safety Foundation, Inc; 2005. Available at: “http://www.nyssf.org”. Accessed July 16, 2005. 19. Sane J, Ylipaavalniemi P, Turtola L, Niemi T, Laaka V. Traumatic injuries among university students in Finland. J Am Coll Health 1997;46(1);21-4 20. Ngyuyen PM, Kenny DJ, Barret EJ. Socio-economic burden of permanent incisor replantation on children and parents. Dent Traumatol 2004;20(3);123-33.
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21. Gift HC, Reisine ST, Larach DC. The social impact of dental problems and visits. Am J Public Health 1992;82(12);1663-8. 22. McIntyre JD, Lee JY, Trope M, Vann WF. Elementary school staff knowledge about dental injuries. Dent Traumatol 2008;24(3);289-98. 23. Takeda T, Ishigami K, Nakajima K, et al. Are all mouthguards the same and safe to use? Part 2. The influence of anterior occlusion against a direct impact on maxillary incisors. Dent Traumatol 2008;24(3);360-5. 24. Onyeaso C, Adegbesan O. Knowledge and attitudes of coaches of secondary school athletes in Ibadan, Nigeria regarding orofacial injuries and mouthguard use by the athletes. Dent Traumatol 2003;19(5):204-8. 25. Fos P, Pinkham JR, Ranalli DN. Prediction of sportsrelated dental traumatic injuries. Dent Clin North Am 2000;44(1):19-33. 26. Lalloo R. Risk factors for major injuries to the face and teeth. Dent Traumatol 2003;19(1):12-14. 27. Bauss O, Rohling J, Schwestka-Polly R. Prevalence of traumatic injuries to the permanent incisors in candidates for orthodontic treatment. Dent Traumatol 2004;20(2):61-6. 28. Forsberg C, Tedestam G. Etiological and predisposing factors related to traumatic injuries to permanent teeth. Swed Dent J 1993;17(5):183-90. 29. 1st World Congress of Sports Injury Prevention. Abstracts. Br J Sports Med 2005;39:373-408. 30. Mills S. Can we mandate prevention? J Pediatr Dent Care 2005;11(2):7-8. 31. Kumamoto D. Establishing a mouthguard program in your community. Gen Dent 2000;48:160-4. 32. Patrick DG, van Noort R, Found MS. Scale of protection and the various types of sports mouthguard. Br J Sports Med 2005;39(5):278-81. 33. Biasca N, Wirth S, Tegner Y. The avoidability of head and neck injuries in ice hockey: A historical review. Br J Sports Med 2002;36(6):410-27. 34. McClelland C, Kinirons M, Geary L. A preliminary study of patient comfort associated with customised mouthguards. Br J Sports Med 1999;33(3):186-9. 35. American Society for Testing and Materials. Standard practice for care and use of athletic mouth protectors. ASTM F697-00. Philadelphia, Pa: American Society for Testing and Materials; Reapproved 2006.
36. Warnet L, Greasley A. Transient forces generated by projectiles on variable quality mouthguards monitored by instrumented impact testing. Br J Sports Med 2001;35 (4):257-62. 37. Greasley A, Imlach G, Karet B. Application of a standard test to the in vitro performance of mouthguards. Br J Sports Med 1998;32(1):17-9. 38. Bureau of Dental Health Education and Bureau of Economic Research and Statistics. Evaluation of mouth protectors used by high school football players. J Am Dent Assoc 1964;68:430-42. 39. DeYoung AK, Robinson E, Godwin WC. Comparing comfort and wearability: Custom-made vs self-adapted mouthguards. J Am Dent Assoc 1994;125(8):1112-8. 40. Ranalli DN. Prevention of craniofacial injuries in football. Dent Clin North Am 1991;35(4);627-45. 41. Academy for Sports Dentistry. Position statement: Mouthguard mandates. 2010. Available at: “http://www. academyforsportsdentistry.org/Organization/PositionStatement/tabid/58/Default.aspx”. Accessed June 23, 2010. 42. Waliko T, Bir C, Godwin W, King A. Relationship between temporomandibular joint dynamics and mouthguards: Feasibility of a test method. Dent Traumatol 2004;20(5): 255-60. 43. Croll T, Castaldi CR. Custom sports mouthguard modified for orthodontic patients and children in the transitional dentition. Pediatr Dent 2004;26(5):417-20. 44. Walker J. Parents plus: Getting mouthguards into kids’ mouths. J Pediatr Dent Care 2005;11(2):39-40. 45. Walker J, Jakobsen J, Brown S. Attitudes concerning mouthguard use in 7- to 8-year-old children. J Dent Child 2002;69(2):207-11. 46. Gardiner D, Ranalli DN. Attitudinal factors influencing mouthguard utilization. Dent Clin North Am 2000;44 (1):53-65. 47. Diab N, Mourino A. Parental attitudes toward mouthguards. Pediatr Dent 1997;19(8):455-60. 48. Woodmansey K. Athletic mouth guards prevent orofacial injuries: A review. Gen Dent 1999;47(1):64-9.
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Policy on the Use of Dental Bleaching for Child and Adolescent Patients Originating Council Council on Clinical Affairs
Review Council Council on Clinical Affairs
Adopted 2004
Revised 2009
Purpose The American Academy of Pediatric Dentistry (AAPD) recognizes that the desire for dental whitening in pediatric and adolescent patients has increased. This policy is intended to help professionals and patients make informed decisions about the indications, efficacy, and safety of internal and external bleaching of primary and young permanent teeth and incorporate such care into a comprehensive treatment plan.
Methods This revision included a new systematic literature search of the MEDLINE/Pubmed electronic database using the following parameters: Terms: “dental bleaching”, “dental whitening”, and “tooth bleaching”; Field: all fields; Limits: within the last 10 years, humans, English, clinical trials, and birth through age 18. Sixty-two articles matched these criteria. Papers for review were chosen from this list and from the references within selected articles. When data did not appear sufficient or were inconclusive, recommendations were based upon expert and/ or consensus opinion by experienced researchers and clinicians.
Background Through news stories and advertisements, the public has become more aware of advances in cosmetic dentistry. Both the variety and availability of bleaching products on the market have increased. Consequently, parents and the news media request information on dental whitening for children and adolescents with increasing frequency. Clinical indications for internal or external dental whitening for individual teeth may include discoloration resulting from a traumatic injury (ie, calcific metamorphosis, darkening with devitalization), irregularities in enamel coloration of a permanent tooth due to trauma or infection of the related primary tooth, or intrinsic discoloration/staining (eg, fluorosis, tetracycline staining).1-8 A negative self-image due to a discolored tooth or teeth can have serious consequences on adolescents and could be considered an appropriate indication for bleaching.9 Due to the
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difference in the thickness of enamel of primary and permanent teeth, tooth coloration within a dental arch may vary significantly during the mixed dentition. Full arch cosmetic bleaching during this developmental stage, however, would result in mismatched dental appearance once the child is in the permanent dentition. Dental whitening may be accomplished by using either professional or at-home bleaching modalities. Advantages of inoffice whitening include: 1. an initial professional examination to help identify causes of discoloration and clinical concerns with treatment (eg, existing restorations, side effects); 2. professional control, including use of accelerants (eg, lights, lasers) and soft-tissue protection; 3. patient compliance; 4. rapid results; 5. stability of results. The pretreatment professional assessment helps identify pulp pathology that may be associated with a single discolored tooth. This examination also identifies restorations that are faulty or could be affected by the bleaching process, and the associated costs for replacing such restorations to maximize esthetic results.1,4,6,10-13 By using photographs and/or a shade guide, the dentist can document the effectiveness of treatment. In addition to providing in-office bleaching procedures, a dentist may fabricate custom trays for at-home use of a bleaching product. Custom trays ensure intimate fit and greater efficiency of bleaching agents. Over-the-counter products for at-home use include bleaching gels, whitening strips, and brush-on agents. Their main advantages include patient convenience and lower associated costs. Peroxide-containing whiteners or bleaching agents improve the appearance by changing the tooth’s intrinsic color. The professional-use products usually range from 10% carbamide peroxide (equivalent to about 3% hydrogen peroxide) to 38% carbamide peroxide (equivalent to approximately 13% hydrogen peroxide). Carbamide peroxide is the most commonly used
american academy of pediatric dentistry
active ingredient in dentist-dispensed home-use tooth-bleaching products.10 These agents sometimes are used sequentially. Inoffice bleaching products require isolation with a rubber dam or a protective gel to shield the gingival soft tissues. Home-use bleaching products contain lower concentrations of hydrogen peroxide or carbamide peroxide.1-3,14-16 Many whitening toothpastes contain polishing or chemical agents to improve tooth appearance by removing surface stains through gentle polishing, chemically chelating, or other nonbleaching action.10 Side effects from bleaching vital and nonvital teeth have been documented. It should be noted that most of the research on bleaching has been performed on adult patients, with only a small amount of published bleaching research using child or adolescent patients.1-3,14-16 The more common side effects associated with bleaching vital teeth are tooth sensitivity and tissue irritation. Sensitivity affects 8% to 66% of patients and often occurs during the early stages of treatment.4,9,11,17-21 Tissue irritation, in most cases, results from an ill-fitting tray rather than the bleaching agents and no longer occurs once a more accurately fitted tray is used. Both sensitivity and tissue irritation usually are temporary and cease with the discontinuance of treatment.4,11,22 Another side effect associated with bleaching vital teeth is increased marginal leakage of an existing restoration.4,11,22 The more common side effects from internal bleaching of nonvital teeth are external root resorption12,23-26 and ankylosis. With external bleaching of nonvital teeth, the most common side effect is increased marginal leakage of an existing restoration.26-30 One of the degradation byproducts of hydrogen peroxide or carbamide peroxide results in a hydroxyl-free radical. This byproduct has been associated with periodontal tissue damage and root resorption. Due to the concern of the hydroxyl free radical31-36 and the potential side effects of dental bleaching, minimizing exposure at the lowest effective concentration of hydrogen peroxide or carbamide peroxide is recommended. Current literature and clinical studies support the use of sodium perborate mixed with water for bleaching nonvital teeth.13,37 Studies have shown higher incidences of root resorption when hydrogen peroxide is mixed with sodium perborate12,38-41 or any mixture of sodium perborate is heated. 42 Therefore, the use of hydrogen peroxide and heating any mixture of sodium perborate are not recommended.
Policy statement The AAPD encourages: 1. the judicious use of bleaching for vital and nonvital teeth; 2. patients to consult their dentists to determine appropriate methods for and the timing of dental whitening within the context of an individualized, comprehensive, and sequenced treatment plan; 3. dental professionals and consumers to consider side effects when contemplating dental bleaching for child and adolescent patients; 4. further research of dental whitening agents in children.
The AAPD discourages full-arch cosmetic bleaching for patients in the mixed dentition.
References 1. Zekonis R, Matis BA, Cochran MA, Al Shetri SE, Eckert GJ, Carlson TJ. Clinical evaluation of in-office and at-home bleaching treatments. Oper Dent 2003;28(2):114-21. 2. Whitman FJ, Simon JF. A clinical comparison of two bleaching systems. J Calif Dent Assoc 1995;23(1):59-64. 3. Matis BA, Wang Y, Jiang T, Eckert GJ. Extended athome bleaching of tetracycline-stained teeth with different concentrations of carbamide peroxide. Quintessence Int 2002;33(9):645-55. 4. Matis BA, Cochran MA, Eckert G, Carlson TJ. The efficacy and safety of a 10% carbamide peroxide bleaching gel. Quintessence Int 1998;29(9):555-63. 5. Barnes DM, Kihn PW, Romberg E, George D, DePaola L, Medina E. Clinical evaluation of a new 10% carbamide peroxide tooth-whitening agent. Compend Contin Educ Dent 1998;19(10):968-72, 977-8. 6. Croll TP. Esthetic correction for teeth with fluorosis and fluorosis-like enamel dysmineralization. J Esthet Dent 1998;10(1):21-9. 7. Croll TP, Sasa IS. Carbamide peroxide bleaching of teeth with dentinogenesis imperfecta discoloration: Report of a case. Quintessence Int 1995;26(10):683-6. 8. Croll TP, Segura A. Tooth color improvement for children and teens: Enamel microabrasion and dental bleaching. J Dent Child 1996;63(1):17-22. 9. Donly KJ. The adolescent patient: Special whitening challenges. Compend Contin Educ Dent 2003;24(4A):390-6. 10. American Dental Association. Statement on the safety and effectiveness of tooth whitening products; June 2002. Available at: “http://www.ada.org/prof/resources/positions/ statements/whiten2.asp”. Accessed October 10, 2008. 11. Haywood VB, Leonard RH, Nelson CF, Brunson WD. Effectiveness, side effects and long-term status of nightguard vital bleaching. J Am Dent Assoc 1994;125(9):1219-26. 12. Haywood VB. Bleaching of vital and nonvital teeth. Curr Opin Dent 1992;2:142-9. 13. Fieldhouse J. Teeth whitening debate I. Br Dent J 2002; 193(6):300-1. 14. Kwon YH, Huo MS, Kim KH, Kim SK, Kim YJ. Effects of hydrogen peroxide on the light reflectance and morphology of bovine enamel. J Oral Rehabil 2002;29(5):473-7. 15. Slezak B, Santarpia P, Xu T, et al. Safety profile of a new liquid whitening gel. Compend Contin Educ Dent 2002; 11(suppl 1):4-11. 16. Kugel G, Aboushala A, Zhou X, Gerlach RW. Daily use of whitening strips on tetracycline-stained teeth: Comparative results after 2 months. Compend Contin Educ Dent 2002;23(1A):29-34; quiz 50.
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17. MacIsaac AM, Hoen CM. Intracoronal bleaching: Concerns and considerations. J Can Dent Assoc 1994;60(1): 57-64. 18. Donly KJ, Donly AS, Baharloo L, et al. Tooth whitening in children. Compend Contin Educ Dent 2002;23(1A): 22-28; quiz 49. 19. Donly KJ, Gerlach RW. Clinical trials on the use of whitening strips in children and adolescents. Gen Dent 2002;50(3):242-5. 20. Almas K, Albaker A, Felembam N. Knowledge of dental health and diseases among dental patients, a multicentre study in Saudi Arabia. Indian J Dent Res 2000;11(4): 145-55. 21. Marin PD, Heithersay GS, Bridges TE. A quantitative comparison of traditional and non-peroxide bleaching agents. Endod Dent Traumatol 1998;14(2):64-7. 22. Schulte JR, Morrissette DB, Gasior EJ, Czajewski MV. The effects of bleaching application time on the dental pulp. J Am Dent Assoc 1994;125(10):1330-5. 23. Szajkis S, Tagger M, Tamse A. Bleaching of root canal treated teeth and cervical external resorption: Review of the literature. Refuat Hashinayim 1986;4(2):10-2. 24. Lado EA, Stanley HR, Weisman MI. Cervical resorption in bleached teeth. Oral Surg Oral Med Oral Pathol 1983;55(1):78-80. 25. Heller D, Skriber J, Lin LM. Effect of intracoronal bleaching on external cervical root resorption. J Endod 1992;18(4):145-8. 26. Madison S, Walton R. Cervical root resorption following bleaching of endodontically treated teeth. J Endod 1990;16(12):570-4. 27. Haywood VB. Greening of the tooth-amalgam interface during extended 10% carbamide peroxide bleaching of tetracycline-stained teeth: A case report. J Esthet Restor Dent 2002;14(1):12-7. 28. Barkhordar RA, Kempler D, Plesh O. Effect of nonvital tooth bleaching on microleakage of resin composite restorations. Quintessence Int 1997;28(5):341-4. 29. Teixeira EC, Hara AT, Turssi CP, Serra MC. Effect of nonvital tooth bleaching on resin/enamel shear bond strength. J Adhes Dent 2002;4(4):317-22.
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30. Teixeira EC, Hara AT, Turssi CP, Serra MC. Effect of nonvital tooth bleaching on microleakage of coronal access restorations. J Oral Rehabil 2003;30(11):1123-7. 31. Anderson DG, Chiego DJ Jr, Clickman GN, McCauley LK. A clinical assessment of the effects of 10% carbamide peroxide gel on human pulp tissue. J Endod 1999;25(4): 247-50. 32. Kinomoto Y, Carnes DL Jr, Ebisu S. Cytotoxicity of intracanal bleaching agents on periodontal ligament cells in vitro. J Endod 2001;27(9):574-7. 33. Rotstein I, Friedman S, Mor C, Katznelson J, Sommer M, Bab I. Histological characterization of bleaching-induced external root resorption in dogs. J Endod 1991;17(9): 436-41. 34. Weiger R, Kuhn A, Löst C. Radicular penetration of hydrogen peroxide during intra-coronal bleaching with various forms of sodium perborate. Int Endod J 1994; 27(6):313-7. 35. Li Y. [Safety of peroxide containing tooth whiteners]. Shanghai Kou Qiang Yi Xue 2001;10(2):97-9. 36. Li Y. Tooth bleaching using peroxide-containing agents: Current status of safety issue. Compend Contin Educ Dent 1998;19(3):783-6, 788, 790. 37. Macey-Dare LV, Williams B. Bleaching of a discoloured non-vital tooth: Use of a sodium perborate/water paste as the bleaching agent. Int J Paediatr Dent 1997;7(1):35-8. 38. Heithersay GS. Invasive cervical resorption following trauma. Aust Endod J 1999;25(2):79-85. 39. Heithersay GS. Treatment of invasive cervical resorption: An analysis of results using topical application of trichloracetic acid, curettage, and restoration. Quintessence Int 1999;30(2):96-110. 40. Heithersay GS. Invasive cervical resorption: An analysis of potential predisposing factors. Quintessence Int 1999;30(2):83-95. 41. Weiger R, Kuhn A, Lost C. In vitro comparison of various types of sodium perborate used for intracoronal bleaching of discolored teeth. J Endod 1994;20(7):338-41. 42. Attin T, Paqué F, Ajam F, Lennon AM. Review of the current status of tooth whitening with the walking bleach technique. Int Endod J 2003;36(5):313-29.
american academy of pediatric dentistry
Policy on Minimizing Occupational Health Hazards Associated With Nitrous Oxide Originating Committee
Clinical Affairs Committee Review Council Council on Clinical Affairs
Adopted 1987
Revised 1993, 1996, 2000, 2003, 2008
Purpose The American Academy of Pediatric Dentistry (AAPD) recommends that exposure to ambient nitrous oxide be minimized to reduce occupational health hazards for dental personnel.
Methods This document is based on current dental, medical, and public health literature regarding the potential risks of ambient nitrous oxide exposure. A MEDLINE search was conducted using the terms “nitrous oxide”, “occupational exposure to nitrous oxide”, and “nitrous oxide and dentistry”. Guidelines and recommendations from the National Institute for Occupational Safety and Health (NIOSH) also were reviewed.1-2 Expert opinions and best current practices were relied upon when sufficient scientific data were not available.
Background Epidemiologic studies provide strong evidence that there are increased general health problems and reproductive difficulties among dental personnel chronically exposed to significant levels of ambient nitrous oxide.3-7 Nitrous oxide acts by oxidizing vitamin B12 from the active, reduced cobalamin to the inactive form. In turn, this inactivates the enzyme methionine synthetase, which requires both the active cobalamin and folate as cofactors. The inactivation of methionine synthetase decreases DNA production, thereby interfering with cell proliferation.8 Nitrous oxide has been linked epidemiologically to reproductive, hematologic, immunologic, neurologic, hepatic, and renal disorders; symptoms are time and dose dependent.9 Symptoms are reported most frequently in cases where scavenging has not been used or with chronic (recreational) abuse.9 Absolute occupational effects are still uncertain.9 Epidemiologic conclusions have been challenged.10 Adverse reproductive outcomes are linked to B12 deficient individuals and those exposed to “high nitrous oxide levels”.9 A maximum safe level of ambient nitrous oxide in the dental environment has not been determined.9-14 Reduction of ambient nitrous oxide through system maintenance, scavenging, ventilation, use of the minimal effective dose,
and patient management is critical to maintaining the lowest practical levels in the dental environment.1,2,14,15 Frequent and regular inspection and maintenance of the nitrous oxide delivery system, together with the use of a scavenging system, can reduce ambient nitrous oxide significantly.16,17 Using a well-fitted mask and an appropriate amount of suction via the scavenging system will minimize leakage, reducing ambient nitrous oxide levels.17 NIOSH has recommended that the exhaust ventilation of nitrous oxide from the patient’s mask be maintained at an air flow rate of 45 L/min and vented outside the building away from fresh air intakes.2 However, scavenging at this rate has been shown to reduce the level of pyschosedation achieved with nitrous oxide inhalation.20 Where possible, 100% clean outdoor air should be used for dental operatory ventilation.1 Supply and exhaust vents should be well separated to allow good mixing and prevent ‘short-circuiting’. 1 Appropriate patient selection is an important consideration in reducing ambient nitrous oxide levels.15 Patients who are unwilling or unable to tolerate the nasal hood and those with medical conditions (eg, obstructive respiratory diseases, emotional disturbances, drug dependencies) that contraindicate the use of nitrous oxide should be managed by other behavior guidance techniques.15 In the dental environment, patient behaviors such as talking, crying, and moving have been shown to result in significant increases in baseline ambient nitrous oxide levels despite the use of the mask-type scavenging systems.19 Use of supplemental measures, including a rubber dam and/or a high-volume dental aspirator, placed near or within 20 cm of the patient’s mouth, has been shown to reduce significantly ambient nitrous oxide levels.21-23 During the first 3-5 minutes after terminating nitrous oxide administration, a significant amount of the gas is exhaled by the patient.24 Once nitrous oxide administration is discontinued, the gas delivery system should be flushed by administering 100% oxygen to the patient for at least 5 minutes.2 This post-procedural oxygenation also decreases the risk of diffusion hypoxia to the patient. Diligent use of the above practices in the pediatric dental environment has allowed for the reduction of ambient nitrous oxide to the levels recommended oral he alth policies
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by NIOSH.14,23 Measurement of nitrous oxide levels in the dental operatory can be helpful in determining the type and extent of remediation necessary to decrease occupational exposure.
Policy statement The AAPD recommends that dentists and dental auxiliaries minimize their exposure to nitrous oxide by maintaining the lowest practical levels in the dental environment. Adherence to the recommendations below can help minimize occupational exposure to nitrous oxide. 1. Use scavenging systems that remove nitrous oxide during patient’s exhalation. 2. Ensure that exhaust systems adequately vent scavenged air and gases to the outside of the building and away from fresh air intake vents. 3. Use, where possible, 100% clean outdoor air for dental operatory ventilation. 4. Implement careful, regular inspection and maintenance of the nitrous oxide/oxygen delivery equipment. 5. Carefully consider patient selection criteria (ie, indications and contraindications) prior to administering nitrous oxide. 6. Select a properly-fitted mask size for each patient. 7. During administration, visually monitor the patient and titrate the flow/percentage to the minimal effective dose of nitrous oxide. 8. Encourage patients to minimize talking and mouth breathing during nitrous oxide administration. 9. Use rubber dam and high volume oral aspiration when possible. 10. Flush the delivery system of nitrous oxide after completion, by administering 100% oxygen to the patient for at least 5 minutes.
References 1. National Institute of Occupational Safety and Health. Control of nitrous oxide in dental operatories. Appl Occup Environ Hyg 1999;14(4):218-20. 2. National Institute of Occupational Safety and Health. Controlling exposures of nitrous oxide during anesthetic administration. Cincinnati, Ohio: National Institute of Occupational Safety and Health; 1994. DHHS/NIOSH Publication No. 94-100. 3. Rowland AS, Baird DD, Weinberg CR, Shore DL, Shy CM, Wilcox AJ. Reduced fertility among women employed as dental assistants exposed to high levels of nitrous oxide. N Engl J Med 1992;327(14):993-7. 4. Cohen EN, Brown BW Jr, Bruce DL, et al. A survey of anesthetic health hazards among dentists. J Am Dent Assoc 1975;90(6):1291-6. 5. Cohen EN, Gift HC, Brown BW Jr, et al. Occupational disease in dentistry and chronic exposure to trace anesthetic gases. J Am Dent Assoc 1980(1);101:21-31. 6. Brodsky JB, Cohen EN, Brown BW Jr, Wu ML, Whitcher CE. Exposure to nitrous oxide and neurologic disease among dental professionals. Anesth Analg 1981;60(5):297-301. 66
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7. Rowland AS, Baird DD, Shore DL, Weinberg CR, Savitz DA, Wilcox AJ. Nitrous oxide and spontaneous abortion in female dental assistants. Am J Epidemiol 1995;141(6):531-7. 8. Emmanouil DE, Quock RM. Advances in understanding the actions of nitrous oxide. Anesth Prog 2007;54(1):9-18. 9. Louis-Ferdinand RT. Myelotoxic, neurotoxic, and reproductive adverse effects of nitrous oxide. Adverse Drug React Toxicol Rev 1994;13(4):193-206. 10. Clark MS, Renehan BW, Jeffers BW. Clinical use and potential biohazards of nitrous oxide/oxygen. Gen Dent 1997; 45(5):486-91. 11. Howard WR. Nitrous oxide in the dental environment: Assessing the risk and reducing the exposure. J Am Dent Assoc 1997;128(3):356-60. 12. American Dental Association Council on Scientific Affairs, American Dental Association Council on Dental Practice. Nitrous oxide in the dental office. J Am Dent Assoc 1997; 128(3):364-5. 13. Donaldson D, Meechan JG. The hazards of chronic exposure to nitrous oxide: An update. Br Dent J 1995;178(3):95-100. 14. Johnston J. Nitrous oxide: Your health not theirs. Br J Theatre Nurs 1993;3(6):29-30. 15. American Academy of Pediatric Dentistry. Guideline on appropriate use of nitrous oxide for pediatric dental patients. Pediatr Dent 2008;30(suppl):140-2. 16. Sass-Kortasak AM, Wheeler IP, Purdham JT. Exposure of operating room personnel to anaesthetic agents: An examination of the effectiveness of scavenging systems and the importance of maintenance programs. Can Anaesth Soc J 1981;28(1):22-8. 17. Flowerdew RM, Brummitt WM. Reduction of nitrous oxide contamination in a pediatric hospital. Can Anaesth Soc J 1979;26(5):370-4. 18. Henry RJ, Primosch RE, Courts FJ. The effects of various dental procedures and patient behaviors upon nitrous oxide scavenger effectiveness. Pediatr Dent 1992;14(1):19-25. 19. Crouch KG, Johnston OE. Nitrous oxide control in the dental operatory: Auxiliary exhaust and mask leakage, design, and scavenging flow rate as factors. Am Ind Hyg Assoc J 1996;57(3):272-8. 20. Primosch R, McLellan M, Jerrell G, Venezie R. Effect of scavenging on the psychomotor and cognitive function of subjects sedated with nitrous oxide and oxygen inhalation. Pediatr Dent 1992;14(1):19-25. 21. Borganelli GN, Primosch RE, Henry RJ. Operatory ventilation and scavenger evacuation rate influence on ambient nitrous oxide levels. J Dent Res 1993;72(9):1275-8. 22. Carlsson P, Ljungqvist B, Hallén B. The effect of local scavenging on occupational exposure to nitrous oxide. Acta Anaesthesiol Scand 1983;27(6):470-5. 23. Henry RJ, Borganelli GN. High-volume aspiration as a supplemental scavenging method for reducing ambient nitrous oxide levels in the operatory: A laboratory study. Int J Paediatr Dent 1995;5(2):157-61. 24. Crouch KG, McGlothin JD, Johnston OE. A long-term study of the development of N2O controls at a pediatric dental facility. AIHAJ 2000;61(5):753-6.
american academy of pediatric dentistry
Policy on the Use of Deep Sedation and General Anesthesia in the Pediatric Dental Office Originating Council Ad Hoc Committee on Sedation and Anesthesia
Review Council Council on Clinical Affairs
Adopted 1999
Revised 2004, 2007
Purpose The American Academy of Pediatric Dentistry (AAPD), as the advocate for oral health in infants, children, adolescents, and persons with special health care needs, recognizes that there exists a patient population for whom routine dental care using nonpharmacologic behavior guidance techniques is not a viable approach. It also recognizes that a population of patients, because of their need for extensive treatment, acute situational anxiety, uncooperative age-appropriate behavior, immature cognitive functioning, disabilities, or medical conditions, would benefit from deep sedation or general anesthesia.1
Background Pediatric dentists have long sought to provide dental care to their young and disabled patients in a manner which will promote excellence in quality of care and concurrently induce a positive attitude in the patient toward dental treatment. Behavior guidance techniques have allowed most children to receive treatment in the dental office with minimal discomfort and without expressed fear. Sedation has provided others with the ability to accept treatment. However, some children and developmentally disabled patients require general anesthesia to receive comprehensive dental care in a safe and humane fashion. Many pediatric dentists (and others who treat children) have sought to provide for the administration of general anesthesia by properly-trained individuals in their offices or other facilities (eg, outpatient care clinics) outside of the traditional hospital setting. In 1998, the AAPD established its Guideline on the Elective Use of Minimal, Moderate, and Deep Sedation and General Anesthesia in Pediatric Dental Patients.2 In an effort to unify guidelines for sedation used by medical and dental practitioners, the American Academy of Pediatrics and the AAPD in 2006 coauthored a statement entitled Guideline for Monitoring and Management of Pediatric Patients During and After Sedation for Diagnostic and Therapeutic Procedures.3 This revised guideline reflects the current understanding of appropriate monitoring needs and, further, provide
definitions and characteristics of 3 levels of sedation (minimal, moderate, and deep) and general anesthesia involving pediatric patients. When deep sedation or general anesthesia is provided in a private pediatric dental office, the pediatric dentist must be responsible for evaluating the educational and professional qualifications of the general anesthesia or deep sedation provider (if it is other than himself ) and determining that the provider is in compliance with state rules and regulations associated with the provision of deep sedation and general anesthesia. The pediatric dentist is also responsible for establishing a safe environment that complies with local, state, and federal rules and regulations, as well as the Guideline for Monitoring and Management of Pediatric Patients During and After Sedation for Diagnostic and Therapeutic Procedures3 for the protection of the patient.
Educational requirements Deep sedation and general anesthesia must be provided only by qualified and appropriately-trained individuals and in accordance with state regulations. Such providers may include pediatric dentists who have completed advanced education in anesthesiology beyond their pediatric residency advanced training program, dental or medical anesthesiologists, certified registered nurse anesthetists, or anesthesia assistants. The expertise in providing deep sedation and general anesthesia cannot be gained through the undergraduate dental school curriculum or continuing education. Only dentists who have completed an advanced education program which meets the requirements of the American Dental Association (ADA) are considered qualified to provide deep sedation and general anesthesia in practice. This includes: 1. completion of an advanced training program in anes thesia and related subjects beyond the predoctoral dental curriculum that satisfies the requirements de scribed in Part Two of the ADA Guidelines for Teaching the Comprehensive Control of Anxiety and Pain in Dentistry4 at the time training was commenced; oral he alth policies
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2. completion of an ADA-accredited post-doctoral training program (eg, oral and maxillofacial surgery) which affords comprehensive and appropriate train ing necessary to administer and manage deep sedation/general anesthesia.
Risk management As stated above, the pediatric dentist is responsible for providing a safe environment for the in-office provision of deep sedation and general anesthesia. In addition to evaluating the qualifications of the anesthesia provider, he/she must be involved with the following aspects of care to minimize risks for the patient: 1. facilities and equipment; 2. monitoring and documentation; 3. patient selection utilizing medical history, physical status, and indications for anesthetic management; 4. preoperative evaluation; 5. appropriately-trained support personnel; 6. emergency medications, equipment, and protocols; 7. preoperative and postoperative patient instructions; 8. criteria and management of recovery and discharge.
Continuous quality improvement To reduce the chance of medical error and determine root cause, aspects of continuous quality improvement are applied in the outpatient setting during the administration of deep sedation and general anesthesia as described in the Guideline for Monitoring and Management of Pediatric Patients During and After Sedation for Diagnostic and Therapeutic Procedures.3 Adverse events are recorded and examined for assessment of risk reduction and improvement in patient satisfaction.
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Policy statement The AAPD endorses the in-office use of deep sedation or general anesthesia on select pediatric dental patients administered either by a trained, credentialed, and licensed pediatric dentist, dental or medical anesthesiologist, nurse anesthetist, or anesthesia assistant in an appropriately-equipped and staffed facility.
References 1. American Academy of Pediatric Dentistry. Guideline on behavior guidance for the pediatric dental patient. Pediatr Dent 2006;28(suppl):97-105. 2. American Academy of Pediatric Dentistry. Guideline on the elective use of minimal, moderate, and deep sedation and general anesthesia in pediatric dental patients. Pediatr Dent 2004;26(suppl):95-103. 3. American Academy of Pediatrics, American Academy of Pediatric Dentistry. Guideline for monitoring and management of pediatric patients during and after sedation for diagnostic and therapeutic procedures. Pediatr Dent 2006;28(suppl):115-32. 4. American Dental Association. Guidelines for teaching the comprehensive control of anxiety and pain in dentistry. Chicago, Ill: ADA House of Delegates; 2005. Available at: “http://www.ada.org/prof/resources/positions/statements/ anxiety_guidelines.pdf ”. Accessed May 6, 2007.
american academy of pediatric dentistry
Policy on Hospitalization and Operating Room Access for Dental Care of Infants, Children, Adolescents, and Persons With Special Health Care Needs Originating Committee
Dental Care Committee
Review Council Council on Clinical Affairs
Adopted 1989
Revised 1997, 2001, 2005, 2010
Reaffirmed 1993
Purpose The American Academy of Pediatric Dentistry (AAPD) advocates, when indicated, hospitalization and equal access to operating room facilities for dental care of infants, children, adolescents, and persons with special health care needs. The AAPD recognizes that barriers to hospital dental care for patients best treated in that setting need to be addressed.
Method This policy is an update of the previous document revised in 2005. An updated electronic search was performed using the parameters: Terms: “access to care for dental care in hospitals”, “operating room access for dental care”; Fields: all fields; Limits: within the last 10 years.
Background Pediatric dentists often treat patients who present special challenges related to their age, behavior, medical status, developmental disabilities, intellectual limitations, or special needs. Caries, periodontal diseases, and other oral conditions, if left untreated, can lead to pain, infection, and loss of function.1-4 These undesirable outcomes adversely can affect learning, communication, nutrition, and other activities necessary for normal growth and development.5-7 Many medical conditions (eg, hematological, oncological) are compounded by the presence of oral maladies and disease. To address these challenges and meet these treatment needs effectively, pediatric dentists have developed and employ a variety of management techniques, including accessing anesthesia services and/or the provision of dental care in a hospital setting with or without general anesthesia. Hospital dentistry is an integral part of the curriculum of all accredited advanced pediatric dental training
programs. Pediatric dentists are, by virtue of training and experience, qualified to recognize the indications for such an approach and to render such care.8 Pediatric dentists occasionally have experienced difficulty in gaining an equal opportunity to schedule operating room time, postponement/delay of nonemergency dental care, and economic credentialing. Economic credentialing (ie, the use of economic criteria not related to quality of care or professional competency) to determine qualifications for granting/renewing an individual’s clinical staff membership or privileges should be opposed.9 The AAPD and the American Dental Association urge hospital insurance carriers to include hospitalization benefits for dental treatment in both private and public insurance programs so that the resources of a hospital are available to patients whose condition, in the judgment of the dentist, warrants treatment in the operating room.10 The mutual objective of both the governing board and the medical staff is to improve the quality and efficiency of patient care in the hospital. Decisions regarding hospital privileges should be based upon the training, experience, and demonstrated competence of candidates, taking into consideration the availability of facilities and the overall medical needs of the community, the hospital, and especially the patients. Privileges should not be based on numbers of patients admitted to the facility or the patient’s economic or insurance status.11
Policy statement The AAPD shall work with all concerned medical and dental colleagues and organizations to remove barriers to hospital and operating room access for dental care for patients best treated in those settings. The AAPD affirms that hospitals or
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outpatient settings providing surgical treatment should not discriminate against pediatric dental patients requiring care under general anesthesia. Such patients and their care providers need access to these facilities. The dental patient, as with any other patient, should have the right to be seen in a timely manner.
References 1. Acs G, Pretzer S, Foley M, Ng MW. Perceived outcomes and parental satisfaction following dental rehabilitation under general anesthesia. Pediatr Dent 2001;23(5): 419-23. 2. Low W, Tan S, Schwartz S. The effect of severe caries on the quality of life in young children. Pediatr Dent 1999;21(6):325-6. 3. Milano M, Seybold SV. Dental care for special needs patients: A survey of Texas pediatric dentists. J Dent Child 2002;69(2):212-5. 4. American Academy of Pediatric Dentistry. Definition of dental disability. Pediatr Dent 2009;31(special issue):12. 5. American Academy of Pediatric Dentistry. Definition of dental neglect. Pediatr Dent 2009;31(special issue):11. 6. Kay L, Killian C, Lindemeyer R. Special Patients. In: Nowak AJ, Casamassimo PS, eds. Pediatric Dentistry: The Handbook. 3rd ed. Chicago, Ill: American Academy of Pediatric Dentistry; 2007:260.
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7. Thomas CW, Primosch RE. Changes in incremental weight and well-being of children with rampant caries following complete dental rehabilitation. Pediatr Dent 2002;24(2):109-13. 8. American Dental Association Commission on Dental Accreditation. Accreditation standards for advanced specialty education programs in pediatric dentistry: Hospital and adjunctive experiences. Chicago, Ill; 1998:25-9. 9. American Medical Association. Policy H-230.975 Economic credentialing. Adopted 1991; reaffirmed 1998. Available at: “http://www.ama-assn.org/ama/pub/ physician-resources/legal-topics/medical-staff-topics/ economic-credentialing.shtml\”. Accessed Jun 22, 2010. 10. American Dental Association. Current policies, economic credentialing (1993:692). Available at: “http://www.ada. org/sections/about/pdfs/doc_policies.pdf ”. Accessed June 22, 2010. 11. American Medical Association. Policy E-4.07 Staff privileges. Issued July, 1983; updated June, 1994. Available at: “http://www.ama-assn.org/ama/pub/physician-resources/ medical-ethics/code-medical-ethics/opinion407.shtml”. Accessed June 22, 2010.
american academy of pediatric dentistry
Policy on Hospital Staff Membership Originating Committee
Hospital Guidelines for Pediatric Dentistry Ad Hoc Committee Review Council Council on Clinical Affairs
Adopted 1977
Revised 1979, 1991, 1999, 2002, 2005, 2010
Purpose The American Academy of Pediatric Dentistry (AAPD) recognizes that dentists have the opportunity to play a significant role within a hospital. Staff membership is necessary to provide comprehensive, consultative, and/or emergency dental services for infants, children, adolescents, and persons with special health care needs within the hospital setting.
Method This document is an update of the previous policy, revised in 2005. The update included an electronic search using the parameters: Terms: “hospital staff ” AND “dentistry”; Fields: all fields; Limits: within the last 10 years; humans; English.
Background Pediatric dentists contribute in multiple ways as members of the hospital staff. Most commonly, the pediatric dentist can provide comprehensive dental services to patients within an operating room setting. Additionally, the pediatric dentist can provide consultative and emergency services.1 “Team” (eg, cleft lip/palate, hemophilia) evaluations of patients often require dental input, and certain medical protocols (eg, hematopoietic cell transplantation) require an oral examination. Beyond patient services, a pediatric dentist may participate within the hospital’s organizational structure through committee memberships of either clinical or administrative purpose. A pediatric dentist can partner with medical colleagues in self-development through hospital-sponsored continuing medical education. Pediatric dentists seeking hospital staff membership must contact the medical staff office at an area hospital. Board certification or candidacy (previously known as board eligibility) increasingly is being required for hospital staff membership. Following a credentialing process and appointment to a medical staff, a pediatric dentist must accept and fulfill certain responsibilities. Among them are patient care within the limits of approved clinical privileges, possible participation in emergency department on-call rotations, timely completion of medical records, and compliance with the rules and regula-
tions of the medical/dental staff and the policies and procedures of the hospital. Although hospital and medical/dental staffs have some individual latitude, the standards for all hospital services are issued by national commissions such as the Joint Commission on Accreditation of Health Care Organizations (JCAHO).2 Standards for dental services are integrated intimately and inseparably within the overall hospital organizational structure and, therefore, are stringently subject to the standards established by these commissions. Economic credentialing (ie, the use of economic criteria not related to quality of care or professional competency) to determine qualifications for granting/renewing an individual’s clinical staff membership or privileges should be opposed. The mutual objective of both the governing board and the medical staff is to improve the quality and efficiency of patient care in the hospital. Decisions regarding privileges should be based upon the training, experience, and demonstrated competencies of candidates, taking into consideration the availability of facilities and the overall medical needs of the community, the hospital, and especially the patient. Privileges should not be based on numbers of patients admitted to the facility or the patient’s economic or insurance status.4
Policy statement The AAPD: 1. Encourages the participation of pediatric dentists on hospital medical/dental staffs. Beyond having the capability to provide valuable services to patients, the pediatric dentist can be an effective, contributing member to the hospital through consultative services, educational opportunities, leadership initiatives, and committee membership. 2. Recognizes the American Dental Association as a corporate member of the JCAHO and further recognizes the standards for hospital governance, as established by the JCAHO.
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3. Encourages hospital member pediatric dentists to maintain strict adherence to the rules and regulations of the medical/dental staff and the policies and procedures of the hospital. 4. Is opposed to the use of economic credentialing to determine qualifications for granting/renewing a practitioner’s clinical staff membership or privileges.
References 1. Weddell JA, Jones JE. Hospital dental services for children and the use of general anesthesia. In: Dean JA, Avery DR, McDonald RE, eds. McDonald and Avery’s Dentistry for the Child and Adolescent. 9th ed. Maryland Heights, Mo: Mosby Elsevier; 2011:277.
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2. Joint Commission on Accreditation of Health Care Organizations. Medical staff chapter (MS). In: 2009 Comprehensive Accreditation Manual for Hospitals: The Official Handbook. Oakbrook Terrace, Ill: Joint Commission on Accreditation of Health Care Organizations; 2009. 3. American Medical Association. Policy H-230.975 Economic credentialing. Adopted 1991; reaffirmed 1998. Available at: “http://www.ama-assn.org/ama/pub/physicianresources/legal-topics/medical-staff-topics/economiccredentialing.shtml\”. Accessed Jun 22, 2010. 4. American Medical Association. Policy E-4.07 Staff privileges. Issued July, 1983; updated June, 1994. Available at: “http://www.ama-assn.org/ama/pub/physician-resources/ medical-ethics/code-medical-ethics/opinion407.shtml”. Accessed June 22, 2010.
american academy of pediatric dentistry
Policy on Model Dental Benefits for Infants, Children, Adolescents, and Individuals With Special Health Care Needs Originating Councils Council on Dental Benefit Programs/Council on Clinical Affairs
Adopted 2008
Purpose
Policy Statement
The American Academy of Pediatric Dentistry (AAPD) believes that all infants, children, adolescents, and individuals with special health care needs must have access to comprehensive preventive and therapeutic oral health care benefits that contribute to their optimal health and well-being. This policy is intended to assist policy makers, third-party payors, and consumer groups/benefits purchasers to make informed decisions about the appropriateness of oral health care services for these patient populations.
The AAPD encourages all policy makers and third party payors to consult the AAPD in the development of benefit plans that best serve the oral health interests of infants, children, adolescents, and individuals with special health care needs. These model services are predicated on establishment of a dental home, defined as the ongoing relationship between the dentist (ie, the primary oral health care provider) and the patient, inclusive of all aspects of oral health care, starting no later than 12 months of age.14 Expected benefits of care should outweigh potential risks. Value of services is an important consideration, and all stakeholders should recognize that cost-effective care is not necessarily the least expensive treatment. Consistent with AAPD clinical guidelines, the following services should be included in health benefit plans.
Methods This policy is based upon a review of AAPD’s systematicallydeveloped oral health policies and clinical practice guidelines as well as clinical practice guidelines that have been developed by other professional organizations and endorsed by the AAPD.
Background The AAPD, in accordance with its vision and mission, advocates optimal oral health and health care for all infants, children, adolescents, and individuals with special health care needs. Oral diseases are progressive and cumulative; ignoring oral health problems can lead to needless pain and suffering, infection, loss of function, increased health care costs, and life-long consequences in educational, social, and occupational environments. When oral health care is not accessible, the health implications, effects on quality of life, and societal costs are enormous.1 The AAPD’s oral health policies and clinical guidelines2 encourage the highest possible level of care to children and patients with special health care needs. The AAPD also sponsors a national consensus conference or symposium each year on pediatric oral health care and publishes those proceedings in a special issue of Pediatric Dentistry. Those documents,2-6 as well as clinical practice guidelines from other organizations with recognized professional expertise and stature,7-13 serve as the basis for the recommendations below. Such recommendations ideally are evidence based but, in the absence of conclusive evidence, may rely on expert opinion and clinical observations.
A. Preventive services: (1) Initial and periodic examinations of the dentition and oral cavity, including medical and dental histories, furnished in accordance with the attached periodicity schedule15 or when oral screenings by other health care providers indicate a risk of caries or other dental or oral disease; (2) Education for the patient and the patient’s family on measures that promote oral health as part of initial and periodic well-child assessment; (3) Age-appropriate anticipatory guidance and counseling on non-nutritive habits, injury prevention, and tobacco use/ substance abuse; (4) Application of topical fluoride at a frequency based upon caries risk factors; (5) Prescription of dietary fluoride supplement12 based upon a child’s age, caries risk, and fluoride level of the water supply or supplies; (6) Application of pit and fissure sealants based on caries risk factors, not based upon patient age or time lapsed since eruption;16 (7) Dental prophylactic services at a frequency based on caries and periodontal risk factors.
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B. Diagnostic procedures consistent with guidelines developed by organizations with recognized professional expertise and stature, including radiographs in accordance with recommendations by the US Food and Drug Administration and the American Dental Association.9 C. Restorative and endodontic services to relieve pain, resolve infection, restore teeth, and maintain dental function and oral health. This would include interim therapeutic restorations, a beneficial provisional technique in contemporary pediatric restorative dentistry.17 D. Orthodontic services including space maintenance and services to diagnose, prevent, intercept, and treat malocclusions, including management of children with cleft lip or palate and/or congenital or developmental defects. These services include, but are not limited to, initial appliance construction and replacement of appliances as the child grows. E. Dental and oral surgery which shall include sedation/general anesthesia and related medical services that shall be furnished on an inpatient basis when medically necessary. F. Periodontal services to resolve gingivitis, periodontitis, and other periodontal diseases or conditions in children. G. Prosthodontic services, including implants to restore oral function, that are consistent with guidelines developed by organizations with recognized professional expertise and stature. H. Diagnostic and therapeutic services related to the management of orofacial trauma. When the injury involves a primary tooth, benefits should cover complications for the developing succedaneous tooth. I. Drug prescription for preventive services, relief of pain, or treatment of infection. J. Medically necessary services for preventive and therapeutic care in patients with medical, physical, or behavioral conditions. These services include, but are not limited to, the care of hospitalized patients, sedation, and general anesthesia in outpatient or inpatient hospital facilities. K. Behavior guidance services necessary for the provision of optimal therapeutic and preventive oral care to patients with medical, physical, or behavioral conditions. These services may include both pharmacologic and non-pharmacologic management techniques. L. Consultative services provided by a pediatric dentist when the dental home has been established with a general practitioner or when requested by another dental specialist or medical care provider.
References 1. US Dept of Health and Human Services. Oral health
in America: A report of the Surgeon General–Executive
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summary. Rockville, Md: US Dept of Health and Human Services, National Institute of Dental and Craniofacial Research, National Institutes of Health; 2000. Available at: “http://www2.nidcr.nih.gov/sgr/execsumm.htm”. Accessed April 3, 2008. 2. American Academy of Pediatric Dentistry. Reference manual. Pediatric Dentistry Supplement. Chicago, Ill. Available at: “http://www.aapd.org/media/policies.asp”. Accessed June 7, 2008. 3. American Academy of Pediatric Dentistry. Pediatric dentistry restorative consensus conference. Pediatr Dent 2002; 24(5):374-516. 4. American Academy of Pediatric Dentistry. Symposium on behavior guidance. Pediatr Dent 2004;26(2):110-83. 5. American Academy of Pediatric Dentistry. Symposium on the prevention of oral disease in children and adolescents. Pediatr Dent 2006;28(2):96-198. 6. Proceedings of the Joint Symposium on Emerging Science in Pulp Therapy: New Insights into Dilemmas and Controversies. November 2-3, 2007. Chicago, Ill. Pediatr Dent 2008;30(3):190-267. 7. American Association of Endodontists. Guide to Clinical Endodontics. 4th ed. Chicago, Ill. American Association of Endodontists; 2004. 8. A merican Academy of Periodontology. Periodontal diseases of children and adolescents. J Periodontol 2003; 74:1696-704. 9. American Dental Association, US Dept of Health and Human Services. The Selection of Patients for X-Ray Examination: Dental Radiographic Examinations. Rockville, Md.: Food and Drug Administration, 2004; HHS Publication Number 88-8273. Available at: “http://www. ada.org/prof/resources/topics/radiography.asp”. Accessed April 3, 2008. 10. American Cleft Palate-Craniofacial Association. Parameters for evaluation and treatment of patients with cleft lip/ palate or other craniofacial anomalies. Chapel Hill, NC: The Maternal and Child Health Bureau, Title V, Social Security Act, Health Resources and Services Administration, US Public Health Service, DHHS; November 2007. Grant # MCJ-425074. Available at: “http://www.acpacpf.org/teamcare/parameters07rev.pdf ”. Accessed April 1, 2008. 11. National Foundation for Ectodermal Dysplasias. Parameters of oral health care for individuals affected by ectodermal dysplasias. National Foundation for Ectodermal Dysplasias. Mascoutah, Ill. 2003. Available at: “http://www. nfed.org”. Accessed June 7, 2008. 12. American Academy of Pediatrics Committee on Nutrition. Fluoride supplementation for children: Interim policy recommendations. Pediatrics 1995;95(5):777. 13. Casamassimo P, Holt K, eds. Bright Futures in Practice: Oral Health—Pocket Guide. Washington, DC: National Maternal and Child Oral Health Resource Center; 2004. 14. American Academy of Pediatric Dentistry. Policy on the dental home. Pediatr Dent 2008;30(suppl):22-3.
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15. American Academy of Pediatric Dentistry. Guideline on periodicity of examination, preventive dental services, anticipatory guidance, and oral treatment for infants, children, and adolescents. Pediatr Dent 2009;31(special issue):118-25.
16. Feigal RJ, Donly KJ. The use of pit and fissure sealants. Pediatr Dent 2006;28(2):143-50. 17. American Academy of Pediatric Dentistry. Guideline on pediatric restorative dentistry. Pediatr Dent 2008;30 (suppl):163-9.
Recommendations for Pediatric Oral Health Assessment, Preventive Services, and Anticipatory Guidance/Counseling Since each child is unique, these recommendations are designed for the care of children who have no contributing medical conditions and are developing normally. These recommendations will need to be modified for children with special health care needs or if disease or trauma manifests variations from normal. The American Academy of Pediatric Dentistry (AAPD) emphasizes the importance of very early professional intervention and the continuity of care based on the individualized needs of the child. Refer to the text in the Guideline on Periodicity of Examination, Preventive Dental Services, Anticipatory Guidance, and Oral Treatment for Infants, Children, and Adolescents ( www.aapd.org/media/Policies_Guidelines/G_Periodicity.pdf) for supporting information and references.
AGE
American Academy of Pediatric Dentistry
6 TO 12 MONTHS
12 TO 24 MONTHS
2 TO 6 YEARS
6 to 12 YEARS
12 YEARS AND OLDER
1
•
•
•
•
•
Assess oral growth and development
20
•
•
•
•
•
Caries-risk assessment
30
•
•
•
•
•
4
•
•
•
•
•
3,4
•
•
•
•
•
5
•
•
•
•
•
6 80
•
•
•
•
•
7
Parent
Parent
Patient/parent
Patient/parent
Patient
8 10
•
•
•
•
•
9
•
•
•
•
•
12 10
•
•
•
•
•
•
•
• •
•
•
•
•
•
•
•
•
•
Clinical oral examination
Radiographic assessment Prophylaxis and topical fluoride Fluoride supplementation Anticipatory guidance/counseling Oral hygiene counseling Dietary counseling Injury prevention counseling Counseling for nonnutritive habits Counseling for speech/language development Substance abuse counseling
1
Counseling for intraoral/perioral piercing Assessment and treatment of developing malocclusion
1 0
10
Assessment for pit and fissure sealants
11
Assessment and/or removal of third molars
10
•
Transition to adult dental care
•
1 First examination at the eruption of the first tooth and no later than 12 months. Repeat every 6 months or as indicated by child’s risk status/susceptibility to disease. Includes assessment of pathology and injuries. 2 By clinical examination. 3 Must be repeated regularly and frequently to maximize effectiveness. 4 Timing, selection, and frequency determined by child’s history, clinical findings, and susceptibility to oral disease. 5 Consider when systemic fluoride exposure is suboptimal. Up to at least 16 years. 6 Appropriate discussion and counseling should be an integral part of each visit for care. 7 Initially, responsibility of parent; as child matures, jointly with parent; then, when indicated, only child. 8 At every appointment; initially discuss appropriate feeding practices, then the role of refined carbohydrates and frequency of snacking in caries development and childhood obesity. 9 Initially play objects, pacifiers, car seats; when learning to walk; then with sports and routine playing, including the importance of mouthguards. 10 At first, discuss the need for additional sucking: digits vs pacifiers; then the need to wean from the habit before malocclusion or skeletal dysplasia occurs. For school-aged children and adolescent patients, counsel regarding any existing habits such as fingernail biting, clenching, or bruxism. 11 For caries-susceptible primary molars, permanent molars, premolars, and anterior teeth with deep pits and fissures; placed as soon as possible after eruption.
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Policy on Third-party Reimbursement of Medical Fees Related to Sedation/General Anesthesia for Delivery of Oral Health Services Originating Committee
Dental Care Committee
Review Council Council on Clinical Affairs
Adopted 1989
Revised 1995, 2000, 2003, 2006
Reaffirmed 1993
Purpose The American Academy of Pediatric Dentistry (AAPD), to ensure that all children have access to the full range of oral health delivery systems, advocates that if sedation or general anesthesia and related facility fees are payable benefits of a health care plan, these same benefits shall apply for the delivery of oral health services.
Methods This policy is based on a review of the current dental literature related to guidelines for sedation and general anesthesia, as well as issues pertaining to medically-necessary oral health care. A MEDLINE search was conducted using the terms “general anesthesia/sedation costs”, “general anesthesia/sedation reimbursement”, and “general anesthesia/sedation insurance coverage”. Relevant policies and guidelines of the AAPD are included.
Background For some infants, children, adolescents, and persons with special health care needs, treatment under sedation/general anesthesia in a hospital, outpatient facility, or dental office or clinic represents the only appropriate method to deliver necessary oral health care.1,2 The patient’s age, dental needs, disabilities, medical conditions, and/or acute situational anxiety may preclude the patient’s being treated safely in a traditional outpatient setting.3-8 These patients may be denied access to oral health care when insurance companies refuse to provide reimbursement for sedation/general anesthesia and related facility services. Most denials cite the procedure as not medically necessary. This determination appears to be based on arbitrary and inconsistent criteria.9-14 For instance, medical policies often provide 76
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reimbursement for sedation/general anesthesia or facility fees related to myringotomy for a 3-year-old child, but deny these benefits when related to treatment of dental disease and/or infection for the same patient. American Dental Association (ADA) Resolution 1989-546 states that insurance companies should not deny benefits that would otherwise be payable “solely on the basis of the professional degree and licensure of the dentist or physician providing treatment, if that treatment is provided by a legally qualified dentist or physician operating within the scope of his or her training and licensure”.15
Policy statement The AAPD strongly believes that the dentist providing the oral health care for the patient determines the medical necessity of sedation/general anesthesia consistent with accepted guidelines on sedation and general anesthesia.1,7 The AAPD encourages third party payors to: 1. recognize that sedation and/or general anesthesia is necessary to deliver compassionate, quality oral health care to some infants, children, adolescents, and persons with special health care needs; 2. include sedation, general anesthesia, and related facility services as benefits of health insurance without discrimination between the “medical” or “dental” nature of the procedure; 3. end arbitrary and unfair refusal of reimbursement for sedation, general anesthesia, and facility costs related to the delivery of oral health care; 4. regularly consult the AAPD and the ADA with respect to the development of benefit plans that best serve the oral health interests of infants, children, adolescents, and patients with special care needs.16
american academy of pediatric dentistry
References 1. American Academy of Pediatric Dentistry. Definition of medically necessary care. Pediatr Dent 2005;27(suppl):14. 2. American Academy of Pediatrics. Model contractual language for medical necessity for children. Pediatr 2005; 116(1):261-2. 3. Low W, Tan S, Schwartz S. The effect of severe caries on the quality of life in young children. Pediatr Dent 1999;21 (6):325-6. 4. Eidelman E, Faibis S, Peretz B. A comparison of restorations for children with early childhood caries treated under general anesthesia or conscious sedation. Pediatr Dent 2000;22(1):33-8. 5. Acs G, Pretzer S, Foley M, Ng MW. Perceived outcomes and parental satisfaction following dental rehabilitation under general anesthesia. Pediatr Dent 2001;23(5):419-23. 6. Ferretti GA. Guidelines for outpatient general anesthesia to provide comprehensive dental treatment. Dent Clin North Am 1984;28(1):107-20. 7. American Academy of Pediatric Dentistry. Guideline on the elective use of minimal, moderate, and deep sedation and general anesthesia in pediatric dental patients. Pediatr Dent 2005;27(suppl):110-8. 8. Wilson S. Pharmacological management of the pediatric dental patient. Pediatr Dent 2004;26(2):131-6.
9. Patton LL, White BA, Field MJ. State of the evidence base for medically necessary oral health care. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2001;92(3):272-5. 10. Flick WG, Claybold S. Who should determine the medical necessity of dental sedation and general anesthesia? A clinical commentary supported by Illinois patient and practitioner surveys. Anesth Prog 1998;45(2):57-61. 11. Conway TE. What is currently available in terms of medically necessary oral care? Spec Care Dentist 1995;15 (5):187-91. 12. White BA. The costs and consequences of neglected medically necessary oral care [review]. Spec Care Dentist 1995;15(5):180-6. 13. Cameron CA, Litch CS, Liggett M, Heimberg S. National alliance for oral health consensus conference on medically necessary oral health care: Legal issues. Spec Care Dentist 1995;15(5):192-200. 14. Crall J. Behavior management conference Panel II report– Third party payor issues. Pediatr Dent 2004;26(2):171-4. 15. American Dental Association. Transactions of the ADA: Benefits for services by qualified practitioners. Chicago, Ill; 1989:546. 16. American Dental Association. Transactions of the ADA: Standards for dental benefit plans. Chicago, Ill; 2000:458.
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Policy on Third-party Reimbursement for Oral Health Care Services Related to Congenital Orofacial Anomalies Originating Committee
Clinical Affairs Committee Review Council Council on Clinical Affairs
Adopted 1996
Revised 2000, 2003, 2006
Purpose The American Academy of Pediatric Dentistry (AAPD), recognizing that patients with craniofacial anomalies require oral health care as a direct result of their craniofacial condition and that these services are an integral part of the rehabilitative process,1 advocates compensation for provision of comprehensive oral health care services throughout life.
Methods This policy is based on review of current dental and medical literature, as well as policies and guidelines established by stakeholders in the health of infants, children, and adolescents affected by craniofacial anomalies. A MEDLINE search was conducted using the terms “orofacial anomalies”, “congenital anomalies”, “cleft lip/palate”, “third party reimbursement”, and “insurance”. Data is not available to determine the effectiveness of various insurance coverage or limitations of that coverage on children with craniofacial anomalies.
Background Congenital orofacial anomalies that result in malformed or missing teeth, such as but not limited to ectodermal dysplasia sia and cleft defects, can have significant negative functional, esthetic, and psychological effects on individuals and their families.1,2 Young children benefit from esthetic and functional restorative techniques and readily adapt to appliances that replace missing teeth and improve function, appearance, and self-image. During the period of facial and oral growth, appliances require frequent adjustment and have to be remade as the individual grows. These patients often are denied coverage for initial appliance construction and, more frequently, replacement of appliances as the child grows. Third-party payors legally may control the
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coverage of these services by limiting contractual benefits. The distinction between congenital anomalies involving the orofacial complex and those involving other parts of the body is often arbitrary and unfair. For instance, health care policies may provide reimbursement for the necessary prosthesis required for congenitally missing extremities and its replacement as the individual grows, but deny benefits for the initial prosthesis and the necessary periodic replacement for congenitally missing teeth. Third-party payors frequently will refuse to pay for oral health care services even when they clearly are associated with the complete habilitation of the craniofacial condition.3 Furthermore, clerical personnel and professional consultants employed by third-party payors often make benefit determinations based on arbitrary distinction between medical vs dental anomalies, ignoring important functional and medical relationships. Evaluation and care provided for an infant, child, or adolescent by a cleft lip/palate, orofacial, or craniofacial deformities team have been described as the optimal way to coordinate and deliver complex services.3 This approach may provide additional documentation to facilitate “medical necessity” of dental rehabilitation.4
Policy statement The AAPD strongly believes that the dentist providing the oral health care for the patient determines the medical indication and justification for treatment in these cases. The AAPD encourages third party payors to: 1. recognize that malformed and missing teeth and resultant anomalies of facial development seen in orofacial anomalies are congenital defects, just as the congenital absence of other body parts, requiring care over the lifetime of the patient;
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2. include oral health care services related to these facial and dental anomalies as benefits of health insurance without discrimination between the medical and dental nature of the congenital defect. These services, optimally provided by the craniofacial team, include, but are not limited to, initial appliance construction, periodic examinations, and replacement of appliances; 3. end arbitrary and unfair refusal of compensation for oral health care services related to these facial and dental anomalies; 4. regularly consult the AAPD with respect to the development of benefit plans that best serve the oral health interests of infants, children, and adolescents with craniofacial anomalies.
References 1. American Cleft Palate-Craniofacial Association. Parameters for evaluation and treatment of patients with cleft lip/palate or other craniofacial anomalies. Revised ed. Chapel Hill, NC: American Cleft Palate-Craniofacial Association; April 2000. 2. National Foundation for Ectodermal Dysplasias. Parameters of oral health care for individuals affected by ectodermal dysplasias. National Foundation for Ectodermal Dysplasias. Mascoutah, Ill; 2003:9. 3. Strauss RP. The organization and delivery of craniofacial services: The state of the art. Cleft Palate Craniofac J 1999; 36(3):189-95. 4. American Academy of Pediatrics. Policy statement: Model contractual language for medical necessity for children. Pediatr 2005;116(1):261-2.
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Policy on Third-party Reimbursement of Fees Related to Dental Sealants Originating Committee Clinical Affairs Committee
Review Council Council on Clinical Affairs
Adopted 1999
Revised 2000, 2006
Purpose
Recommendations
The American Academy of Pediatric Dentistry (AAPD) recognizes that the placement of sealants and their continued maintenance are scientifically-sound and cost-effective techniques for prevention of pit and fissure caries.
1. The dentition should be evaluated periodically for developmental defects and deep pits and fissures that may contribute to caries risk. Dental sealants should be placed on susceptible teeth and should be evaluated for repair or replacement as part of a periodic dental examination. 2. Third party coverage for sealants should not be based upon a patient’s age. Timing of the eruption of teeth can vary widely. Furthermore, caries risk may increase at any time during a patient’s life. 3. The AAPD shall work with other dental organizations, the insurance industry, and consumer groups to make the advantages of dental sealants understood and to seek reimbursement for fees associated with their placement, maintenance, and repair.
Methods This revision is based upon a review of current dental literature related to dental sealants. A MEDLINE search was conducted using the terms “dental sealants”, “indications”, and “insurance”.
Background According to national estimates, by 17 years of age, 78% of children in the United States have experienced caries.1 As much as 90% of all caries in school-aged children occurs in pits and fissures. The teeth at highest risk by far are permanent first and second molars where fluoride has its least preventive effect on the pits and fissures. Any tooth, including primary teeth and permanent teeth other than molars, may benefit from sealant application due to fissure anatomy and caries risk factors.2,3 Caries risk may increase due to changes in patient habits, oral microflora, or physical condition, and unsealed teeth subsequently might benefit from sealant application.2,3 Current data also show that, although initial sealant retention rates are high, sealant loss does occur.2 It is in the patient’s interest to receive periodic evaluation of sealants for maintenance or replacement. Without recall and maintenance, sealant failure will compound over time, leaving previously sealed surfaces with a caries susceptibility equal to that of surfaces that never were sealed. With appropriate followup care, the success rate of sealants may be 80 to 90%, even after a decade.2 Although sealants are safe and effective, their use continues to be low.4 Sealants are particularly effective in preventing pit and fissure caries and providing cost savings if placed on patients during periods of greatest risk.5,6 However, initial insurance coverage for sealants often is denied, and insurance coverage for repair and/or replacement may be limited.7
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References 1. US Dept of Health and Human Services. Oral Health in America: A Report of the Surgeon General. Rockville, Md: US Dept of Health and Human Services, National Institute of Dental and Craniofacial Research, National Institutes of Health; 2000. 2. Feigal RJ. The use of pit and fissure sealants. Pediatr Dent 2002;24(5):415-22. 3. American Academy of Pediatric Dentistry. Guideline on pediatric restorative dentistry. Pediatr Dent 2005;27 (suppl):122-9. 4. US Dept of Health and Human Services. Healthy people 2010. Rockville, Md: US Dept of Health and Human Services, National Institutes of Health; 2000. 5. Weintraub JA. Pit and fissure sealants in high-caries risk individuals. J Dent Educ 2001;65(10):1084-90. 6. American Dental Association Council on Access, Prevention, and Interprofessional Relations, American Dental Association Council on Scientific Affairs. Dental sealants. J Am Dent Assoc 1997;128(4):485-8. 7. American Dental Association. Statement on preventive coverage in dental benefits plans. Chicago, Ill; 1992:602; 1994:656.
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Policy on the Role of Pediatric Dentists as Both Primary and Specialty Care Providers Originating Council Council on Clinical Affairs
Review Council Council on Clinical Affairs
Adopted 2003
Revised 2008
Purpose The American Academy of Pediatric Dentistry (AAPD) emphasizes that health care providers and other interested third parties must recognize the dual role that pediatric dentists play in the provision of professional oral health care, which includes both primary and specialty care services.
Methods
The AAPD respects the rights of employers to negotiate health care benefits for their employees. Unfortunately, thirdparty payors sometimes do not recognize pediatric dentists as primary care providers. This position restricts access to pediatric dentists for children who have reached a predetermined age.
Policy statement
This statement was based on a review of the accreditation standards for advanced specialty training programs in pediatric dentistry and the AAPD position paper on the role of pediatric dentists as primary and specialty care providers.1,2 A MEDLINE search was conducted using the terms “pediatric dentist”, “pediatric specialist”, “primary care provider”, and “specialty care provider”.
The AAPD recognizes that infants, children, adolescents, and individuals with special health care needs have the right to quality oral healthcare. The AAPD encourages third party payors to recognize pediatric dentists as both primary and specialty oral health care providers and to refrain from age-related restrictions when a parent or referring clinician desires to utilize the services and expertise of a pediatric dentist to establish a dental home or for limited specialized care.
Background
References
“Pediatric dentistry is an age-related specialty that provides both primary and comprehensive preventive and therapeutic oral health needs for infants and children through adolescence, including those with special health care needs.”1 The American Dental Association, the American Academy of General Dentistry, and the AAPD all recognize the pediatric dentist as both a primary care provider and specialty care provider. The dual role of pediatric dentists is similar to that of pediatricians, gynecologists, and internists in medicine. Within the medical profession, clinicians and third-party payors recognize these physicians in a dual role and have designed payment plans to accommodate this situation.
1. American Dental Association Commission on Dental Ac-
creditation. Accreditation standards for advanced specialty education programs in pediatric dentistry. Chicago, Ill; 2000. 2. American Academy of Pediatric Dentistry Council on Dental Benefits Programs. Position paper: The role of pediatric dentists as primary and specialty care providers. Chicago, Ill; 2002.
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Policy on Patient Safety Originating Council
Council on Clinical Affairs Adopted 2008
Purpose The American Academy of Pediatric Dentistry (AAPD) recognizes patient safety as an essential component of quality oral health care for infants, children, adolescents, and those with special health care needs. The AAPD encourages dentists to consider thoughtfully the environment in which they deliver healthcare services and to implement practices that decrease a patient’s risk of injury or harm during the delivery of care. This policy is not intended to duplicate safety recommendations for medical facilities accredited by national commissions such as the Joint Commission on Accreditation of Healthcare Organizations (JCAHO) or those related to workplace safety such as Occupational Safety & Health Administration (OSHA).
Methods This guideline is based on a review of the current dental and medical literature related to patient safety. A MEDLINE literature search was conducted using the terms “patient safety”, “risk management”, “patient’s rights”, and “dentistry”.
Background All health care systems should be designed to promote patient health and protection. Dental practices must be in compliance with federal laws that help protect patients from misuse of personal information [eg, Health Insurance Portability and Accountability Act (HIPAA)]1-4 and potential dangers such as the transmission of disease. State and local laws help regulate potential chemical and environmental hazards (eg, radiation) and facilities (eg, fire prevention systems, emergency exits). Furthermore, state dental practice acts are intended to regulate the competency of and provision of services by dental health professionals. Designing health care systems that focus on preventing errors is critical to assuring patient safety. Some possible sources of error in the dental office are miscommunication, failure to review the patient’s medical history (eg, current drugs and medications), and lack of standardized records, abbreviations, and processes.5 Standardization helps assure clerical and clinical personnel execute their responsibilities in a safe and effective manner. Policy and procedure manuals that describe each facility’s established protocols serve as a valuable training tool for new employees and reinforce a consistent approach for safe, quality patient care. Identifying deviations from such protocols and studying patterns of occurrence can help reduce
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the likelihood of adverse events.6 Reducing clinical errors requires a careful examination of adverse events and root cause analysis of how the event could be avoided in the future. The environment in which dental care is delivered impacts patient safety. In addition to structural issues regulated by state and local laws, other design features should be planned and periodically evaluated for patient safety, especially as they apply to young children. Play structures, games, and toys are possible sources for accidents and infection. Scientific knowledge and technology continually advance, and patterns of care evolve due, in part, to recommendations by organizations with recognized professional expertise and stature. Some recommendations can be based only on suggestive evidence or theoretical rationale (eg, infection control); other concerns of clinical practice remain in flux (eg, materials utilized in restorative dentistry). Consequently, the dental patient would benefit from a practitioner who follows current literature and participates in professional continuing education courses to increase awareness and knowledge of best current practices. The AAPD emphasizes safe, age-appropriate, nonpharmacological or pharmacological behavior guidance techniques for use with pediatric dental patients. It is important to base behavior guidance on each patient’s individual needs with goals of fostering a positive dental attitude, safety, and providing quality dental care.7 Appropriate diagnosis of behavior and safe and effective implementation of advanced behavior guidance techniques (ie, protective stabilization, sedation, general anesthesia) necessitate knowledge and experience that generally are beyond the core knowledge that students receive during predoctoral education.7
Policy Statement To promote patient health and protection, the AAPD recommends: 1. Professional continuing education by all licensed dental professionals to maintain familiarity with current regulations, technology, and clinical practices. 2. Compliance with federal laws such as HIPAA to protect patients against misuse of information identifiable to them.1 3. Compliance and recognition of the importance of infection control policies, procedures, and practices in dental health care settings in order to prevent disease transmission from patient to care provider, from care provider to patient, and from patient to patient.2-4
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4. Routine inspection of physical facility in regards to patient safety. This would include development of office emergency and fire safety protocols and routine inspection and maintenance of clinical equipment. 5. Recognition that informed consent by the parent is essential in the delivery of health care and effective relationship/ communication practices can help avoid problems and adverse events.8 The parent should be encouraged to be an active participant in the child’s care. 6. Accuracy of patient identification with the use of at least 2 patient identifiers, such as name and date of birth, when providing care, treatment, or services.5,9 7. An accurate and complete patient chart that can be interpreted by a knowledgeable third party.10 Standardizing abbreviations, acronyms, and symbols throughout the record is recommended. 8. An accurate, comprehensive, and up-to-date medical/ dental history including medications and allergy list to ensure patient safety during each visit.10 Ongoing communication with health care providers, both medical and dental, who manage the child’s health helps ensure comprehensive, coordinated care of each patient. 9. Appropriate staffing and supervision of patients treated in the dental office. 10. Adherence to AAPD recommendations on behavior guidance, especially as they pertain to use of advanced behavior guidance techniques (ie, protective stabilization, sedation, general anesthesia).7 11. Standardization and consistency of processes within the practice. A policies and procedures manual, with ongoing review and revision, could help increase employee awareness and decrease the likelihood of untoward events. Dentists should emphasize procedural protocols that protect the patient’s airway (eg, rubber dam isolation)11 and minimize opportunity for injury during delivery of care (eg, protective eyewear). 12. Minimizing exposure to nitrous oxide by maintaining the lowest practical levels in the dental environment. This would include routine inspection and maintenance of nitrous oxide delivery equipment as well as adherence to clinical guidelines for patient selection and delivery of inhalation agents.12 13. Minimizing radiation exposure through adherence to ALARA (as low as reasonably achievable) principle, equipment inspection and maintenance, and patient selection criteria.13 14. All facilities performing sedation for diagnostic and therapeutic procedures to maintain records that track adverse events. Such events then can be examined for assessment of risk reduction and improvement in patient safety.14 15. Dentists who utilize in-office anesthesia care providers take all necessary measures to minimize risk to patients. Prior to delivery of sedation/general anesthesia, appropriate documentation shall address rationale for sedation/general
anesthesia, informed consent, instructions to parent, dietary precautions, preoperative health evaluation, and any prescriptions along with the instructions given for their use. The dentist and anesthesia care provider must communicate during treatment to share concerns about the airway or other details of patient safety.15 16. Ongoing quality improvement strategies. Routine assessment of risk, adverse events, and mistakes with a plan for reduction and improvement in patient safety and satisfaction.5
References 1. US Dept of Health and Human Services. Medical Privacy National Standards to Protect the Privacy of Personal Health Information: Available at: “http://www.hhs.gov/ocr/hipaa/”. Accessed July 30, 2007. 2. World Health Organization. WHO Guidelines On Hand Hygiene In Health Care (advanced draft): A Summary. Available at: “http://www.who.int/patientsafety/events/05/ HH_en.pdf ”. Accessed July 30, 2007. 3. Boyce JM, Pittet D. Guideline for Hand Hygiene in HealthCare Settings. Recommendations of the Healthcare Infection Control Practices Advisory Committee and the HICPAC/ SHEA/APIC/IDSA Hand Hygiene Task Force. Available at: “http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5116a1. htm”. Accessed July 30, 2007. 4. American Academy of Pediatric Dentistry. Policy on Infection control. Pediatr Dent 2007;29(suppl):76. 5. Joint Commission on Accreditation of Health Care Organizations. 2008 National Patient Safety Goals Ambulatory Care Program. Available at: “http://www.jointcommission. org/PatientSafety/NationalPatientSafetyGoals/”. Accessed July 30, 2007. 6. American Academy of Pediatrics. Principles of Patient Safety in Pediatrics. Available at: “http://aappolicy.aap publications.org/cgi/content/full/pediatrics;107/6/ 1473”. Accessed July 30, 2007. 7. American Academy of Pediatric Dentistry. Guideline on behavior guidance for the pediatric dental patient. Pediatr Dent 2008;30(suppl):125-33. 8. American Academy of Pediatric Dentistry. Guideline on informed consent. Pediatr Dent 2008;30(suppl):234-5. 9. Joint Commission on Accreditation of Health Care Organizations. Implementation Expectations for the Universal Protocol for Preventing Wrong Site, Wrong Procedure and Wrong Person Surgery. Available at: “http://www.joint commission.org/NR/rdonlyres/DEC4A816-ED52-4C04AF8C-FEBA74A732EA/0/up_guidelines.pdf ”. Accessed July 30, 2007. 10. American Academy of Pediatric Dentistry. Guideline on record-keeping. Pediatr Dent 2007;29(suppl):211-8. 11. American Academy of Pediatric Dentistry. Guideline on pediatric restorative dentistry. Pediatr Dent 2008;30 (suppl):163-9.
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12. American Academy of Pediatric Dentistry. Policy on minimizing occupational health hazards associated with nitrous oxide. Pediatr Dent 2008;30(suppl):64-5. 13. American Dental Association, US Dept of Health and Human Services. The Selection of Patients for X-Ray Examination: Dental Radiographic Examinations. Rockville, Md: Food and Drug Administration, 2004; HHS Publication No. 88-8273. Available at: “http://www. ada.org/prof/resources/topics/radiography.asp”. Accessed August 8, 2008.
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14. American Academy of Pediatric Dentistry, American Academy of Pediatrics. Guideline for monitoring and management of pediatric patients during and after sedation for diagnostic and therapeutic procedures. Pediatr Dent 2007;29(suppl):134-51. 15. American Academy of Pediatric Dentistry. Guideline on use of anesthesia personnel in the administration of officebased deep sedation/general anesthesia to the pediatric dental patient. Pediatr Dent 2007;29(suppl):152-4.
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Policy on the Ethical Responsibility to Treat or Refer Originating Council
Council on Clinical Affairs Review Council Council on Clinical Affairs
Adopted 2003
Reaffirmed 2008
Purpose The American Academy of Pediatric Dentistry (AAPD) believes that all infants, children, adolescents, and individuals with special health care needs are entitled to oral health care that meets the treatment and ethical standards set by our specialty. If a dentist is unable to provide or fails to offer treatment for a diagnosed dental disease or condition, he or she has an ethical responsibility to refer the patient to a specific practitioner capable of providing the necessary care.
Methods Documents relating to principles of ethics of dental and medical organizations were reviewed. A MEDLINE search using the terms “ethics” and “dentistry” was performed. Experts on dental and medical ethics were consulted.
Background Dentists have an obligation to act in an ethical manner in the care of patients. Commonly accepted virtues of ethics include autonomy, beneficence, nonmaleficence, and justice.1,2 Autonomy reflects the patient’s or, if the patient is a minor, the parent’s or guardian’s right to be involved in treatment decisions. The caregiver must be informed of the problem and that treatment is recommended. Beneficence indicates the dentist has the obligation to act for the benefit of the patient in a timely manner, even when there may be conflicts with the dentist’s personal self interests. Nonmaleficence dictates that the dentist’s care does not result in harm to the patient. In situations where a dentist is not able to meet the patient’s needs, referral to a practitioner capable of providing the needed care is indicated. Justice expresses that the dentist should deal fairly with patients, colleagues, and the public.
A patient may suffer progression of his/her oral disease if treatment is not provided because of age, behavior, inability to cooperate, disability, or medical status. Postponement or denial of care can result in unnecessary pain, discomfort, increased treatment needs and costs, unfavorable treatment experiences, and diminished oral health outcomes.
Policy statement Infants, children, and adolescents, including those with special health care needs, have a right to dental care. The AAPD believes it is unethical for a dentist to ignore a disease or condition because of the patient’s age, behavior, or disabilities. Dentists have an ethical obligation to provide therapy for patients with oral disease or refer for treatment patients whose needs are beyond the skills of the practitioner.
References 1. American Dental Association. Principles of Ethics and Code of Professional Conduct. With official advisory opinions revised to January 2005. Available at: “http://www.ada.org/ prof/prac/law/code/index.asp”. Accessed July 15, 2007. 2. American College of Dentists. Ethics Handbook for Dentists. An Introduction to Ethics, Professionalism, and Ethical Decision Making. Gaithersburg, Md: American College of Dentists; 2004.
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Policy on Second Opinions for Pediatric Oral Health Care Originating Council
Council on Clinical Affairs Adopted 2010
Purpose The American Academy of Pediatric Dentistry (AAPD) recognizes that second opinions are one avenue for additional information regarding health care issues. Parents frequently seek additional information and/or other opinions in order to address their child’s health care needs and make informed decisions. This policy is intended to provide guidance to the pediatric dentist by addressing what should be obtained and documented when providing a second opinion, as well as an understanding of the ethical and legal obligations involved in the process.
Methods This policy is based on a review of the current dental and medical literature related to the concept of second opinion in dentistry and medicine. An electronic search and a MEDLINE search was conducted using the search terms: “second opinion”, “medical second opinion”, and “dental second opinion”. Documents relating to principles of ethics of dental and medical organizations also were reviewed.
Background Patients today are more informed about their medical and dental problems and treatment options and are playing an active role in decision making with their doctors. Medical and dental knowledge and available treatment options are evolving at a rapid pace, and it is becoming increasingly difficult for health care providers to be fully aware of all the latest advances and information. As a result, patients and health care providers are seeking second opinions so that more informed decisions based on the risks and benefits can be made regarding the patient’s health care. For minor health problems, second opinions usually are unnecessary. However, a second opinion is recommended if the patient disagrees with or questions the diagnosis or the treatment plan of the health care provider, has multiple medical problems, or is diagnosed with a life-threatening disease such as cancer. Second opinions also are recommended when there is no improvement in the patient’s condition, when there is a communication barrier between the patient and the provider and, additionally, when extensive oral care needs or high cost may make treatment prohibitive. For health care practitioners, a second opinion or referral may be warranted if they
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are unsure of the diagnosis or the diagnosis/treatment is beyond the scope of their expertise. Furthermore, a second opinion may be necessary when required by a third party payor. There is a debate among health care providers about whether to provide a patient with a “blind” second opinion (ie, when medical/dental records, test results and first provider’s opinion are not made available to the second provider) or if the patient’s diagnostic information and diagnosis should be shared with the provider giving the second opinion. The advantage of the “blind” second opinion is that it cannot be influenced by previous information. The provider will develop his/her own unbiased opinion. The disadvantage is that the provider performing the second opinion may have to repeat diagnostic tests and the patient will incur additional costs. The second provider may not be able to explain to the patient why his/her opinion is different without knowing the patient’s previous history and the basis of the first provider’s opinion. A third option would be to provide test results, radiographs, and other information without the first doctor’s written diagnosis and treatment recommendations. This would allow for an unbiased opinion without having the patient incur unnecessary charges or radiation exposure from repeated radiographs. When presented with requests for second opinions, practitioners should consider the legal implications of such requests. Health care providers rendering second opinions could be unwarily involved in litigation, either on behalf of the patient or in defending themselves against other practitioners, as a result of the consult. The fact that one is the second or third professional consulted does not mean that the provider is exempt from liability.1 A dissatisfied patient could file a lawsuit naming not only the treating doctor, but also the doctor rendering the second opinion as defendants. In addition, a colleague who believes his or her professional reputation has been damaged by statements made to a patient during a consultation could file a lawsuit for defamation of character. Patients should be advised of their health status without disparaging comments about their prior treatment or previous provider.
Policy statement The AAPD recognizes that: 1. A patient has a right to a second opinion. A provider who is trained and experienced in diagnosing and treating the condition should provide the second
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opinion. Internet sites or a telephone conversation cannot be relied upon and should not constitute a second opinion.2 2. A health care practitioner has the right to request a second opinion from one or multiple practitioners/ specialists as deemed necessary to facilitate the optimal clinical outcome.3 3. Educating the patient regarding the diagnosis and available treatment options, including their risks and benefits, should be the goal of a second opinion consultation. Health care providers may disagree on the best treatment for an individual patient. Any opinion should be rendered only on careful consideration of all the facts and with due attention given to current and previous states of the patient. Instances of gross or continual faulty diagnosis or treatment by other providers may require that the provider be reported to an appropriate reviewing agency as determined by the local component or constituent dental society.3 4. A provider has the ethical obligation on request of either the patient or the patient’s new provider to furnish records, including radiographs or copies of them. These may be beneficial for the future treatment of that patient.3 Health Insurance Portability and Accountability Act (HIPAA) privacy rules4 and state laws apply to all exchanges of health care information. 5. Second opinions may be mandatory by third party payors. The provider should be independent and the opinion should be based on best outcomes for the patient and not financial incentives.
6. Most second opinions are voluntary. It is the responsibility of the patient to check with his/her insurance carrier for specific policies and benefits regarding coverage of second opinions. 7. When presented with requests for second opinions, practitioners should consider the legal implications of such request. Patients should be fully advised of their health status without disparaging comments about their prior treatment or previous provider.
References 1. Machen DE. Legal aspects of orthodontic practice: Risk management concepts. Am J Orthod Dentofacial Orthop 1990;93(3)269-70. 2. US Dept of Health and Human Services, Office on Women’s Health. How to get a second opinion. Available at: “http://www.womenshealth.gov/tools/secondopinion. cfm”. Accessed July 8, 2010. 3. American Dental Association. Principles of ethics and code of professional conduct. With official advisory opinions revised to January, 2010. Available at: “http:// www.ada.org/sections/about/pdfs/ada_code.pdf ”. Accessed July 8, 2010. 4. US Dept of Health and Human Services. Health Information Privacy. Available at: “http://www.hhs.gov/ocr/ privacy/”. Accessed July 8, 2010.
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Policy on a Patient’s Bill of Rights and Responsibilities Originating Council
Council on Clinical Affairs Adopted 2009
Purpose The American Academy of Pediatric Dentistry (AAPD) recognizes that pediatric oral health care should be rendered under conditions that are acceptable to both patient and dentist. The expectation is that oral health care providers, their staff, and patients/parents will support this policy, thereby enhancing patient care.
Methods This policy is based on a systematic literature search of the MEDLINE/Pubmed electronic database using the following parameters: Terms: “patient freedoms”, “patient’s Bill of Rights”, “Bill of Rights”, “Consumer Bill of Rights”; Fields: all fields; Limits: within the last 10 years and English. Eighty-one articles met these criteria. Papers for review were chosen from this list and from the references within selected articles. Documents of health care and public policy organizations relating to the concept of patient rights and responsibilities also were reviewed.1-3
Background AAPD is the leader in representing the oral health interests of infants, children, adolescents, and persons with special health care needs1. Effective oral health care requires collaboration between patients/parents and pediatric dentists and other health care professionals. Open and honest communication, respect for personal and professional values, and sensitivity to differences are integral to optimal patient care. The delivery of contemporary pediatric oral health care many times can be confusing to parents. It is normal for parents whose children have planned oral health care treatment to have a set of expectations about the proposed care. Likewise, it is desirable for these parents to have a clear understanding of their responsibilities in the delivery of care to their children. A Patient’s Bill of Rights is a statement of the rights to which patients are entitled as recipients of medical/dental care. These rights can be exercised on the patient’s behalf by a parent or legal guardian if the patient is a minor, lacks decisionmaking capacity, or is legally incompetent. It articulates the positive rights that health care providers and facilities should provide patients, thereby providing information, offering fair treatment, and granting them autonomy over medical decisions. The collaborative nature of health care requires that patients, or their families/surrogates, participate in their care.
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The effectiveness of care and patient satisfaction with the course of treatment depend, in part, on the patient fulfilling certain responsibilities. As such, the American Academy of Pediatric Dentistry proposes this Policy on a Patient’s Bill of Rights and Responsibilities in the planning and delivery of pediatric oral health care. The AAPD encourages oral health care providers to tailor this Bill of Rights and Responsibilities to their patient community by translating and/or simplifying it as may be necessary to ensure that patients and their families understand their rights and responsibilities.
Bill of Rights These rights can be exercised on the patient’s behalf by a parent or legal guardian if the patient is a minor, lacks decision-making capacity, or is legally incompetent. The patient has the right to: 1. a dental home that provides comprehensive, considerate, and respectful care. 2. have oral health diagnoses made by a dentist. 3. a choice of oral health care provider. The parent has a right to designate a pediatric dentist as a primary oral health care provider for the child. 4. participate fully in all the decisions related to his/her care. 5. receive accurate, relevant, current, and easilyunderstood information concerning diagnosis, treatment, and prognosis. The patient is entitled to the opportunity to discuss and request information related to the specific procedures and/or treatments, the risks involved, and the medically reasonable alternatives and their accompanying risks and benefits. Life threatening emergency care could be an exception. 6. make decisions about the plan of care prior to and during the course of treatment, to refuse a recommended treatment or plan of care to the extent permitted by law, and to be informed of the health consequences of this action. In case of such refusal, the patient is entitled to other appropriate care and services that the pediatric dentist offers or to transfer to another dentist. 7. consent to or decline to participate in proposed research studies affecting care and treatment or requiring direct patient involvement and to have those
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8. 9. 10. 11.
12.
13. 14.
15.
16.
studies explained fully prior to consent. A patient who declines to participate in research is entitled to the most effective care that the pediatric dentist can otherwise provide. expect reasonable continuity of care. emergency care for acute dental trauma and odontogenic infections, as needed. know the identity, education, and training of the providers involved in his/her care, as well as when those involved are students, residents, or other trainees. know the immediate and long-term financial implications of treatment choices, insofar as they are known. The patient has the right to be informed of the charges for services and available payment methods. be informed of the provider’s policies and practices that relate to patient care, treatment, and responsibilities. The patient has the right to be informed of available resources for resolving disputes, grievances, and conflicts, such as ethics committees, patient representatives, or other mechanisms available in an organization. every consideration of privacy. Case discussion, consultation, examination, and treatment should be conducted so as to protect each patient’s privacy. expect that all communications and records pertaining to his/her care will be treated as confidential, except in cases such as suspected abuse and public health hazards when reporting is permitted or required by law. The patient has the right to expect that the provider will emphasize the confidentiality of information released to other parties entitled to review this information. review the records pertaining to his/her medical care and to have the information explained or interpreted as necessary, except when restricted by law. The patient has the right to request amendments to his/her record. ask and be informed of the existence of business relationships among institutions, other health care providers, or payors that may influence the patient’s treatment and care.
Bill of Responsibilities These responsibilities can be exercised on the patient’s behalf by a parent or legal guardian if the patient is a minor, lacks decision-making capacity, or is legally incompetent. 1. The patient is responsible for providing, to the best of his/her knowledge, accurate and complete information about past illnesses, hospitalizations, medications, and other matters related to his/her health status. 2. The patient must take responsibility for requesting additional information or clarification about his/her health status or treatment when he/she does not fully understand information and instructions. 3. The patient is responsible for his/her actions if he/she refuses treatment or does not follow the instructions of the provider. It is the patient’s responsibility to inform dentists and other caregivers of anticipated problems in following prescribed treatment, including follow-up treatment instructions. 4. The patient has a responsibility to keep appointments and when unable to do so, to notify the dental office as soon as possible. 5. The patient is responsible for being considerate of the rights of other patients and health care workers and for not interfering with the general functioning of the facility. 6. The patient is responsible for providing accurate insurance information and for accepting the financial obligations associated with the services rendered.
References 1. American Academy of Pediatric Dentistry. AAPD Vision Statement. Pediatr Dent 2008;29(suppl):3. 2. American Hospital Association. A Patient’s Bill of Rights. AHA 1992. Catalog no. 157759. 3. President’s Advisory Commission on Consumer Protection and Quality in the Health Care Industry. Consumer Bill of Rights and Responsibilities, 1998. Washington, DC. July 17, 1998. Available at: “http://www.hcqualitycommission. gov/final/append_a.html”. Accessed June 22, 2009.
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Policy on Stem Cells Originating Council
Council on Clinical Affairs Adopted 2008
Stem cells are pluripotential cells that can divide and multiply for an extended period of time, differentiating into a diverse range of specialized cell types and tissues. Adult mesenchymal stem cells, of which dental stem cells are a subset, display inherent plasticity, the ability to proliferate and differentiate into many cell lines. The most familiar application of adult stem cell therapy is bone marrow transplantation to treat hematopoietic cancers, metabolic disorders, and congenital immunodeficiency syndromes. Stem cell therapy is undergoing clinical testing for other conditions such as Parkinson’s disease, diabetes, and brain trauma/spinal cord injuries. Suggested applications related to oral health care have included healing and regeneration of dental and periodontal tissues as well as craniofacial structures (eg, repair of cleft lip/palate). Parents may elect to preserve umbilical cord blood of their child for future harvesting of stem cells if autologous regenerative
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therapies are indicated. Pulpal tissue of primary teeth and surgically removed third molars may serve as a source of adult mesenchymal stem cells. While sources of dental stem cells are readily accessible, those cells must be secured and stored properly to maintain the potential to proliferate and differentiate. The public is increasingly aware of this emerging science, and more parents are expressing interest in harvesting/banking dental stem cells. The American Academy of Pediatric Dentistry recognizes the emerging field of regenerative medicine and encourages dentists to follow future evidence-based literature in order to educate parents about the collection, storage, viability, and use of dental stem cells with respect to autologous regenerative therapies. As the technology continues to evolve, the process of procurement of dental stems cells should be accomplished only with deliberate integrity and appropriate informed consent to assure the highest ethical standards and quality of outcomes.
american academy of pediatric dentistry
Policy on Infection Control Originating Committee Clinical Affairs Committee - Infectious Disease Control Subcommittee
Review Council
Council on Clinical Affairs Adopted 1989
Revised 1993, 2001, 2004, 2009
The American Academy of Pediatric Dentistry (AAPD) recognizes the importance of infection control policies, procedures, and practices in dental health care settings in order to prevent disease transmission from patient to care provider, from care provider to patient, and from patient to patient. The AAPD acknowledges Guidelines for Infection Control in the Dental Health-Care Setting—20031 and Guidelines for Disinfection and Sterilization in Healthcare Facilities—20082 as in-depth reviews of infection control measures for dental settings and supports the strategies therein. Aware that some recommendations are based only on suggestive evidence or theoretical rationale, and because many concerns regarding infection control in the dental setting remain unresolved, the AAPD
encourages dental practitioners to follow current literature and consider carefully infection control measures in their practices so as to minimize the risk of disease transmission.
Reference 1. Kohn WG, Collins AS, Cleveland JL, et al. CDC Guidelines for infection control in dental health-care settings— 2003. MMWR Recomm Rep 2003;52:(RR-17):1-61. 2. Rutula WA, Weber DJ, Healthcare Infection Control Practices Advisory Committee. CDC Guidelines for disinfection and sterilization in healthcare facilities—2008. Available at: “http://www.cdc.gov/ncidod/dhqp/pdf/ guidelines/Disinfection_Nov_2008.pdf ”. Accessed January 19, 2009.
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Guideline on Periodicity of Examination, Preventive Dental Services, Anticipatory Guidance/Counseling, and Oral Treatment for Infants, Children, and Adolescents Originating Committee
Clinical Affairs Committee Review Council Council on Clinical Affairs
Adopted 1991
Revised 1992, 1996, 2000, 2003, 2007, 2009
Purpose The American Academy of Pediatric Dentistry (AAPD) intends this guideline to help practitioners make clinical decisions concerning preventive oral health interventions, including anticipatory guidance and preventive counseling, for infants, children, and adolescents.
Methods This guideline is a compilation of related policies and guidelines developed by the AAPD, in addition to pediatric oral health literature and national reports and recommendations. The related policies and guidelines provide additional references for individual recommendations.
Background Professional care is necessary to maintain oral health.1 The AAPD emphasizes the importance of initiating professional oral health intervention in infancy and continuing through adolescence and beyond.1,2 The periodicity of professional oral health intervention and services is based on a patient’s individual needs and risk indicators.3,4 Each age group has distinct developmental needs to be addressed at specific intervals as part of a comprehensive evaluation.5-7 Continuity of care is based on the assessed needs of the individual patient and assures appropriate management of all oral conditions, dental disease, and injuries.8-10 The early dental visit to establish a dental home provides a foundation upon which a lifetime of preventive education and oral health care can be built.11 Anticipatory guidance and counseling are essential components of the dental visit.5,7,11-18
Recommendations This guideline addresses periodicity and general principles of examination, preventive dental services, anticipatory guidance/ counseling, and oral treatment for children who have no
contributory medical conditions and are developing normally. An accurate, comprehensive, and up-to-date medical history is necessary for correct diagnosis and effective treatment planning. Recommendations may be modified to meet the unique requirements of patients with special needs. Clinical oral examination The first examination is recommended at the time of the eruption of the first tooth and no later than 12 months of age.11 The developing dentition and occlusion should be monitored throughout eruption at regular clinical examinations. Unrecognized dental disease can result in exacerbated problems which lead to more extensive and expensive care,19-21 whereas early detection and management of oral conditions can improve a child’s oral health, general health and well-being, and school readiness.12,22-27 Early diagnosis of developing malocclusions may allow for timely therapeutic intervention.28 Components of a comprehensive oral examination include assessment of: • General health/growth • Pain • Extraoral soft tissue • Temporomandibular joint • Intraoral soft tissue • Oral hygiene and periodontal health • Intraoral hard tissue • The developing occlusion • Caries risk • Behavior of child Based upon the visual examination, the dentist may employ additional diagnostic aids (eg, radiographs, photographs, pulp testing, laboratory tests, study casts). The most common interval of examination is 6 months; however, some patients may require examination and preventive
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services at more frequent intervals, based upon historical, clinical, and radiographic findings.3,29-34 Caries and its sequelae are among the most prevalent health problems facing infants, children, and adolescents in America.1 Caries is cumulative and progressive and, in the primary dentition, is highly predictive of caries occurring in the permanent dentition.35,36 Reevaluation and reinforcement of preventive activities contribute to improved instruction for the caregiver of the child or adolescent, continuity of evaluation of the patient’s health status, and repetitive exposure to dental procedures, potentially allaying anxiety and fear for the apprehensive child or adolescent. Caries-risk assessment Risk assessment is the key element of contemporary preventive care for infants, children, adolescents, and persons with special health care needs. Its goal is to prevent disease by identifying and minimizing causative factors (eg, microbial burden, dietary habits, plaque accumulation) and optimizing protective factors (eg, fluoride exposure, oral hygiene, sealants).37 A caries-risk assessment tool (CAT) simplifies and clarifies the process.13 Sufficient evidence demonstrates certain groups of children at greater risk for development of early childhood caries (ECC) would benefit from infant oral health care.12,22,38,39 Infants and young children have unique caries-risk factors such as ongoing establishment of oral flora and host defense systems, susceptibility of newly erupted teeth, and development of dietary habits. Children are most likely to develop caries if mutans streptococci are acquired at an early age.39,40 The characteristics of ECC and the availability of preventive methods support anticipatory guidance/counseling as an important strategy in addressing this significant pediatric health problem. ECC can be a costly, devastating disease with lasting detrimental effects on the dentition and systemic health.12,19-27 Adolescence can be a time of heightened caries activity due to an increased intake of cariogenic substances and inattention to oral hygiene procedures.41,42 Risk assessment can assure preventive care is tailored to each individual’s needs and direct resources to those for whom preventive interventions provide the greatest benefit. Because a child’s risk for developing dental disease can change over time due to changes in habits (eg, diet, home care), oral microflora, or physical condition, risk assessment must be repeated regularly and frequently to maximize effectiveness. Prophylaxis and topical fluoride treatment The interval for frequency of professional preventive services is based upon assessed risk for caries and periodontal disease. Gingivitis is nearly universal in children and adolescents43; it usually responds to thorough removal of bacterial deposits and improved oral hygiene.43,44 Self-administered plaque control programs without periodic professional reinforcement are inconsistent in providing long-term inhibition of gingivitis.44 Many patients lack the skill or motivation to become and remain plaque-free for a significant time.44 Hormonal fluctuations, including those occurring during the onset of puberty, can modify the gingival inflammatory response to dental plaque.43
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Children can develop any of the several forms of periodontitis, with aggressive periodontitis occurring more commonly in children and adolescents than adults.43 Caries risk may change quickly during active dental eruption phases. Newly erupted teeth may be at higher risk of developing caries, especially during the post-eruption maturation process. Children who exhibit higher risk of developing caries would benefit from recall appointments at greater frequency than every 6 months. This allows increased professional fluoride therapy application, microbial monitoring, antimicrobial therapy reapplication, and reevaluating behavioral changes for effectiveness.3,45,46 An individualized preventive plan increases the probability of good oral health by demonstrating proper oral hygiene methods/techniques and removing plaque, stain, calculus47, and the factors that influence their build-up.48-50 Professional topical fluoride treatments should be based on caries risk assessment.13,14,51-53 A pumice prophylaxis is not an essential prerequisite to this treatment.54 Appropriate precautionary measures should be taken to prevent swallowing of any professionally-applied topical fluoride. Children at moderate caries risk should receive a professional fluoride treatment at least every 6 months; those with high caries risk should receive greater frequency of professional fluoride applications (eg, every 3-6 months).52,55,56,57-62 Ideally, this would occur as part of a comprehensive preventive program in a dental home.11 Fluoride supplementation Fluoride contributes to the prevention, inhibition, and reversal of caries.53,62,63 The AAPD encourages optimal fluoride exposure for every child, recognizing fluoride in the community water supplies as the most beneficial and inexpensive preventive intervention. Fluoride supplementation should be considered when fluoride exposure is not optimal.62 Supplementation should be in accordance with the guidelines jointly recommended by the AAPD62, the American Academy of Pediatrics63, and the American Dental Association (ADA)64, and endorsed by the Centers for Disease Control and Prevention.14 Anticipatory guidance/counseling Anticipatory guidance is the process of providing practical, developmentally-appropriate information about children’s health to prepare parents for the significant physical, emotional, and psychological milestones.65 Appropriate discussion and counseling should be an integral part of each visit. Topics to be included are oral hygiene and dietary habits, injury prevention, nonnutritive habits, substance abuse, intraoral/perioral piercing, and speech/language development. Oral hygiene counseling involves the parent and patient. Initially, oral hygiene is the responsibility of the parent. As the child develops, home care is performed jointly by parent and child. When a child demonstrates the understanding and ability to perform personal hygiene techniques, the health care professional should counsel the child. The effectiveness of home care should be monitored at every visit and includes a discussion on the consistency of daily preventive activities.3
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High-risk dietary practices appear to be established early, probably by 12 months of age, and are maintained throughout early childhood.66.67 Frequent bottle feeding at night, breastfeeding on demand, and extended and repetitive use of a no-spill training cup are associated with, but not consistently implicated in, ECC.68 The role of carbohydrates in caries initiation is unequivocal. Acids in carbonated beverages can have a deleterious effect (ie, erosion) on enamel. Excess consumption of carbohydrates, fats, and sodium contribute to poor systemic health. Dietary analysis and the role of dietary choices on oral health, malnutrition, and obesity should be addressed through nutritional and preventive oral health counseling at periodic visits.15 The US Department of Agriculture’s Food Pyramid69 and Center for Disease Control and Prevention/National Center for Health Statistics’ Growth Charts70 provide guidance for parents and their children and promote better understanding of the relationship between healthy diet and development. Facial trauma that results in fractured, displaced, or lost teeth can have significant negative functional, esthetic, and psychological effects on children.71 Practitioners should provide age-appropriate injury prevention counseling for orofacial trauma.16,17 Initially, discussions would include play objects, pacifiers, car seats, and electrical cords. As motor coordination develops, the parent/patient should be counseled on additional safety and preventive measures, including mouthguards for sporting activities. The greatest incidence of trauma to the primary dentition occurs at 2 to 3 years of age, a time of increased mobility and developing coordination. 72 The most common injuries to permanent teeth occur secondary to falls, followed by traffic accidents, violence, and sports.73-76 Dental injuries could have improved outcomes if the public were aware of first-aid measures and the need to seek immediate treatment. Nonnutritive oral habits (eg, digital and pacifier habits, bruxism, abnormal tongue thrusts) may apply forces to teeth and dentoalveolar structures.18 Although early use of pacifiers and digit sucking are considered normal, habits of sufficient frequency, intensity, and duration can contribute to deleterious changes in occlusion and facial development. It is important to discuss the need for early additional sucking, then the need to wean from the habits before malocclusion or skeletal dysplasias occur. Early dental visits provide an opportunity to encourage parents to help their children stop sucking habits by age 3 years or younger. For school-aged children and adolescent patients, counseling regarding any existing habits (eg, fingernail biting, clenching, bruxism) is appropriate.18 Speech and language is an integral component of a child’s early development.77 Deficiencies and abnormal delays in speech and language production can be recognized early and referral made to address the concerns appropriately. Communication and coordination of appliance therapy with a speech and language professional can assist in the timely treatment of these disorders. Smoking and smokeless tobacco use almost always are initiated and established in adolescence.78-80 During this time period, children may be exposed to opportunities to experiment
with other substances that negatively impact their health and well-being. Practitioners should provide education regarding the serious health consequences of tobacco use and exposure to second hand smoke.81 The practitioner may need to obtain information regarding tobacco use and alcohol/drug abuse confidentially from an adolescent patient.6 When substance abuse has been identified, referral for appropriate intervention is indicated. Complications from intraoral/perioral piercings can range from pain, infection, and tooth fracture to life-threatening conditions of bleeding, edema, and airway obstruction.82 Although piercings most commonly are observed in the teenaged pediatric dental patient, education regarding pathologic conditions and sequelae associated with these piercings should be initiated for the preteen child/parent and reinforced during subsequent periodic visits. Radiographic assessment Appropriate radiographs are a valuable adjunct in the oral health care of infants, children and adolescents.29,30 Timing of initial radiographic examination should not be based upon the patient’s age.29 Rather, after review of an individual’s history and clinical findings, judicious determination of radiographic needs and examination can optimize patient care while minimizing radiation exposure.29,30 The US Food and Drug Administration/ ADA guidelines were developed to assist the dentist in deciding under what circumstances specific radiographs are indicated.30 Treatment of dental disease/injury Healthcare providers who diagnose oral disease or trauma should either provide therapy or refer the patient to an appropriatelytrained individual for treatment.83 Immediate intervention is necessary to prevent further dental destruction, as well as more widespread health problems. Postponed treatment can result in exacerbated problems that may lead to the need for more extensive care.19-21 Early intervention could result in savings of healthcare dollars for individuals, community health care programs, and third party payors. Treatment of developing malocclusion Guidance of eruption and development of the primary, mixed, and permanent dentitions is an integral component of comprehensive oral health care for all pediatric dental patients.28 Early diagnosis and successful treatment of developing malocclusions can have both short-term and long-term benefits, while achieving the goals of occlusal harmony and function and dentofacial esthestics.84-87 Early treatment is beneficial for many patients, but may not be indicated for every patient. When there is a reasonable indication that an oral habit will result in unfavorable sequelae in the developing permanent dentition, any treatment must be appropriate for the child’s development, comprehension, and ability to cooperate. Use of an appliance is indicated only when the child wants to stop the habit and would benefit from a reminder.28 At each stage of occlusal development, the objectives of intervention/treatment include: (1) reversing adverse growth;
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(2) preventing dental and skeletal disharmonies; (3) improving esthetics of the smile; (4) improving self-image; and (5) improving the occlusion.28 Sealants Sealants reduce the risk of pit and fissure caries in susceptible teeth and are cost-effective when maintained.88.89 They are indicated for primary and permanent teeth with pits and fissures that are predisposed to plaque retention. At-risk pits and fissures should be sealed as soon as possible. Because caries risk may increase at any time during a patient’s life due to changes in habits (eg, dietary, home care), oral microflora, or physical condition, unsealed teeth subsequently might benefit from sealant application.88 The need for sealant placement should be reassessed at periodic preventive care appointments. Sealants should be monitored and repaired or replaced as needed. Third Molars Panoramic or periapical radiographic assessment is indicated during late adolescence to assess the presence, position, and development of third molars.29,30 A decision to remove or retain third molars should be made before the middle of the third decade.90 Consideration should be given to removal when there is a high probability of disease or pathology and/or the risks associated with early removal are less than the risks of later removal.10 Referral for regular and periodic dental care As adolescent patients approach the age of majority, it is important to educate the patient and parent on the value of transitioning to a dentist who is knowledgeable in adult oral health care. At the time agreed upon by the patient, parent, and pediatric dentist, the patient should be referred to a specific practitioner in an environment sensitive to the adolescent’s individual needs.6,91 Until the new dental home is established, the patient should maintain a relationship with the current care provider and have access to emergency services. Proper communication and records transfer allow for consistent and continuous care for the patient. Recommendations by Age 6 to 12 months 1. Complete the clinical oral examination with adjunctive diagnostic tools (eg, radiographs as determined by child’s history, clinical findings, and susceptibility to oral disease) to assess oral growth and development, pathology, and/or injuries; provide diagnosis. 2. Provide oral hygiene counseling for parents, including the implications of the oral health of the caregiver. 3. Remove supragingival and subgingival stains or deposits as indicated. 4. Assess the child’s systemic and topical fluoride status (including type of infant formula used, if any, and exposure to fluoridated toothpaste) and provide counseling regarding fluoride. Prescribe systemic fluoride supplements,
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5. 6. 7. 8. 9. 10. 11. 12. 13.
if indicated, following assessment of total fluoride intake from drinking water, diet, and oral hygiene products. Assess appropriateness of feeding practices, including bottle and breast-feeding, and provide counseling as indicated. Provide dietary counseling related to oral health. Provide age-appropriate injury prevention counseling for orofacial trauma. Provide counseling for nonnutritive oral habits (eg, digit, pacifiers). Provide required treatment and/or appropriate referral for any oral diseases or injuries. Provide anticipatory guidance. Consult with the child’s physician as needed. Complete a caries risk assessment. Determine the interval for periodic reevaluation.
12 to 24 months 1. Repeat 6 to 12-month procedures every 6 months or as indicated by individual patient’s risk status/susceptibility to disease. 2. Assess appropriateness of feeding practices–including bottle, breast-feeding, and no-spill training cups–and provide counseling as indicated. 3. Review patient’s fluoride status–including any childcare arrangements which may impact systemic fluoride intake– and provide parental counseling. 4. Provide topical fluoride treatments every 6 months or as indicated by the individual patient’s needs. 2 to 6 years 1. Repeat 12- to 24-month procedures every 6 months or as indicated by individual patient’s risk status/susceptibility to disease. Provide age-appropriate oral hygiene instructions. 2. Scale and clean the teeth every 6 months or as indicated by individual patient’s needs. 3. Provide pit and fissure sealants for caries-susceptible primary molars and permanent molars, premolars, and anterior teeth. 4. Provide counseling and services (eg, mouthguards) as needed for orofacial trauma prevention. 5. Provide assessment/treatment or referral of developing malocclusion as indicated by individual patient’s needs. 6. Provide required treatment and/or appropriate referral for any oral diseases, habits, or injuries as indicated. 7. Assess speech and language development and provide appropriate referral as indicated. 6 to 12 years 1. Repeat 2- to 6-year procedures every 6 months or as indicated by individual patient’s risk status/susceptibility to disease. 2. Provide substance abuse counseling (eg, smoking, smokeless tobacco). 3. Provide counseling on intraoral/perioral piercing.
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12 years and older 1. Repeat 6- to 12-year procedures every 6 months or as indicated by individual patient’s risk status/susceptibility to disease. 2. During late adolescence, assess the presence, position, and development of third molars, giving consideration to removal when there is a high probability of disease or pathology and/or the risks associated with early removal are less than the risks of later removal. 3. At an age determined by patient, parent and pediatric dentist, refer the patient to a general dentist for continuing oral care.
References 1. US Dept of Health and Human Services. Oral Health in America: A Report of the Surgeon General. Rockville, Md: US Dept of Health and Human Services, National Institute of Dental and Craniofacial Research, National Institutes of Health; 2000. 2. Lewis DW, Ismail AI. Periodic health examination, 1995 Update: 2. Prevention of dental caries. The Canadian Task Force on the Periodic Health Examination. Can Med Assoc J 1995;152(6):836-46. 3. U S Preventive Services Task Force. Guide to Clinical Preventive Services. 2nd ed. Baltimore, Md: Williams and Wilkins; 1996. 4. Beirne P, Forgie A, Clarkson J, Worthington HV. Recall intervals for oral health in primary care patients. Evid Based Dent 2005;6(3):62-3. 5. American Academy of Pediatric Dentistry. Guideline on infant oral health care. Pediatr Dent 2009;31(special issue):95-9. 6. American Academy of Pediatric Dentistry. Guideline on adolescent oral health care. Pediatr Dent 2008;30(suppl): 94-101. 7. American Academy of Pediatric Dentistry. Guideline on the role of prophylaxis in pediatric dentistry. Pediatr Dent 2008;30(suppl):119-20. 8. A merican Academy of Pediatric Dentistry. Guideline on pediatric restorative dentistry. Pediatr Dent 2008;30 (suppl):169-9. 9. American Academy of Pediatric Dentistry. Guideline on acquired temporomandibular disorders in infants, children, and adolescents. Pediatr Dent 2008;30(suppl): 202-4. 10. American Academy of Pediatric Dentistry. Guideline on pediatric oral surgery. Pediatr Dent 2008;30(suppl):205-11. 11. American Academy of Pediatric Dentistry. Policy on the dental home. Pediatr Dent 2008;30(suppl):22-3. 12. American Academy of Pediatric Dentistry. Policy on early childhood caries: Classifications, consequences, and preventive strategies. Pediatr Dent 2008;30(suppl):40-3. 13. A merican Academy of Pediatric Dentistry. Policy on the use of a caries-risk assessment tool (CAT) for infants, children, and adolescents. Pediatr Dent 2008;30(suppl): 29-33.
14. CDC. Recommendations for using fluoride to prevent and control dental caries in the Unites States. MMWR Recomm Rep 2001;50(RR14):1-42. 15. American Academy of Pediatric Dentistry. Policy on dietary recommendations for infants, children, and adolescents. Pediatr Dent 2008;30(suppl):47-8. 16. American Academy of Pediatric Dentistry. Policy on prevention of sports-related orofacial injuries. Pediatr Dent 2008;30(suppl):58-60. 17. American Academy of Pediatric Dentistry. Guideline on management of acute dental trauma. Pediatr Dent 2008; 30(suppl):175-83. 18. American Academy of Pediatric Dentistry. Policy on oral habits. Pediatr Dent 2006;28(suppl):43. 19. Lee JY, Bouwens TJ, Savage MF, Vann WF Jr. Examining the cost-effectiveness of early dental visits. Pediatr Dent 2006;28(2):102-5, discussion 192-8. 20. Griffin SO, Gooch BF, Beltrán E, Sutherland JN, Barsley R. Dental services, costs, and factors associated with hospitalization for Medicaid-eligible children, Louisiana 1996-97. J Public Health Dent 2000;60(1):21-7. 21. Ramos-Gomez FJ, Huang GF, Masouredis CM, Braham RL. Prevalence and treatment costs of infant caries in Northern California. ASDC J Dent Child 1996;63: 108-12. 22. American Academy of Pediatric Dentistry. Policy on early childhood caries: Unique challenges and treatment options. Pediatr Dent 2008;30(suppl):44-6. 23. Acs G, Lodolini G, Kaminsky S, Cisneros GJ. Effect of nursing caries on body weight in a pediatric population. Pediatr Dent 1992;14(5):302-5. 24. Ramage S. The impact of dental disease on school performance. J Southeast Soc Pediatr Dent 2000;6:26. 25. National Center for Education in Maternal and Child Health. Oral health and learning. Bethesda, Md. National Center for Education in Maternal and Child Health and Georgetown University; 2001. 26. Clarke M, Locker D, Berall G, Pencharz P, Kenny DJ, Judd P. Malnourishment in a population of young children with severe early childhood caries. Pediatr Dent 2006;28(3):254-9. 27. Ayhan H, Suskan E, Yildirim S. The effect of nursing or rampant caries on height, body weight, and head circum-ference. J Clin Pediatr Dent 1996;20(3):209-12. 28. American Academy of Pediatric Dentistry. Guideline on management of the developing dentition and occlusion in pediatric dentistry. Pediatr Dent 2009;31(special issue): 196-208. 29. American Academy of Pediatric Dentistry. Guideline on prescribing dental radiographs. Pediatr Dent 2009;31 (special issue):250-2. 30. American Dental Association, US Dept of Health and Human Services. The selection of patients for dental radiographic examinations – 2004. Available at: “http:// www.ada.org/prof/resources/topics/topics_radiography_examinations.pdf ”. Accessed June 16, 2009. clinical guidelines
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31. Greenwell H, Committee on Research, Science and Therapy American Academy of Periodontology. Guidelines for periodontal therapy. J Periodontol 2001;72(11):1624-8. 32. Flores MT, Andreasen JO, Bakland LK, et al. Guidelines for the evaluation and management of traumatic dental injuries (part 3 of the series). Dental Traumatol. 2001;17(3): 97-102. 33. Flores MT, Andreasen JO, Bakland LK, et al. Guidelines for the evaluation and management of traumatic dental injuries (part 4 of the series). Dental Traumatol 2001;17 (4):145-8. 34. Flores MT, Andreasen JO, Bakland LK, et al. Guidelines for the evaluation and management of traumatic dental injuries (part 5 of the series). Dental Traumatol 2001;17 (5):193-6. 35. Li Y, Wang W. Predicting caries in permanent teeth from caries in primary teeth: An eight-year cohort study. J Dent Res 2002;81(8):561-6. 36. Helfenstein V, Steiner M, Marthaler TM. Caries prediction on the basis of past caries including precavity lesions. Caries Res 1991;25(5):372-6. 37. Fontana M, Zero DT. Assessing patients’ caries risk. J Am Dent Assoc 2006;137(9):1231-9. 38. Marino R, Bonze K, Scholl T, Anhalt H. Nursing bottle caries: Characteristics of children at risk. Clin Pediatr 1989;28(3):129-31. 39. Harris R, Nicoll AD, Adair PM, Pine CM. Risk factors for dental caries in young children: A systematic review of the literature. Community Dent Health 2004;21(suppl): 71-85. 40. Berkowitz RJ. Mutans streptococci: Acquisition and transmission. Pediatr Dent 2006;28(2):106-9. 41. American Psychological Association. Developing adolescents: A reference for professionals. Washington, DC. American Psychological Association; 2002. 42. Macgregor ID, Regis D, Balding J. Self-concept and dental health behaviors in adolescents. J Clin Periodontol 1997;24(5):335-9. 43. Califano JV, Research Science and Therapy Committee American Academy of Periodontology. Periodontal diseases of children and adolescents. J Periodontol 2003;74 (11):1696-704. 44. Research Science and Therapy Committee American Aca-demy of Periodontology. Treatment of plaque-induced gingivitis, chronic periodontitis, and other clinical conditions. J Periodontol 2001;72:1790-800. Erratum J Periodontol 2003;74(10):1568. 45. Featherstone JDB. Caries prevention and reversal based on the caries balance. Pediatr Dent 2006;28(2);128-32. 46. Anderson MH, Shi W. A probiotic approach to caries management. Pediatr Dent 2006;28(2):151-3. 47. Clerehugh V, Tugnait A. Periodontal diseases in children and adolescents: 2. Management. Dent Update 2001;28 (6):274-81.
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48. Roulet JF, Roulet-Mehrens TK. The surface roughness of restorative materials and dental tissues after polishing with prophylaxis and polishing pastes. J Periodontol 1982;53(4):257-66. 49. Hosoya Y, Johnston JW. Evaluation of various cleaning and polishing methods on primary enamel. J Pedod 1989;13(3):253-69. 50. Quirynen M, Bollen CML. The influence of surface roughness and surface-free energy on supra- and subgingival plaque formation in man. A review of the literature. J Clin Periodontol 1995;22(1):1-14. 51. Facts about Fluoride. CDS Rev 2006;99(1):44. 52. American Dental Association Council on Scientific Affairs. Professionally-applied topical fluoride: Evidencebased clinical recommendations. J Am Dent Assoc 2006; 137(8):1151-9. 53. Adair SM. Evidence-based use of fluoride in contemporary pediatric dental practice. Pediatr Dent 2006;28(2): 133-42. 54. Johnston DW, Lewis DW. Three-year randomized trial of professionally applied topical fluoride gel comparing annual and biannual applications with/without prior prophylaxis. Caries Res 1995;29(5):331-6. 55. Bader JD, Shugars DA, Bonito AJ. A systematic review of selected caries prevention and management methods. Community Dent Oral Epidemiol 2001;29(6):399-411. 56. Axelsson S, Söder B, Norderam G, et al. Effect of combined caries-preventive methods: A systematic review of controlled clinical trials. Acta Odontol Scand 2004;62 (3):163-9. 57. Källestål C. The effect of five years’ implementation of caries-preventive methods in Swedish high-risk adolescents. Caries Res 2005;39(1):20-6. 58. Featherstone JD, Adair SM, Anderson MH, et al. Caries management by risk assessment: Consensus statement, April 2002. J Calif Dent Assoc 2003;331(3):257-69. 59. Featherstone JD. The caries balance: The basis for caries management by risk assessment. Oral Health Prev Dent 2004;2(suppl 1):259-64. 60. Bader JD, Shugars DA, Rozier G, et al. Diagnosis and management of dental caries. Evid Rep Technol Assess (Summ) 2001;36:1-4. 61. Bader JD, Shugars DA, Bonito AJ. A systematic review of the performance of methods for indentifying carious lesions. J Public Health Dent 2002;62(4):201-13. 62. American Academy of Pediatric Dentistry. Guideline on fluoride therapy. Pediatr Dent 2008;30(suppl):121-5. 63. American Academy of Pediatrics Committee on Nutrition. Fluoride supplementation for children: Interim policy recommendations. Pediatrics 1995;95:777. 64. Meskin LH, ed. Caries diagnosis and risk assessment: A review of preventive strategies and management. J Am Dent Assoc 1995;126(suppl):1s-24s.
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65. Lewis CW, Grossman DC, Domoto PK, Deyo RA. The role of the pediatrician in the oral health of children: A national survey. Pediatrics 2000;106(6):E84. 66. Douglass JM. Response to Tinanoff and Palmer: Dietary determinants of dental caries and dietary recommendations for preschool children. J Public Health Dent 2000; 60(3):207-9. 67. Kranz S, Smiciklas-Wright H, Francis LA. Diet quality, added sugar, and dietary fiber intakes in American preschoolers. Pediatr Dent 2006;28(2):164-71. 68. Reisine S, Douglass JM. Pyschosocial and behavorial issues in early childhood caries. Comm Dent Oral Epidem 1998;26(suppl):132-44. 69. US Dept of Agriculture. Food pyramid. Available at: “http://www.mypyramid.gov”. Accessed March 18, 2007. 70. CDC, National Center for Health Statistics. Growth charts. Available at: “http://www.cdc.gov/growthcharts/”. Accessed June 16, 2009. 71. Cortes MI, Marcenes W, Shelham A. Impact of traumatic injuries to the permanent teeth on the oral health-related quality of life in 12- to 14-year old children. Comm Dent Oral Epidemiol 2002;30(3):193-8. 72. Flores MT. Traumatic injuries in the primary dentition. Dental Traumatol 2002;18(6):287-98. 73. Rocha MJdC, Cardoso M. Traumatized permanent teeth in Brazilian children assisted at the Federal University of Santa Catarina, Brazil. Dental Traumatol 2001;17(6): 245-9. 74. Caldas FA Jr, Burgos ME. A retrospective study of traumatic dental injuries in a Brazilian dental trauma clinic. Dental Traumatol 2001;17(6):250-3. 75. Skaare AB, Jacobsen I. Dental injuries in Norwegians aged 7-18 years. Dental Traumatol 2003;19(2):67-71. 76. Tapias MA, Jiménez-García R, Lamas F, Gil AA. Prevalence of traumatic crown fractures to permanent incisors in a childhood population: Mostoles, Spain. Dental Traumatol 2003;19(3):119-22. 77. American Speech-Language-Hearing Association. Available at: “http://www.asha.org/public/speech/development/ chart.htm”. Accessed June 16, 2009. 78. American Lung Association. Smoking and teen fact sheet – April 2006. Available at: “http://www.lungusa.org/ site/pp.asp?c=dvLUK9O0E&b=39871”. Accessed June 16, 2009.
79. CDC. Preventing tobacco use among young people: A report of the Surgeon General (executive summary). MMWR Recommend Reports 1994;43(RR-4):[inclusive page numbers]. 80. Albert DA, Severson HH, Andrews JA. Tobacco use by adolescents: The role of the oral health professional in evidence-based cessation program. Pediatr Dent 2006;28 (2):177-87. 81. American Academy of Pediatric Dentistry. Policy on tobacco use. Pediatr Dent 2008;30(suppl):53-5. 82. American Academy of Pediatric Dentistry. Policy on intraoral and perioral piercing. Pediatr Dent 2008;30(suppl): 56-7. 83. American Academy of Pediatric Dentistry. Policy on ethical responsibility to treat or refer. Pediatr Dent 2008; 30(suppl):83. 84. Kanellis MJ. Orthodontic treatment in the primary dentition. In Bishara SE, ed. Textbook of orthodontics. Philadelphia, Pa: WB Saunders Co:2001;248-56. 85. Woodside DG. The significance of late developmental crowding to early treatment planning for incisor crowding. Am J Orthod Dentofacial Orthop 2000;117(5): 559-61. 86. Kurol J. Early treatment of tooth-eruption disturbances. Am J Orthod Dentofacial Orthop 2002;121(6):588-91. 87. Sankey WL, Buschang PH, English J, Owen AH III. Early treatment of vertical skeletal dysplasia: The hyperdivergent phenotype. Am J Orthod Dentofacial Orthop 2000;118(3):317-27. 88. Feigal RJ. The use of pit and fissure sealants. Pediatr Dent 2002;24(5):415-22. 89. Feigal RJ, Donly KJ. The use of pit and fissure sealants. Pediatr Dent 2006;28(2):143-50. 90. American Association of Oral and Maxillofacial Surgeons. Parameters and Pathways: Clinical Practice Guidelines for Oral and Maxillofacial Surgery (AAOMS ParPath01). J Oral Maxillofac Surg 2001. 91. American Academy of Pediatric Dentistry. Guideline on management of persons with special health care needs. Pediatr Dent 2008;30(suppl):107-11.
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Injury prevention counseling
Counseling for nonnutritive habits
Counseling for speech/language development
7 Initially, responsibility of parent; as child matures, jointly with parent; then, when indicated, only child.
6 Appropriate discussion and counseling should be an integral part of each visit for care.
5 Consider when systemic fluoride exposure is suboptimal. Up to at least 16 years.
4 Timing, selection, and frequency determined by child’s history, clinical findings, and susceptibility to oral disease.
11 For caries-susceptible primary molars, permanent molars, premolars, and anterior teeth with deep pits and fissures; placed as soon as possible after eruption.
10 At first, discuss the need for additional sucking: digits vs pacifiers; then the need to wean from the habit before malocclusion or skeletal dysplasia occurs. For school-aged children and adolescent patients, counsel regarding any existing habits such as fingernail biting, clenching, or bruxism.
9 Initially play objects, pacifiers, car seats; when learning to walk; then with sports and routine playing, including the importance of mouthguards.
3 Must be repeated regularly and frequently to maximize effectiveness.
2 By clinical examination.
• • 8 At every appointment; initially discuss appropriate feeding practices, then the role of refined carbohydrates and frequency of snacking in caries development and childhood obesity.
10
•
1 First examination at the eruption of the first tooth and no later than 12 months. Repeat every 6 months or as indicated by child’s risk status/susceptibility to disease. Includes assessment of pathology and injuries.
Transition to adult dental care
Assessment and/or removal of third molars
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American Academy of Pediatric Dentistry
Since each child is unique, these recommendations are designed for the care of children who have no contributing medical conditions and are developing normally. These recommendations will need to be modified for children with special health care needs or if disease or trauma manifests variations from normal. The American Academy of Pediatric Dentistry (AAPD) emphasizes the importance of very early professional intervention and the continuity of care based on the individualized needs of the child. Refer to the text of this guideline for supporting information and references.
Recommendations for Pediatric Oral Health Assessment, Preventive Services, and Anticipatory Guidance/Counseling reference manual 10 / 11
AMERICAN ACADEMY OF PEDIATRIC DENTISTRY
Guideline on Caries-risk Assessment and Management for Infants, Children, and Adolescents Originating Council Council on Clinical Affairs
Review Council Council on Clinical Affairs
Adopted 2002
Revised 2006, 2010
Purpose The American Academy of Pediatric Dentistry (AAPD) recognizes that caries-risk assessment and management protocols can assist clinicians with decisions regarding treatment based upon caries risk and patient compliance and are essential elements of contemporary clinical care for infants, children, and adolescents. This guideline is intended to educate healthcare providers and other interested parties on the assessment of caries risk in contemporary pediatric dentistry and aid in clinical decision making regarding diagnostic, fluoride, dietary, and restorative protocols.
Methods This guideline is an update of AAPD’s “Policy on Use of a Caries-risk Assessment Tool (CAT) for Infants, Children, and Adolescents, Revised 2006” that includes the additional concepts of dental caries management protocols. The update used electronic and hand searches of English written articles in the medical and dental literature within the last 10 years using the search terms “caries risk assessment”, “caries management”, and “caries clinical protocols”. From this search, 1,909 articles were evaluated by title or by abstract. Information from 75 articles was used to update this document. When data did not appear sufficient or were inconclusive, recommendations were based upon expert and/or consensus opinion by experienced researchers and clinicians.
Background Caries-risk assessment Risk assessment procedures used in medical practice normally have sufficient data to accurately quantitate a person’s disease susceptibility and allow for preventive measures.1 Even though caries-risk data in dentistry still are not sufficient to quantitate the models, the process of determining risk should be a component in the clinical decision making process.2 Risk assessment: 1. fosters the treatment of the disease process instead of treating the outcome of the disease;
2. gives an understanding of the disease factors for a specific patient and aids in individualizing preventive discussions; 3. individualizes, selects, and determines frequency of preventive and restorative treatment for a patient; and 4. anticipates caries progression or stabilization. Caries-risk assessment models currently involve a combination of factors including diet, fluoride exposure, a susceptible host, and microflora that interplay with a variety of social, cultural, and behavioral factors.3-6 Caries risk assessment is the determination of the likelihood of the incidence of caries (ie, the number of new cavitated or incipient lesions) during a certain time period7 or the likelihood that there will be a change in the size or activity of lesions already present. With the ability to detect caries in its earliest stages (ie, white spot lesions), health care providers can help prevent cavitation.8-10 Caries risk indicators are variables that are thought to cause the disease directly (eg, microflora) or have been shown useful in predicting it (eg, socioeconomic status) and include those variables that may be considered protective factors. Currently, there are no caries-risk factors or combinations of factors that have achieved high levels of both positive and negative predictive values.2 Although the best tool to predict future caries is past caries experience, it is not particularly useful in young children due to the importance of determining caries risk before the disease is manifest. Children with white spot lesions should be considered at high risk for caries since these are precavitated lesions that are indicative of caries activity.11 Plaque accumulation also is strongly associated with caries development in young children.12,13 As a corollary to the presence of plaque,14 a child’s mutans streptococci levels3 and the age at which a child becomes colonized with cariogenic flora15,16 are valuable in assessing risk, especially in preschool children. While there is no question that fermentable carbohydrates are a necessary link in the causal chain for dental caries, a systematic study of sugar consumption and caries risk has concluded that the relationship between sugar consumption and
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caries is much weaker in the modern age of fluoride exposure than previously thought.17 However, there is evidence that night-time use of the bottle, especially when it is prolonged, may be associated with early childhood caries.18 Despite the fact that normal salivary flow is an extremely important intrinsic host factor providing protection against caries, there is little data about the prevalence of low salivary flow in children.19,20 Sociodemographic factors have been studied extensively to determine their effect on caries risk. Children with immigrant backgrounds have 3 times higher caries rates than nonimmigrants.21 Most consistently, an inverse relationship between socioeconomic status and caries prevalence is found in studies of children less than 6 years of age.22 Perhaps another type of sociodemographic variable is the parents’ history of cavities and abscessed teeth; this has been found to be a predictor of treatment for early childhood caries.23,24 The most studied factors that are protective of dental caries include systemic and topical fluoride, sugar substitutes, and tooth brushing with fluoridated toothpaste. Teeth of children who reside in a fluoridated community have been shown to have higher fluoride content than those of children who reside in suboptimal fluoridated communities.25 Additionally, both pre- and post-eruption fluoride exposure maximize the caries-preventive effects.26,27 For individuals residing in nonfluoridated communities, fluoride supplements have shown a significant caries reduction in primary and permanent teeth.28 With regard to fluoridated toothpaste, studies have shown
consistent reduction in caries experience.29 Professional topical fluoride applications performed semiannually also reduce caries,30 and fluoride varnishes generally are equal to that of other professional topical fluoride vehicles.31 The effect of sugar substitutes on caries rates have been evaluated in several populations with high caries prevalence.32 Studies indicate that xylitol can decrease mutans streptococci levels in plaque and saliva and can reduce dental caries in young children and adults, including children via their mothers.33 With regard to toothbrushing, there only is a weak relationship between frequency of brushing and decreased dental caries, which is confounded because it is difficult to distinguish whether the effect is actually a measure of fluoride application or whether it is a result of mechanical removal of plaque.34 The dental home or regular periodic care by the same practitioner is included in many caries-risk assessment models because of its known benefit for dental health.35 Risk assessment tools can aid in the identification of reliable predictors and allow dental practitioners, physicians, and other nondental health care providers to become more actively involved in identifying and referring high-risk children. Tables 1, 2, and 3 incorporate available evidence into practical tools to assist dental practitioners, physicians, and other nondental health care providers in assessing levels of risk for caries development in infants, children, and adolescents. As new evidence emergences, these tools can be refined to provide greater predictably of caries in children prior to disease initiation.
Table 1. Caries-risk Assessment Form for 0-3 Year Olds 59,60 (For Physicians and Other Non-Dental Health Care Providers)
High Risk
Factors
Moderate Risk
Protective
Biological Mother/primary caregiver has active cavities Parent/caregiver has low socioeconomic status Child has >3 between meal sugar-containing snacks or beverages per day Child is put to bed with a bottle containing natural or added sugar Child has special health care needs Child is a recent immigrant
Yes Yes Yes Yes Yes Yes
Protective Child receives optimally-fluoridated drinking water or fluoride supplements Child has teeth brushed daily with fluoridated toothpaste Child receives topical fluoride from health professional Child has dental home/regular dental care
Yes Yes Yes Yes
Clinical Findings Child has white spot lesions or enamel defects Child has visible cavities or fillings Child has plaque on teeth
Yes Yes Yes
Circling those conditions that apply to a specific patient helps the health care worker and parent understand the factors that contribute to or protect from caries. Risk assessment categorization of low, moderate, or high is based on preponderance of factors for the individual. However, clinical judgment may justify the use of one factor (eg, frequent exposure to sugar containing snacks or beverages, visible cavities) in determining overall risk.
Overall assessment of the child’s dental caries risk:
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High
Moderate
Low
AMERICAN ACADEMY OF PEDIATRIC DENTISTRY
Table 2. Caries-risk Assessment Form for 0-5 Year Olds 59,60 (For Dental Providers)
High Risk
Factors
Moderate Risk
Protective
Biological Mother/primary caregiver has active caries Parent/caregiver has low socioeconomic status Child has >3 between meal sugar-containing snacks or beverages per day Child is put to bed with a bottle containing natural or added sugar Child has special health care needs Child is a recent immigrant
Yes Yes Yes Yes Yes Yes
Protective Child receives optimally-fluoridated drinking water or fluoride supplements Child has teeth brushed daily with fluoridated toothpaste Child receives topical fluoride from health professional Child has dental home/regular dental care
Yes Yes Yes Yes
Clinical Findings Child has >1 decayed/missing/filled surfaces (dmfs) Child has active white spot lesions or enamel defects Child has elevated mutans streptococci levels Child has plaque on teeth
Yes Yes Yes Yes
Circling those conditions that apply to a specific patient helps the practitioner and parent understand the factors that contribute to or protect from caries. Risk assessment categorization of low, moderate, or high is based on preponderance of factors for the individual. However, clinical judgment may justify the use of one factor (eg, frequent exposure to sugar-containing snacks or beverages, more than one dmfs) in determining overall risk.
Overall assessment of the child’s dental caries risk:
High
Moderate
Low
Table 3. Caries-risk Assessment Form for >6 Years Olds 60-62 (For Dental Providers)
High Risk
Factors
Moderate Risk
Protective
Biological Patient is of low socioeconomic status Patient has >3 between meal sugar containing snacks or beverages per day Patient has special health care needs Patient is a recent immigrant
Yes Yes Yes Yes
Protective Patient receives optimally-fluoridated drinking water Patient brushes teeth daily with fluoridated toothpaste Patient receives topical fluoride from health professional Additional home measures (eg, xylitol, MI paste, antimicrobial) Patient has dental home/regular dental care
Yes Yes Yes Yes Yes
Clinical Findings Patient has >1 interproximal lesions Patient has active white spot lesions or enamel defects Patient has low salivary flow Patient has defective restorations Patient wearing an intraoral appliance
Yes Yes Yes Yes Yes
Circling those conditions that apply to a specific patient helps the practitioner and patient/parent understand the factors that contribute to or protect from caries. Risk assessment categorization of low, moderate, or high is based on preponderance of factors for the individual. However, clinical judgment may justify the use of one factor (eg, >1 interproximal lesions, low salivary flow) in determining overall risk.
Overall assessment of the dental caries risk:
High
Moderate
Low
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Furthermore, the evolution of caries-risk assessment tools and protocols can assist in providing evidence for and justifying periodicity of services, modification of third-party involvement in the delivery of dental services, and quality of care with outcomes assessment to address limited resources and workforce issues.
Caries management protocols Clinical management protocols are documents designed to assist in clinical decision-making; they provide criteria regarding diagnosis and treatment and lead to recommended courses of action. The protocols are based on evidence from current
Table 4. Example of a Caries Management Protocol for 1-2 Year Olds Risk Category
Diagnostics
Interventions Fluoride
Restorative
Diet
Low risk
– Recall every 6-12 months – Baseline MS a
– Twice daily brushing with fluoridated toothpaste b
Counseling
– Surveillance χ
Moderate risk parent engaged
– Recall every 6 months – Baseline MS a
– Twice daily brushing with fluoridated toothpaste b – Fluoride supplements d – Professional topical treatment every 6 months
Counseling
– Active surveillance e of incipient lesions
Moderate risk parent not engaged
– Recall every 6 months – Baseline MS a
– Twice daily brushing with fluoridated toothpaste b – Professional topical treatment every 6 months
Counseling, with limited expectations
– Active surveillance e of incipient lesions
High risk parent engaged
– Recall every 3 months – Baseline and follow up MS a
– Twice daily brushing with fluoridated toothpaste b – Fluoride supplements d – Professional topical treatment every 3 months
Counseling
– Active surveillance e of incipient lesions – Restore cavitated lesions with ITRf or definitive restorations
High risk parent not engaged
– Recall every 3 months – Baseline and follow up MS a
– Twice daily brushing with fluoridated toothpaste b – Professional topical treatment every 3 months
Counseling, with limited expectations
– Active surveillance e of incipient lesions – Restore cavitated lesions with ITRf or definitive restorations
Table 5. Example of a Caries Management Protocol for 3-5 Year Olds Risk Category
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Diagnostics
Interventions Fluoride
Restorative
Diet
Sealants l
No
Yes
– Surveillance χ
Low risk
– Recall every 6-12 months – Radiographs every 12-24 months – Baseline MS a
– Twice daily brushing with fluoridated toothpaste g
Moderate risk parent engaged
– Recall every 6 months – Radiographs every 6-12 months – Baseline MS a
– Twice daily brushing with fluoridated toothpaste g – Fluoride supplements d – Professional topical treatment every 6 months
Counseling
Yes
– Active surveillance e of incipient lesions – Restoration of cavitated or enlarging lesions
Moderate risk parent not engaged
– Recall every 6 months – Radiographs every 6-12 months – Baseline MS a
– Twice daily brushing with fluoridated toothpaste g – Professional topical treatment every 6 months
Counseling, with limited expectations
Yes
– Active surveillance e of incipient lesions – Restoration of cavitated or enlarging lesions
High risk parent engaged
– Recall every 3 months – Radiographs every 6 months – Baseline and follow up MS a
– Brushing with 0.5% fluoride (with caution) – Fluoride supplements d – Professional topical treatment every 3 months
Counseling
Yes
– Active surveillance e of incipient lesions – Restoration of cavitated or enlarging lesions
High risk parent not engaged
– Recall every 3 months – Radiographs every 6 months – Baseline and follow up MS a
– Brushing with 0.5% fluoride (with caution) – Professional topical treatment every 3 months
Counseling, with limited expectations
Yes
– Restore incipient, cavitated, or enlarging lesions
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AMERICAN ACADEMY OF PEDIATRIC DENTISTRY
Table 6. Example of a Caries Management Protocol for >6 Year-Olds Risk Category
Interventions
Diagnostics
Fluoride
Restorative
Diet
Sealants l
No
Yes
– Surveillance χ
Low risk
– Recall every 6-12 months – Radiographs every 12-24 months
– Twice daily brushing with fluoridated toothpaste m
Moderate risk patient/parent engaged
– Recall every 6 months – Radiographs every 6-12 months
– Twice daily brushing with fluoridated toothpaste m – Fluoride supplements d – Professional topical treatment every 6 months
– Counseling
Yes
– Active surveillance e of incipient lesions – Restoration of cavitated or enlarging lesions
Moderate risk patient/parent not engaged
– Recall every 6 months – Radiographs every 6-12 months
– Twice daily brushing with toothpastee m – Professional topical treatment every 6 months
– Counseling, with limited expectations
Yes
– Active surveillance e of incipient lesions – Restoration of cavitated or enlarging lesions
High risk patient/parent engaged
– Recall every 3 months – Radiographs every 6 months
– Brushing with 0.5% fluoride – Fluoride supplements d – Professional topical treatment every 3 months
– Counseling – Xylitol
Yes
– Active surveillance e of incipient lesions – Restoration of cavitated or enlarging lesions
High risk patient/parent not engaged
– Recall every 3 months – Radiographs every 6 months
– Brushing with 0.5% fluoride – Professional topical treatment every 3 months
– Counseling, with limited expectations – Xylitol
Yes
– Restore incipient, cavitated, or enlarging lesions
Legends for Tables 4-6 a Salivary mutans streptococci bacterial levels. χ Periodic monitoring for signs of caries progression. e Careful monitoring of caries progression and prevention program. γ Parental supervision of a “pea sized” amount of toothpaste. μ Less concern about the quantity of tooth paste.
b Parental supervision of a “smear” amount of tooth paste. d Need to consider fluoride levels in drinking water. f Interim Therapeutic Restoration.63 λ Indicated for teeth with deep fissure anatomy or developmental defects.
peer-reviewed literature and the considered judgment of expert panels, as well as clinical experience of practitioners. The protocols should be updated frequently as new technologies and evidence develop. Historically, the management of dental caries was based
on the notion that it was a progressive disease that eventually destroyed the tooth unless there was surgical/restorative intervention. Decisions for intervention often were learned from unstandardized dental school instruction, and then refined by clinicians over years of practice. Little is known about the criteria dentists use when making decisions involving restoration of carious lesions.36 It is now known that surgical intervention of dental caries alone does not stop the disease process. Additionally, many lesions do not progress, and tooth restorations have a finite longevity. Therefore, modern management of dental caries should be more conservative and includes early detection of noncavitated lesions, identification of an individual’s risk for caries progression, understanding of the disease process for that individual, and “active surveillance” to apply preventive measures and monitor carefully for signs of arrestment or progression.
Caries management protocols for children further refine the decisions concerning individualized treatment and treatment thresholds based on a specific patient’s risk levels, age, and compliance with preventive strategies (Tables 4, 5, 6). Such protocols should yield greater probability of success and better cost effectiveness of treatment than less standardized treatment. Additionally, caries management protocols free practitioners of the necessity for repetitive high level treatment decisions, standardize decision making and treatment strategies,36-38 eliminate treatment uncertainties, and guarantee morecorrect strategies.39 Content of the present caries management protocol is based on results of clinical trials, systematic reviews, and expert panel recommendations that give better understanding to, and recommendations for, diagnostic, preventive, and restorative treatments. The radiographic diagnostic guidelines are based on the latest guidelines from the American Dental Association (ADA).40 Systemic fluoride protocols are based on the Centers for Disease Control and Prevention’s (CDC) recommendations for using fluoride.29 Guidelines for the use of topical fluoride treatment are based on the ADA’s Council on Scientific Affairs’ recommendations for professionally-applied
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topical fluoride,41 the Scottish Intercollegiate Guideline Network guideline for the management of caries in pre-school children,42 a Maternal and Child Health Bureau Expert Panel,43 and the CDC’s fluoride guidelines.29 Guidelines for pit and fissure sealants are based on ADA’s Council on Scientific Affairs recommendations for the use of pit-and-fissure sealants.44 Guidelines on diet counseling to prevent caries are based on 2 review papers.45,46 Guidelines for the use of xylitol are based on the AAPD’s oral health policy on use of xylitol in caries prevention,32 a well-executed clinical trial on high caries-risk infants and toddlers,47 and 2 evidence-based reviews.48,49 Active surveillance (prevention therapies and close monitoring) of enamel lesions is based on the concept that treatment of disease may only be necessary if there is disease progression,50 that caries progression has diminished over recent decades,51 and that the majority of proximal lesions, even in dentin, are not cavitated.52 Other approaches to the assessment and treatment of dental caries will emerge with time and, with evidence of effectiveness, may be included in future guidelines on caries risk assessment and management protocols. For example, there are emerging trends to use calcium and phosphate remineralizing solution to reverse dental caries.53 Other fluoride compounds, such as silver diamine fluoride54 and stannous fluoride55, may be more effective than sodium fluoride for topical applications. There has been interest in antimicrobials to affect the caries rates, but evidence from caries trials is still inconclusive.56 However, some other proven methods, such as prescription fluoride drops and tablets, may be removed from this protocol in the future due to attitudes, risks, or compliance.57,58
Recommendations
1. Dental-caries risk assessment, based on a child’s age, biological factors, protective factors, and clinical find ings, should be a routine component of new and periodic examinations by oral health and medical providers. 2. While there is not enough information at present to have quantitative caries-risk assessment analyses, esti mating children at low, moderate, and high caries risk by a preponderance of risk and protective factors will enable a more evidence-based approach to medical provider referrals, as well as establish periodicity and intensity of diagnostic, preventive, and restorative services. 3. Clinical management protocols, based on a child’s age, caries risk, and level of patient/parent cooperation, provide health providers with criteria and protocols for determining the types and frequency of diagnos tic, preventive, and restorative care for patient speci fic management of dental caries.
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References 1. Lauer MS, Fontanarosa BP. Updated guidelines for cholesterol management. JAMA 2001;285(19):2486-97. 2. Zero D, Fontana M, Lennon AM. Clinical applications and outcomes of using indicators of risk in caries management. J Dent Educ 2001;65(10):1126-32. 3. Litt MD, Reisine S, Tinanoff N. Multidimensional causal model of dental caries development in low-income preschool children. Public Health Reports 1995;110(4):607-17. 4. Nicolau B, Marcenes W, Bartley M, Sheiham A. A life course approach to assessing causes of dental caries experience: The relationship between biological, behavioural, socio-economic and psychological conditions and caries in adolescents. Caries Res 2003;37(5):319-26. 5. Featherstone JD. The caries balance: Contributing factors and early detection. J Calif Dent Assoc 2003;31(2): 129-33. 6. Featherstone JD. The caries balance: The basis for caries management by risk assessment. Oral Health Prev Dent 2004;2(Suppl 1):259-64. 7. Reich E, Lussi A, Newbrun E. Caries-risk assessment. Int Dent J 1999;49(1):15-26. 8. Ismail AI, Nainar SM, Sohn W. Children’s first dental visit: Attitudes and practices of US pediatricians and family physicians. Pediatr Dent 2003;25(5):425-30. 9. Tsang P, Qi F, Shi W. Medical approach to dental caries: Fight the disease, not the lesion. Pediatr Dent 2006;28(2): 188-98. 10. Crall JJ. Development and integration of oral health services for preschool-age children. Pediatr Dent 2005;27(4): 323-30. 11. Vadiakas G. Case definition, aetiology and risk assessment of early childhood caries (ECC): A revisited review. European Arch Paed Dent 2008;9(9):114-25. 12. Alaluusua S, Malmivirta R. Early plaque accumulation – A sign for caries risk in young children. Community Dent Oral Epidemiol 1994;22(10):273-6. 13. Roeters J, Burgesdijk R, Truin GJ, van ’t Hof M. Dental caries and its determinants in 2- to-5-year old children. ASDC J Dent Child 1995;62(6):401-8. 14. Lee C, Tinanoff N, Minah G, Romberg E. Effect of Mutans streptococcal colonization on plaque formation and regrowth in young children – A brief communication. J Public Health Dent 2008;68(1):57-60. 15. Thibodeau EA, O’Sullivan DM, Tinanoff N. Mutans streptococci and caries prevalence in preschool children. Community Dent Oral Epidemiol 1993;21(5):288-91. 16. Grindefjord M, Dahllöf G, Nilsson B, Modéer T. Prediction of dental caries development in 1-year old children. Caries Res 1995;29(5):343-8. 17. Burt BA, Satishchandra P. The relationship between low birthweight and subsequent development of caries: A systematic review. J Dent Ed 2001;65(10):1017-23.
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18. Reisine S, Douglass JM. Psychosocial and behavioral issues in early childhood caries. Community Dent Oral Epidemiol 1998;26(1 Suppl):45-8. 19. C ataldo WL, Oppenheim FG. Physical and chemical aspects of saliva as indicators of risk for dental caries in humans. J Dent Ed 2001;65(10):1054-62. 20. Vanobbergen J, Martens L, Lesaffre E, Bogaerts K, Declerck D. The value of a baseline caries risk assessment model in the primary dentition for the prediction of caries increment in the permanent dentition. Caries Res 2001;35(6): 442-50. 21. Nunn ME, Dietrich T, Singh HK, Henshaw MM, Kressin NR. Prevalence of early childhood caries among very young urban Boston children compared with US Children. J Public Health Dent 2009;69(3):156-62. 22. Vargas CM, Crall JJ, Schneider DA. Sociodemographic distribution of pediatric dental caries: NHANES III, 1988-1994. J Am Dent Assoc 1998;129(9):1229-38. 23. Southward LH, Robertson A, Edelstein BL, et al. Oral health of young children in Mississippi Delta child care centers: A second look at early childhood caries risk assessment. J Public Health Dent 2008;68(4):188-95. 24. Thitasomakul S, Piwat S, Thearmontree A, Chankanka O, Pithpornchaiyakul W. Madyusoh S. Risks for early childhood caries analyzed by negative binomial models. J Dent Res 2009;88(2):137-41. 25. Weatherell J, Deutsch D, Robinson C, Hallsworth AS. Assimilation of fluoride by enamel throughout the life of the tooth. Caries Res 1977;11(2):85-115. 26. Backer Dirks O, Houwink B, Kwant GW. The results of 6½ years of artificial fluoridation of drinking water in The Netherlands – The Tiel Cumemborg experiment. Arch Oral Biol 1961;5(12):284-300. 27. Singh KA, Spencer AJ, Armfield JM. Relative effects of pre-and posteruption water fluoride on caries experience of permanent first molars. J Pub Heath Dent 2003;63(1): 11-9. 28. Murray JJ, Naylor MN. Fluorides and dental caries. In: Murray JJ, ed. Prevention of Oral Disease. Oxford University Press, Oxford; 1996:32-67. 29. CDC. Recommendations for using fluoride to prevent and control dental caries in the United States. MMWR Recomm Rep 2001;50(RR14):1-42. 30. Ripa LW. A critique of topical fluoride methods (dentifrice, mouthrinses, operator-, and self-applied gels) in an era of decreased caries and increased fluorosis prevalence. J Pub Health Dent 1991;51(1):23-41. 31. Beltrán-Aguilar ED, Goldstein JW, Lockwood SA. Fluoride varnishes: A review of their clinical use, cariostatic mechanism, efficacy and safety. J Am Dent Assoc 2000; 131(5):589-96. 32. American Academy of Pediatric Dentistry. Policy on use of xylitol in caries prevention. Pediatr Dent 2010;32 (special issue):36-8.
33. Ly KA, Milgrom P, Rothen M. Xylitol, sweeteners, and dental caries. Pediatr Dent 2006;28(2):154-63. 34. Reisine ST, Psoter W. Socioeconomic status and selected behavioral determinants and risk factor for dental caries. J Dent Ed 2001;65(10):1009-16. 35. Nowak AJ, Casamassimo PS. The dental home. A primary care oral health concept. J Am Dent Assoc 2002;133(1): 93-8. 36. Bader JD, Shugars DA. What do we know about how dentists make caries-related treatment decisions? Community Dent Oral Epidemiol 1997;25(1):97-103. 37. Anusavice K. Management of dental caries as a chronic infectious disease. J Dent Ed 1998;62(10):791-802. 38. Benn DK, Clark TD, Dankel DD, Kostewicz SH. Practical approach to evidence-based management of caries. J Am Coll Dent 1999;66(1):27-35. 39. White BA, Maupome G. Clinical decision-making for dental caries management. J Dent Ed 2001;65(10): 1121-5. 40. American Dental Association Council on Scientific Affairs. The use of dental radiographs. Update and recommendations. J Am Dent Assoc 2006;137(9):1304-12. 41. American Dental Association Council on Scientific Affairs. Professionally applied topical fluoride: Evidencebased clinical recommendations. J Am Dent Assoc 2006; 137(8):1151-9. 42. Scottish Intercollegiate Guideline Network (SIGN). Prevention and management of dental decay in the preschool child. 2005. Available at: “http://www.sign.ac.uk/ pdf/sign83.pdf ”. Accessed July 2, 2010. 43. Maternal and Child Health Bureau Expert Panel. Topical fluoride recommendations for high-risk children: Development of decision support matrix. October 22–23, 2007, Altarum Institute, Washington, DC. Available at: “http://mohealthysmiles.typepad.com/Topical%20fl% 20recommendations%20for%20hi%20risk%20children. pdf ”. Accessed July 3, 2010. 44. American Dental Association Council on Scientific Affairs. Evidence-based clinical recommendations for the use of pit-and-fissure sealants. J Am Dent Assoc 2008;139(4):257-67. 45. Tinanoff N. Association of diet with dental caries in preschool children. Dental Clin North Am 2005;49(4): 725-7. 46. Burt BA, Pai S. Sugar consumption and caries risk: A systematic review. J Dent Ed 2001;65(10):1017-23. 47. Milgrom P, Ly KA, Tut OK, et al. Xylitol pediatric topical oral syrup to prevent dental caries. Arch Pediatr Adolesc Med 2009;163(7):601-7. 48. Maguire A, Rugg-Gunn AJ. Xylitol and caries prevention – Is it a magic bullet? British Dent J 2003;194(8):429-36. 49. Hayes C. The effect of non-cariogenic sweeteners on the prevention of dental caries: A review of the evidence. J Dent Ed 2001;65(10):1106-9.
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50. Parker C. Active surveillance: Toward a new paradigm in the management of early prostate cancer. Lancet Oncol 2004;5(2):101-6. 51. Warren JJ, Levy SM, Broffitt B, Kanellis MJ. Longitudinal study of non-cavitated carious lesion progression in the primary dentition J Public Health Dent 2006;66(2):83-7. 52. Anusavice KJ. Present and future approaches for the control of caries J Dent Ed 2005;69(5):538-54. 53. Hicks J, García-Godoy F, Flaitz C. Biological factors in dental caries: Role of remineralization and fluoride in the dynamic process of demineralization and remineralization. J Clin Ped Dent 2004;28(1):203-14. 54. Rosenblatt A, Stamford TCM, Niederman R. Silver diamine fluoride: A caries “silver-fluoride bullet”. J Dent Res 2009;88(2):116-25. 55. Tinanoff N. Progress regarding the use of stannous fluoride in clinical dentistry. J Clinical Dent 1995;6(Special issue):37-40. 55. Twetman S. Prevention of early childhood caries (ECC). Review of literature published 1998-2007. Europ Archives Paed Dent 2008;9(1):12-8. 56. Caufield PW, Desanayke AP, Li Y. The antimicrobial approach to caries management. J Dent Ed 2001;65(10): 1091-5. 57. Ismail AI, Hassen H. Fluoride supplements, dental caries and fluorosis. A systematic review. J Am Dent Assoc 2008;139(11):1457-68.
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58. Tinanoff N. Use of fluorides. In: Berg J, Slayton RL, eds. Early Childhood Oral Health. Wiley-Blackwell: Ames, Iowa; 2009:92-109. 59. Ramos-Gomez FJ, Crall J, Gansky SA, Slayton RL, Featherstone JDB. Caries risk assessment appropriate for the age 1 visit (infants and toddlers). J Calif Dent Assoc 2007;35(10):687-702. 60. American Dental Association Councils on Scientific Affairs and Dental Practice. Caries Risk Assessment Form (Ages 0-6). American Dental Association: Chicago, Ill; 2008. Available at: “http://www.ada.org/sections/professionalResources/docs/topics_caries_under6.doc”. Accessed July 3, 2010. 61. American Dental Association Councils on Scientific Affairs and Dental Practice. Caries Risk Assessment Form (Age >6). American Dental Association: Chicago, Ill; 2008. Available at: “http://www.ada.org/sections/ professionalResources/docs/topics_caries_over6.doc\”. Accessed July 3, 2010 62. Featherstone JDB, Domejean-Orliaguet S, Jenson L, Wolff M, Young DA. Caries risk assessement in practice for age 6 through adult. J Calif Dent Assoc 2007;35(10): 703-13. 63. American Academy of Pediatric Dentistry. Policy on interim therapeutic restorations. Pediatric Dent 2009;31(special issue):38-9.
american academy of pediatric dentistry
Guideline on Perinatal Oral Health Care Originating Council Council on Clinical Affairs
Adopted 2009
Purpose The American Academy of Pediatric Dentistry (AAPD) recognizes that perinatal oral health, along with infant oral health, is one of the foundations upon which preventive education and dental care must be built to enhance the opportunity for a child to have a lifetime free from preventable oral disease. Aware that dentists, physicians, allied health professionals, and community organizations must be involved as partners to achieve this goal, the AAPD proposes recommendations for perinatal oral healthcare, including caries risk assessment, anticipatory guidance, preventive strategies, and appropriate therapeutic interventions, to be followed by the stakeholders in perinatal and pediatric oral health.
Method This guideline is based on a review of the current dental and medical literature related to perinatal oral health care. An electronic search was conducted using the following parameters: Terms: “early childhood caries”, “perinatal”, and “perinatal oral health”; Fields: all fields; Limits: within the last 10 years, humans, English, and clinical trials. Papers for review were chosen from the resultant list and from references within selected articles. When data did not appear sufficient or were inconclusive, recommendations were based upon expert and/ or consensus opinion by experienced researchers and clinicians.
Background The perinatal period is defined as the period around birth, beginning with the completion of the 20-28th week of gestation and ending 7-28 days after birth.1-4 Perinatal oral health plays a crucial role in the overall health and well being of pregnant women.5 It is also essential for the health and well being of their newborn children. Many women do not seek dental care during their pregnancy, and those that do often confront unwillingness by dentists to provide care.6,7 Many expectant mothers are unaware of the implications of poor oral health for themselves, their pregnancy, and/or their unborn child. Research continues to show links between periodontal disease and adverse outcomes in pregnancy including preterm deliveries, low birth weight babies, and preeclampsia.8-14 Furthermore, mothers with poor oral health and high levels of cariogenic oral bacteria are at greater risk for infecting their children with the bacteria and increasing their children’s caries risk at an early age.15 Dental caries in infants is a disease that is,
by and large, preventable. Determining those mothers at highest risk for transferring cariogenic bacteria to their children improves opportunities for preventive intervention. The primary goal of perinatal oral health care, with regard to caries transmission, is to lower the numbers of cariogenic bacteria in an expectant mother’s mouth so that Mutans streptococci (MS) colonization of the infant can be delayed as long as possible.16 Timely delivery of educational information and preventive therapies to these parents can help prevent the later need for dental rehabilitation in their children. Physicians, nurses, and other health care professionals are far more likely to see expectant or new mothers and their infants than are dentists. Therefore, it is essential that these providers be aware of the infectious etiology and associated risk factors of caries and early childhood caries (ECC), make appropriate decisions regarding timely and effective interventions for pregnant women, and facilitate the establishment of a dental home.17-19
Perinatal Oral Health Caries Caries results from an overgrowth of specific organisms that are part of the normally-occurring human oral flora.20 MS is considered to be a principal indicator group of bacterial organisms responsible for dental caries.21 MS colonization of an infant has been shown to occur from the time of birth.22-28 While colonization had been thought to occur after dental eruption (as teeth provide non-shedding surfaces for adherence), current data show that other surfaces also may harbor MS.26,29-30 The furrows of the tongue appear to be an important ecological niche in harboring the bacteria in predentate infants.27,29 Vertical colonization of MS from mother to infant is well documented;31-33 genotypes of MS in infants appear identical to those present in mothers in approximately 71% of motherinfant pairs.34 The higher the levels of maternal salivary MS, the greater the risk of the infant being colonized.35 The success of transmission and resulting colonization of the mother’s salivary MS may be related to several factors including the magnitude of the inoculum, frequency of inoculation, and a minimum infective dose.36-38 Along with maternal salivary levels of MS, the mother’s oral hygiene, periodontal disease, snack frequency, and socioeconomic status also are associated with infant colonization.30 Recent reports have indicated that horizontal transmission (ie, transmission between members of a group) may be of concern. 39-41 Horizontal sources may include siblings of similar age or children in a daycare center. clinical guidelines
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Caries risk assessment can be performed to determine the patient’s relative risk for caries. Its goal is to prevent disease by identifying and minimizing causative factors (eg, microbial burden, dietary habits, plaque accumulation) and optimizing protective factors (eg, fluoride exposure, oral hygiene, sealants).42 Caries risk assessment tools can aid in the identification of reliable predictors and allow health care professionals to identify and refer high-risk patients.43 The early establishment of a dental home provides time-critical opportunities to implement preventive oral health practices, including a caries risk assessment, and reduces the risk of preventable oral/dental conditions or disease for children.44 Anticipatory guidance 45 Anticipatory guidance for the mother and/or other caregivers can help delay the onset and reduce the impact of MS colonization of the infant. Modification of the mother’s oral hygiene and diet and the use of topical chlorhexidine and/or fluoride can have a significant effect on MS levels and, correspondingly, the child’s caries rate.46-48 Perinatal anticipatory guidance includes the following: • Oral health education: The perinatal period is an opportune time to educate and perform dental treatment on expectant mothers.7,10,49,50 Pregnancy offers an opportunity to educate women regarding oral health by providing a “teachable moment” in self-care and future child-care.51 Early intervention and counseling during the perinatal period from all health care providers (eg, physicians, dentists, nurses) are essential to ensure good oral health for the mother and infant. • Oral hygiene: Tooth-brushing and flossing by the mother on a daily basis are important to help dislodge food and reduce bacterial plaque levels. Systematic literature reviews suggest an association between periodontal disease and an increased risk of adverse pregnancy outcomes, including preterm deliveries and low birth weight babies.52,53 Periodontal infections, which can be a reservoir for inflammatory mediators, can pose a threat to the placenta and fetus which can increase the likelihood of preterm delivery.54,55 Mothers with severe periodontitis have high levels of prostaglandin in their gingival crevicular fluid and blood. In turn, these increased levels of prostaglandins may be associated with uterine contractions leading to preterm deliveries.54,56 Fortunately, research shows that scaling and root planning during pregnancy can reduce the likelihood of preterm deliveries and low birth weight babies.8,57-61 These data thus emphasize the need for perinatal intervention. The effects of pregnancy negatively may affect oral health behaviors among pregnant women. Nausea and vomiting may lead to avoidance of tooth brushing, resulting in an increased caries rate. For a pregnant woman experiencing frequent vomiting, rinsing with a cup of water containing a teaspoon of baking soda and waiting an hour before brushing can help minimize dental erosion.7 Using a fluoridated toothpaste, chewing sugarless or 110
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xylitol-containing gum, and eating small amounts of nutritious food through out the day can help minimize their caries risk.7 Diet: Important components of the mother’s diet need to be discussed fully. A healthy diet is necessary to provide adequate amounts of nutrients for the mother-to-be and unborn child. Food cravings may lead to the consumption of foods that increase the mother’s caries risk. The caries potential of the mother’s diet, (ie, cariogenicity of certain foods, beverages, medicines) as well as its effect on her child, should be addressed. The frequency of consumption of cariogenic substances and resulting demineralization process also are important discussion topics. Fluoride: Daily use of a fluoridated toothpaste approved by the American Dental Association and rinsing nightly with an alcohol-free, over-the-counter mouth rinse containing 0.05% sodium fluoride have been suggested to help reduce plaque levels and help promote enamel remineralization.16 Professional oral health care: Routine professional dental care for the mother can help optimize her oral health. Every pregnant woman should have an oral evaluation, be counseled on proper oral hygiene, and be referred for preventive and therapeutic oral health care.7,10 Removal of active caries with subsequent restoration is important to suppress maternal MS reservoirs and has the potential to minimize the transfer of MS to the infant, thereby decreasing the infant’s risk of developing ECC.7 The safest time to perform dental treatment during pregnancy is in the second trimester, or the 14th–20th weeks.7,10,51,62 The risk of pregnancy loss is lower compared to that in the first trimester, and organogenesis is complete.7 Even though the second trimester is usually optimal, dental treatment can be accomplished safely at any time during pregnancy. Treatment options may include diagnostic x-rays,7,63-67 dental prophylaxis, periodontal treatment, and restorations68-73 with the administration of local anesthetics containing epinephrine.7,74 Amalgam may be considered as a restorative material in pregnant women. There is no evidence that fetal exposure to mercury releases from the mother’s existing amalgam restorations causes any adverse effects.68-70,72 Since mercury vapor released during removal and placement of amalgam restoration may be absorbed into the blood stream and cross the placental barrier, the use of rubber dam and high speed evacuation is recommended.72 Antibiotics and analgesics for treating infection and controlling pain may be administered.7 Acute conditions, such as pain and swelling, should be treated as soon as possible.7,75 Delay in necessary treatment could result in significant risk to the mother and indirectly to the fetus.7 The consequences of not treating an active infection during pregnancy outweigh the possible risks presented by most of the medications required for dental treatment.76 Due to patient positioning, comfort is a consideration for treatment during the third trimester. In these cases, elective treatment sometimes is best deferred until after delivery.
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• Delay of colonization: Reducing maternal MS reservoirs, avoiding or delaying MS transmission, and implementing preventive practices for the child can help delay the colonization process.77-79 Maternal MS reservoirs can be suppressed by dietary counseling, reducing the frequency of simple carbohydrate intake, applying topical chlorhexidine and/or fluoride, removing and restoring active caries, and chewing xylitol-containing chewing gum.7 Evidence suggests that the use of xylitol chewing gum (4 pieces per day by the mother) has a significant impact on decreasing the child’s caries rate. 48,80,81 Avoidance or delay of MS transmission can be accomplished by educating the mother or caregiver on behaviors that directly pass saliva to the child (eg, sharing utensils or cups, cleaning a dropped pacifier by mouth).77,82,83 Routine preventive efforts should include toothbrushing, optimizing the child’s fluoride exposure, and limiting the child’s frequency of carbohydrate intake.
Recommendations The AAPD recommends: 1. Every expectant mother receive a comprehensive oral health evaluation from a dentist and, if not previously accomplished, establish a dental home as early as possible during pregnancy. The first visit should consist of review of medical, dental, and dietary histories, risk assessment for caries and periodontal disease, diagnosis of disease and other conditions, oral health education, and anticipatory guidance. Radiographic assessment and treatment of oral conditions should be performed with attention to maternal and fetal safety and patient comfort. 2. All primary health care professionals who serve pregnant women provide education on the etiology and prevention of ECC. Oral health counseling and referral for a comprehensive oral examination and treatment during pregnancy is especially important for the mother. 3. The curriculum of all medical, nursing, and allied health professional programs include education in perinatal oral health, including the infectious etiology of ECC, methods of oral health risk assessment, anticipatory guidance, and the need for early establishment of a dental home. 4. Parents/caregivers establish a dental home for infants by 12 months of age. 5. Legislators, policy makers and third party payors be educated about the benefits of perinatal intervention in order to support efforts that improve access to oral health care for pregnant women, including more frequent and comprehensive services.
References 1. Center for Cancer Education, University of Newcastle upon Tyne. Dictionary of Cell and Molecular Biology. Available at: “http://cancerweb.ncl.ac.uk/cgi-bin/omd? query=perinatal”. Accessed June 11, 2009. 2. Datasegment.com. Online dictionary. Available at: “http: //onlinedictionary.datasegment.com/word/perinatal”. Accessed June 11, 2009.
3. The Free Encyclopedia Wikimedia Foundation Inc. Wikipedia. Available at: “http://www.en.wikipedia.org/wiki/ Perinatal”. Accessed June 11, 2009. 4. Merriam-Webster Online Dictionary. Available at: “http:// www.merriam-webster.com/dictionary/perinatal”. Accessed June 11, 2009. 5. Brown A. Access or Oral Health Care During the Perinatal Period: A Policy Brief. National Maternal and Child Oral Health Resource Center. Georgetown University, Washington, DC; 2008. Available at: “http://www.mchoralhealth. org/PDFs/PerinatalBrief.pdf ”. Accessed August 30, 2009. 6. Gaffield ML, Gilbert BJ, Malvitz DM. Oral Health during pregnancy: An analysis of information collected by the pregnancy risk assessment monitoring system. J Am Dent Assoc 2001;132(7):1009-16. 7. New York State Department of Health. Oral health care during pregnancy and early childhood: Practice Guidelines. August, 2006. Available at: “http://www.health.state. ny.us/publications/0824.pdf ”. Accessed December 29, 2008. 8. D asanayake AP, Gennaro S, Hendricks-Muñoz KD, Chhun N. Maternal periodontal disease, pregnancy, and neonatal outcomes. MCN Am J Matern Child Nurs 2008;33(1):45-9. 9. Sacco G, Carmagnola D, Abati S, et al. Periodontal disease and preterm birth relationship: A review of the literature. Minerva Stomatol 2008;57(5):233-50. 10. Silk H, Douglass AB, Douglass JM, Silk L. Oral health during pregnancy. Am Fam Physician 2008;77(8):1139-44. 11. Xiong X, Buekens P, Fraser WD, Beck J, Offenbacher S. Periodontal disease and adverse pregnancy outcomes: A systematic review. BJOG 2006;113(2):135-43. 12. Siqueira FM, Cota LO, Costa JE, Haddad JP, Lana AM, Costa FO. Maternal periodontitis as a potential risk variable for preeclampsia: A case-control study. J Periodontol 2008;79(2):207-15. 13. Oettinger-Barak O, Barak S, Ohel G, et al. Severe pregnancy complication (preeclampsia) is associated with greater periodontal destruction. J Periodontol 2005;76 (1):134-7. 14. McKeown D. The link between periodontal disease and adverse birth outcomes. Toronto Staff Report 2006. Available at: “http://www.toronto.ca/legdocs/2006/agendas/com mittees/hl/hl060227/it002.pdf ”. Accessed June 23, 2006. 15. Ramos-Gomez FJ, Weintraub JA, Gansky SA, Hoover CI, Featherstone JD. Bacterial, behavioral and environmental factors associated with early childhood caries. J Clin Pedi Dent 2002;26(2):165-73. 16. American Academy of Pediatrics. Policy on oral health risk assessment timing and establishment of the dental home. Pediatrics 2003;111(5Pt1):1113-6. 17. Nowak AJ, Warren JJ. Infant oral health and oral habits. Pediatr Clin North Am 2000;47(5):1043-66. 18. Lewis CW, Grossman DC, Domoto PK, Deyo RA. The role of the pediatrician in the oral health of children: A national survey. Pediatrics 2000;106(6):E84. clinical guidelines
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19. Harrison R. Oral health promotion for high-risk children: Case studies from British Columbia. J Can Dent Assoc 2003;69(5):292-6. 20. Loesche WJ. Clinical and microbiological aspects of chemotherapeutic agents used according to the specific plaque hypothesis. J Dent Res 1979;58(12):2404-12. 21. Ge Y, Caufield PW, Fisch GS, Li Y. Streptococcus mutans and Streptococcus sanguinis colonization correlated with caries experience in children. Caries Res 2008;42(6):444-8. 22. Stiles HM, Meyers R, Brunnelle JA, Wittig AB. Occurrence of Streptococcus mutans and Streptococcus sanguis in the oral cavity and feces of young children. In: Stiles M, Loesch WJ, O’Brien T, eds. Microbial Aspects of Dental Caries. Washington, DC: Information Retrieval; 1976:187. 23. Loesche WJ. Microbial Adhesion and Plaque. In: Dental Caries: A Treatable Infection. 2nd ed. Grand Haven, Mich. Automated Diagnostic Documentation, Inc; 1993:81-116. 24. Berkowitz RJ, Jordan HV, White G. The early establish-ment of Streptococcus mutans in the mouth of infants. Arch Oral Biol 1975;20(3):171-4. 25. Wan AK, Seow WK, Purdie DM, Bird PS, Walsh LJ, Tudehope DI. A longitudinal study of Streptococcus mutans colonization in infants after tooth eruption. J Dent Res 2003;82(7):504-8. 26. Wan AK, Seow WK, Walsh LJ, Bird P, Tudehope DI, Purdie DM. Association of Streptococcus mutans infection and oral developmental nodules in pre-dentate infants. J Dent Res 2001;80(10):1945-8. 27. Berkowitz RJ. Mutans streptococci: Acquisition and transmission. Pediatr Dent 2006;28(2):106-9; discussion 192-8. 28. Law V, Seow WK, Townsend G. Factors influencing oral colonization of mutans streptococci in young children. Aust Dent J 2007;52(2):93-100; quiz 159. 29. Tanner AC, Milgrom PM, Kent R Jr, et al. The microbiota of young children from tooth and tongue samples. J Dent Res 2002;81(1):53-7. 30. Wan AK, Seow WK, Purdie DM, Bird PS, Walsh LJ, Tudehope DI. Oral colonization of Streptococcus mutans in six-month-old predentate infants. J Dent Res 2001;80 (12):2060-5. 31. Davey AL, Rogers AH. Multiple types of the bacterium Streptococcus mutans in the human mouth and their intrafamily transmission. Arch Oral Biol 1984;29(6):453-60. 32. Berkowitz R, Jones P. Mouth-to-mouth transmission of the bacterium Streptococcus mutans between mother and child. Arch Oral Biol 1985;30(4):377-9. 33. Douglass JM, Li Y, Tinanoff N. Association of Mutans streptococci between caregivers and their children. Pediatr Dent 2008;29(5):375-87. 34. Li Y, Caufield PW. The fidelity of initial acquisition of Mutans streptococci by infants from their mothers. J Dent Res 1995;74(2):681-5. 35. American Academy of Pediatric Dentistry. Policy on early childhood caries (ECC): Classifications, consequences, and prevention strategies. Pediatr Dent 2008;29(suppl):39-41. 112
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36. Acs G, Lodolini G, Kaminshy S, Cisneros GJ. Effect of nursing caries on body weight in pediatric populations. Pediatr Dent 1992;14(5):302-5. 37. Clarke M, Locker D, Berall G, Pencharz P, Kenny DJ, Judd P. Malnourishment in a population of young children with severe early childhood caries. Pediatr Dent 2006;28 (3):254-9. 38. Ismail AI. Prevention of early childhood caries. Comm Dent Oral Epidemiol 1998;26(suppl):49-61. 39. Mattos-Graner RO, Li Y, Caufield PW, Duncan M, Smith JD. Genotypic diversity of Mutans streptococci in Brazilian nursery children suggests horizontal transmission. J Clin Microbiol 2001;39(6):2313-6. 40. Van Loveren C, Buijs JF, ten Cate JM. Similarity of bacteriocin activity profiles of Mutans streptococci within the family when the children acquire strains after the age of 5. Caries Res 2000;34(6):481-5. 41. Redmo Emanuelsson IM, Wang XM. Demonstration of identical strains of Mutans streptococci within Chinese families by genotyping. Eur J Oral Sci 1998;106(3):778-94. 42. American Academy of Pediatric Dentistry. Guideline on periodicity of examination, preventive dental services, anticipatory guidance, and oral treatment for infants, children, and adolescents. Pediatr Dent 2009;31(special issue):118-25. 43. American Academy of Pediatric Dentistry. Policy on the use of a caries-risk assessment tool (CAT) for infants, children, and adolescents. Pediatr Dent 2009;30(suppl):29-33. 44. American Academy of Pediatric Dentistry. Policy on the dental home. Pediatr Dent 2009;30(suppl):22-23. 45. Nowak AJ, Casamassimo PS. Using anticipatory guidance to provide early dental intervention. J Am Dent Assoc 1995;126(8):1156-63. 46. Köhler B, Andréen I, Jonsson B. The effects of cariespreventive measures in mothers on dental caries and the oral presence of the bacteria Streptococcus mutans and lactobacilli in their children. Arch Oral Biol 1984;29(11):879-83. 47. Brambilla E, Felloni A, Gagliani M, Malerba A, GarcíaGodoy F, Strohmenger L. Caries prevention during pregnancy: Results of a 30-month study. J Am Dent Assoc 1998;129(7):871-7. 48. Isokangas P, Söderling E, Pienihäkkinen K, Alanen P. Occurrence of dental decay in children after maternal consumption of xylitol chewing gum: A follow-up from 0 to 5 years of age. J Dent Res 2000;79(11):1885-9. 49. Boggess KA, Society for Maternal-Fetal Medicine Publications Committee. Maternal oral health in pregnancy. Obstet Gynecol 2008;111(4):976-86. 50. De La Cruz GG, Rozier RG, Slade G. Dental screening and referral of young children by pediatric primary care providers. Pediatrics 2004;114(5):e642-52. 51. Boggess KA, Edelstein BL. Oral health in women during preconception and pregnancy: Implications for birth outcomes and infant oral health. Matern Child Health J 2006;10(5 suppl):S169-74. 52. Xiong X, Buekens P, Vastardis S, Yu SM. Periodontal disease and pregnancy outcomes: State-of-the-science. Obstet Gynecol Surv 2007;62(9):605-15.
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53. Khader YS, Ta’ani Q. Periodontal diseases and the risk of preterm birth and low birth weight: A meta-analysis. J Periodontol 2005;76(2):161-5. 54. Offenbacher S, Katz V, Fertik G, et al. Periodontal infections as a possible risk factor for preterm low birth weight. J Periodontol 1996;67(suppl 10):1103-13. 55. Jeffcoat MK, Geurs NC, Reddy MS, Cliver SP, Goldenberg RL, Hauth JC. Periodontal infection and preterm birth: Results of a prospective survey. J Am Dent Assoc 2001;132(7):875-80. 56. Offenbacher S, Jared HL, O’Reily PG, et al. Potential pathogenic mechanisms of periodontitis associated pregnancy complications. Ann Periodontol 1998;3(1):233-50. 57. López NJ, Da Silva I, Ipinza J, Gutiérrez J. Periodontal therapy reduces the rate of preterm low birth weight in women with pregnancy-associated gingivitis. J Periodontol 2005;76(11 suppl):2144-53. 58. Jeffcoat MK, Hauth JC, Geurs NC, et al. Periodontal disease and preterm birth: Results of a pilot intervention study. J Periodontal 2003;74(8):1214-8. 59. Scannapieco FA, Bush RB, Paju S. Periodontal disease as a risk factor for adverse pregnancy outcomes. A systemic review. Ann Periodontol 2003;8(1):70-8. 60. Dasanayake AP, Li Y, Wiener H, Ruby JD, Lee, MJ. Salivary actinomyces naeslundii genospecies 2 and lactobacillus casei levels predict pregnancy outcomes. J Periodontol 2005;76(2):171-7. 61. López NJ, Smith PC, Gutiérrez J. Periodontal therapy may reduce the risk of preterm low birth weight in women with periodontal disease: A randomized controlled trial. J Periodontol 2002;73(8):911-24. 62. Gajendra S, Kumar JV. Oral health and pregnancy: A review. NY State Dent J 2004;70(1):40-4. 63. American College of Obstetrics and Gynecology. Committee Opinion, Number 299, September 2004 Guidelines for diagnostic imaging during pregnancy. Obstet Gynecol 2004;104(3):647-51. 64. National Council on Radiation Protection and Measurement. Report No. 54: Medical radiation exposure of pregnant and potentially pregnant women. Bethesda, Md; 1977. 65. Toppenberg KS, Hill DA, Miller DP. Safety of radiographic imaging during pregnancy. Am Fam Physician 1999;59(7):1813-8, 1820. 66. Matteson SR, Joseph LP, Bottomley W, et al. The report of the panel to develop radiographic selection criteria for dental patients. Gen Dent 1991;39(4):264-70. 67. American Dental Association, US Dept of Health and Human Services. The selection of patients for x-ray examinations: Dental radiographic examinations. Rockville, Md. Food and Drug Administration, 2004; HHS Publication Number 88-8273. Available at: “http://www.ada.org/prof/ resources/topics/radiography.asp#radiographs”. Accessed December 30, 2008.
68. Life Sciences Research Office. Review and analysis of the literature on the potential adverse effects of dental amalgam. Bethesda, Md. December 9, 2004. Available at: “http: //www.lsro.org/presentation_files/amalgam/amalgam_pressrelease.pdf ”. Accessed June 15, 2009. 69. US Food and Drug Administration, Center for Devices and Radiological Health Consumer Information. Consumer Update: Dental Amalgam. Available at: “http://www.fda. gov/cdrh/consumer/amalgams.html”. Accessed December 30, 2008. 70. Hujoel PP, Lydon-Rochelle M, Bollen AM, Woods JS, Geurtsen W, del Aguila MA. Mercury exposure from dental filling replacement during pregnancy and low birth weight risk. Am J Epidemiol 2005;161(8):734-40. 71. March of Dimes. During your pregnancy: Things to avoid: Mercury. 2008. Available at: “http://www.marchofdimes. com/pnhec/159_15759.asp”. Accessed December 30, 2008. 72. Whittle KW, Whittle JG, Sarll DW. Amalgam fillings during pregnancy. Br Dent J 1998;185(10):500. 73. Olea N, Pulgar R, Perez P, et al. Estrogenicity of resin-based composites and sealants used in dentistry. Environ Health Perspect 1996;104(3):298-305. 74. Rosen MA. Management of anesthesia for the pregnant surgical patient. Anesthesiol 1999;91(4):1159-63. 75. Chiodo GT, Rosenstein DI. Dental treatment during pregnancy: A preventive approach. J Am Dent Assoc 1985; 110(3). 76. Moore PA. Selecting drugs for the dental patient. J Am Dent Assoc 1998;129(9):1281-6. 77. Berkowitz RJ. Causes, treatments and prevention of early childhood caries: A microbiologic perspective. J Can Dent Assoc 2003;69(5):304-7. 78. Kohler B, Andreen I. Influence of caries-preventive measures in mothers on cariogenic bacteria and caries experience in their children. Arch Oral Biol 1994;39(10): 907-11. 79. Li Y, Dasanayake AP, Caufield PW, Elliot RR. Butts JT III. Characterization of maternal Mutans streptococci transmission in an African American population. Dent Clin North Am 2003;47(1):87-101. 80. Söderling E, Isokongas P, Pienihäkkien K, Tenovuo J, Alanen P. Influence of maternal xylitol consumption on mother-child transmission of Mutans streptococci: 6-year follow-up. Caries Res 2001;35(3):173-7. 81. Gomez SS, Weber AA. Effectiveness of a caries preventive program in pregnant women and new mothers on their offspring. Int J Paediatr Dent 2001;11(2):117-22. 82. Berkowitz RJ. Acquisition and transmission of Mutans streptococci. J Calif Dent Assoc 2003;31(2):135-8. 83. Caufield PW, Wannemuehler YM, Hansen JB. Familial clustering of Streptococcus mutans cryptic plasmid strain in a dental clinic population. Infect Immun 1982;38(2): 907-11.
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Guideline on Infant Oral Health Care Originating Committee
Clinical Affairs Committee – Infant Oral Health Subcommittee Review Council Council on Clinical Affairs
Adopted 1986
Revised 1989, 1994, 2001, 2004, 2009
Purpose The American Academy of Pediatric Dentistry (AAPD) recognizes that infant oral health, along with perinatal oral health, is one of the foundations upon which preventive education and dental care must be built to enhance the opportunity for a lifetime free from preventable oral disease. Recognizing that allied health professionals and community organizations must be involved as partners to achieve this goal, the AAPD proposes recommendations for preventive strategies, oral health risk assessment, anticipatory guidance, and appropriate therapeutic interventions to be followed by the stakeholders in pediatric oral health.
Methods
This revision included a new systematic literature search of the MEDLINE/Pubmed electronic database using the following parameters: Terms: infant oral health, infant oral health care, and early childhood caries; Field: all fields; Limits: within the last 10 years, humans, English, and clinical trials. Papers for review were chosen from the resultant list and from references within selected articles. When data did not appear sufficient or were inconclusive, recommendations were based upon expert and/or consensus opinion by experienced researchers and clinicians.
Background Introduction The Centers for Disease Control and Prevention reports that caries is perhaps the most prevalent infectious disease in our nation’s children.1 More than 40% of children have caries by the time they reach kindergarten.2 Early childhood caries (ECC) can be a particularly virulent form of caries, beginning soon after tooth eruption, developing on smooth surfaces, progressing rapidly, and having a lasting detrimental impact on the dentition.3-8 This disease affects the general population but is 32 times more likely to occur in infants who are of low socioeconomic status, who consume a diet high in sugar, and whose mothers have a low education level.9 Caries in primary teeth can affect children’s growth, result in significant pain and potentially life-threatening infection, and diminish overall quality
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of life.10-17 Since physicians, nurses, and other health care professionals are far more likely to see new mothers and infants than are dentists, it is essential that they be aware of the infectious etiology and associated risk factors of ECC, make appropriate decisions regarding timely and effective intervention, and facilitate the establishment of the dental home.3,18-21 Caries Caries results from an overgrowth of specific organisms that are part of normally-occurring human oral flora.22 Mutans streptococci (MS) is considered to be a principal indicator group of bacterial organisms responsible for dental caries.23 MS colonization of an infant has been shown to occur from the time of birth.24-30 While colonization had been thought to occur after dental eruption (as teeth provided non-shedding surfaces for adherence), current data show that other surfaces also may harbor MS.28,31,32 For example, the furrows of the tongue appear to be an important ecological niche in harboring the bacteria in predentate infants.29,31 Vertical colonization of MS from mother to infant is well documented;33-35 genotypes of MS in infants appear identical to those present in mothers in approximately 71% of motherinfant pairs.36 The higher the levels of maternal salivary MS, the greater the risk of the infant being colonized.37 Along with salivary levels of MS, mother’s oral hygiene, periodontal disease, snack frequency, and socioeconomic status also are associated with infant colonization.32 Recent reports have indicated that horizontal transmission (ie, transmission between members of a group) also may be of concern.38-40 Horizontal sources may include siblings of similar age or children in a daycare center. Preventive strategies Caries is a disease that is, by and large, preventable. Early risk assessment allows for identification of parent-infant groups who are at risk for ECC and would benefit from early preventive intervention. The ultimate goal of early assessment is the timely delivery of educational information to populations at high risk for developing caries in order to prevent the need for later surgical intervention.
american academy of pediatric dentistry
Oral health risk assessment An oral health risk assessment for infants by 6 months of age allows for the institution of appropriate preventive strategies as the primary dentition begins to erupt. Caries risk assessment can be used to determine the patient’s relative risk for caries. Even the most judiciously designed and implemented cariesrisk assessment tool, however, can fail to identify all infants at risk for developing ECC. In these cases, the mother may not be the colonization source of the child’s oral flora, the dietary intake of simple carbohydrates may be extremely high, or other uncontrollable factors may combine to place the patient at risk for developing caries. Therefore, screening for risk of caries in the parent and patient coupled with oral health counseling, although a feasible and equitable approach to ECC control, is not a substitute for the early establishment of the dental home.37 Whenever possible, the ideal approach to infant oral health care, including ECC prevention and management, is the early establishment of a dental home.21,41
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Anticipatory guidance42
General anticipatory guidance for the mother (or other intimate caregiver) includes the following: • Oral hygiene: Tooth-brushing and flossing by the mother on a daily basis are important to help dislodge food and reduce bacterial plaque levels. • Diet: Important components of dietary education for the parents include the cariogenicity of certain foods and beverages, role of frequency of consumption of these substances, and the demineralization/remineralization process. • Fluoride: Using a fluoridated toothpaste approved by the American Dental Association and rinsing every night with an alcohol-free, over-the-counter mouth rinse containing 0.05% sodium fluoride have been suggested to help reduce plaque levels and help enamel remineralization.18 • Caries removal: Routine professional dental care for the mothers can help keep their oral health in optimal condition. Removal of active caries with subsequent restoration is important to suppress maternal MS reservoirs and has the potential to minimize the transfer of MS to the infant, thereby decreasing the infant’s risk of developing ECC. 46 • Delay of colonization: Education of the parents, especially mothers, on avoiding saliva-sharing behaviors (eg, sharing spoons and other utensils, sharing cups, cleaning a dropped pacifier or toy with their mouth) can help prevent early colonization of MS in their infants. • Xylitol chewing gums: Evidence demonstrates that mothers’ use of xylitol chewing gum can prevent dental caries in their children by prohibiting the transmission of MS.47 General anticipatory guidance for the young patient (0 to 3 years of age) includes the following: • Oral hygiene: Oral hygiene measures should be implemented no later than the time of the eruption of the first primary tooth. Cleansing the infant’s teeth as soon as they erupt with either a washcloth or soft toothbrush will help
•
•
reduce bacterial colonization. Children’s teeth should be brushed twice daily with fluoridated toothpaste and a soft, age-appropriate sized toothbrush.37 A “smear” of toothpaste is recommended for children less than 2 years of age,48 while a “pea-size” amount of paste is recommended for children 2-5 years of age.48-50 Flossing should be initiated when adjacent tooth surfaces can not be cleansed with a toothbrush.37 Diet: High-risk dietary practices appear to be established early, probably by 12 months of age, and are maintained throughout early childhood.51,52 Frequent night time bottle feeding, ad libitum breast-feeding, and extended and repeated use of a sippy or no-spill cup are associated with, but not consistently implicated in ECC.53 Likewise, frequent consumption of snacks or drinks containing fermentable carbohydrates (eg, juice, milk, formula, soda) also can increase the child’s caries risk.54 Fluoride: Optimal exposure to fluoride is important to all dentate infants and children. The use of fluoride for the prevention and control of caries is documented to be both safe and effective.55-59 Twice-daily brushing with fluoridated toothpaste is recommended for all children as a preventive procedure.55.60 Professionally-applied fluoride, as well as athome fluoride treatments, should be considered for children at high caries risk based upon caries risk assessment.55,58,59,61,62 Systemically-administered fluoride should be considered for all children drinking fluoride deficient water (<0.6 ppm).63 Caution is indicated in the use of all fluoride-containing products. Fluorosis has been associated with cumulative fluoride intake during enamel development, with the severity dependent on the dose, duration, and timing of intake.58 Decisions concerning the administration of additional fluoride are based on the unique needs of each patient.43-45 Injury prevention: Practitioners should provide ageappropriate injury prevention counseling for orofacial trauma. Initially, discussions would include play objects, pacificers, car seats, and electric cords.64 Non-nutritive habits: Non-nutritive oral habits (eg, digit or pacifier sucking, bruxism, abnormal tongue thrust) may apply forces to teeth and dentoalveolar structures. It is important to discuss the need for early sucking and the need to wean infants from these habits before malocclusion or skeletal dysplasias occur.64
Recommendations The AAPD recommends that: 1. All primary health care professionals who serve mothers and infants provide parent/caregiver education on the etiology and prevention of ECC. Oral health counseling and referral for a comprehensive oral examination and treatment during pregnancy is especially important for the mother. 2. The infectious and transmissible nature of bacteria that cause ECC and methods of oral health risk assessment,
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anticipatory guidance, and early intervention be included in the curriculum of all medical, nursing, and allied health professional programs. Every infant receive an oral health risk assessment from his/her primary health care provider or qualified health care professional by 6 months of age. This initial visit should consist of the following: • assessing the patient’s risk of developing oral disease using a caries risk assessment; • providing education on infant oral health; and • evaluating and optimizing fluoride exposure. Parents or caregivers establish a dental home for infants by 12 months of age. The following should be accomplished at that visit: • recording thorough medical (infant) and dental (mother or primary caregiver and infant) histories; • completing a thorough oral examination; • assessing the infant’s risk of developing caries and determining an appropriate prevention plan and interval for periodic reevaluation based upon that assessment; • providing anticipatory guidance regarding dental and oral development, fluoride status, non-nutritive sucking habits, teething, injury prevention, oral hygiene instruction, and the effects of diet on the dentition; • planning for comprehensive care in accordance with accepted guidelines and periodicity schedules for pediatric oral health; • referring patients to the appropriate health professional if intervention is necessary. Health care professionals and all other stakeholders in children’s oral health should support the identification of a dental home for all infants at 12 months of age. Legislators, policy makers, and third party payors be educated about the benefits of early interventions in order to support efforts that improve access to oral health care for infants and children.
References 1. US Dept of Health and Human Services. Oral health in America: A report of the Surgeon General. Rockville, Md: US Dept of Health and Human Services, National Institute of Dental and Craniofacial Research, National Institutes of Health; 2000. 2. Pierce KM, Rozier RG, Vann WF Jr. Accuracy of pediatric primary care providers’ screening and referral for early childhood caries. Pediatrics 2002;109(5):E82-2. 3. Nowak AJ, Warren JJ. Infant oral health and oral habits. Pediatr Clin North Am 2000;47(5):1043-66. 4. Gray MM, Marchment MD, Anderson RJ. The relationship between caries experience in deciduous molars at 5 years and in first permanent molars of the same child at 7 years. Community Dent Health 1991;8(1):3-7.
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5. Grindefjord M, Dahllöf G, Modéer T. Caries development in children from 2.5 to 3.5 years of age: A longitudinal study. Caries Res 1995;29(6):449-54. 6. O’Sullivan DM, Tinanoff N. The association of early dental caries patterns with caries incidence in preschool children. J Public Health Dent 1996;56(2):81-3. 7. Johnsen DC, Gerstenmaier JH, DiSantis TA, Berkowitz RJ. Susceptibility of nursing-caries children to future approximal molar decay. Pediatr Dent 1997;19(1):37-41. 8. Heller KE, Eklund SA, Pittman J, Ismail AA. Associations between dental treatment in the primary and permanent dentitions using insurance claims data. Pediatr Dent 2000;22(6):469-74. 9. Drury TF, Horowitz AM, Ismail AA, et al. Diagnosing and reporting early childhood caries for research purposes. J Public Health Dent 1999;59(3):192-7. 10. Acs G, Lodolini G, Kaminsky S, Cisneros GJ. Effect of nursing caries on body weight in a pediatric population. Pediatr Dent 1992;14(5):302-5. 11. Ayhan H, Suskan E, Yildirim S. The effect of nursing or rampant caries on height, body weight, and head circumference. J Clin Pediatr Dent 1996;20(3):209-12. 12. Fleming P, Gregg TA, Saunders ID. Analysis of an emergency dental service provided at a children’s hospital. Int J Paediatr Dent 1991;1(1):25-30. 13. Schwartz S. A one-year statistical analysis of dental emergencies in a pediatric hospital. J Can Dent Assoc 1994;60(11):959-62, 966-8. 14. Sheller B, Williams BJ, Lombardi SM. Diagnosis and treatment of dental caries-related emergencies in a children’s hospital. Pediatr Dent 1997;19(8):470-5. 15. Low W, Tan S, Schwartz S. The effect of severe caries on the quality of life in young children. Pediatr Dent 1999; 21(6):325-6. 16. Acs G, Pretzer S, Foley M, Ng MW. Perceived outcomes and parental satisfaction following dental rehabilitation under general anesthesia. Pediatr Dent 2001;23(5): 419-23. 17. Thomas CW, Primosch RE. Changes in incremental weight and well-being of children with rampant caries following complete dental rehabilitation. Pediatr Dent 2002;24(2):109-13. 18. American Academy of Pediatrics. Policy on oral health risk assessment timing and establishment of the dental home. Pediatrics 2003;111(5Pt1):1113-6. 19. Lewis CW, Grossman DC, Domoto PK, et al. The role of the pediatrician in the oral health of children: A national survey. Pediatrics 2000;106(6):E84. 20. Harrison R. Oral health promotion for high-risk children: Case studies from British Columbia. J Can Dent Assoc 2003;69(5):292-6. 21. American Academy of Pediatrics, Section on Pediatric Dentistry and Oral Health. A policy statement: Preventive intervention for pediatricians. Pediatrics 2008;122 (6):1387-94.
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22. Loesche WJ. Clinical and microbiological aspects of chemotherapeutic agents used according to the specific plaque hypothesis. J Dent Res 1979;58(12):2404-12. 23. Ge Y, Caufield PW, Fisch GS, Li Y. Streptococcus mutans and Streptococcus sanguis colonization correlated with caries experience in children. Caries Res 2008;42(6):444-8. Epub 2008 Oct 3. 24. Berkowitz RJ, Jordan HV, White G. The early establishment of Streptococcus mutans in the mouths of infants. Arch Oral Biol 1975;20(3):171-4. 25. Stiles HM, Meyers R, Brunnelle JA, Wittig AB. Occurrence of Streptococcus mutans and Streptococcus sanguis in the oral cavity and feces of young children. In: Stiles M, Loesch WJ, O’Brien T, eds. Microbial Aspects of Dental Caries. Washington, DC: Information Retrieval; 1976:187. 26. Loesche WJ. Microbial adhesion and plaque. In: Dental Caries: A Treatable Infection. 2nd ed. Grand Haven, Mich; Automated Diagnostic Documentation, Inc; 1993:81-116. 27. Wan AK, Seow WK, Purdie DM, Bird PS, Walsh LJ, Tudehope DI. A longitudinal study of Streptococcus mutans colonization in infants after tooth eruption. J Dent Res 2003;82(7):504-8. 28. Wan AK, Seow WK, Walsh LJ, Bird P, Tudehope DI, Purdie DM. Association of Streptococcus mutans infection and oral developmental nodules in predentate infants. J Dent Res 2001;80(10):1945-8. 29. Berkowitz RJ. Mutans streptococci: Acquisition and transmission. Pediatr Dent 2006;28(2):106-9, discussion192-8. 30. Law V, Seow WK, Townsend G. Factors influencing oral colonization of mutans streptococci in young children. Aust Dent J 2007;52(2):93-100, quiz 159. 31. Tanner ACR, Milgrom PK, Kent R Jr, et al. The microbiotia of young children from tooth and tongue samples. J Dent Res 2002;81(1):53-7. 32. Wan AK, Seow WK, Purdie DM, Bird PS, Walsh LJ, Tudehope DI. Oral colonization of Streptococcus mutans in six-month-old predentate infants. J Dent Res 2001; 80(12):2060-5. 33. Davey AL, Rogers AH. Multiple types of the bacterium Streptococcus mutans in the human mouth and their intrafamily transmission. Arch Oral Biol 1984;29(6):453-60. 34. Berkowitz R, Jones P. Mouth-to-mouth transmission of the bacterium Streptococcus mutans between mother and child. Arch Oral Biol 1985;30(4):377-9. 35. Douglass JM, Li Y, Tinanoff N. Association of Mutans streptococci between caregivers and their children. Pediatr Dent 2008;29(5):375-87. 36. Li Y, Caufield PW. The fidelity of initial acquisition of Mutans streptococci by infants from their mothers. J Dent Res 1995;74(2):681-5. 37. American Academy of Pediatric Dentistry. Policy on early childhood caries (ECC): Classifications, consequences, and preventive strategies. Pediatr Dent 2008;30(suppl):40-2.
38. Mattos-Graner RO, Li Y, Caufield PW, Duncan M, Smith DJ. Genotypic diversity of Mutans streptococci in Brazilian nursery children suggests horizontal transmission. J Clin Microbiol 2001:39(6):2313-6. 39. Van Loveren C, Bujis JF, ten Cate JM. Similarity of bacteriocin activity profiles of Mutans streptococci within the family when the children acquire strains after the age of 5. Caries Res 2000;34(6):481-5. 40. Emanuelsson L, Wang X. Demonstration of Identical strains of Mutans streptococci within Chinese families by genotyping. Eur J Oral Sci 1998;106(3):778-94. 41. American Academy of Pediatric Dentistry. Policy on the dental home. Pediatr Dent 2008;30(suppl):22-3. 42. Nowak AJ, Casamassimo PS. Using anticipatory guidance to provide early dental intervention. J Am Dent Assoc 1995;126(8):1156-63. 43. American Academy of Pediatric Dentistry. Policy on use of fluoride. Pediatr Dent 2008;30(suppl):34-5. 44. Hale K, Heller K. Fluorides: Getting the benefits, avoiding the risks. Contemp Pediatr 2000;2:121. 45. American Dental Association. Caries diagnosis and risk assessment: A review of preventive strategies and management. J Am Dent Assoc 1995;126(suppl):1S-24S. 46. New York State Department of Health. Oral health care during pregnancy and early childhood: Practice Guidelines. Aug, 2006. Available at: “http://www.health.state.ny.us/publications/0824.pdf ”. Accessed December 29, 2008. 47. Isokangas P, Söderling E, Pienihäkkinen K, Alanen P. Occurrence of dental decay in children after maternal consumption of xylitol chewing gum: A follow-up from 0 to 5 years of age. J Dent Res 2000;79(11):1885-9. 48. Scottish Intercollegiate Guideline Network. Prevention and management of dental decay in the pre-school child. A national guideline # 83. November, 2005. Available at: “http://www.sign.ac.uk/pdf/qrg83.pdf ”. Accessed March 6, 2009. 49. Pang DT, Vann WF Jr. The use of fluoride-containing toothpastes in young children: The scientific evidence for recommending a small amount. Pediatr Dent 1992;14(6): 384-7. 50. Ramos-Gomez FJ, Crall JJ, Gansky SA, Slayton RL, Featherstone JD. Caries risk assessment appropriate for the age 1 visit (infants and toddlers). J Calif Dent Assoc 2007;35(10):687-702. 51. Douglass JM. Response to Tinanoff and Palmer: Dietary determinants of dental caries and dietary recommendations for pre-school children. J Public Health Dent 2000;60(3):207-9. 52. Kranz S, Smiciklas-Wright H, Francis LA. Diet quality, added sugar, and dietary fiber intake in American preschoolers. Pediatr Dent 2006;28(2):164-71. 53. Reisine S, Douglass JM. Psychosocial and behavioral issues in early childhood caries. Commun Dent Oral Epidem 1998;26(suppl):32-44.
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54. Marino R, Bonze K, Scholl T, Anhalt H. Nursing bottle caries: Characteristics of children at risk. Clin Pediatr 1989;28(3):129-31. 55. Adair SM. Evidence-based use of fluoride in contemporary pediatric dental practice. Pediatr Dent 2006;28(2): 133-42. 56. Whitford GM. The physiological and toxicological characteristics of fluoride. J Dent Res 1990;69(special issue):539-49, discussion 556-7. 57. Workshop Reports I, II, III from “A symposium on changing patterns of fluoride intake” held at UNC-Chapel Hill, April 23-25, 1991. J Dent Res 1992;71(5):1214-27. 58. CDC. Recommendations for using fluoride to prevent and control dental caries in the United States. MMWR Recomm Rep 2001;50(RR-14):1-42. 59. Facts about fluoride. CDS Rev 2006;99(1):44.
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60. Featherstone JDB. Caries prevention and reversal based on caries balance. Pediatr Dent 2006;28(2):90-2. 61. American Dental Association, Council on Scientific Affairs. Professionally-applied topical fluoride: Evidencebased clinical recommendations. J Amer Dent Assoc 2006;137(8):1151-9. 62. American Academy of Pediatric Dentistry. Policy on use of a caries risk assessment tool (CAT) for infants, children, and adolescents. Pediatr Dent 2008;30(suppl):29-33. 63. American Academy of Pediatric Dentistry. Guideline on fluoride therapy. Pediatr Dent 2008;30(suppl):121-4. 64. American Academy of Pediatric Dentistry. Guideline on periodicity of examination, preventive dental services, anticipatory guidance, and oral treatment for children. Pediatr Dent 2009;31(special issue):118-25.
american academy of pediatric dentistry
Guideline on Adolescent Oral Health Care Originating Committee
Clinical Affairs Committee Review Council
Council on Clinical Affairs, Committee on the Adolescent
Adopted 1986
Revised 1999, 2003, 2005, 2010
Purpose The American Academy of Pediatric Dentistry (AAPD) recognizes that the adolescent patient has unique needs. This guideline addresses these unique needs and proposes general recommendations for their management.
Methods This guideline is an update of the previous document, revised in 2005. The update includes an electronic search using the following parameters: Terms: “adolescent” combined with “dental”, “gingivitis”, “oral piercing”, “sealants”, “oral health”, “caries”, “tobacco use”, “dental trauma”, “orofacial trauma”, periodontal”, “dental esthetics”, “smokeless tobacco”, “nutrition”, and “diet”; Fields: all fields; Limits: within the last 10 years; humans; English; clinical trials. The reviewers agreed upon the inclusion of 83 electronic and hand searched articles that met the defined criteria. When data did not appear sufficient or were inconclusive, recommendations were based upon expert and/or consensus opinion by experienced researchers and clinicians.
Background There is no standard definition of “adolescent”.1 Adolescents are defined very broadly as youths between the ages of 10 to 18. Using this definition, there were approximately 41.5 million adolescents in the United States in 2008, according to the US Census Bureau.2 The adolescent patient is recognized as having distinctive needs3,4 due to: (1) a potentially high caries rate; (2) increased risk for traumatic injury and periodontal disease; (3) a tendency for poor nutritional habits; (4) an increased esthetic desire and awareness; (5) complexity of combined orthodontic and restorative care (eg, congenitally missing teeth); (6) dental phobia; (7) potential use of tobacco, alcohol, and other drugs; (8) pregnancy; (9) eating disorders; and (10) unique social and psychological needs.5-8 Treatment of the adolescent patient can be multifaceted and complex. An accurate, comprehensive, and up-to-date medical history is necessary for correct diagnosis and effective treatment planning. Familiarity with the patient’s
medical history is essential to decreasing the risk of aggravating a medical condition while rendering dental care. If the parent is unable to provide adequate details regarding a patient’s medical history, consultation with the medical health care provider may be indicated. The practitioner also may need to obtain additional information confidentially from an adolescent patient.
Recommendations This guideline addresses some of the special needs within the adolescent population and proposes general recommendations for their management. Caries Adolescence marks a period of significant caries activity for many individuals. Current research suggests that the overall caries rate is declining, yet remains highest during adolescence.9 Immature permanent tooth enamel,10 a total increase in susceptible tooth surfaces, and environmental factors such as diet, independence to seek care or avoid it, a low priority for oral hygiene, and additional social factors also may contribute to the upward slope of caries in adolescence.1,11-13 It is important for the dental provider to emphasize the positive effects that fluoridation, routine professional care, patient education, and personal hygiene can have in counteracting the changing pattern of caries in the adolescent population.5,6,14,15
Management of Caries Primary prevention Fluoride: Fluoridation has proven to be the most economical and effective caries prevention measure. The adolescent can benefit from fluoride throughout the teenage years and into early adulthood. Although the systemic benefit of fluoride incorporation into developing enamel is not considered necessary past 16 years of age, topical benefits can be obtained through optimally-fluoridated water, professionally-applied and prescribed compounds, and fluoridated dentifrices.16 Recommendations: The adolescent should receive maximum fluoride benefit dependent on risk assessment17:
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1. Brushing teeth twice a day with a fluoridated dentifrice is recommended to provide continuing topical benefits.14,18 2. Professionally-applied fluoride treatments should be based on the individual patient’s caries-risk assessment, as determined by the patient’s dental provider.18 3. Home-applied prescription strength topical fluoride products [eg, 0.4% stannous fluoride gel, 0.5% fluoride gel or paste, 0.2% sodium fluoride (NaF) rinse] may be used when indicated by an individual’s caries pattern or caries risk status.18 4. Systemic fluoride intake via optimal fluoridation of drinking water or professionally-prescribed supplements is recommended to 16 years of age. Supplements should be given only after all other sources of fluoride have been evaluated.18 5. The criteria for determination of need and the methods of delivery should be those currently recommended by the American Dental Association and the AAPD.18 Oral hygiene: Adolescence can be a time of heightened caries activity and periodontal disease due to an increased intake of cariogenic substances and inattention to oral hygiene procedures.1,19 Tooth brushing with a fluoridated dentifrice and flossing can provide benefit through the topical effect of the fluoride and plaque removal from tooth surfaces.20 Recommendations: 1. Adolescents should be educated and motivated to maintain personal oral hygiene through daily plaque removal, including flossing, with the frequency and pattern based on the individual’s disease pattern and oral hygiene needs.19,20 2. Professional removal of plaque and calculus is recommended highly for the adolescent, with the frequency of such intervention based on the individual’s assessed risk for caries/periodontal disease, as determined by the patient’s dental provider.20,21 Diet management: The role of carbohydrates in caries initiation is unequivocal. Adolescents are exposed to and consume high quantities of refined carbohydrates and acid-containing beverages.11,12,22 The adolescent can benefit from diet analysis and modification. Recommendations: Diet analysis, along with professionallydetermined recommendations for maximal general and dental health, should be part of an adolescent’s dental health management.23
A diet analysis and management should consider:
1. dental disease patterns; 2. overall nutrient and energy needs; 3. psychosocial aspects of adolescent nutrition; 4. dietary carbohydrate intake and frequency; 5. intake and frequency of acid-containing beverages; 6. wellness considerations.
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Sealants: Sealant placement is an effective caries-preventive technique that should be considered on an individual basis. Sealants have been recommended for any tooth, primary or permanent, that is judged to be at risk for pit and fissure caries.6,12,24-27 Caries risk may increase due to changes in patient habits, oral microflora, or physical condition, and unsealed teeth subsequently might benefit from sealant applications.27 Recommendations: Adolescents at risk for caries should have sealants placed. An individual’s caries risk may change over time; periodic reassessment for sealant need is indicated throughout adolescence.27 Secondary prevention Professional preventive care: Professional preventive dental care, on a routine basis, may prevent oral disease or disclose existing disease in its early stages. The adolescent patient whose oral health has not been monitored routinely by a dentist may have advanced caries, periodontal disease, or other oral involvement urgently in need of professional evaluation and extensive treatment. Recommendations: 1. Timing of periodic oral examinations should take into consideration the individual’s needs and risk indicators to determine the most cost-effective, disease-preventive benefit to the adolescent.17 2. Initial and periodic radiographic evaluation should be a part of a clinical evaluation. The type, number, and frequency of radiographs should be determined only after an oral examination and history taking. Previously exposed radiographs should be available, whenever possible, for comparison. Currently accepted guidelines for radiographic exposures (ie, appropriate films based upon medical history, caries risk, history of periodontal disease, and growth and development assessments) should be followed.28 Restorative dentistry: In cases where remineralization of noncavitated, demineralized tooth surfaces is not successful, as demonstrated by progression of carious lesions, dental restorations are necessary. Preservation of tooth structure, esthetics, and each individual patient’s needs must be considered when selecting a restorative material.29 Molars with extensive caries or malformed, hypoplastic enamel—for which traditional amalgam or composite resin restorations are not feasible—may require full coverage restorations.27,30 Recommendations: Each adolescent patient and restoration must be evaluated on an individual basis. Preservation of noncarious tooth structure is desirable. Referral should be made when treatment needs are beyond the treating dentist’s scope of practice.27 Periodontal diseases Adolescence can be a critical period in the human being’s periodontal status. Epidemiologic and immunologic data suggest
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that irreversible tissue damage from periodontal disease begins in late adolescence and early adulthood.8 Adolescents have a higher prevalence of gingivitis than prepubertal children or adults. The rise of sex hormones during adolescence is suspected to be a cause of the increased prevalence. Studies suggest that the increase in sex hormones during puberty affects the composition of the subgingival microflora.31 Other studies suggest circulating sex hormones may alter capillary permeability and increase fluid accumulation in the gingival tissues. This inflammatory gingivitis is believed to be transient as the body accommodates to the ongoing presence of the sex hormones.32 Acute conditions: The adolescent may be subjected to acute conditions such as acute necrotizing ulcerative gingivitis and periodontitis, which can require immediate and occasional long-term management. In most cases, early diagnosis, treatment, and appropriate management can prevent irreversible damage. 33-35 Recommendations: Acute intraoral infection involving the periodontium and oral mucosa requires immediate treatment. Therapeutic management should be based on currently accepted techniques of periodontal therapy.36,37 Referral should be made when the treatment needs are beyond the treating dentist’s scope of practice. Chronic conditions: Chronic conditions affecting the adolescent include, but are not limited to, gingivitis, puberty gingivitis, hyperplastic gingivitis related to orthodontic therapy, gingival recession that may or may not be related to orthodontic therapy, drug-related gingivitis, pregnancy gingivitis, localized juvenile periodontitis, and periodontitis.24,31-33 Personal oral hygiene and regular professional intervention can minimize occurrence of these conditions and prevent irreversible damage. Recommendations: The adolescent will benefit from an individualized preventive dental health program, which includes the following items aimed specifically at periodontal health: 1. Patient education emphasizing the etiology, characteristics, and prevention of periodontal diseases, as well as selfhygiene skills.32-34 2. A personal, age-appropriate oral hygiene program including plaque removal, oral health self-assessment, and diet. Sulcular brushing and flossing should be included in plaque removal, and frequent follow-up to determine adequacy of plaque removal and improvement of gingival health should be considered.32-36 3. Regular professional intervention, the frequency of which should be based on individual needs and should include evaluation of personal oral hygiene success, periodontal status, and potential complicating factors such as medical conditions, malocclusion, or handicapping conditions. Periodontal probing, periodontal charting, and radiographic periodontal diagnosis should be a consideration
when caring for the adolescent. The extent and nature of the periodontal evaluation should be determined professionally on an individual basis. Those patients with progressive periodontal disease should be referred when the treatment needs are beyond the treating dentist’s scope of practice.32-34,36 4. Appropriate evaluation for procedures to facilitate orthodontic treatment including, but not limited to, tooth exposure, frenectomy, fiberotomy, gingival augmentation, and implant placement.37 Occlusal considerations Malocclusion can be a significant treatment need in the adolescent population as both environmental and genetic factors come into play. Although the genetic basis of much malocclusion makes it unpreventable, numerous methods exist to treat the occlusal disharmonies, temporomandibular joint dysfunction, periodontal disease, and disfiguration which may be associated with malocclusion. Within the area of occlusal problems are several tooth/jaw-related discrepancies that can affect the adolescent. Third molar malposition and temporomandibular disorders require special attention to avoid long-term problems. Congenitally missing teeth present complex problems for the adolescent and often require combined orthodontic and restorative care for satisfactory resolution. Malocclusion: Any tooth/jaw positional problems that present significant esthetic, functional, physiologic, or emotional dysfunction are potential difficulties for the adolescent. These can include single or multiple tooth malpositions, tooth/jaw size discrepancies, and craniofacial disfigurements. Recommendations: Malposition of teeth, malrelationship of teeth to jaws, tooth/jaw size discrepancy, skeletal malrelationship, or craniofacial malformations or disfigurement that presents functional, esthetic, physiologic, or emotional problems to the adolescent should be referred for evaluation when the treatment needs are beyond the treating dentist’s scope of practice. Treatment of malocclusion by a dentist should be based on professional diagnosis, available treatment options, patient motivation and readiness, and other factors to maximize progress.38 Third molars: Third molars can present acute and chronic problems for the adolescent. Impaction or malposition leading to such problems as pericoronitis, caries, cysts, or periodontal problems merits evaluation for removal.36,39 The role of the third molar as a functional tooth also should be considered. Although prophylactic removal of all impacted or unerupted disease-free third molars is not indicated, consideration should be given to removal by the third decade when there is a high probability of disease or pathology and/or the risks associated with early removal are less than the risks of later removal. Recommendations: Evaluation of third molars, including radiographic diagnostic aids, should be an integral part of the dental examination of the adolescent.28 For diagnostic and
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extraction criteria, refer to AAPD’s Guideline on Pediatric Oral Surgery.40 Referral should be made if treatment is beyond the treating dentist’s scope of practice. Temporomandibular joint (TMJ) problems: Disorders of the TMJ can occur at any age, but appears to be more prevalent in adolescence .40-42 Recommendations: Evaluation of the TMJ and related structures should be a part of the examination of the adolescent. Referral should be made when the diagnostic and/or treatment needs are beyond the treating dentist’s scope of practice.43,44 Congenitally missing teeth: The impact of a congenitally missing permanent tooth on the developing dentition can be significant.3 When treating adolescent patients with congenitally missing teeth, many factors must be taken into consideration including, but not limited to, esthetics, patient age, and growth potential, as well as periodontal and oral surgical needs.38,45,46 Recommendations: Evaluation of congenitally missing permanent teeth should include both immediate and long-term management. Referral should be made when the treatment needs are beyond the treating dentist’s scope of practice. A team approach may be indicated.47 Ectopic eruption: Abnormal eruption patterns of the adolescent’s permanent teeth can contribute to root resorption, bone loss, gingival defects, space loss, and esthetic concerns. Early diagnosis and treatment of ectopically erupting teeth can result in a healthier and more esthetic dentition. Prevention and treatment may include extraction of deciduous teeth, surgical intervention, and/or endodontic, orthodontic, periodontal, and/ or restorative care.48-50 Recommendations: The dentist should be proactive in diagnosing and treating ectopic eruption and impacted teeth in the young adolescent. Early diagnosis, including appropriate radiographic examination,28 is important. Referral should be made when the treatment needs are beyond the treating dentist’s scope of practice.47 Traumatic injuries The most common injuries to permanent teeth occur secondary to falls, followed by traffic accidents, violence, and sports.51-54 All sporting activities have an associated risk of orofacial injuries due to falls, collisions, and contact with hard surfaces.55 The administrators of youth, high school, and college organized sports have demonstrated that dental and facial injuries can be reduced significantly by introducing mandatory protective equipment such as face guards and mouthguards. Additionally, youths participating in leisure activities such as skateboarding, rollerskating, and bicycling also benefit from appropriate protective equipment.56,57 Recommendations: Dentists should introduce a comprehensive trauma prevention program to help reduce the incidence
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of traumatic injury to the adolescent dentition. This prevention plan should consider assessment of the patient’s sport or activity, including level and frequency of activity.58 Once this information is acquired, recommendation and fabrication of an age-appropriate, sport-specific, and properly-fitted mouthguard/faceguard can be initiated.58 Players must be warned about altering the protective equipment that will disrupt the fit of the appliance. In addition, players and parents must be informed that injury may occur, even with properly-fitted protective equipment.58 Additional considerations in oral/dental management of the adolescent The adolescent can present particular psychosocial characteristics that impact the health status of the oral cavity, care seeking, and compliance. The self-concept development process, emergence of independence, and the influence of peers are just a few of the psychodynamic factors impacting dental health during this period.1,5,7,16 Discolored or stained teeth: Desire to improve esthetics of the dentition by tooth whitening and removal of stained areas or defects can be a concern of the adolescent. Indications for the appropriate use of tooth-whitening methods and products are dependent upon correct diagnosis.59 The dentist must determine the appropriate mode of treatment. Use of bleaching agents, microabrasion, placement of an esthetic restoration, or a combination of treatments all can be considered.60 Recommendations: For the adolescent patient, judicious use of bleaching can be considered part of a comprehensive, sequenced treatment plan that takes into consideration the patient’s dental developmental stage, oral hygiene, and caries status. A dentist should monitor the bleaching process, ensuring the least invasive, most effective treatment method. Dental professionals also should consider possible side effects when contemplating dental bleaching for adolescent patients.61,62 Tobacco use: Significant oral, dental, and systemic health consequences and death are associated with all forms of tobacco use. Smoking and other tobacco use almost always are initiated and established in adolescence.63-68 Recommendations: Education of the adolescent patient on the oral and systemic consequences of tobacco use should be part of each patient’s oral health education. For those adolescent patients who use tobacco products, the practitioner should provide or refer the patient to appropriate educational and counseling services.69-71 When associated pathology is present, referral should be made when the treatment needs are beyond the treating dentist’s scope of practice. Positive youth development: Treatment and management of adolescent oral health that takes into account the adolescent’s psychological and social needs can be approached through the
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framework of positive youth development (PYD).72 The approach goes beyond traditional prevention, intervention, and treatment of risky behaviors and problems and suggests that a strong interpersonal relationship between the adolescent patient and the pediatric dentist can be influential in improving adolescent oral health and transitioning patients to adult care. In the office, dental professionals have a unique opportunity to serve as positive role models. Recommendations: Integrating PYD into clinical practice can be attained through continuing education on adolescent development issues, as well as partnerships with communitybased organizations and schools. The dentist can be a part of the myriad of adolescent support and services.72 Psychosocial and other considerations: Behavioral considerations when treating an adolescent may include anxiety, phobia, or intellectual dysfunction.1 Referral should be made when the treatment needs are beyond the treating dentist’s scope of practice and nondental professionals or a team approach may be indicated. Additional examples of oral problems associated with adolescent behaviors include, but are not limited to: 1. oral manifestations of venereal diseases; 2. effects of oral contraceptives or antibiotics on periodontal structures; 3. perimyolysis (severe enamel erosion) in bulimia73; 4. traumatic injury to teeth and oral structures in athletic or other activities (short- and long-term management)56,74-76; 5. intraoral and perioral piercing with possible local and systemic effects.77,78 The impact of psychosocial factors relating to oral health must include consideration of the following: 1. changes in dietary habits (eg, fads, freedom to snack, increased energy needs, access to carbohydrates); 2. use of tobacco, alcohol, and drugs; 3. motivation for maintenance of good oral hygiene; 4. potential for traumatic injury; 5. adolescent as responsible for care; 6. lack of knowledge about periodontal disease. Physiologic changes also can contribute to significant oral concerns in the adolescent. These changes include: 1. loss of remaining primary teeth; 2. eruption of remaining permanent teeth; 3. gingival maturity; 4. facial growth; 5. hormonal changes. Recommendations: 1. An adolescent’s oral health care should be provided by a dentist who has appropriate training in managing the patient’s specific needs. Referral should be made when the treatment needs are beyond the treating dentist’s scope of practice. This may include both dental and nondental problems.72 2. Attention should be given to the particular psychosocial aspects of adolescent dental care. Other issues such as
consent, confidentiality, and compliance should be addressed in the care of these patients.79,80 3. A complete oral health care program for the adolescent requires an educational component that addresses the particular concerns and needs of the adolescent patient and focuses on: a. specific behaviorally-and physiologically-induced oral manifestations in this age group;20 b. shared responsibility for care and health by the ado lescent and provider;20 c. consequences of adolescent behavior on oral health.81,82 Transitioning to adult care: As adolescent patients approach the age of majority, it is important to educate the patient and parent on the value of transitioning to a dentist who is knowledgeable in adult oral health care. The adult’s oral health needs may go beyond the scope of the pediatric dentist’s training. The transitioning adolescent should continue professional oral health care in an environment sensitive to his/her individual needs. Many adolescent patients independently will choose the time to seek care from a general dentist and may elect to seek treatment from a parent’s primary care provider. In some instances, however, the treating pediatric dentist will be required to suggest transfer to adult care. Pediatric dentists are concerned about decreased access to oral health care for persons with special health care needs (SHCN)83 as they transition beyond the age of majority. Pediatric hospitals, by imposing age restrictions, can create a barrier to care for these patients. Transitioning to a dentist who is knowledgeable and comfortable with adult oral health care needs often is difficult due to a lack of trained providers willing to accept the responsibility of caring for SHCN patients. Recommendations: At a time agreed upon by the patient, parent, and pediatric dentist, the patient should be transitioned to a dentist knowledgeable and comfortable with managing that patient’s specific oral care needs. For the SHCN patient, in cases where it is not possible or desired to transition to another practitioner, the dental home can remain with the pediatric dentist and appropriate referrals for specialized dental care should be recommended when needed.83
References 1. American Psychological Association. Developing Adolescents: A Reference for Professionals. Washington, DC: American Psychological Association; 2002. 2. MacKay AP, Duran C. Adolescent health in the United States, 2007. National Center for Health Statistics, 2007. Available at: “http://www.cdc.gov/nchs/data/misc/adolescent2007.pdf ”. Accessed July 6, 2010. 3. Pinkham JR, Adair SM, Casamassimo PS, et al. Adolescence. In: Pinkham JR, Adair SM, Casamassimo PS, Fields HW Jr, McTigue DJ, Nowak AJ, eds. Pediatric Dentistry: Infancy Through Adolescence. 4th ed. Philadelphia, Pa: WB Saunders Co; 2005:649-718.
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4. National Institutes of Health. Consensus development conference statement: Diagnosis and management of dental caries throughout life, March 26-28, 2001. J Am Dent Assoc 2001;132(8):1153-61. 5. Macgregor ID, Regis D, Balding J. Self-concept and dental health behaviors in adolescents. J Clin Periodontol 1997;24(5):335-9. 6. Yu SM, Bellamy HA, Schwalberg RH, Drum MA. Factors associated with use of preventive dental and health services among US adolescents. J Adolesc Health 2001;29 (6):395-405. 7. American Academy of Pediatric Dentistry. Policy on prevention of sports-related orofacial injuries. Pediatr Dent 2004;26(suppl):44. 8. US Dept of Health and Human Services. Oral Health In America: A Report of the Surgeon General—Executive Summary. Rockville, Md: US Dept of Health and Human Services, National Institute of Dental and Craniofacial Research, National Institutes of Health; 2000. 9. Kaste LM, Selwitz RH, Oldakowski JA, Brunelle JA, Winn DM, Brown LJ. Coronal caries in the primary and permanent dentition of children and adolescents 1-17 years of age: United States, 1988-1991. J Dent Res 1996;75 (special issue):631-41. 10. Kirkham J, Robinson C, Strong M, Shore RC. Effects of frequency of acid exposure on demineralization/ remineralization behavior of human enamel in vitro. Caries Res 1994;28(1):9-13. 11. Howze KA. Health for Teens in Care: A Judge’s Guide 2002. Washington, DC: American Bar Association; 2002. 12. Majewski RF. Dental caries in adolescents associated with caffeinated carbonated beverages. Pediatr Dent 2001;23 (3):198-203. 13. Marshall TA, Levy SM, Broffitt B, et al. Dental caries and beverage consumption in young children. Pediatrics 2003;112(3Pt1):e184-e191. 14. Burt BA. Prevention policies in light of the changed distribution of dental caries. Acta Odontol Scand 1998;56(3): 179-86. 15. Ir win CE, Millstein SG. Biophysical correlates of risk–taking behaviors during adolescence. J Adolesc Health Care 1986;7:825-965. 16. CDC. Recommendations for using fluoride to prevent and control dental caries in the United States. MMWR Recomm Rep 2001;50(RR14):1-42. 17. American Academy of Pediatric Dentistry. Guideline on caries-risk assessment and management in infants, children, and adolescents. Pediatr Dent 2010;32(special issue): 101-8. 18. American Academy of Pediatric Dentistry. Guideline on fluoride therapy. Pediatr Dent 2009;31(suppl):128-31. 19. Macgregor ID, Balding J, Regis D. Tooth-brushing schedule, motivation, and ‘lifestyle’ behaviours in 7,770 young adolescents. Community Dent Health 1996;13(4):232-7.
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20. Dean JA, Hughes CV. Mechanical and chemotherapeutic home oral hygiene. In: Dean JA, Avery DR, McDonald RE, eds. McDonald and Avery’s Dentistry for the Child and Adolescent. 9th ed. Maryland Heights, Mo: Mosby Elsevier;2011:205-22. 21. American Academy of Pediatric Dentistry. Guideline on periodicity of examination, preventive dental services, anticipatory guidance, and oral treatment for children. Pediatr Dent 2009;31(special issue):118-25. 22. Freeman R, Sheiham A. Understanding decision-making process for sugar consumption in adolescents. Community Dent Oral Epidemiol 1997;25(3):228-32. 23. American Academy of Pediatric Dentistry. Policy on dietary recommendations for infants, children, and adolescents. Pediatr Dent 2009;31(special issue):47-8. 24. Feigal RJ. The use of pit and fissure sealants. Pediatr Dent 2002;24(5):415-22. 25. Ahovuo-Saloranta A, Hiiri A, Nordblad A, Worthington H, Makela M. Pit and fissure sealants for preventing dental decay in the permanent teeth of children and adolescents [review]. Cochrane Database Syst Rev 2004;3: CD001830. 26. Macek MD, Beltrán-Aguilar ED, Lockwood SA, Malvitz DM. Updated comparison of the caries susceptibility of various morphological types of permanent teeth. J Public Health Dent 2003;63(3):174-82. 27. American Academy of Pediatric Dentistry. Guideline on pediatric restorative dentistry. Pediatr Dent 2009;31 (special issue):172-8. 28. American Academy of Pediatric Dentistry. Guideline on prescribing dental radiographs for infants, children, adolescents, and persons with special health care needs. Pediatr Dent 2009;31(special issue):250-2. 29. Donly K. Pediatric Restorative Dentistry Consensus Conference April 15-16, 2002, San Antonio, Texas. Pediatr Dent 2002;24(5):374-6. 30. Croll TP, Castaldi CR. The preformed stainless steel crown for restoration of permanent posterior teeth in special cases. J Am Dent Assoc 1978;97(4):644-9. 31. Beck JD, Arbes SI Jr. Epidemiology of gingival and periodontal disease. In: Newman MG, Taki HH, Klokkevold PR, Carranza FA, eds. Carranza’s Clinical Periodontology. 10th ed. St Louis, Mo: Saunders Elsevier; 2006:117-9. 32. Wilson TG Jr, Kornman KS. Fundamentals of Periodontics. 2nd ed. Hanover Park, Ill: Quintessence Publishing; 2003;196-7. 33. Modeer T, Wondimu B. Periodontal diseases in children and adolescents. Dent Clin North Am 2000;44(3): 633-58. 34. Grossi SG, Zambon JJ, Ho AW, et al. Assessment of risk for periodontal disease. I. Risk indicators for attachment loss. J Periodontol 1994;65(3):260-7. 35. Grossi SG, Genco RJ, Machtei EE, et al. Assessment of risk for periodontal disease. II. Risk indicators for alveolar bone loss. J Periodontol 1995;66(1):23-9.
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36. Litonjua LS. Pericoronitis, deep fascial space infections, and the impacted third molar. J Philipp Dent Assoc 1996; 47(4):43-7. 37. American Academy of Periodontology. Periodontal therapy. J Periodontol 2001;72(11):1624-8. 38. Richardson G, Russell KA. Congenitally missing maxillary incisors and orthodontic treatment considerations for the single tooth implant. J Can Dent Assoc 2001;67 (1):25-8. 39. Waller JH, Malden N. Rapid cystic involvement of a lower third molar. Dent Update 1999;26(4):166-7. 40. American Academy of Pediatric Dentistry. Guideline on pediatric oral surgery. Pediatr Dent 2010;32(special issue): 238-45. 41. American Academy of Pediatric Dentistry. Guideline on acquired temporomandibular disorders in infants, children, and adolescents. Pediatr Dent 2010;32(special issues):232-7. 42. Riolo ML, tenHave TR, Brandt D. Clinical validity of the relationship between TMJ signs and symptoms in children and youth. J Dent Child 1988;55(2):110-3. 43. National Institutes of Health. Management of Temporomandibular Disorders. National Institutes of Health Technology Assessment Conference Statement. J Am Dent Assoc 1996;127(11):1595-606. 44. Skeppar J, Nilner M. Treatment of craniomandibular disorders in children and young adults. J Orofac Pain 1993;7(4):362-9. 45. Garg AK. Treatment of congenitally missing maxillary incisors: Orthodontics, bone grafts, and osseointegrated implants. Dent Implantol Update 2002;13(2):9-14. 46. Wexler G. Missing upper lateral incisors: Orthodontic considerations in young patients. Ann R Australas Coll Dent Surg 2000;15:136-40. 47. American Academy of Pediatric Dentistry. Guideline on management of the developing dentition and occlusion in pediatric dentistry. Pediatr Dent 2009;31(special issue): 196-208. 48. Chaushu S, Sharabi S, Becker A. Dental morphologic characteristics of normal versus delayed developing dentitions with palatally displaced canines. Am J Orthod Dentofacial Orthop 2002;121(4):339-46. 49. Kojima R, Taguchi Y, Kabayashi H, Noda T. External root resorption of the maxillary permanent incisors caused by ectopically erupting canines. J Clin Pediatr Dent 2002; 26(2):193-7. 50. Ericson S, Kurol PJ. Resorption of incisors after ectopic eruption of maxillary canines. Angle Orthod 2000;70(6): 415-23. 51. Kurol J. Early treatment of tooth eruption disturbances. Am J Orthod Dentofacial Orthop 2002;121(6):588-91. 52. Rocha MJdC, Cardoso M. Traumatized permanent teeth in Brazilian children assisted at the Federal University of Santa Catarina, Brazil. Dent Traumatol 2001;17(6):245-9.
53. deFranca Caldas A Jr, Burgos MEA. A retrospective study of traumatic dental injuries in a Brazilian dental trauma clinic. Dent Traumatol 2001;17(6):250-3. 54. Skaare AB, Jacobsen I. Dental injuries in Norwegians aged 7-18 years. Dent Traumatol 2003;19(2):67-71. 55. Gassner R, Bösch R, Tuli T, Emshoff R. Prevalence of dental trauma in 6,000 patients with facial injuries: Implications for prevention. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1999;87(1):27-33. 56. Tesini DA, Soporowski NJ. Epidemiology of orofacial sports-related injuries. Dent Clin North Am 2000;44(1): 1-18. 57. Ranalli DN. Prevention of sport-related dental traumatic injuries. Dent Clin North Am 2000;44(1):19-33. 58. Ranalli DN. A sports dentistry trauma control plan for children and adolescents. J Southeast Soc Pediatr Dent 2002;8:8-9. 59. Sarrett DC. Tooth whitening today. J Am Dent Assoc 2002;133(11):1535-8. 60. Donly KJ. The adolescent patient: Special whitening challenges. Compend Contin Educ Dent 2003;24(4A):390-6. 61. Li Y. Tooth bleaching using peroxide containing agents: Current status of safety issues. Compend Continu Educ Dent 1998;19(8):783-96, 790. 62. American Academy of Pediatric Dentistry. Policy on use of dental bleaching for child and adolescent patients. Pediatr Dent 2009;31(special issue):59-61. 63. US Dept of Health and Human Services. Preventing Tobacco Use Among Young People: Report of the Surgeon General. Atlanta, Ga: US Dept of Health and Human Services, Public Health Service, CDC, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health; 1994. 64. CDC. Cigarette use among high school students-United States,1991-2009. MMWR Morb Mortal Weekly Rep 2010;59(26):797-801. 65. Tomar SL, Winn DM, Swango PA, Giovino GA, Kleinman DV. Oral mucosal smokeless tobacco lesions among adolescents in the United States. J Dent Res 1997;76(6): 1277-86. 66. Audrain-McGovern J, Rodriguez D, Tercyak KP, Cuevas J, Rodgers K, Patterson F. Identifying and characterizing adolescent smoking trajectories. Cancer Epidemiol Biomarkers Prev 2004;13(12):2023-34. 67. Zullig KJ, Valois RF, Huebner ES, Drane JW. Evaluating the performance of the Centers for Disease Control and Prevention core health-related quality of life scale with adolescents. Public Health Rep 2004;119(6):577-84. 68. Johnson CC, Myers L, Webber LS, Boris NW. Profiles of the adolescent smoker: Models of tobacco use among 9th grade high school students; Acadiana Coalition of Teens against Tobacco (ACTT). Prev Med 2004;39(3):551-8.
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69. American Dental Association. Summary of policy and recommendations regarding tobacco: 1964-present. ADA Resolution 1H-1992. In: ADA Transactions 1992. Chicago, Ill: ADA; 1993:598. 70. American Cancer Society, National Cancer Institute, National Institutes of Health. How to Help Your Patients Stop Using Tobacco: A National Cancer Institute Manual for the Oral Health Team. Bethesda, Md: National Institutes of Health, US Dept of Health and Human Services, Public Health Service; 1998. NIH publication No. 98-3191. 71. American Academy of Pediatric Dentistry. Policy on tobacco use. Pediatr Dent 2010;32(special issue):49-52. 72. Larson RW. Toward a psychology of positive youth development. Am Psychologist 2000;55(1):170-83. 73. Christensen GJ. Oral care for patients with bulimia. J Am Dent Assoc 2002;133(12):1689-91. 74. Cortes MI, Marcenes W, Sheiham A. Impact of traumatic injuries to the permanent teeth on the oral health-related quality of life in 12- to 14-year-old children. Community Dent Oral Epidemiol 2002;30(3):193-8. 75. Gassner R, Tuli T, Hächl O, Moreira R, Ulmer H. Craniomaxillofacial trauma in children: A review of 3,385 cases with 6,060 injuries in 10 years. J Oral Maxillofac Surg 2004;62(4):399-407. 76. Barnett F. Prevention of sports-related dental trauma: The role of mouthguards. Pract Proced Aesthet Dent 2003;15(5):391-4.
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77. American Academy of Pediatric Dentistry. Policy on intraoral and perioral piercing. Pediatr Dent 2009;31 (special issue):54-5. 78. Boardman R, Smith RA. Dental implications of oral piercing. J Calif Dent Assoc 1997;25(3):200-7. 79. American Academy of Pediatric Dentistry. Guideline on record-keeping. Pediatr Dent 2009;31(special issue): 239-46. 80. American Academy of Pediatric Dentistry. Guideline on informed consent. Pediatr Dent 2009;31(special issue):247-9. 81. Romito L, McDonald JL Jr. Nutritional considerations for the dental patient. In: Dean JA, Avery DR, McDonald RE, eds. McDonald and Avery’s Dentistry for the Child and Adolescent. 9th ed. Maryland Heights, Mo: Mosby Inc; 2011;223-240. 82. Macgregor ID, Balding JW. Self-esteem as a predictor of toothbrushing behavior in young adolescents. J Clin Periodontol 1991;18(5);312-6. 83. American Academy of Pediatric Dentistry. Guideline on management of persons with special health care needs. Pediatr Dent 2009;31(special issue):113-7.
American Academy of pediatric dentistry
Guideline on Oral Health Care for the Pregnant Adolescent Originating Council
Council on Clinical Affairs, Committee on the Adolescent Adopted 2007
Purpose The American Academy of Pediatric Dentistry (AAPD), as the oral health advocate for infants, children, adolescents, and persons with special needs, recognizes that adolescent pregnancy remains a significant social and health issue in the US. This guideline is intended to address management of oral health care particular to the pregnant adolescent rather than provide specific treatment recommendations for oral conditions.
Methods This guideline is based on a review of the current dental and medical literature related to adolescent pregnancy. Some recommendations are evidence-based, while others represent best clinical practice and expert opinion. A MEDLINE search was conducted using the terms “pregnancy”, “adolescent pregnancy”, “maternal”, and “pre-term birth” with “oral health”.
Background General considerations Even though the birth rate for US females aged 15 to 19 declined 1 percent between 2003 and 2004 to 41.2 births per 1,000, approximately 900,000 teenagers become pregnant each year.1 Approximately 50 percent of adolescent pregnancies occur within the first 6 months of initial sexual intercourse, even with increasing use of contraceptives by adolescents.2 The correlation between poverty and adolescent pregnancy is great, for as many as 83 percent of adolescent females who give birth are from low-income families.3 Once an adolescent has given birth to one child, she is at increased risk for giving birth to another child during adolescence.1 Medical complications involving mother and child occur more frequently in pregnant females aged 11 through 15 years than those aged 20 to 22 years.4 These include the delivery of low birth weight infants, increased neonatal death rate, and increased mortality rate for the mother.4 In addition, pregnancyinduced hypertension, anemia, sexually transmissible diseases, and premature delivery are concerns for the pregnant adolescent.5 Hypertension increases the risk of bleeding during procedures. Blood pressure ≥ 140/90 mmHg is considered mild hypertension, whereas values ≥ 160/110 mmHg are considered severe.6 The diet of the pregnant adolescent can affect the health of the child. A healthy diet is necessary to provide adequate amounts of nutrients to the mother-to-be and the unborn child.7
Nutrients of particular importance include folate, vitamin B6, vitamin B12, calcium, and zinc.8 During pregnancy, a woman’s nutritional needs are increased, but certainly “the eating for 2” concept is not recommended.9 The total energy needs during pregnancy range between 2,500 to 2,700 kcal a day for most women, but pre-pregnancy body mass index, rate of weight gain, maternal age, and physiological appetite must be considered in tailoring this recommendation to the individual.10 Nausea and vomiting occur in 50 to 90 percent of all pregnancies during the first trimester and often are associated with young age and low socioeconomic status.11 An expectant female may modify food choices due to morning sickness and/or taste aversions, but appropriate nutrition for the health of the mother and fetus is crucial. A study of over 152,000 women who gave birth between 1996 and 2000 found almost half were prescribed medications for which there was no clinical evidence of safety for use during pregnancy.12 The goal of any drug therapy during pregnancy is to improve maternal/fetal health while avoiding adverse drug reactions.13 The US Food and Drug Administration has defined 5 categories of drugs according to the risk they pose to pregnant women and their fetuses.14 These categories provide some guidance to the relative safety of the medication for use by pregnant women. Category A includes drugs that have been studied in humans and have evidence supporting their safe use; Category B drugs show no evidence of risk to humans. Generally, these drugs are considered acceptable for use during pregnancy.13 Category C drugs, such as aspirin and aspirin-containing products, may be used with caution, whereas drugs in categories D (eg, tetracycline) and X are not intended for use during pregnancy. The Organization of Teratology Information Services (“http:// orpheus.ucsd.edu/otis”; 866-626-6847) provides useful national information for drug safety during pregnancy. Low socioeconomic status and lack of parental involvement can place an adolescent at increased risk of initiating tobacco use.15 Smoking during pregnancy is associated with adverse outcomes.15,16 Women who smoke may have increased risks for ectopic pregnancy, spontaneous abortion, and preterm delivery.15,16 Infants born to women who smoke during pregnancy are more likely to be small for gestational age and have low birthweight.15-18 The longer the mother smokes during pregnancy, the greater the effect on the infant’s birth weight.16 Increasing evidence shows that maternal tobacco use is associated with CLINICAL GUIDELINES
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mental retardation and birth defects such as oral clefts.15 The risk for perinatal mortality (ie, stillbirths and neonatal deaths) and sudden infant death syndrome (SIDS) is increased for infants of women who smoke.15,16 Infants and children exposed to environmental tobacco smoke (ie, second hand smoke) have higher rates of lower respiratory illness, middle ear infections, asthma, and caries in the primary dentition.15-20 Women are more likely to stop smoking during pregnancy, both spontaneously and with assistance, than at other times in their lives.16 Use of ionizing radiation in the US is a well-regulated activity.21 The federal government establishes performance standards for manufacture and installation of x-ray generating equipment. States implement regulations that govern users; these regulations pertain to facility design, shielding, and use and maintenance of equipment.21 Major biological risks from radiation exposure are carcinogenesis, fetal effects, and mutations. Health benefits will outweigh the risk from radiation exposure from any radiographic examination if: 1. the examination is clinically indicated and justified, 2. technique is optimized to ensure high quality diagnostic images, and 3. principles are followed to minimize exposure.21 Oral conditions associated with pregnancy Changes in the oral cavity have been associated with pregnancy. These include alterations in both the hard and soft tissues. An increase in caries has been associated with carbohydrate loading as snacking becomes more frequent.7 In some instances, morning sickness and vomiting may contribute to the onset of perimyolysis, an erosion of the lingual surfaces of the teeth caused by exposure to gastric acids. A confounding factor is that pregnancyassociated hormonal changes may cause dryness of the mouth. Approximately 44 percent of pregnant participants in one study reported persistent xerostomia.22 From a periodontal perspective, the effects of hormonal levels on the gingival status of pregnant women may be accompanied by increased levels of Bacteroides, Prevotella, and Porphyromonas.23 Signs of gingivitis (eg, bleeding, redness, swelling, tenderness) are evident in the second trimester and peak in the eighth month of pregnancy, with anterior teeth affected more than posterior teeth.24 These findings are exacerbated by poor plaque control and mouth breathing.24 Increased tooth mobility has been associated with microbial shifts from aerobic to anaerobic bacteria.23 These bacterial shifts are accompanied by increased inflammation in the attachment apparatus, as well as mineral disturbances in the lamina dura, causing tooth mobility. This condition appears to reverse postpartum.23 Periodontitis during pregnancy, if left untreated, has been shown to contribute to preterm, low birth weight infants.24 One study compared 74 pregnant teenagers who received periodontal treatment during pregnancy to 90 who did not. The rate of preterm/low birth weight delivery was 18.9 percent in the control and 13.5 percent in the treatment group.25 This relationship continues to be investigated in large clinical trials.27,28 Periodontal disease, as a risk for pre-term birth, may be related to the presence of prostaglandins, certain cytokines, and tumor 128
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necrosis factor-alpha. Prospective studies may provide more direct evidence of this relationship. Another association being investigated is the effect of periodontitis and the development of preeclampsia, a rapidly progressing condition occurring in pregnancy characterized by hypertension and the presence of proteinuria.28 Oral health care during pregnancy A multi-state study concluded that, besides neglecting medical care during pregnancy, most expectant females of all ages do not seek dental care, even though 50 percent of them have a dental problem.5 The expectant mother might question the safety of dental treatment during pregnancy. Untreated oral disease may compromise the health of the pregnant female and the unborn child.29 The consequences of not treating an active infection during pregnancy outweigh the possible risks presented by most of the medications required for dental care.13 In addition, deferring elective dental treatment during a healthy pregnancy is not justified.29 During dental radiographic examination of a pregnant patient, optimizing techniques, shielding the thyroid and abdomen, choosing the fastest available image receptor (ie, high-speed film, rare earth screen-film systems, digital radiography), and avoiding retakes help minimize radiation exposure to the fetus.21,30 The health care provider must be aware that the primary dental x-ray beam may pass near or through the thyroid gland, even with attention to proper radiographic techniques. The juvenile thyroid is among the most sensitive organs to radiation-induced tumors, both benign and malignant.21 Risk decreases significantly with age at exposure, essentially disappearing after age 20.21 Evidence shows that radiation exposure to the thyroid during pregnancy is associated with low birth weight.31 Common dental projections rarely, if ever, deliver a measurable absorbed dose to the embryo or fetus.21 Gonadal absorbed dose from a typical dental x-ray procedure is equivalent to about 1 hour of natural background radiation.21 The National Council on Radiation Protection and Measurements recommends if dental treatment is to be deferred until after the delivery, so should the dental radiographs.21 The objectives of professional oral health care during the first trimester include avoiding fetal hypoxia, premature labor/ abortion, and teratogenic effects.29 Due to the increased risk of pregnancy loss, use of nitrous oxide may be contraindicated in the first trimester of pregnancy.32 The safest and most comfortable time for dental treatment is during weeks 14 to 20 of gestation. Because the pregnant uterus is below the umbilicus, the woman is generally more comfortable at this time. Pregnant women are considered to have a “full stomach” due to delayed gastric emptying and, therefore, are at increased risk for aspiration, particularly during the last trimester.33,34 Elective restorative and periodontal therapies during the second trimester may prevent any dental infections or other complications from occurring in the third trimester.29 In the final trimester, a prophylaxis may be repeated, especially if home oral care is inadequate or if soft tissue is abnormal. Evidence is insufficient to support or refute that mercury exposure from dental amalgams contributes to adverse pregnancy
American Academy of pediatric dentistry
outcomes.35,36 Currently, there is no evidence that the exposure of a fetus to mercury releases from the mother’s existing amalgam fillings causes any adverse effects.35-38 Mercury vapor released during the removal or placement of amalgam restorations may be inhaled and absorbed into the blood stream and does cross the placental barrier. The use of rubber dam and high speed suction can reduce the risk of vapor inhalation.38 Suppression of the mother’s reservoirs of Streptococcus mutans (SM) by dental rehabilitation and antimicrobial treatments may prevent or at least delay infant acquisition of these cariogenic microorganisms.39 SM, present in all children with early childhood caries, is predominantly acquired from mother’s saliva, and transmission may occur as early as the first year of life.40 Improving oral health during pregnancy leads to a reduction in salivary SM in the offspring.40 Beginning in the sixth month of pregnancy, a daily rinse of 0.05 percent sodium fluoride and 0.12 percent chlorhexidine has resulted in significant reduction in levels of caries-causing bacteria, consequently delaying the colonization of such bacteria among offspring.39 Xylitol, a naturally occurring sweetener, has been added to a variety of products because of its potential to reduce caries incidence. Although xylitol chewing gum has been shown to reduce the mother-child transmission of SM, there is still uncertainty regarding the frequency, amount, and duration of chewing required to reduce bacterial transmission.41 Education is an important component of prenatal oral health care and may have a significant effect on the oral health of both the mother and the child. Counseling for the pregnant adolescent includes topics directed toward all adolescent patients (eg, dietary habits, injury prevention, third molars), as well as oralchanges that may occur during pregnancy and infant oral health care. Since the pregnant adolescent may be receptive to information that will improve the infant’s health, anticipatory guidance, a proactive developmentally-based counseling technique, can be introduced to focus on the needs of the child at each stage of life. Legal considerations Statutes and case law concerning consent involving pregnant patients less than 18 years of age vary from state to state. In some states, dentists are required to obtain parental consent for nonemergency dental services provided to a child 17 years of age or younger who remains under parental care.42 This would involve obtaining consent from the parent who must be aware of the pregnancy in order to understand the risks and benefits of the proposed dental treatment.29 However, if the parent is unaware of the pregnancy, the pregnant adolescent may be entitled to confidentiality regarding health issues such as the pregnancy.43 In other states, there are “mature minor” laws that allow minors to consent for their own health care when a dentist deems the minor competent to provide informed consent. In addition, some states emancipate minors who are pregnant or by court order. Practitioners are obligated to be familiar with and abide by the laws particular to where they practice and where the patient resides. Recommendations The AAPD recommends that all pregnant adolescents seek pro-
fessional oral health care during the first trimester. After obtaining a thorough medical history, the dental professional should perform a comprehensive evaluation which includes a thorough dental history, dietary history, clinical examination, and caries risk assessment. The dental history includes, but is not limited to, discussion of preexisting oral conditions, signs/symptoms of such, current oral hygiene practices and preventive home care, previous radiographic exposures, and tobacco use. The adolescent’s dietary history should focus on exposures to carbohydrates, especially due to increased snacking, and acidic beverages/foods. During the clinical examination, the practitioner should pay particular attention to health status of the periodontal tissues. The AAPD’s caries-risk assessment tool44, utilizing historical and clinical findings, will aid the practitioner in identifying risk factors in order to develop an individualized preventive program. Based upon the historical indicators, clinical findings, and previous radiographic surveys, radiographs may be indicated. Because risk of carcinogenesis or fetal effects is very small but significant, radiographs should be obtained only when there is expectation that diagnostic yield (including the absence of pathology) will influence patient care. If dental treatment must be deferred until after delivery, radiographic assessment also should be deferred. All radiographic procedures should be conducted in accordance with radiation safety practices. These include optimizing the radiographic techniques, shielding the pelvic region and thyroid gland, and using the fastest imaging system consistent with the imaging task. Image receptors of speeds slower than American National Standards Institute (ANSI) speed group E shall not be used. Counseling for all pregnant patients should address: 1. Relationship of maternal oral health with fetal health (eg, association of periodontal disease with preterm birth and pre-eclampsia), 2. An individualized preventive plan including oral hygiene instructions, rinses, and/or xylitol gum to decrease the likelihood of SM transmission postpartum, 3. Dietary considerations (eg, maintaining a healthy diet, avoiding frequent exposures to cariogenic foods and beverages, overall nutrient and energy needs), 4. Anticipatory guidance for the infant’s oral health including the benefits of early establishment of a dental home, 5. Anticipatory guidance for the adolescent’s oral health to include injury prevention, oral piercings, tobacco and substance abuse, sealants, and third molars, 6. Oral changes that may occur secondary to pregnancy (eg, xerostomia, shifts in oral flora), 7. Individualized treatment recommendations based upon the specific oral findings for each patient. Preventive services must be a high priority for the adolescent pregnant patient. Ideally, a dental prophylaxis should be performed during the first trimester and again during the third trimester if oral home care is inadequate or periodontal conditions warrant professional care. Referral to a periodontist should be considered in the presence of progressive periodontal disease. While fluoridated dentifrice and professionally-applied CLINICAL GUIDELINES
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topical fluoride treatments can be effective caries preventive measures for the expectant adolescent, the AAPD does not support the use of prenatal fluoride supplements to benefit the fetus.45 A pregnant adolescent experiencing morning sickness should be instructed to rinse with a cup of water containing a teaspoon of sodium bicarbonate and to avoid tooth brushing for about 1 hour after vomiting to minimize dental erosion caused by stomach acid exposure.6 Where there is established erosion, fluoride may be used to minimize hard tissue loss and control sensitivity. A daily neutral sodium fluoride mouth rinse or gel to combat enamel softening by acids and control pulpal sensitivity may be prescribed.46 A palliative approach to alleviate dry mouth may include increased water consumption or chewing sugarless gum to increase salivation. Customary practice regarding invasive dental procedures requires certain precautions during pregnancy, particularly during the first trimester. Elective restorative and periodontal therapies should be performed during the second trimester. Dental treatment for a pregnant patient who is experiencing pain or infection should not be delayed until after delivery. When selecting therapeutic agents for local anesthesia, infection, postoperative pain, or sedation, the dentist must evaluate the potential benefits of the dental therapy versus the risk to the pregnant patient and the fetus. The practitioner should select the safest medication, limit the duration of the drug regimen, and minimize dosage. Health care providers should avoid the use of aspirin, aspirin-containing products, erythromycin estolate, and tetracycline in the pregnant patient.6 Patients requiring restorative care should be counseled regarding the risk and benefits and alternatives to amalgam fillings. The dental practitioner should use rubber dam and high speed suction during the placement or removal of amalgam to reduce the risk of vapor inhalation.38 Consultation with the prenatal medical provider should precede use of nitrous oxide/oxygen analgesia/anxiolysis during pregnancy. Nitrous oxide inhalation should be limited to cases where topical and local anesthetics alone are inadequate. Precautions must be taken to prevent hypoxia, hypotension, and aspiration.33 The pediatric dentist should incorporate positive youth development (PYD)47 into care for the adolescent patient. This approach goes beyond traditional prevention, intervention, and treatment of risky behaviors and problems and suggests that a strong interpersonal relationship between the adolescent and the pediatric dentist can be influential in improving adolescent oral health and transitioning to adult care. Through PYD, the dentist can promote healthy lifestyles, teach positive patterns of social interaction, and provide a safety net in times of need. At a time agreed upon by the patient, parent, and pediatric dentist, the patient should be transitioned to a practitioner knowledgeable and comfortable with managing that patient’s specific oral care needs. Dental practitioners must be familiar with state statutes that govern consent for care for a pregnant patient less than the age of majority. If a pregnant adolescent’s parents are unaware of the pregnancy, and state laws require parental consent for dental treatment, the practitioner should encourage the 130
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adolescent to inform them so appropriate informed consent for dental treatment can occur.
References 1. Kirby D. Emerging Answers: Research Findings on Programs to Reduce Teen Pregnancy (summary), Washington, DC: National Campaign to Prevent Teenage Pregnancy; 2001. 2. Haffner DW, ed. Facing Facts: Sexual Health for America’s Adolescents: The Report of the National Commission on Adolescent Sexual Health. New York, NY: Sexuality Information and Education Council of the United States; 1995. 3. Klein JD, Committee on Adolescence. Adolescent pregnancy: Current trends and issues. Pediatrics 2005;116 (1):281-6. 4. Forrest JD. Timing of the reproductive life stages. Obstet Gynecol 1993;82(1):105-11. 5. Gaffield ML, Colley Gilbert BJ, Malvitz DM, Romaguera R. Oral health during pregnancy. J Am Dent Assoc 2001;132 (7):1009-16. 6. New York State Dept of Health. Oral health care during pregnancy and early childhood practice guidelines. Available at: “http://www.health.state.ny.us/prevention/dental/ oral_health_care_pregnancy_early_childhood.htm”. Accessed March 12, 2007. 7. American Dental Association. Pregnancy: Frequently asked questions. Available at: “http://www.ada.org/public/topics/ pregnancy_faq.asp”. Accessed March 12, 2007. 8. National Research Council. Recommended Dietary Allowances, 10th ed. Washington, DC, National Academy Press; 1989. 9. McCann AL, Bonci L. Maintaining women’s oral health. Dent Clin N Amer 2001;45(3):571-601. 10. Kaiser LL, Allen L. Position of the American Dietetic Association: Nutrition and lifestyle for a healthy pregnancy outcome. J Am Diet Assoc 2002;102(10):1479-90. 11. Koren G, Bishai R, eds. Nausea and Vomiting in Pregnancy. State of the Art 2000. Toronto, Canada, Motherisk Hospital for Children; 2000:5-9. 12. Andrade SE, Gurwitz JH, Davis RL, et al. Prescription drug use in pregnancy. Am J Obstet Gynecol 2004;191(2): 398-407. 13. Moore PA. Selecting drugs for the pregnant dental patient. J Am Dent Assoc 1998;129(9):1281-6. 14. US Food and Drug Administration. Labeling and prescription drug advertising: Content and format for labeling for human prescription drugs. Fed Regist 1979;44 (124):434-67. 15. US Dept of Health and Human Services. Healthy people 2010: Tobacco use and healthy people 2010 objectives– tobacco priority area. Washington, DC. Available at: “http:// www.healthypeople.gov/document/html/Volume2/27 tobacco.htm”. Accessed March 24, 2007. 16. US Dept of Health and Human Services, CDC, National Center for Chronic Disease Prevention and Health Promotion Office on Smoking and Health. Report of the Surgeon General–Women and smoking: Tobacco use and
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reproductive outcomes – Fact sheet. US Public Health Service. Office of the Surgeon General. 2001. Available at: “http://www.cdc.gov/tobacco/data_statistics/sgr/ sgr_2001/highlight_outcomes.htm”. Accessed March 24, 2007. 17. Matthews TJ. Smoking during pregnancy in the 1990s. National vital statistics report. Hyattsville, Md: National Center for Health Statistics; 2001:49;7. CDC. Dept of Health and Human Services. Publication No. (PHHS) 2001-1120; PRS 01-0539 (8/2001). 18. World Health Organization. International consultation on environmental tobacco smoke (ETS) and child health – Consultation report. Geneva, Switzerland: World Health Organization; 1999. 19. US Dept of Health and Human Services. Preventing Tobacco Use Among Young People: Report of the Surgeon General. Atlanta, Ga: US Dept of Health and Human Services, Public Health Service, CDC, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health; 1994. 20. Aligne CA, Moss ME, Auinger P, Weitzman M. Association of pediatric dental caries with passive smoking. JAMA 2003;289(10):1258-64. 21. National Council on Radiation Protection and Measurements. Radiation protection in dentistry. Report No. 145. NRCP Publications, Bethesda, Md; 2003. 22. Steinberg BJ. Women’s oral health issues. J Dent Educ 1999;63(3):271-5. 23. Raber-Durlacher JE, van Steenbergen TJM, van der Velden U, de Graaff J, Abraham-Inpijn L. Experimental gingivitis during pregnancy and postpartum: Clinical, endocrinological, and microbiological aspects. J Clin Periodontol 1994;21(8):549-58. 24. McGaw T. Periodontal disease and preterm delivery of low-birth-weight infants. J Can Dent Assoc 2002;68(3): 165-9. 25. Mitchell-Lewis D, Engebretson SP, Chen J, Lamster IB, Papapanou PN. Periodontal infections and pre-term birth: Early findings from a cohort of young minority women in New York. Eur J Oral Sci 2001;109(1):34-9. 26. Jeffcoat MK, Geurs NC, Reddy MS, Cliver SP, Goldenberg RL, Hauth JC. Periodontal infection and preterm birth: Results of a prospective study. J Am Dent Assoc 2001;132(7):875-80. 27. Davenport ES, Williams CE, Sterne JA, Murad S, Sivapathasundram V, Curtis MA. Maternal periodontal disease and preterm low birthweight: Case-controlled study. J Dent Res 2002;81(5):313-8. 28. Contreras A, Herrera JA, Soto JE, Arce RM, Jaramillo A, Botero JE. Periodontitis is associated with preeclampsia in pregnant women. J Periodontol 2006;77(2):182-8. 29. Hilgers KK, Douglass J, Mathieu G. Adolescent pregnancy: A review of dental treatment guidelines. Pediatr Dent 2003;25(5):459-67.
30. American Dental Association, US Dept Health Human Services. The selection of patients for dental radiographic examinations –2004. Available at: “http://www.ada.org/ prof/resources/topics/radiography.asp”. Accessed March 12, 2007. 31. Berthold M. JAMA dental radiography study bolsters ADA recommendations. Available at: “http://www.ada. org/prof/resources/pubs/adanews/adanewsarticle.asp? articleid=853”. Accessed March 12, 2007. 32. Rowland AS, Baird DD, Shore DL, Weinberg CR, Savitz DA, Wilcox AJ. Nitrous oxide and spontaneous abortion in female dental assistants. Am J Epidemiol 1995;141(6):531-8. 33. Rosen MA. Management of anesthesia for the pregnant surgical patient. Anesthesiology 1999;91(4):1159-63. 34. Creasy RK, Resnik R. Maternal-Fetal Medicine: Principles and Practice. 5th ed. Philadelphia, Pa: WB Saunders, 2004. 35. Life Sciences Research Office. Review and analysis of the literature on the potential adverse health effects of dental amalgam. Bethesda, Md; 2004. 36. Hujoel PP, Lydon-Rochelle M, Bollen AM, Woods JS, Geurtsen W, del Aguila MA. Mercury exposure from dental filling placement during pregnancy and low birth weight risk. Am J Epidemiol 2005;161(8):734-40. 37. US Food and Drug Administration Center for Devices and Radiological Health Consumer Information. Consumer Update: Dental Amalgam. [updated 2002 Dec 31; cited 2005 Aug, 30]. Available at: “http://www.fda.gov/cdrh/ consumer/amalgams.html”. Accessed March 12, 2007. 38. Whittle KW, Whittle JG, Sarll DW. Amalgam fillings during pregnancy. Br Dent J 1998;185(10):500. 39. Brambilla E, Felloni A, Gagliani M, Malerba A, GarcíaGodoy F, Strohmenger L. Caries prevention during pregnancy: Results of a 30-month study. J Am Dent Assoc 1998;129(7):871-7. 40. Caulfield PW. Dental caries – A transmissible and infectious disease revisited: A position paper. Pediatr Dent 1997;19(8):491-8. 41. Söderling E, Isokangas P, Pienihäkkinen K, Tenovuo J, Alanen P. Influence of maternal xylitol consumption on mother-child transmission of Mutans streptococci: 6-year follow-up. Caries Res 2001;35(3):173-7. 42. Weber TJ, Fernsler HL. Treating the minor patient. Penn Dent J 2002;69(3):11-4. 43. H asegawa TK, Matthews M Jr. Confidentiality for a pregnant adolescent? Texas Dent J 1994;111(2):23-5. 44. American Academy of Pediatric Dentistry. Policy on the use of a caries-risk assessment tool (CAT) for infants, children, and adolescents. Pediatr Dent 2006;28(suppl):24-8. 45. American Academy of Pediatric Dentistry. Guideline on fluoride therapy. Pediatr Dent 2007;29(suppl):111-4. 46. Linnett V, Seow WK. Dental erosion in children: A literature review. Pediatr Dent 2001;23:37-43. 47. American Academy of Pediatric Dentistry. Guideline on adolescent oral health care. Pediatr Dent 2006;28(suppl): 77-84.
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Guideline on Management of Dental Patients With Special Health Care Needs Originating Council
Council on Clinical Affairs Review Council
Council on Clinical Affairs Adopted 2004
Revised 2008
Purpose The American Academy of Pediatric Dentistry (AAPD) recognizes that providing both primary and comprehensive preventive and therapeutic oral health care to individuals with special health care needs (SHCN) is an integral part of the specialty of pediatric dentistry.1 The AAPD values the unique qualities of each person and the need to ensure maximal health attainment for all, regardless of developmental or other special health care needs. This guideline is intended to educate health care providers, parents, and ancillary organizations about the management of oral health care needs particular to individuals with SHCN rather than provide specific treatment recommendations for oral conditions.
Methods
This guideline is based on a review of the current dental and medical literature related to individuals with SHCN. A MEDLINE search was conducted using the terms “special needs”, “disabled patients”, “handicapped patients”, “dentistry”, and “oral health”. Papers and workshop reports from the AAPD-sponsored symposium “Lifetime Oral Health Care for Patients with Special Needs” (Chicago, IL: November, 2006) were reviewed.2
Background The AAPD defines special health care needs as “any physical, developmental, mental, sensory, behavioral, cognitive, or emotional impairment or limiting condition that requires medical management, health care intervention, and/or use of specialized services or programs. The condition may be developmental or acquired and may cause limitations in performing daily selfmaintenance activities or substantial limitations in a major life activity. Health care for individuals with special needs requires specialized knowledge, increased awareness and attention, adaptation, and accommodative measures beyond what are considered routine.”3 Individuals with SHCN are at increased risk for oral diseases.4 Oral diseases can have a direct and devastating impact
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on the health of those with certain systemic health problems or conditions. Patients with compromised immunity (eg, leukemia or other malignancies, human immunodeficiency virus) or cardiac conditions associated with endocarditis may be especially vulnerable to the effects of oral diseases. Patients with mental, developmental, or physical disabilities who do not have the ability to understand and assume responsibility for or cooperate with preventive oral health practices are susceptible as well. Oral health is an inseparable part of general health and well-being.4 SHCN also includes disorders or conditions which manifest only in the orofacial complex (eg, amelogenesis imperfecta, dentinogenesis imperfecta, cleft lip/palate, oral cancer). While these patients may not exhibit the same physical or communicative limitations of other SHCN patients, their needs are unique, impact their overall health, and require oral health care of a specialized nature. Currently, 52 million Americans have some type of disabling condition and 25 million Americans have a severe disability.5 Due to improvements in medical care, SHCN patients will continue to grow in number; many of the formerly acute and fatal conditions have become chronic and manageable problems. Historically, many of these patients received care in nursing homes and state-operated institutions. Today, society’s trend is to mainstream these individuals to traditional community-based centers, with many seeking care from private dental practitioners. The Americans with Disabilities Act (AwDA) defines the dental office as a place of public accommodation.6 Thus, dentists are obligated to be familiar with these regulations and ensure compliance. Failure to accommodate patients with SHCN could be considered discrimination and a violation of federal and/or state law. Although regulations require practitioners to provide physical accessibility to an office (eg, wheelchair ramps, handicapped-parking spaces), individuals with SHCN can face many other barriers to obtaining oral health care. Financing and reimbursement have been cited as common barriers for medically necessary oral health care.5 Families with SHCN children
American Academy of pediatric dentistry
experience much higher expenditures than required for healthy children. Most individuals with SHCN rely more on government funding to pay for medical and dental care and generally lack adequate access to private insurance for health care services.6,7 Insurance plays an important role for families with SHCN children, but it still provides incomplete protection.8,9 Lack of preventive and timely therapeutic care may increase the need for costly episodic care.10 Optimal health of children is more likely to be achieved with access to comprehensive health care benefits.11 Nonfinancial barriers such as language and psychosocial, structural, and cultural considerations may interfere with access to oral health care.9 Effective communication is essential and, for hearing impaired patients/parents, can be accomplished through a variety of methods including interpreters, written materials, and lip-reading. Psychosocial factors associated with utilization include oral health beliefs, norms of caregiver responsibility, and positive caregiver dental experience. Structural barriers include transportation, school absence policies, discriminatory treatment, and difficulty locating providers who accept Medicaid.12 Community-based health services, with educational and social programs, may assist dentists and their patients with SHCN.13 Priorities and attitudes can serve as impediments to oral care. Parental and primary physician lack of awareness and knowledge may limit a SHCN patient from seeking preventive dental care.14 Other health conditions may seem more important than dental health, especially when the relationship between oral health and general health is not well understood.15 SHCN patients may express a greater level of anxiety about dental care than those without a disability, which may adversely impact the frequency of dental visits and, subsequently, oral health.16 Pediatric dentists are concerned about decreased access to oral health care for SHCN patients as they transition beyond the age of majority. Pediatric hospitals, by imposing age restrictions, can create another barrier to care for these patients. Transitioning to a dentist who is knowledgeable and comfortable with adult oral health care needs often is difficult due to a lack of trained providers willing to accept the responsibility of caring for SHCN patients.17 Furthermore, as children with disabilities reach adulthood, health insurance coverage may be restricted.18
Recommendations Scheduling appointments The parent’s/patient’s initial contact with the dental practice (usually via telephone) allows both parties an opportunity to address the child’s primary oral health needs and to confirm the appropriateness of scheduling an appointment with that particular practitioner. Along with the child’s name, age, and chief complaint, the receptionist should determine the presence and nature of any SHCN and, when appropriate, the name(s) of the child’s medical care provider(s). The office staff, under the guidance of the dentist, also should determine the need for an increased length of appointment and/or additional auxiliary staff in order to accommodate the patient in an effective and efficient manner. The need for a higher level of dentist and team time as
well as customized services should be documented so the office staff is prepared to accommodate the patient’s unique circumstances at each subsequent visit. When scheduling patients with SHCN, it is imperative that the dentist be familiar and comply with Health Insurance Portability and Accountability Act (HIPAA) and AwDA regulations applicable to dental practices.19 HIPAA insures that the patient’s privacy is protected and AwDA prevents discrimination on the basis of a disability. Dental home Patients with SHCN who have a dental home20 are more likely to receive appropriate preventive and routine care. The dental home provides an opportunity to implement individualized preventive oral health practices and reduces the child’s risk of preventable dental/oral disease. When SHCN patients reach adulthood, their oral health care needs may go beyond the scope of the pediatric dentist’s training. It is important to educate and prepare the patient and parent on the value of transitioning to a dentist who is knowledgeable in adult oral health needs. At a time agreed upon by the patient, parent, and pediatric dentist, the patient should be transitioned to a dentist knowledgeable and comfortable with managing that patient’s specific health care needs. In cases where this is not possible or desired, the dental home can remain with the pediatric dentist and appropriate referrals for specialized dental care should be recommended when needed.21 Patient assessment Familiarity with the patient’s medical history is essential to decreasing the risk of aggravating a medical condition while rendering dental care. An accurate, comprehensive, and up-to-date medical history is necessary for correct diagnosis and effective treatment planning. Information regarding the chief complaint, history of present illness, medical conditions and/or illnesses, medical care providers, hospitalizations/surgeries, anesthetic experiences, current medications, allergies/sensitivities, immunization status, review of systems, family and social histories, and thorough dental history should be obtained.22 If the patient/parent is unable to provide accurate information, consultation with the caregiver or with the patient’s physician may be required. At each patient visit, the history should be consulted and updated. Recent medical attention for illness or injury, newly diagnosed medical conditions, and changes in medications should be documented. A written update should be obtained at each recall visit. Significant medical conditions should be identified in a conspicuous yet confidential manner in the patient’s record. Comprehensive head, neck, and oral examinations should be completed on all patients. A caries-risk assessment should be performed.23 A caries-risk assessment tool (CAT) provides a means of classifying caries risk at a point in time and, therefore, should be applied periodically to assess changes in an individual’s risk status. An individualized preventive program, including a dental recall schedule, should be recommended after evaluation of the patient’s caries risk, oral health needs, and abilities.
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A summary of the oral findings and specific treatment recommendations should be provided to the patient and parent/ caregiver. When appropriate, the patient’s other health care providers should be informed. Medical consultations The dentist should coordinate care via consultation with the patient’s other care providers including physicians, nurses, and social workers. When appropriate, the physician should be consulted regarding medications, sedation, general anesthesia, and special restrictions or preparations that may be required to ensure the safe delivery of oral health care. The dentist and staff always should be prepared to manage a medical emergency. Patient communication When treating patients with SHCN, an assessment of the patient’s mental status or degree of intellectual functioning is critical in establishing good communication. Often, information provided by a parent or caregiver prior to the patient’s visit can assist greatly in preparation for the appointment.24 An effort should be made to communicate directly with the patient during the provision of dental care. A patient who does not communicate verbally may communicate in a variety of non-traditional ways. At times, a parent, family member, or caretaker may need to be present to facilitate communication and/or provide information that the patient cannot. According to the requirements of the AwDA, if attempts to communicate with the SHCN patient/parent are unsuccessful because of a disability such as impaired hearing, the dentist must work with those individuals to establish an effective means of communications.6 Informed consent All patients must be able to provide appropriate signed informed consent for dental treatment or have someone who legally can provide it for them. Informed consent/assent must comply with state laws and, when applicable, institutional requirements. Informed consent should be well documented in the dental record through a signed and witnessed form.25 Behavior guidance Behavior guidance of the patient with SHCN can be challenging. Demanding and resistant behaviors may be seen in the person with mental retardation and even in those with purely physical disabilities and normal mental function. These behaviors can interfere with the safe delivery of dental treatment. With the parent/caregiver’s assistance, most patients with physical and mental disabilities can be managed in the dental office. Protective stabilization can be helpful in patients for whom traditional behavior guidance techniques are not adequate.26 When protective stabilization is not feasible or effective, sedation or general anesthesia is the behavioral guidance armamentarium of choice. When in-office behavior guidance including sedation/ general anesthesia is not feasible or effective, a hospital or outpatient surgical care facility is necessary to provide treatment.
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Preventive strategies Individuals with SHCN are at increased risk for oral diseases; these diseases further jeopardize the patient’s health.3 Education of parents/caregivers is critical for ensuring appropriate and regular supervision of daily oral hygiene. Dental professionals should demonstrate oral hygiene techniques, including the proper positioning of the person with a disability. They also should stress the need to brush with a fluoridated dentifrice twice daily to help prevent caries and to brush and floss daily to prevent gingivitis. Toothbrushes can be modified to enable individuals with physical disabilities to brush their own teeth. Electric toothbrushes may improve patient compliance. Floss holders may be beneficial when it is difficult to place hands into the mouth. Caregivers should provide the appropriate oral care when the patient is unable to do so adequately. Dietary counseling should be discussed for long term prevention of dental disease. Dentists should encourage a noncariogenic diet and advise patients/parents about the high cariogenic potential of oral pediatric medications rich in sucrose and dietary supplements rich in carbohydrates.27 As well, other oral side effects (eg, xerostomia, gingival overgrowth) of medications should be reviewed. Patients with SHCN may benefit from sealants. Sealants reduce the risk of caries in susceptible pits and fissures of primary and permanent teeth.28 Topical fluorides (eg, brush-on gel, mouth rinse, varnish, professional application during prophylaxis) may be indicated when caries risk is increased.29 Interim therapeutic restoration (ITR),30 using materials such as glass ionomers that release fluoride, may be useful as both preventive and therapeutic approaches in patients with SHCN.28 In cases of gingivitis and periodontal disease, chlorhexidine mouth rinse may be useful. For patients who might swallow a rinse, a toothbrush can be used to apply the chlorhexidine. Patients having severe dental disease may need to be seen every 2 to 3 months or more often if indicated. Those patients with progressive periodontal disease should be referred to a periodontist for evaluation and treatment. Barriers Dentists should be familiar with community-based resources for patients with SHCN and encourage such assistance when appropriate. While local hospitals, public health facilities, rehabilitation services, or groups that advocate for those with SHCN can be valuable contacts to help the dentist/patient address language and cultural barriers, other community-based resources may offer support with financial or transportation considerations that prevent access to care. Patients with developmental or acquired orofacial conditions The oral health care needs of patients with developmental or acquired orofacial conditions necessitate special considerations. While these individuals usually do not require longer appointments or advanced behavior guidance techniques commonly associated with SHCN patients, management of their oral conditions presents other unique challenges.31 Developmental
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defects such as hereditary ectodermal dysplasia, where most teeth are missing or malformed, cause lifetime problems that can be devastating to children and adults.4 From the first contact with the child and family, every effort must be made to assist the family in adjusting to the anomaly and the related oral needs.32 The dental practitioner must be sensitive to the psychosocial wellbeing of the patient, as well as the effects of the condition on growth, function, and appearance. Congenital oral conditions may entail therapeutic intervention of a protracted nature, timed to coincide with developmental milestones. Patients with conditions such as ectodermal dysplasia, epidermolysis bullosa, cleft lip/palate, and oral cancer frequently require an interdisciplinary team approach to their care. Coordinating delivery of services by the various health care providers can be crucial to successful treatment outcomes. Patients with oral involvement of conditions such as osteogenesis imperfecta, ectodermal dysplasia, and epidermolysis bullosa often present with unique financial barriers. Although the oral manifestations are intrinsic to the genetic and congenital disorders, medical health benefits often do not provide for related professional oral health care. The distinction made by third party payors between congenital anomalies involving the orofacial complex and those involving other parts of the body is often arbitrary and unfair.33 For children with hereditary hypodontia, removable or fixed prostheses (including complete dentures or over-dentures) and/or implants may be indicated.34 Dentists should work with the insurance industry to recognize the medical indication and justification for such treatment in these cases. Referrals A patient may suffer progression of his/her oral disease if treatment is not provided because of age, behavior, inability to cooperate, disability, or medical status. Postponement or denial of care can result in unnecessary pain, discomfort, increased treatment needs and costs, unfavorable treatment experiences, and diminished oral health outcomes. Dentists have an obligation to act in an ethical manner in the care of patients.35 When the patient’s needs are beyond the skills of the practitioner, the dentist should make appropriate referrals in order to ensure the overall health of the patient.
References 1. American Academy of Pediatric Dentistry. Reference Manual Overview: Definition and scope of pediatric dentistry. Pediatr Dent 2008;30(suppl):1. 2. American Academy of Pediatric Dentistry. Symposium on lifetime oral health care for patients with special needs. Pediatr Dent 2007;29(2):92-152. 3. American Academy of Pediatric Dentistry. Definition of special health care needs. Pediatr Dent 2008;30(suppl):15. 4. US Dept of Health and Human Services. Oral health in America: A report of the Surgeon General. Rockville, Md: US Dept of Health and Human Services, National Institute of Dental and Craniofacial Research, National Institutes of Health; 2000.
5. University of Florida College of Dentistry. Oral health care for persons with disabilities. Available at: “http://www. dental.ufl.edu/Faculty/Pburtner/disabilities/introduction. htm”. Accessed March 23, 2008. 6. US Dept of Justice. Americans with Disabilities Act. Available at: “http://www.usdoj.gov/crt/ada/adahom1.htm”. Accessed March 23, 2008. 7. Crall JJ. Improving oral health for individuals with special health care needs. Pediatr Dent 2007;29(2):98-104. 8. Newacheck PW, Kim SE. A national profile of health care utilization and expenditures for children with special health care needs. Arch Pediatr Adolesc Med 2005;159(1):10-7. 9. Chen AY, Newacheck PW. Insurance coverage and financial burden for families of children with special health care needs. Ambul Pediatr 2006;6(4):204-9. 10. Newacheck PW, McManus M, Fox HB, Hung YY, Halfon N. Access to health care for children with special health care needs. Pediatrics 2000;105(4Pt1):760-6. 11. American Academy of Pediatrics, Committee on Child Health Financing. Scope of health care benefits for children from birth through age 21. Pediatrics 2006;117(3): 979-82. 12. Kelly SE, Binkley CJ, Neace WP, Gale BS. Barriers to care-seeking for children’s oral health among low-income care-givers. Am J Public Health 2005;95(8):1345-51. 13. Halfon N, Inkelas M, Wood D. Nonfinancial barriers to care for children and youth. Annu Rev Public Health 1995; 16:447-72. 14. Shenkin JD, Davis MJ, Corbin SB. The oral health of special needs children: Dentistry’s challenge to provide care. J Dent Child 2001;86(3):201-5. 15. Barnett ML. The oral-systemic disease connection. An update for the practicing dentist. J Am Dent Assoc 2006; 137(suppl 10):5S-6S. 16. Gordon SM, Dionne RA, Synder J. Dental fear and anxiety as a barrier to accessing oral health care among patients with special health care needs. Spec Care Dentist 1998;18 (2):88-92. 17. Woldorf JW. Transitioning adolescents with special health care needs: Potential barriers and ethical conflicts. J Spec Pediatr Nurs 2007;12(1):53-5. 18. Callahan ST, Cooper WO. Continuity of health insurance coverage among young adults with disabilities. Pediatrics 2007;119(6):1175-80. 19. US Dept of Health and Human Services. Health Insurance Portability and Accountability Act (HIPAA). Available at: “http://:aspe.hhs.gov/admnsimp/pl104191.htm”. Accessed March 23, 2008. 20. American Academy of Pediatric Dentistry. Policy on dental home. Pediatr Dent 2007;29(suppl):22-3. 21. Nowak AJ. Patients with special health care needs in pediatric dental practices. Pediatr Dent 2002;24(3):227-8. 22. American Academy of Pediatric Dentistry. Guideline on record-keeping. Pediatr Dent 2007;29(suppl):29-33.
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23. American Academy of Pediatric Dentistry. Policy on use of a caries-risk assessment tool (CAT) for infants, children and adolescents. Pediatr Dent 2007;29(suppl):29-33. 24. Klein U, Nowak AJ. Autistic disorder: A review for the pediatric dentist. Pediatr Dent 1998;20(5):312-7. 25. American Academy of Pediatric Dentistry. Guideline on informed consent. Pediatr Dent 2007;29(suppl):219-20. 26. American Academy of Pediatric Dentistry. Guideline on behavior guidance for the pediatric dental patient. Pediatr Dent 2008;30(suppl):125-33. 27. American Academy of Pediatric Dentistry. Policy on dietary recommendations for infants, children, and adolescents. Pediatr Dent 2008;30(suppl):47-8. 28. American Academy of Pediatric Dentistry. Guideline on pediatric restorative dentistry. Pediatr Dent 2008;30 (suppl):163-9. 29. American Academy of Pediatric Dentistry. Guideline on fluoride therapy. Pediatr Dent 2008;30(suppl):121-4. 30. American Academy of Pediatric Dentistry. Policy on interim therapeutic restorations (ITR). Pediatr Dent 2008; 30(suppl):38-9. 31. American Academy of Pediatric Dentistry. Guideline on oral health care/dental management of heritable dental developmental anomalies. Pediatr Dent 2008;30(suppl): 196-201.
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32. American Cleft Palate-Craniofacial Association. Parameters for evaluation and treatment of patients with cleft lip/ palate or other craniofacial anomalies. Chapel Hill, NC: The Maternal and Child Health Bureau, Title V, Social Security Act, Health Resources and Services Administration, US Public Health Service, Dept of Health and Human Services; Revised edition November 2007. Grant #MCJ-425074. 33. American Academy of Pediatric Dentistry. Policy on third party reimbursement for oral health care services related to congenital orofacial anomalies. Pediatr Dent 2007;29 (suppl):71-2. 34. National Foundation for Ectodermal Dysplasias. Parameters of oral health care for individuals affected by ectodermal dysplasias. National Foundation for Ectodermal Dysplasias. Mascoutah, Ill; 2003. 35. American Academy of Pediatric Dentistry. Policy on the ethical responsibility to treat or refer. Pediatr Dent 2008; 30(suppl):83.
american academy of pediatric dentistry
Guideline on Oral and Dental Aspects of Child Abuse and Neglect Originating Group American Academy of Pediatrics Committee on Child Abuse and Neglect and the American Academy of Pediatric Dentistry
Review Group American Academy of Pediatrics Committee on Child Abuse and Neglect and the American Academy of Pediatric Dentistry Council on Clinical Affairs
Adopted 1999
Revised 2005
Reaffirmed 2010
Abstract In all 50 states, physicians and dentists are required to report suspected cases of abuse and neglect to social service or law enforcement agencies. The purpose of this report is to review the oral and dental aspects of physical and sexual abuse and dental neglect and the role of physicians and dentists in evaluating such conditions. This report addresses the evaluation of bite marks as well as perioral and intraoral injuries, infections, and diseases that may be suspicious for child abuse or neglect. Physicians receive minimal training in oral health and dental injury and disease and, thus, may not detect dental aspects of abuse or neglect as readily as they do child abuse and neglect involving other areas of the body. Therefore, physicians and dentists are encouraged to collaborate to increase the prevention, detection, and treatment of these conditions.
Physical abuse Craniofacial, head, face, and neck injuries occur in more than half of the cases of child abuse.1-10 A careful and thorough intraoral and perioral examination is necessary in all cases of suspected abuse and neglect. In addition, all suspected victims of abuse or neglect, including children in state custody or foster care, should be examined carefully not only for signs of oral trauma but also for caries, gingivitis, and other oral health problems. Some authorities believe that the oral cavity may be a central focus for physical abuse because of its significance in communication and nutrition.11 Oral injuries may be inflicted with instruments such as eating utensils or a bottle during forced feedings, hands, fingers, or scalding liquids or caustic substances. The abuse may result in: contusions, burns, or lacerations of the tongue, lips, buccal mucosa, palate (soft and hard), gingivae, alveolar mucosa, or frenum; fractured, displaced, or avulsed teeth; or facial bone and jaw fractures.
In one study,12 the lips were the most common site for inflicted oral injuries (54%), followed by the oral mucosa, teeth, gingivae, and tongue. Discolored teeth, indicating pulpal necrosis, may result from previous trauma.13,14 Gags applied to the mouth may result in bruises, lichenification, or scarring at the corners of the mouth.15 Some serious injuries of the oral cavity, including posterior pharyngeal injuries and retropharyngeal abscesses, may be inflicted by caregivers with factitious disorder by proxy16 to simulate hemoptysis or other symptoms requiring medical care; regardless of caregiver motive, all inflicted injuries should be reported for investigation. Unintentional or accidental injuries to the mouth are common and must be distinguished from abuse by judging whether the history, including the timing and mechanism of injury, is consistent with the characteristics of the injury and the child’s developmental capabilities. Multiple injuries, injuries in different stages of healing, or a discrepant history should arouse a suspicion of abuse. Consultation with or referral to a knowledgeable dentist may be helpful.
Sexual abuse Although the oral cavity is a frequent site of sexual abuse in children,17 visible oral injuries or infections are rare. When oral-genital contact is suspected, referral to specialized clinical settings equipped to conduct comprehensive examinations is recommended. The American Academy of Pediatrics statement “Guidelines in the Evaluation of Sexual Abuse of Children”18 provides information regarding these examinations.
Oral and perioral gonorrhea in prepubertal children, diagnosed with appropriate culture techniques and confirmatory testing, is pathognomonic of sexual abuse19 but rare among prepubertal girls evaluated for sexual abuse.20 Pharyngeal gonorrhea is frequently asymptomatic.21 When oral-genital contact is confirmed by history or examination
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findings, universal testing for sexually transmitted diseases within the oral cavity is controversial; the clinician should consider risk factors (eg, chronic abuse, perpetrator with a known sexually transmitted disease) and the child’s clinical presentation in deciding whether to conduct such testing. Although human papillomavirus infection may result in oral or perioral warts, the mode of transmission remains uncertain and debatable. Human papillomavirus infections may be sexually transmitted through oral-genital contact, vertically transmitted from mother to infant during birth, or horizontally transmitted through nonsexual contact from a child or caregiver’s hand to the genitals or mouth.22 Unexplained injury or petechiae of the palate, particularly at the junction of the hard and soft palate, may be evidence of forced oral sex.23 As with all suspected child abuse or neglect, when sexual abuse is suspected or diagnosed in a child, the case must be reported to child protective services and/or law enforcement agencies for investigation.24-27 A multidisciplinary child abuse evaluation for the child and family should be initiated. Children who present acutely with a recent history of sexual abuse may require specialized forensic testing for semen and other foreign materials resulting from assault. If a victim provides a history for oral-penile contact, the buccal mucosa and tongue can be swabbed with a sterile cotton-tipped applicator, then the swab can be air-dried and packaged appropriately for laboratory analysis. However, specialized hospitals and clinics equipped with protocols and experienced personnel are best suited for collecting such material and maintaining a chain of evidence necessary for investigations.
Bite marks Acute or healed bite marks may indicate abuse. Dentists trained as forensic odontologists can assist physicians in the detection and evaluation of bite marks related to physical and sexual abuse.28 Bite marks should be suspected when ecchymoses, abrasions, or lacerations are found in an elliptical or ovoid pattern. Bite marks may have a central area of ecchymoses (contusions) caused by 2 possible phenomena: positive pressure from the closing of the teeth with disruption of small vessels or negative pressure caused by suction and tongue thrusting. Bites produced by dogs and other carnivorous animals tend to tear flesh, whereas human bites compress flesh and can cause abrasions, contusions, and lacerations but rarely avulsions of tissue. An intercanine distance (ie, the linear distance between the central point of the cuspid tips) measuring more than 3.0 cm is suspicious of an adult human bite.29
The pattern, size, contour, and color of the bite mark should be evaluated by a forensic odontologist or a forensic pathologist if an odontologist is not available. If neither specialist is available, a physician or dentist experienced in the patterns of child abuse injuries should observe and document the bite mark characteristics photographically with an identification tag and scale marker (eg, ruler) in the photograph. The photograph
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should be taken such that the angle of the camera lens is directly over the bite and perpendicular to the plane of the bite to avoid distortion. A special photographic scale was developed by the American Board of Forensic Odontology (ABFO) for this purpose, as well as for documenting other patterned injuries, and can be obtained from the vendor (ABFO No. 2 reference scale, available from Lightening Powder Co Inc, Salem, Ore). Names and contact information for ABFO certified odontologists can be obtained from the ABFO Web site (www.abfo.org).
In addition to photographic evidence, every bite mark that shows indentations should have a polyvinyl siloxane impression made immediately after swabbing the bite mark for secretions containing DNA. This impression will help provide a 3- dimensional model of the bite mark. Written observations and photographs should be repeated daily for at least 3 days to document the evolution of the bite. Because each person has a characteristic bite pattern, a forensic odontologist may be able to match dental models (casts) of a suspected abuser’s teeth with impressions or photographs of the bite. Blood group substances can be secreted in saliva. DNA is present in epithelial cells from the mouth and may be deposited in bites. Even if saliva and cells have dried, they should be collected using the double-swab technique. First, a sterile cotton swab moistened with distilled water is used to wipe the area in question, dried, and placed in a specimen tube. A second sterile dry cotton swab cleans the same area, then is dried and placed in a specimen tube. A third control sample should be obtained from an uninvolved area of the child’s skin. All samples should be sent to a certified forensic laboratory for prompt analysis. 30 The chain of custody must be maintained on all samples submitted for forensic analysis. Questions regarding evidentiary procedure should be directed to a law enforcement agency.
Dental neglect Dental neglect, as defined by the American Academy of Pediatric Dentistry,31 is the “willful failure of parent or guardian to seek and follow through with treatment necessary to ensure a level of oral health essential for adequate function and freedom from pain and infection.” Dental caries, periodontal diseases, and other oral conditions, if left untreated, can lead to pain, infection, and loss of function. These undesirable outcomes can adversely affect learning, communication, nutrition, and other activities necessary for normal growth and development.32 Some children who first present for dental care have severe early childhood caries (formerly termed “baby bottle” or “nursing” caries); caregivers with adequate knowledge and willful failure to seek care must be differentiated from caregivers without knowledge or awareness of their child’s need for dental care in determining the need to report such cases to child protective services. Failure to seek or obtain proper dental care may result from factors such as family isolation, lack of finances, parental
american academy of pediatric dentistry
ignorance, or lack of perceived value of oral health.33 The point at which to consider a parent negligent and to begin intervention occurs after the parent has been properly alerted by a health care professional about the nature and extent of the child’s condition, the specific treatment needed, and the mechanism of accessing that treatment.33 Because many families face challenges in their attempts to access dental care or insurance for their children, the clinician should determine whether dental services are readily available and accessible to the child when considering whether negligence has occurred. The physician or dentist should be certain that the caregivers understand the explanation of the disease and its implications and, when barriers to the needed care exist, attempt to assist the families in finding financial aid, transportation, or public facilities for needed services. Parents should be reassured that appropriate analgesic and anesthetic procedures will be used to ensure the child’s comfort during dental procedures. If, despite these efforts, the parents fail to obtain therapy, the case should be reported to the appropriate child protective services agency.31,33
Conclusions Pediatricians should be aware that physical or sexual abuse may result in oral or dental injuries or conditions that sometimes can be confirmed by laboratory findings. Furthermore, injuries inflicted by one’s mouth or teeth may leave clues regarding the timing and nature of the injury as well as the identity of the perpetrator. Pediatricians are encouraged to be knowledgeable about such findings and their significance and to meticulously observe and document them. When questions arise or when consultation is needed, a pediatric dentist or a dentist with formal training in forensic odontology can ensure appropriate testing, diagnosis, and treatment. Pediatric dentists and oral and maxillofacial surgeons, whose advanced education programs include a mandated child abuse curriculum, can provide valuable information and assistance to physicians about oral and dental aspects of child abuse and neglect. The Prevent Abuse and Neglect Through Dental Awareness [also known as PANDA; telephone (501) 661-2595 or e-mail
[email protected]] coalition, which has trained thousands of physicians, nurses, teachers, child care providers, dentists, and dental auxiliaries, is another resource for physicians seeking information on this issue. Physician members of multidisciplinary child abuse and neglect teams are encouraged to identify such dentists in their communities to serve as consultants for these teams. In addition, physicians with experience or expertise in child abuse and neglect can make themselves available to dentists and to dental organizations as consultants and educators. Such efforts will strengthen our ability to prevent and detect child abuse and neglect and enhance our ability to care for and protect children.
References 1. Mouden LD, Bross DC. Legal issues affecting dentistry’s role in preventing child abuse and neglect. J Am Dent Assoc 1995;126:1173-80. 2. Schwartz S, Woolridge E, Stege D. The role of the dentist in child abuse. Quintessence Int 1976;7:79-81. 3. Sognnaes RF, Blain SM. Child abuse and neglect. I: Diagnostic criteria of special interest to dentists [abstract]. J Dent Res 1979;58(special issue A):367. 4. Donly KJ, Nowak AJ. Maxillofacial, neck, and dental lesions of child abuse. In: Reece RM, ed. Child Abuse: Medical Diagnosis and Management. Philadelphia, Pa: Lea & Febiger; 1994:150-66. 5. Baetz K, Sledziewski W, Margetts D, Koren L, Levy M, Pepper R. Recognition and management of the battered child syndrome. J Dent Assoc S Afr 1977;32:13-8. 6. Becker DB, Needleman HL, Kotelchuck M. Child abuse and dentistry: Orofacial trauma and its recognition by dentists. J Am Dent Assoc 1978;97:24-8. 7. Cameron JM, Johnson HR, Camps FE. The battered child syndrome. Med Sci Law 1966;6:2-21. 8. Jessee SA. Physical manifestations of child abuse to the head, face and mouth: A hospital survey. J Dent Child 1995;62:245-9. 9. Jessee SA, Rieger M. A study of age-related variables among physically abused children. J Dent Child 1996; 63:275-80. 10. Malecz RE. Child abuse, its relationship to pedodontics: A survey. J Dent Child 1979;46:193-4. 11. Needleman HL. Orofacial trauma in child abuse: Types, prevalence, management, and the dental profession’s involvement. Pediatr Dent 1986;8(special issue 1):71-80. 12. O’Neill JA Jr, Meacham WF, Griffin JP, Sawyers JL. Patterns of injury in the battered child syndrome. J Trauma 1973;13:332-9. 13. Skinner AE, Castle RL. Seventy-eight Battered Children: A Retrospective Study. London, England: National Society for the Prevention of Cruelty to Children; 1969. 14. Tate RJ. Facial injuries associated with the battered child syndrome. Br J Oral Surg 1971;9:41-5. 15. Vadiakas G, Roberts MW, Dilley DC. Child abuse and neglect: Ethical issues for dentistry. J Mass Dent Soc 1991; 40:13-5. 16. Naidoo S. A profile of the oro-facial injuries in child physical abuse at a children’s hospital. Child Abuse Negl 2000;24:521-34. 17. Kittle PE, Richardson DS, Parker JW. Two child abuse/ child neglect examinations for the dentist. J Dent Child 1981;48:175-80. 18. Blain SM, Winegarden T, Barber TK, Sognnaes FR. Child abuse and neglect. II: Role of dentistry [abstract]. J Dent Res 1979;58(special issue A):367. 19. McNeese MC, Hebeler JR. The abused child: A clinical approach to identification and management. Clin Symp 1977;29:1-36.
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20. Levin AV. Otorhinolaryngologic manifestations. In: Levin AV, Sheridan MS, eds. Munchausen Syndrome by Proxy: Issues in Diagnosis and Treatment. New York, NY: Lexington Books; 1995:219-30. 21. Folland DS, Burke RE, Hinman AR, Schaffner W. Gonorrhea in preadolescent children: An inquiry into source of infection and mode of transmission. Pediatrics 1977;60: 153-6. 22. American Academy of Pediatrics Committee on Child Abuse. Guidelines for the evaluation of sexual abuse of children: A subject review. Pediatrics 1999;103:186-91. 23. DeJong AR. Sexually transmitted diseases in sexually abused children. Sex Transm Dis 1986;13:123-6. 24. Everett VD, Ingram DL, Flick LAR, Russell TA, TropezSims ST, McFadden AY. A comparison of sexually transmitted diseases (STDs) found in a total of 696 boys and 2973 girls evaluated for sexual abuse [abstract]. Pediatr Res 1998;43:91A. 25. Nelson JD, Mohs E, Dajani AS, Plotkin SA. Gonorrhea in preschool- and school-aged children: Report of the Prepubertal Gonorrhea Cooperative Study Group. JAMA 1976;236:1359-64.
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26. Stevens-Simon C, Nelligan D, Breese P, Jenny C, Douglas JM Jr. The prevalence of genital human papillomavirus infections in abused and nonabused preadolescent girls. Pediatrics 2000;106:645-9. 27. Schlesinger SL, Borbotsina J, O’Neill L. Petechial hemorrhages of the soft palate secondary to fellatio. Oral Surg Oral Med Oral Pathol 1975;40:376-8. 28. Sperber ND. Bite marks, oral and facial injuries: Harbigers of severe child abuse? Pediatrician 1989;16:207-11. 29. Wagner GN. Bitemark identification in child abuse cases. Pediatr Dent 1986;8:96-100. 30. National Research Council, Committee on DNA Technology in Forensic Science, Board of Biology, Commission on Life Sciences. DNA Technology in Forensic Science. Washington, DC: National Academy Press; 1992. 31. American Academy of Pediatric Dentistry. Definition of dental neglect. Pediatr Dent 2003;25(suppl):7. 32. Sanger RG, Bross DC, eds. Clinical Management of Child Abuse and Neglect: A Guide for the Dental Professional. Chicago, Ill: Quintessence Publishing Co, Inc; 1984. 33. California Society of Pediatric Dentists. Dental neglect: When to report. Calif Pediatrician 1989;Fall:31-2.
american academy of pediatric dentistry
Guideline on the Role of Dental Prophylaxis in Pediatric Dentistry Originating Committee
Clinical Affairs Committee Review Council Council on Clinical Affairs
Adopted 1986
Revised 1993, 2000, 2003, 2007
Reaffirmed 1996
Purpose The American Academy of Pediatric Dentistry (AAPD), as an advocate for optimal oral health of infants, children, and adolescents, must educate caregivers and other interested third parties on the indications for and benefits of a dental prophylaxis in conjunction with a periodic oral health assessment.
Methods This guideline is based on a review of current preventive, restorative, and periodontal literature, as well as AAPD’s Policy Statement on the Use of a Caries-risk Assessment Tool (CAT) for Infants, Children, and Adolescents1 and the American Academy of Periodontics’ (AAP) Periodontal Diseases in Children and Adolescents.2 A MEDLINE search was conducted using the terms “dental prophylaxis”, “toothbrushing”, “professional tooth cleaning”, and “professional dental prophylaxis in children”.
Background Microbial plaque is the primary etiological factor in caries and periodontal disease.3,4 Although it may be possible to remove most plaque using mechanical oral hygiene aids, many patients do not have the motivation or skill to maintain a plaque-free state for extended periods of time.5 Clinical studies show that “self-administered plaque control programs alone, without periodic professional reinforcement, are inconsistent in providing long-term inhibition of gingivitis”.5 Indications for a professional dental prophylaxis include: 1. removal of plaque, stain, and calculus;6 2. elimination of factors that influence the build-up and retention of plaque;7-9 3. demonstration of proper oral hygiene methods to the patient/caregiver; 4. facilitation of a thorough clinical examination; 5. introduction of dental procedures to the child. The type and frequency of professional prophylaxis recommended is based on an individual patient’s risk-assessment
for caries and periodontal disease. The AAPD has developed a tool1 to determine caries risk and the AAP has guidelines2 to address periodontal risk. These assessments may include: 1. medical history/current systemic health including medications; 2. age and cooperation of the patient; 3. compliance of the patient and family; 4. past and current caries; 5. family history of caries; 6. past and current periodontal health; 7. family history of periodontal disease; 8. oral hygiene; 9. presence of plaque; 10. presence of gingivitis; 11. presence of calculus; 12. presence of extrinsic stain; 13. local factors that would influence the build-up and retention of plaque. A professional prophylaxis can be performed using toothbrush, rubber cup, flossing, and/or mechanical instruments. In the absence of stain or calculus, a manual toothbrush and non-abrasive paste may fulfill the goals of a professional prophylaxis. Rubber cup prophylaxis, with paste grit as fine as possible, is indicated for the removal of extrinsic staining and smoothing of rough enamel surfaces following scaling.6 A practitioner diagnosing localized stain and/or calculus may elect to polish only selected teeth rather than the full erupted dentition. The benefits of various prophylaxis options are shown in Table 1. Rubber cup prophylaxis using pastes or pumice may be performed prior to the application of a professional fluoride treatment. The use of abrasive toothpastes and whitening products, as well as abrasion during a prophylaxis, can remove the acquired pellicle. This can have an adverse effect on exposed tooth surfaces by increasing the chances of enamel loss through exposure to dietary acids.10 Furthermore, even though CLINICAL GUIDELINES
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Table 1. Benefits of Prophylaxis Options Plaque removal
Stain
Calculus
Polish/smooth
Education of patient/parent
Facilitate Examination
Toothbrush
Yes
No
No
No
Yes
Yes
Power brush
Yes
Yes
No
No
Yes
Yes
Rubber cup
Yes
Yes
No
Yes
Yes
Yes
Hand instruments
Yes
Yes
Yes
No
Yes
Yes
the pellicle begins forming immediately after it is removed, it may take up to 7 days, possibly longer, to mature fully and offer maximal protection against dietary acid challenges.10 Rubber cup prophylaxis with pumice paste can remove up to 0.6–4.0 microns of the outer enamel11-14 which includes the fluoride-rich layer. This is dependent on the speed of the handpiece, abrasivity of the paste, and the amount of time spent cleaning the tooth.11-14 Researchers have concluded that a pumice prophylaxis followed by a topical fluoride application results in “similar” levels of fluoride uptake as a topical fluoride application without a prophylaxis.15,16
Recommendations A periodic professional prophylaxis should be performed to: 1. instruct the caregiver and child or adolescent in proper oral hygiene techniques; 2. remove microbial plaque and calculus; 3. polish hard surfaces to minimize the accumulation and retention of plaque; 4. remove extrinsic stain; 5. facilitate the examination of hard and soft tissues; 6. introduce dental procedures to the young child and apprehensive patient. In addition to establishing the need for a prophylaxis, the clinician should determine the most appropriate type of prophylaxis for each patient. The practitioner should select the least aggressive technique that fulfills the goals of the procedure. To minimize loss of the fluoride-rich layer of enamel during polishing, the least abrasive paste should be used with light pressure. If a rubber cup/pumice prophylaxis is performed, a topical fluoride application is recommended.17 A patient’s risk for caries/periodontal disease, as determined by the patient’s dental provider, should help determine the interval of the prophylaxis. Patients who exhibit higher risk for developing caries and/or periodontal disease should have recall visits at intervals more frequent than every 6 months. This allows increased professional fluoride therapy application, microbial monitoring, antimicrobial therapy reapplication, and reevaluating behavioral changes for effectiveness.18 An individualized preventive plan increases the probability of good oral health by demonstrating proper oral hygiene methods and techniques and removing plaque, stain, calculus6, and the factors that influence their build-up.7-9
References 1. American Academy of Pediatric Dentistry. Policy on use of a caries-risk assessment tool (CAT) for infants, children, and adolescents. Pediatr Dent 2006;28(suppl):24-8.
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2. Califano JV, Research Science and Therapy Committee American Academy of Periodontology. Periodontal diseases of children and adolescents. J Periodontol 2003;74 (11):1690-704. 3. Stookey GK. Current status of caries prevention. Compendium 2000;21(10A):862-7. 4. Clerehugh V, Tugnait A. Periodontal diseases in children and adolescents: 1. Aetiology and diagnosis. Dent Update 2001;28(5):222-30, 232. 5. American Academy of Periodontology Research Science and Therapy Committee. Treatment of plaque-induced gingivitis, chronic periodontitis, and other clinical conditions. J Periodontol 2001;72(12):1790-800. 6. Clerehugh V, Tugnait A. Periodontal diseases in children and adolescents: 2. Management. Dent Update 2001;28(6):274-81. 7. Roulet JF, Roulet-Mehrens TK. The surface roughness of restorative materials and dental tissues after polishing with prophylaxis and polishing pastes. J Periodontol 1982;53:257-66. 8. Hosoya Y, Johnston JW. Evaluation of various cleaning and polishing methods on primary enamel. J Pedod 1989;13 (3):253-69. 9. Quirynen M, Bollen CML. The influence of surface roughness and surface-free energy on supra- and subgingival plaque formation in man. A review of the literature. J Clin Periodontol 1995;22(1):1-14. 10. Zero DT. Dental caries process. Dent Clin North Am 1999; 43(4):635-64. 11. Stookey GK. In vitro estimates of enamel and dentin abrasion associated with a prophylaxis. J Dent Res 1978;57(1):36. 12. Vrbic V, Brudevold F, McCann HG. Acquisition of fluoride by enamel from fluoride pumice pastes. Helv Odontol Acta 1967;11(1):21-6. 13. Koch G, Petersson LG, Johnson G. Abrasive effect and fluorine uptake from polishing and prophylactic pastes. Swed Dent J 1975;68(1):1-7. 14. Mellberg JR. The relative abrasivity of dental prophylactic pastes and abrasives on enamel and dentin. Clin Prev Dent 1979;1(1):13-8. 15. Joyston-Bechal S, Duckworth R, Braden M. The effect of artificially produced pellicle and plaque on the uptake of 18F by human enamel in vitro. Arch Oral Biol 1979;21(2):73-8. 16. Tinanoff N, Wei SHY, Parkins FM. Effect of a pumice prophylaxis on fluoride uptake in tooth enamel. J Am Dent Assoc 1974;88(2):384-9. 17. Adair SM. Evidence-based use of fluoride in contemporary pediatric dental practice. Pediatr Dent 2006;28(2):133-42. 18. US Preventive Services Task Force. Guide to Clinical Preventive Services. 2nd ed. Baltimore, MD: Williams and Wilkins; 1996.
american academy of pediatric Dentistry
Guideline on Fluoride Therapy Originating Committee
Liaison with Other Groups Committee Review Council Council on Clinical Affairs
Adopted 1967
Revised 1978, 1995, 2000, 2003, 2007, 2008
Reaffirmed 1972, 1977
Purpose The American Academy of Pediatric Dentistry (AAPD) intends this guideline to help practitioners and parents make decisions concerning appropriate use of fluoride as part of the comprehensive oral health care for infants, children, adolescents, and persons with special health care needs.
Methods A thorough review of the scientific literature pertaining to the use of systemic and topical fluoride was completed to revise and update this guideline. A MEDLINE search was conducted using the terms “fluoride”, “fluoridation”, “acidulated phosphate fluoride”, “fluoride varnish”, “fluoride therapy”, and “topical fluoride”. Expert opinions and best current practices also were relied upon for this guideline.
Professionally-applied topical fluoride treatments are efficacious in reducing caries in children with moderate or high caries risk.5,7,8,25-32 Two percent sodium fluoride (NaF; 9000 ppm)1, 1.23% acidulated phosphate fluoride (APF; 12,300 ppm) solution or gel1,33-44, and 5% sodium fluoride varnish (NaFV; 22,500ppm)1,41,43,45-54 are the most commonly used agents for professionally-applied fluoride treatments.1,45 Some topical fluoride products are marketed with recommended treatment times of less than 4 minutes, but the majority of studies suggest that 4-minute applications are more efficacious.1,8,36,57,58 Children at higher caries risk may require additional or more frequent fluoride therapies.7,59,60 If an individual’s caries risk level is uncertain, treating this person as high risk is prudent until further experience allows a more accurate assessment.4
Recommendations
Background
Systemically-administered fluoride supplements Use of fluorides for the prevention and control of caries is Fluoride supplements should be considered for all children documented to be both safe and highly effective.1-5 Fluoride has drinking fluoride-deficient (<0.6 ppm) water. After determinseveral caries-protective mechanisms of action, including enamel ing the fluoride level of the water supply or supplies (either remineralization and altering bacterial metabolism to help prevent through contacting public health officials or water analysis), caries.6 Optimizing fluoride levels in water supplies is an ideal evaluating other dietary sources of fluoride, and assessing the public health measure because it is effective and inexpensive and child’s caries risk, the daily fluoride supplement dosage can does not require conscious daily cooperation from individuals.4,7-10 be determined using the Dietary Fluoride Supplementation Daily fluoride exposure through water supplies and monitored Schedule (Table 1). To optimize the topical benefits of systemic use of fluoride toothpaste can be effective preventive procedures. fluoride supplements, the child should be encouraged to chew Determination of dietary sources of fluoride before prescrib- or suck fluoride tablets.1 ing supplements can help reduce intake of excess fluoride.11-15 Sources of dietary fluoride may include drinking water from home, day care, and school; beverages Table 1. dietary fluoride supplementation schedule such as soda12, juice15, and infant formula11,16,17; 18 prepared food ; and toothpaste. Infant formulas Age <0.3 ppm F 0.3-0.6 ppm F >0.6 ppm F (powdered or liquid) and water bottled specifically Birth-6 months 0 0 0 for infants have varying concentrations of fluoride.1624 6 mo-3 years 0.25 mg 0 0 Fluorosis has been associated with cumulative 3-6 years 0.50 mg 0.25 mg 0 fluoride intake during enamel development, with the severity dependant on the dose, duration, and 6 y up to at least 16 years 1.00 mg 0.50 mg 0 timing of intake.4 CLINICAL GUIDELINES
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References
1. Adair SM. Evidence-based use of fluoride in contemporary pediatric dental practice. Pediatr Dent 2006:28(2):133-42. 2. Whitford GM. The physiological and toxicological characteristics of fluoride. J Dent Res 1990;69 (special issue):539-49; discussion 556-7. 3. Workshop Reports I, II, III from “A symposium on changing patterns of fluoride intake” held at UNC-Chapel Hill April 23-25,1991. J Dent Res 1992;71(5):1214-27. 4. CDC. Recommendations for using fluoride to prevent and control dental caries in the United Figure 1. Comparison of a smear (left) with a pea-sized (right) amount of toothpaste. States. MMWR Recomm Rep 2001;50(RR-14): 1-42. Professionally-applied topical fluoride treatment 5. Facts about fluoride. CDS Rev 2006;99(1):44. Professional topical fluoride treatments should be based on 6. Featherstone JD. The science and practice of caries precaries-risk assessment.1,4,5,7,60 A pumice prophylaxis is not an vention. J Am Dent Assoc 2000;131(7):877-99. essential prerequisite to this treatment.61 Appropriate precau- 7. American Dental Association Council on Scientific Aftionary measures should be taken to prevent swallowing of any fairs. Professionally-applied topical fluoride: Evidenceprofessionally-applied topical fluoride. Children at moderate based clinical recommendations. J Am Dent Assoc 2006; caries risk should receive a professional fluoride treatment 137(8):1151-9. at least every 6 months; those with high caries risk should 8. CDC. Achievements in Public Health, 1990-1999: Fluoreceive greater frequency of professional fluoride applications ridation of drinking water to prevent dental caries. JAMA (ie, every 3-6 months).7,32,59,62-67 Ideally, this would occur as part 2000;283(10):1283-6. of a comprehensive preventive program in a dental home. 68 9. Pelletier AR. Maintenance of optimal fluoride levels in When a dental home cannot be established for individuals public water systems. J Public Health Dent 2004;64(4): with increased caries risk as determined by caries risk assess237-9. ment, periodic applications of fluoride varnish by trained 10. CDC. Populations receiving optimally fluoridated pubnon-dental healthcare professionals may be effective in reducing lic drinking water-United States, 2000. MMWR Morb the incidence of early childhood caries.50-54,69,70 Mortal Wkly Rep 2002;51(7):144-7. 11. L evy SM, Kohout FJ, Guha-Chowdhury N, Kiritsy Fluoride-containing products for home use MC, Heilman JR, Wefel JS. Infants’ fluoride intake from drinking water alone, and from water added to formula, Therapeutic use of fluoride for children should focus on regibeverages, and food. J Dent Res 1995;74(7):1399-407. mens that maximize topical contact, preferably in lower-dose, higher-frequency approaches.1 Fluoridated toothpaste should 12. Levy SM, Kohout FJ, Kiritsy MC, Heilman JR, Wefel JS. Infants’ fluoride ingestion from water, supplements be used twice daily as a primary preventive procedure.1,71 Twice and dentifrice. J Am Dent Assoc 1995;126(12):1625-32. daily use has benefits greater than once daily brushing.1 Parents should be counseled on their child’s caries risk, dispensing an 13. Bowen WH. Fluorosis, is it really a problem? J Am Dent Assoc 2002;133(10):1405-7. appropriate volume of toothpaste onto a soft, age-appropriate sized toothbrush, frequency of brushing, and performing/ 14. Heilman JR, Kiritsy MC, Levy SM, Wefel JS. Assessing fluoride levels of carbonated soft drinks. J Am Dent assisting brushing of young children. A ‘smear’of fluoridated Assoc 1999;130(11):1593-9. toothpaste (see Figure 1) for children less than 2 years of age may decrease risk of fluorosis.72 A ‘pea-size’ amount (see Figure 15. Kiritsy MC, Levy SM, Warren JJ, Guha-Chowdhury N, Heilman JR, Marshall T. Assessing fluoride concentra1) of toothpaste is appropriate for children aged 2 through 5 tions of juices and juice-flavored drinks. J Am Dent Assoc years.72-74 To maximize the beneficial effect of fluoride in the 1996;127(7):895-902. toothpaste, rinsing after brushing should be kept to a mini 16. Van Winkle S, Levy SM, Kiritsy MC, Heilman JR, Wefel mum or eliminated altogether. 72,75 JS, Marshall T. Water and formula fluoride concentra Additional at-home topical fluoride regimens utilizing intions: Significance for infants fed formula. Pediatr Dent creased concentrations of fluoride should be considered for 1995;17(4):305-10. children at high risk for caries.1,4,7,60 These may include overthe-counter or prescription strength formulations. Fluoride 17. Levy SM, Kiritsy MC, Warren JJ. Sources of fluoride intake in children. J Public Health Dent 1995;55(1):39-52. mouth rinses or brush-on gels may be incorporated into a 18. Heilman JR, Kiritsy MC, Levy SM, Wefel JS. Fluoride caries-prevention program for a school-aged child at high risk. concentrations of infant foods. J Am Dent Assoc 1997; 128(7):857-63. 144
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19. Erdal S, Buchanan SN. A quantitative look at fluorosis, fluoride exposure, and intake in children using a health risk assessment approach. Environ Health Perspect 2005; 113(1):111-7. 20. Marshall TA, Levy SM, Warren JJ, Broffitt B, EichenbergerGilmore JM, Stumbo PJ. Associations between intakes of fluoride from beverages during infancy and dental fluorosis of primary teeth. J Am Coll Nutr 2004;23(2):108-16. 21. Buzalaf MA, Damante CA, Trevizani LM, Granjeiro JM. Risk of fluorosis associated with infant formulas prepared with bottled water. J Dent Child 2004;71(2):110-3. 22. A nderson WA, Pratt I, Ryan MR, Flynn A. A probabilistic estimation of fluoride intake by infants up to the age of 4 months from infant formula reconstituted with tap water in the fluoridated regions of Ireland. Caries Res 2004;38(5):421-9. 23. Buzalaf MA, Granjeiro JM, Damante CA, de Ornelas F. Fluoride content of infant formulas prepared with deionized, bottled mineral and fluoridated drinking water. J Dent Child 2001;68(1):37-41, 10. 24. Pagliari AV, Moimaz SA, Saliba O, Delbum AC, Sassaki, KT. Analysis of fluoride concentration in mother’s milk substitutes. Pesqui Odontol Bras 2006;20(3):269-74. 25. L alumandier JA, Rozier RG. The prevalence and risk factors of fluorosis among patients in a pediatric dental practice. Pediatr Dent 1995;17(1):19-25. 26. Beltrán-Aguilar ED, Griffin SO, Lockwood SA. Prevalence and trends in enamel fluorosis in the United States from the 1930s to the 1980s. J Am Dent Assoc 2002;133 (2):157-65. 27. Beltrán-Aguilar ED, Barker LK, Canto MT, et al. Surveillance for dental caries, dental sealants, tooth retention, edentulism, and enamel fluorosis-United States, 19881994 and 1999-2002. MMWR Surveill Summ 2005;54 (3):1-43. 28. D enBesten PK, Thariani H. Biological mechanisms of fluorosis and level and timing of systemic exposure to fluoride with respect to fluorosis. J Dent Res 1992;71(5): 1238-43. 29. Evans RW, Stamm JW. Dental fluorosis following downward adjustment of fluoride in drinking water. J Public Health Dent 1991;51(2):91-8. 30. Heller KE, Eklund SA, Burt BA. Dental caries and dental fluorosis at varying water fluoride concentrations. J Public Health Dent 1997;57(3):136-43. 31. R ipa LW. An evaluation of the use of professional (operator-applied) topical fluorides. J Dent Res 1990;69 (Spec No):786-96; discussion 820-3. 32. Bader JD, Shugars DA, Bonito AJ. A systematic review of selected caries prevention and management methods. Community Dent Oral Epidemiol 2001;29(6):399-411. 33. R ozier RG. Effectiveness of methods used by dental professionals for the primary prevention of dental caries. J Dent Educ 2001;65(10):1063-72.
34. Wei SH, Lau EW, Hattab FN. Time dependence of enamel fluoride acquisition from APF gels. II. In vivo study. Pediatr Dent 1988;10(3):173-7. 35. Wei SH, Hattab FN. Time dependence of enamel fluoride acquisition for APF gels. I. In vitro study. Pediatr Dent 1988;10(3):168-72. 36. Wei SH, Chik FF. Fluoride retention following topical fluoride foam and gel application. Pediatr Dent 1990;12 (6):368-74. 37. v an Rijkom HM, Truin GJ, van ‘t Hof MA. Cariesinhibiting effect of professional fluoride gel application in low-caries children initially aged 4.5-6.5 years. Caries Res 2004;38(2):115-23. 38. v an Rijkom HM, Truin GJ, van ‘t Hof MA. A metaanalysis of clinical studies on the caries-inhibiting effect of fluoride gel treatment. Caries Res 1998;32(2):83-92. 39. Truin GJ, van ’t Hof MA. Caries prevention by professional fluoride gel application on enamel and dentinal lesions in low-caries children. Caries Res 2005;39(3): 236-40. 40. Truin GJ, van ‘t Hof MA. Professionally applied fluoride gel in low-caries 10.5-year-olds. J Dent Res 2005;84(5): 418-21. 41. Marinho VC, Higgins JP, Sheiham A, Logan S. Combinations of topical fluoride (toothpastes, mouthrinses, gels, varnishes) versus single topical fluoride for preventing dental caries in children and adolescents. Cochrane Data-base Syst Rev 2004(1):CD002781. 42. M arinho VC, Higgins JP, Logan S, Sheiham A. Systematic review of controlled trials on the effectiveness of fluoride gels for the prevention of dental caries in children. J Dent Educ 2003;67(4):448-58. 43. Marinho VC, Higgins JP, Logan S, Sheiham A. Fluoride gels for preventing dental caries in children and adolescents. Cochrane Database Syst Rev 2002(2):CD002280. 44. Marinho V. Fluoride gel inhibits caries in children who have low caries-risk but this may not be clinically relevant. Evid Based Dent 2004;5(4):95. 45. Bawden JW. Fluoride varnish: A useful new tool for public health dentistry. J Public Health Dent 1998;58 (4):266-9. 46. C hu CH, Lo EC, Lin HC. Effectiveness of silver diamine fluoride and sodium fluoride varnish in arresting dentin caries in Chinese pre-school children. J Dent Res 2002;81(11):767-70. 47. Klein U, Kanellis MJ, Drake D. Effects of four anticaries agents on lesion depth progression in an in vitro caries model. Pediatr Dent 1999;21(3):176-80. 48. Bravo M, Montero J, Bravo JJ, Baca P, Llodra JC. Sealant and fluoride varnish in caries: A randomized trial. J Dent Res 2005;84(12):1138-43. 49. Lo EC, Chu CH, Lin HC. A community-based caries control program for pre-school children using topical fluorides: 18-month results. J Dent Res 2001;80(12): 2071-4. CLINICAL GUIDELINES
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50. Hawkins R, Noble J, Locker D, et al. A comparison of the costs and patient acceptability of professionallyapplied topical fluoride foam and varnish. J Public Health Dent 2004;64(2):106-10. 51. Rozier RG, Sutton BK, Bawden JW, Haupt K, Slade GD, King RS. Prevention of early childhood caries in North Carolina medical practices: Implications for research and practice. J Dent Educ 2003;67(8):876-85. 52. Q uiñonez RB, Stearns SC, Talekar BS, Rozier RG, Downs SM. Simulating cost-effectiveness of fluoride varnish during well-child visits for Medicaid-enrolled children. Arch Pediatr Adolesc Med 2006;160(2):164-70. 53. Petersson LG, Twetman S, Dahlgren H, et al. Professional fluoride varnish treatment for caries control: A systematic review of clinical trials. Acta Odontol Scand 2004;62(3):170-6. 54. D ohnke-Hohrmann S, Zimmer S. Change in caries prevalence after implementation of a fluoride varnish program. J Public Health Dent 2004;64(2):96-100. 55. Kawasaki A, Suge T, Ishikawa K, Ozaki K, Matsuo T, Ebisu S. Ammonium hexafluorosilicate increased acid resistance of bovine enamel and dentine. J Mater Sci Mater Med 2005;16(5):461-6. 56. Knight GM, McIntyre JM, Mulyani. The effect of silver fluoride and potassium iodide on the bond strength of auto cure glass ionomer cement to dentine. Aust Dent J 2006;51(1):42-5. 57. Wei SH, Hattab FN. Fluoride retention following topical application of a new APF foam. Pediatr Dent 1989;11(2): 121-4. 58. Wei SH, Hattab FN. Enamel fluoride uptake from a new APF foam. Pediatr Dent 1988;10(2):111-4. 59. A xelsson S, Soder B, Nordenram G, et al. Effect of combined caries-preventive methods: A systematic review of controlled clinical trials. Acta Odontol Scand 2004;62 (3):163-9. 60. American Academy of Pediatric Dentistry. Policy on use of a caries-risk assessment tool (CAT) for infants, children, and adolescents. Pediatr Dent 2006;28(suppl):24-8. 61. Johnston DW, Lewis DW. Three-year randomized trial of professionally applied topical fluoride gel comparing annual and biannual applications with/without prior prophylaxis. Caries Res 1995;29(5):331-6. 62. Kallestal C. The effect of five years’ implementation of caries-preventive methods in Swedish high-risk adolescents. Caries Res 2005;39(1):20-6.
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63. Featherstone JD, Adair SM, Anderson MH, et al. Caries management by risk assessment: Consensus statement, April 2002. J Calif Dent Assoc 2003;31(3):257-69. 64. Featherstone JD. The caries balance: The basis for caries management by risk assessment. Oral Health Prev Dent 2004;2(suppl 1):259-64. 65. Bader JD, Shugars DA, Rozier G, et al. Diagnosis and management of dental caries. Evid Rep Technol Assess (Summ) 2001;(36):1-4. 66. Bader JD, Shugars DA, Bonito AJ. A systematic review of the performance of methods for identifying carious lesions. J Public Health Dent 2002;62(4):201-13. 67. Bader JD, Perrin NA, Maupome G, Rindal B, Rush WA. Validation of a simple approach to caries risk assessment. J Public Health Dent 2005;65(2):76-81. 68. American Academy of Pediatric Dentistry. Policy on the dental home. Pediatr Dent 2007;29(suppl):22-3. 69. McDonald SP, Sheiham A. A clinical comparison of non-traumatic methods of treating dental caries. Int Dent J 1994;44(5):465-70. 70. Wawrzyniak MN, Boulter S, Giotopoulos C, Zivitski J. Incorporating caries prevention into the well-child visit in a family medicine residency. Fam Med 2006;38(2):90-2. 71. Featherstone JDB. Caries prevention and reversal based on the caries balance. Pediatr Dent 2006:28(2):128-32. 72. Scottish Intercollegiate Guideline Network. Prevention and management of dental decay in the pre-school child. A national guideline #83. November 2005;1-44. Available at: “http://www.sign.ac.uk/guidelines/published/numlist. html”. Accessed February 23, 2008. 73. Pang DT, Vann WF Jr. The use of fluoride-containing toothpastes in young children: The scientific evidence for recommending a small quantity. Pediatr Dent 1992;14 (6):384-7. 74. Ramos-Gomez FJ, Crall JJ, Gansky SA, Slayton RL, Featherstone JDB. Caries risk assessment appropriate for the age 1 visit (infants and toddlers). J Calif Dent Assoc 2007;35(10):687-702. 75. Sjögren K, Birkhed D. Factors related to fluoride retention after toothbrushing and possible connection to caries activity. Caries Res 1993;27(6):474-7.
american academy of pediatric Dentistry
Guideline on Behavior Guidance for the Pediatric Dental Patient Originating Committee
Clinical Affairs Committee – Behavior Management Subcommittee Review Council Council on Clinical Affairs
Adopted 1990
Revised 1991, 1996, 2000, 2005, 2006, 2008*
Purpose The American Academy of Pediatric Dentistry (AAPD) recognizes that, in providing oral health care for infants, children, adolescents, and persons with special health care needs, a continuum of both nonpharmacological and pharmacological behavior guidance techniques may be used by dental health care providers. The various behavior guidance techniques used must be tailored to the individual patient and practitioner. Promoting a positive dental attitude, safety, and quality of care are of the utmost importance. This guideline is intended to educate health care providers, parents, and other interested parties about many behavior guidance techniques used in contemporary pediatric dentistry. It will not attempt to duplicate information found in greater detail in the AAPD’s Guideline on Appropriate Use of Nitrous Oxide for Pediatric Dental Patients,1 Guidelines for Monitoring and Management of Pediatric Patients During and After Sedation for Diagnostic and Therapeutic Procedures: An Update,2 and Guideline on the Use of Anesthesia Care Providers in the Administration of In-office Deep Sedation/General Anesthesia to the Pediatric Dental Patient.3
Methods This guideline was developed following the AAPD’s 1989 consensus conference on behavior management for the pediatric dental patient. In 2003, the AAPD held another symposium on behavior guidance, with proceedings published in Pediatric Dentistry (2004, Vol. 26, No. 2). This revision reflects a review of those proceedings, other dental and medical literature related to behavior guidance of the pediatric patient, and sources of recognized professional expertise and stature including both the academic and practicing pediatric dental communities and the standards of the Commission on Dental Accreditation.4 MEDLINE searches were performed using key terms such as “behavior management in children”, “behavior management in dentistry”, “child behavior and dentistry”, “child and dental anxiety”, “child preschool and dental anxiety”, “child personality and test”, * The
“child preschool personality and test”, “patient cooperation”, “dentists and personality”, “dentist-patient relations”, “patient assessment”, “treatment deferral”, and “restraint”.
Background Overview Dental practitioners are expected to recognize and effectively treat childhood dental diseases that are within the knowledge and skills acquired during dental education. Safe and effective treatment of these diseases often requires modifying the child’s behavior. Behavior guidance is a continuum of interaction involving the dentist and dental team, the patient, and the parent directed toward communication and education. Its goal is to ease fear and anxiety while promoting an understanding of the need for good oral health and the process by which that is achieved. A dentist who treats children should have a variety of behavior guidance approaches and, in most situations, should be able to assess accurately the child’s developmental level, dental attitudes, and temperament and to predict the child’s reaction to treatment. The child who presents with oral/dental pathology and noncompliance tests the skills of every practitioner. By virtue of differences in each clinician’s training, experience, and personality, a behavior guidance approach for a child may vary among practitioners. The behaviors of the dentist and dental staff members play an important role in behavior guidance of the pediatric patient. Through communication, the dental team can allay fear and anxiety, teach appropriate coping mechanisms, and guide the child to be cooperative, relaxed, and self-confident in the dental setting. Successful behavior guidance enables the oral health team to perform quality treatment safely and efficiently and to nurture a positive dental attitude in the child. Some of the behavior guidance techniques in this document are intended to maintain communication, while others are intended to extinguish inappropriate behavior and establish communication. As such, these techniques cannot be evaluated on an individual basis as to validity, but must be assessed within
2008 revision was limited to clarifications within “Advanced Behavior Guidance, Protective Stabilization”.
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the context of the child’s total dental experience. Each technique must be integrated into an overall behavior guidance approach individualized for each child. Therefore, behavior guidance is as much an art as it is a science. It is not an application of individual techniques created to “deal” with children, but rather a comprehensive, continuous method meant to develop and nurture the relationship between patient and doctor, which ultimately builds trust and allays fear and anxiety. This guideline contains definitions, objectives, indications, and contraindications for behavior guidance techniques commonly taught and used in pediatric dentistry.5-7 This document is reflective of the AAPD’s role as an advocate for the improvement of the overall health of the child. Dentists are encouraged to utilize behavior guidance techniques consistent with their level of professional education and clinical experience. Behavior guidance cases that are beyond the training, experience, and expertise of individual practitioners should be referred to practitioners who can render care more appropriately. Dental Team Behavior The pediatric dental staff can play an important role in behavior guidance. The scheduling coordinator or receptionist will have the first contact with a prospective parent, usually through a telephone conversation. Information provided to the parent prior to an appointment will help set expectations for the initial visit. The internet and customized web pages are excellent ways of introducing parents/patients to one’s practice. These encounters serve as educational tools that help the parent and child be better prepared for the first visit and may answer questions that help to allay fears. In addition, the receptionist is usually the first staff member the child meets. The manner in which the child is welcomed into the practice may influence future patient behavior. The clinical staff is an extension of the dentist in terms of using communicative behavior guidance techniques. Therefore, their communicative skills are very important. The dental team should work together in communicating with parents and patients. A child’s future attitude toward dentistry may be determined by a series of successful experiences in a pleasant dental environment. All dental team members are encouraged to expand their skills and knowledge in behavior guidance techniques by reading dental literature, observing video presentations, or attending continuing education courses. Dentist Behavior The health professional may be inattentive to communication style, but patients/parents are very attentive to it.8 The communicative behavior of dentists is a major factor in patient satisfaction.9,10 The dentist should recognize that not all parents may express their desire for involvement.11 Dentist behaviors reported to correlate with low parent satisfaction include rushing through appointments, not taking time to explain procedures, barring parents from the examination room, and generally being impatient.12 Relationship/communication problems have been demonstrated to play a prominent role in initiating malpractice actions. Even
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where no error occurred, perceived lack of caring and/or collaboration were associated with litigation.13,14 Studies of efficacy of various dentist behaviors in management of uncooperative patients are equivocal. Dentist behaviors of vocalizing, directing, empathizing, persuading, giving the patient a feeling of control, and operant conditioning have been reported as efficacious responses to uncooperative patient behaviors.15-17 Communication Communication (ie, imparting or interchange of thoughts, opinions, or information) may be accomplished by a number of means but, in the dental setting, it is affected primarily through dialogue, tone of voice, facial expression, and body language. The 4 “essential ingredients” of communication are: 1. the sender; 2. the message, including the facial expression and body language of the sender; 3. the context or setting in which the message is sent; and 4. the receiver.18 For successful communication to take place, all 4 elements must be present and consistent. Without consistency, there may be a poor “fit” between the intended message and what is understood. Communicating with children poses special challenges for the dentist and the dental team. A child’s cognitive development will dictate the level and amount of information interchange that can take place. It is impossible for a child to perceive an idea for which he has no conceptual framework and unrealistic to expect a child patient to adopt the dentist’s frame of reference. The dentist, therefore, must have a basic understanding of the cognitive development of children so, through appropriate vocabulary, messages consistent with the receiver’s intellectual development can be sent. Communication may be impaired when the sender’s expression and body language are not consistent with the intended message. When body language conveys uncertainty, anxiety, or urgency, the dentist cannot effectively communicate confidence in his/her clinical skills. It is possible to communicate with the child patient briefly at the beginning of a dental appointment to establish rapport and trust. However, once a procedure begins, the dentist’s ability to control and shape behavior becomes paramount, and information sharing becomes secondary. The 2-way interchange of information gives way to 1-way manipulation of behavior through commands. This type of interaction is called “requests and promises”.19 When action must take place to reach a goal (eg, completion of the dental procedure), the dentist assumes the role of the requestor. Requests elicit promises from the patient that, in turn, establish a commitment to cooperate. The dentist may need to frame the request in a number of ways in order to make the request effective. For example, reframing a previous command in an assertive voice with appropriate facial expression and body language is the basis for the technique of voice control. While voice control is classified as one of the means of
american academy of pediatric Dentistry
communicative guidance, it may be considered aversive in nature by some parents.20 The 3 “essential communications” imparted to child patients through primarily non-verbal means are: 1. “I see you as an individual and will respond to your needs as such”; 2. “I am thoroughly knowledgeable and highly skilled”; 3. “I am able to help you and will do nothing to hurt you needlessly”.21 The importance of the context in which messages are delivered cannot be overstated. The dental office may be made “child friendly” by the use of themes in its decoration, age-appropriate toys and games in the reception room or treatment areas, and smaller scale furniture. The operatory, however, may contain distractions (eg, another child crying) that, for the patient, produce anxiety and interfere with communication. Dentists and other members of the dental team may find it advantageous to provide certain information (eg, post-operative instructions, preventive counseling) away from the operatory and its many distractions. Patient Assessment The response of a child patient to the demands of dental treatment is complex and determined by many factors. Multiple studies have demonstrated that a minority of children with uncooperative behavior have dental fears and that not all fearful children present dental behavior guidance problems.22-24 Child age/cognitive level,24-28 temperament/personality characteristics,22,23,29-31 anxiety and fear,23,24,32 reaction to strangers,33 previous dental experiences,24,26,34 and maternal dental anxiety34-36 influence a child’s reaction to the dental setting. The dentist should include an evaluation of the child’s cooperative potential as part of treatment planning. Information can be gathered by observation of and interacting with the child and by questioning the child’s parent. Ideal assessment methods are valid, allow for limited cognitive and language skills, and are easy to use in a clinical setting. Assessment tools that have demonstrated some efficacy in the pediatric dental setting, along with a brief description of their purpose, are listed in Appendix 1.24,27,29,30,36-44 No single assessment method or tool is completely accurate in predicting a child patient’s behavior for dental treatment, but awareness of the multiple influences on child behavior may aid in treatment planning for the pediatric patient. Since children exhibit a broad range of physical, intellectual, emotional, and social development and a diversity of attitudes and temperament, it is important that dentists have a wide range of behavior guidance techniques to meet the needs of the individual child. Barriers Unfortunately, various barriers may hinder the achievement of a successful outcome. Developmental delay, physical/mental disability, and acute or chronic disease all are potential reasons for noncompliance. Reasons for noncompliance in the healthy, communicating child often are more subtle and difficult to
diagnose. Major factors contributing to poor cooperation can include fears transmitted from parents, a previous unpleasant dental or medical experience, inadequate preparation for the first encounter in the dental environment, or dysfunctional parenting practices.24-26 To alleviate these barriers, the dentist should become a teacher. The dentist’s methods should include assessing the patient’s developmental level and comprehension skills, directing a message to that level, and having a patient who is attentive to the message being delivered (ie, good communication). To deliver quality dental treatment safely and develop an educated patient, the “teacher-student” roles and relationship must be established and maintained. Deferred treatment Dental disease usually is not life-threatening and the type and timing of dental treatment can be deferred in certain circumstances. When a child’s behavior prevents routine delivery of oral health care using communicative guidance techniques, the dentist must consider the urgency of dental need when determining a plan of treatment. Rapidly advancing disease, trauma, pain, or infection usually dictates prompt treatment. Deferring some or all treatment or employing therapeutic interventions (eg, alternative restorative technique [ART],45,46 fluoride varnish, antibiotics for infection control) until the child is able to co-operate may be appropriate when based upon an individualized assessment of the risks and benefits of that option. The dentist must explain the risks and benefits of deferred or alternative treatments clearly, and informed consent must be obtained from the parent. Treatment deferral also should be considered in cases when treatment is in progress and the patient’s behavior becomes hysterical or uncontrollable. In such cases, the dentist should halt the procedure as soon as possible, discuss the situation with the patient/parent, and either select another approach for treatment or defer treatment based upon the dental needs of the patient. If the decision is made to defer treatment, the practitioner immediately should complete the necessary steps to bring the procedure to a safe conclusion before ending the appointment. Caries risk should be reevaluated when treatment options are compromised due to child behavior. The AAPD has developed a caries-risk assessment tool (CAT)47 that provides a means of classifying caries risk at a point in time and can be applied periodically to assess changes in an individual’s risk status. An individualized preventive program, including appropriate parent education and a dental recall schedule, should be recommended after evaluation of the patient’s caries risk, oral health needs, and abilities. Topical fluorides (eg, brush-on gels, fluoride varnish, professional application during prophylaxis) may be indicated.48 ART may be useful as both preventive and therapeutic approaches.45,46 Informed consent Regardless of the behavior guidance techniques utilized by the individual practitioner, all guidance decisions must be based on a subjective evaluation weighing benefits and risks to the child. CLINICAL GUIDELINES
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The need for treatment, consequences of deferred treatment, and potential physical/emotional trauma must be considered. Decisions regarding the use of behavior guidance techniques other than communicative management cannot be made solely by the dentist. They must involve a parent and, if appropriate, the child. The dentist serves as the expert on dental care (ie, the timing and techniques by which treatment can be delivered). The parent shares with the practitioner the decision whether or not to treat and must be consulted regarding treatment strategies and potential risks. Therefore, the successful completion of diagnostic and therapeutic services is viewed as a partnership of dentist, parent, and child. Informing the parent about the nature, risk, and benefits of the technique to be used and any professionally-recognized or evidence-based alternative techniques is essential to obtaining informed consent.49 All questions must be answered to the parent’s understanding. Communicative management, by virtue of being a basic element of communication, requires no specific consent. All other behavior guidance techniques require informed consent consistent with the AAPD’s Guideline on Informed Consent49 and applicable state laws. In the event of an unanticipated reaction to dental treatment, it is incumbent upon the practitioner to protect the patient and staff from harm. Following immediate intervention to assure safety, if techniques must be altered to continue delivery of care, the dentist must have informed consent for the alternative methods. Summary 1. Behavior guidance is based on scientific principles. The proper implementation of behavior guidance requires an understanding of these principles. Behavior guidance, however, is more than pure science and requires skills in communication, empathy, coaching, and listening. As such, behavior guidance is a clinical art form and a skill built on a foundation of science. 2. The goals of behavior guidance are to establish communication, alleviate fear and anxiety, deliver quality dental care, build a trusting relationship between dentist and child, and promote the child’s positive attitude toward oral/dental health and oral health care. 3. The urgency of the child’s dental needs must be considered when planning treatment. Deferral or modification of treatment sometimes may be appropriate until routine care can be provided using appropriate behavior guidance techniques. 4. All decisions regarding use of behavior guidance techniques must be based upon a benefit vs risk evaluation. As part of the process of obtaining informed consent, the dentist’s recommendations regarding use of techniques (other than communicative guidance) must be explained to the parent’s understanding and acceptance. Parents share in the decision-making process regarding treatment of their children.
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5. The dental staff must be trained carefully to support the doctor’s efforts and properly welcome the patient and parent into a child-friendly environment that will facilitate behavior guidance and a positive dental visit.
Recommendations Basic behavior guidance Communication and communicative guidance Communicative management and appropriate use of commands are used universally in pediatric dentistry with both the cooperative and uncooperative child. In addition to establishing a relationship with the child and allowing for the successful completion of dental procedures, these techniques may help the child develop a positive attitude toward oral health. Communicative management comprises a host of techniques that, when integrated, enhance the evolution of a cooperative patient. Rather than being a collection of singular techniques, communicative management is an ongoing subjective process that becomes an extension of the personality of the dentist. Associated with this process are the specific techniques of tell-show-do, voice control, nonverbal communication, positive reinforcement, and distraction. The dentist should consider the cognitive development of the patient, as well as the presence of other communication deficits (eg, hearing disorder), when choosing specific communicative management techniques. Tell-show-do • Description: Tell-show-do is a technique of behavior shaping used by many pediatric professionals. The technique involves verbal explanations of procedures in phrases appropriate to the developmental level of the patient (tell); demonstrations for the patient of the visual, auditory, olfactory, and tactile aspects of the procedure in a carefully defined, nonthreatening setting (show); and then, without deviating from the explanation and demonstration, completion of the procedure (do). The tell-show-do technique is used with communication skills (verbal and nonverbal) and positive reinforcement. • Objectives: The objectives of tell-show-do are to: 1. teach the patient important aspects of the dental visit and familiarize the patient with the dental setting; 2. shape the patient’s response to procedures through desensitization and well-described expectations. • Indications: May be used with any patient. • Contraindications: None. Voice control • Description: Voice control is a controlled alteration of voice volume, tone, or pace to influence and direct the patient’s behavior. Parents unfamiliar with this technique may benefit from an explanation prior to its use to prevent misunderstanding. • Objectives: The objectives of voice control are to: 1. gain the patient’s attention and compliance; 2. avert negative or avoidance behavior; 3. establish appropriate adult-child roles.
american academy of pediatric Dentistry
• Indications: May be used with any patient. • Contraindications: Patients who are hearing impaired. Nonverbal communication • Description: Nonverbal communication is the reinforcement and guidance of behavior through appropriate contact, posture, facial expression, and body language. • Objectives: The objectives of nonverbal communication are to: 1. enhance the effectiveness of other communicative management techniques; 2. gain or maintain the patient’s attention and compliance. • Indications: May be used with any patient. • Contraindications: None. Positive reinforcement • Description: In the process of establishing desirable patient behavior, it is essential to give appropriate feedback. Positive reinforcement is an effective technique to reward desired behaviors and, thus, strengthen the recurrence of those behaviors. Social reinforcers include positive voice modulation, facial expression, verbal praise, and appropriate physical demonstrations of affection by all members of the dental team. Nonsocial reinforcers include tokens and toys. • Objective: To reinforce desired behavior. • Indications: May be useful for any patient. • Contraindications: None.
Distraction • Description: Distraction is the technique of diverting the patient’s attention from what may be perceived as an unpleasant procedure. Giving the patient a short break during a stressful procedure can be an effective use of distraction prior to considering more advanced behavior guidance techniques. • Objectives: The objectives of distraction are to: 1. decrease the perception of unpleasantness; 2. avert negative or avoidance behavior. • Indications: May be used with any patient. • Contraindications: None. Parental presence/absence • Description: The presence or absence of the parent sometimes can be used to gain cooperation for treatment. A wide diversity exists in practitioner philosophy and parental attitude regarding parents’ presence or absence during pediatric dental treatment. Parenting styles in America have evolved in recent decades.50 Practitioners are faced with challenges from an increasing number of children who many times are ill-equipped with the coping skills and self-discipline necessary to deal with new experiences in the dental office. Frequently, parental expectations for the child’s behavior are unrealistic, while expectations for the dentist who guides their behavior are great.51 Practitioners agree that good communication is important among the dentist, patient, and parent. Practitioners also are united in the fact that effective communication between the dentist and the child is paramount and requires focus on the part of both parties. Children’s responses to their parents’ presence
or absence can range from very beneficial to very detrimental. Each practitioner has the responsibility to determine the communication and support methods that best optimize the treatment setting recognizing his/her own skills, the abilities of the particular child, and the desires of the specific parent involved. • Objectives: The objectives of parental presence/absence are to: 1. gain the patient’s attention and improve compliance; 2. avert negative or avoidance behaviors; 3. establish appropriate dentist-child roles; 4. enhance effective communication among the dentist, child, and parent; 5. minimize anxiety and achieve a positive dental experience. • Indications: May be used with any patient. • Contraindications: Parents who are unwilling or unable to extend effective support (when asked). Nitrous oxide/oxygen inhalation • Description: Nitrous oxide/oxygen inhalation is a safe and effective technique to reduce anxiety and enhance effective communication. Its onset of action is rapid, the effects easily are titrated and reversible, and recovery is rapid and complete. Additionally, nitrous oxide/oxygen inhalation mediates a variable degree of analgesia, amnesia, and gag reflex reduction. The need to diagnose and treat, as well as the safety of the patient and practitioner, should be considered before the use of nitrous oxide/oxygen analgesia/anxiolysis. Detailed information concerning the indications, contraindications, and additional clinical considerations may be found in the Guideline on Appropriate Use of Nitrous Oxide for Pediatric Dental Patients.1 Advanced behavior guidance Most children can be managed effectively using the techniques outlined in basic behavior guidance. These basic behavior guidance techniques should form the foundation for all of the management activities provided by the dentist. Children, however, occasionally present with behavioral considerations that require more advanced techniques. These children often cannot cooperate due to lack of psychological or emotional maturity and/or mental, physical, or medical disability. The advanced behavior guidance techniques commonly used and taught in advanced pediatric dental training programs include protective stabilization, sedation, and general anesthesia.6 They are extensions of the overall behavior guidance continuum with the intent to facilitate the goals of communication, cooperation, and delivery of quality oral health care in the difficult patient. Appropriate diagnosis of behavior and safe and effective implementation of these techniques necessitate knowledge and experience that are generally beyond the core knowledge students receive during predoctoral dental education. While most predoctoral programs provide didactic exposure to treatment of very young children (ie, aged birth – 2 years), patients with special health care needs, and advanced behavior guidance techniques, hands-on experience is lacking.52 A minority of programs provides educational experiences with these patient populations, while few provide hands-on exposure to advanced behavior guidance techniques.52 CLINICAL GUIDELINES
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“On average, predoctoral pediatric dentistry programs teach students to treat children four years of age and older, who are generally well behaved and have low levels of caries.”52 Dentists considering the use of these advanced behavior guidance techniques should seek additional training through a residency program, a graduate program, and/or an extensive continuing education course that involves both didactic and experiential mentored training. Protective stabilization • Description: The use of any type of protective stabilization in the treatment of infants, children, adolescents, or patients with special health care needs is a topic that concerns health care providers, care givers, and the public.53-61 The broad definition of protective stabilization is the restriction of patient’s freedom of movement, with or without the patient’s permission, to decrease risk of injury while allowing safe completion of treatment. The restriction may involve another human(s), a patient stabilization device, or a combination thereof. The use of protective stabilization has the potential to produce serious consequences, such as physical or psychological harm, loss of dignity, and violation of a patient’s rights. Stabilization devices placed around the chest may restrict respirations; they must be used with caution, especially for patients with respiratory compromise (eg, asthma) and/or who will receive medications (ie, local anesthetics, sedatives) that can depress respirations. Because of the associated risks and possible consequences of use, the dentist is encouraged to evaluate thoroughly its use on each patient and possible alternatives.62 Careful, continuous monitoring of the patient is mandatory during protective stabilization. Partial or complete stabilization of the patient sometimes is necessary to protect the patient, practitioner, staff, or the parent from injury while providing dental care. Protective stabilization can be performed by the dentist, staff, or parent with or without the aid of a restrictive device. The dentist always should use the least restrictive, but safe and effective, protective stabilization. The use of a mouth prop in a compliant child is not considered protective stabilization. The need to diagnose, treat, and protect the safety of the patient, practitioner, staff, and parent should be considered prior to the use of protective stabilization. The decision to use protective stabilization must take into consideration: 1. alternative behavior guidance modalities; 2. dental needs of the patient; 3. the effect on the quality of dental care; 4. the patient’s emotional development; 5. the patient’s medical and physical considerations. Protective stabilization, with or without a restrictive device, performed by the dental team requires informed consent from a parent. Informed consent must be obtained and documented in the patient’s record prior to use of protective stabilization. Due to the possible aversive nature of the technique, informed consent also should be obtained prior to a parent’s performing protective stabilization during dental procedures. Furthermore, when appropriate, an explanation to the patient regarding the
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need for restraint, with an opportunity for the patient to respond, should occur.63 In the event of an unanticipated reaction to dental treatment, it is incumbent upon the practitioner to protect the patient and staff from harm. Following immediate intervention to assure safety, if techniques must be altered to continue delivery of care, the dentist must have informed consent for the alternative methods. The patient’s record must include: 1. informed consent for stabilization; 2. indication for stabilization; 3. type of stabilization; 4. the duration of application of stabilization; 5. behavior evaluation/rating during stabilization. • Objectives: The objectives of patient stabilization are to: 1. reduce or eliminate untoward movement; 2. protect patient, staff, dentist, or parent from injury; 3. facilitate delivery of quality dental treatment. • Indications: Patient stabilization is indicated when: 1. patients require immediate diagnosis and/or limited treatment and cannot cooperate due to lack of maturity or mental or physical disability; 2. the safety of the patient, staff, dentist, or parent would be at risk without the use of protective stabilization; 3. sedated patients require limited stabilization to help reduce untoward movement. • Contraindications: Patient stabilization is contraindicated for: 1. cooperative nonsedated patients; 2. patients who cannot be immobilized safely due to associated medical or physical conditions; 3. patients who have experienced previous physical or psychological trauma from protective stabilization (unless no other alternatives are available); 4. nonsedated patients with nonemergent treatment requiring lengthy appointments. • Precautions: The following precautions should be taken: 1. careful review of the patient’s medical history to ascertain if there are any medical conditions (eg, asthma) which may compromise respiratory function; 2. tightness and duration of the stabilization must be monitored and reassessed at regular intervals; 3. stabilization around extremities or the chest must not actively restrict circulation or respiration; 4. stabilization should be terminated as soon as possible in a patient who is experiencing severe stress or hysterics to prevent possible physical or psychological trauma. Sedation • Description: Sedation can be used safely and effectively with patients unable to receive dental care for reasons of age or mental, physical, or medical condition. Background information and documentation for the use of sedation is detailed in the Guideline for Monitoring and Management of Pediatric Patients During and After Sedation for Diagnostic and Therapeutic Procedures.2
american academy of pediatric Dentistry
The need to diagnose and treat, as well as the safety of the patient, practitioner, and staff, should be considered for the use of sedation. The decision to use sedation must take into consideration: 1. alternative behavioral guidance modalities; 2. dental needs of the patient; 3. the effect on the quality of dental care; 4. the patient’s emotional development; 5. the patient’s physical considerations. Documentation shall include2: 1. informed consent. Informed consent must be obtained from the parent and documented prior to the use of sedation; 2. instructions and information provided to the parent; 3. health evaluation; 4. a time-based record that includes the name, route, site, time, dosage, and patient effect of administered drugs; 5. the patient’s level of consciousness, responsiveness, heart rate, blood pressure, respiratory rate, and oxygen saturation at the time of treatment and until predetermined discharge criteria have been attained; 6. adverse events (if any) and their treatment; 7. time and condition of the patient at discharge. • Objectives: The goals of sedation are to: 1. guard the patient’s safety and welfare; 2. minimize physical discomfort and pain; 3. control anxiety, minimize psychological trauma, and maximize the potential for amnesia; 4. control behavior and/or movement so as to allow the safe completion of the procedure; 5. return the patient to a state in which safe discharge from medical supervision, as determined by recognized criteria, is possible. • Indications: Sedation is indicated for: 1. fearful, anxious patients for whom basic behavior guidance techniques have not been successful; 2. patients who cannot cooperate due to a lack of psychological or emotional maturity and/or mental, physical, or medical disability; 3. patients for whom the use of sedation may protect the developing psyche and/or reduce medical risk. • Contraindications: The use of sedation is contraindicated for: 1. the cooperative patient with minimal dental needs; 2. predisposing medical conditions which would make sedation inadvisable. General anesthesia • Description: General anesthesia is a controlled state of unconsciousness accompanied by a loss of protective reflexes, including the ability to maintain an airway independently and respond purposefully to physical stimulation or verbal command. The use of general anesthesia sometimes is necessary to provide quality dental care for the child. Depending on the patient, this can be done in a hospital or an ambulatory setting, including the dental office. Additional background information may be found in the Guideline on Use of Anesthesia Care Providers
in the Administration of In-office Deep Sedation/General Anesthesia to the Pediatric Dental Patient.3 The need to diagnose and treat, as well as the safety of the patient, practitioner, and staff, should be considered for the use of general anesthesia. The decision to use general anesthesia must take into consideration: 1. alternative behavioral guidance modalities; 2. dental needs of the patient; 3. the effect on the quality of dental care; 4. the patient’s emotional development; 5. the patient’s medical status. Prior to the delivery of general anesthesia, appropriate documentation shall address the rationale for use of general anesthesia, informed consent, instructions provided to the parent, dietary precautions, and preoperative health evaluation. Because laws and codes vary from state to state, minimal requirements for a time-based anesthesia record should include: 1. the patient’s heart rate, blood pressure, respiratory rate, and oxygen saturation at specific intervals throughout the procedure and until predetermined discharge criteria have been attained; 2. the name, route, site, time, dosage, and patient effect of administered drugs, including local anesthesia; 3. adverse events (if any) and their treatment; 4. that discharge criteria have been met, the time and condition of the patient at discharge, and into whose care the discharge occurred. • Objectives: The goals of general anesthesia are to 1. provide safe, efficient, and effective dental care; 2. eliminate anxiety; 3. reduce untoward movement and reaction to dental treatment; 4. aid in treatment of the mentally, physically, or medically compromised patient; 5. eliminate the patient’s pain response. • Indications: General anesthesia is indicated for: 1. patients who cannot cooperate due to a lack of psychological or emotional maturity and/or mental, physical, or medical disability; 2. patients for whom local anesthesia is ineffective because of acute infection, anatomic variations, or allergy; 3. the extremely uncooperative, fearful, anxious, or uncommunicative child or adolescent; 4. patients requiring significant surgical procedures; 5. patients for whom the use of general anesthesia may protect the developing psyche and/or reduce medical risk; 6. patients requiring immediate, comprehensive oral/dental care. • Contraindications: The use of general anesthesia is contra-
indicated for: 1. a healthy, cooperative patient with minimal dental needs; 2. predisposing medical conditions which would make general anesthesia inadvisable.
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Appendix 1. Patient Assessment Tools tool
format
application
Toddler temperament scale
Parent questionnaire
Behavior of 12 to 36 months
30, 37
Behavioral style questionnaire (BSQ)
Parent questionnaire
Child temperament of 3 to 7 years
29, 38
Eyberg Child Behavior Inventory (ECBI)
Parent questionnaire
Frequency and intensity of 36 common problem behaviors
39
Facial Image Scale (FIS)
Drawings of faces, child chooses
Anxiety indicator suitable for young preliterate children
40
Children’s Dental Fear Picture Test (CDFP)
3 picture subtests, child chooses
Dental fear assessment for children >5 years old
41
Child Fear Survey Schedule-Dental Subscale (CFSS-DS)
Parent questionnaire
Dental fear assessment
24, 41, 42
Parent-Child Relationship Inventory (PCRI)
Parent questionnaire
Parent attitudes and behavior that may result in child behavior problems
27, 43
Corah’s dental anxiety scale (DAS)
Parent questionnaire
Dental anxiety of parent
24, 36, 44
References 1. American Academy of Pediatric Dentistry. Guideline on 2.
3.
4.
5. 6. 7.
8. 9. 10.
11.
appropriate use of nitrous oxide for pediatric dental patients. Pediatr Dent 2006;28(suppl):112-4. American Academy of Pedatrics, American Academy of Pediatric Dentistry. Guideline for monitoring and management of pediatric patients during and after sedation for diagnostic and therapeutic procedures: An update. Pediatr Dent 2006;28(suppl):115-32. American Academy of Pediatric Dentistry. Guideline on use of anesthesia care providers in the administration of in-office deep sedation/general anesthesia to the pediatric dental patient. Pediatr Dent 2006;28(suppl):133-5. American Dental Association Commission on Dental Accreditation. Accreditation Standards for Advanced Specialty Education Programs in Pediatric Dentistry. American Dental Association. Chicago, Ill; 1998. Adair SM, Schafer TE, Rockman RA, Waller JL. Survey of behavior management teaching in predoctoral pediatric dentistry programs. Pediatr Dent 2004:26(2):143-50. Adair SM, Rockman RA, Schafer TE, Waller JL. Survey of behavior management teaching in pediatric dentistry advanced education programs. Pediatr Dent 2004:26(2):151-8. Adair SM, Waller JL, Schafer TE, Rockman RA. A survey of members of the American Academy of Pediatric Dentistry on their use of behavior management techniques. Pediatr Dent 2004:26(2):159-66. Hall JA, Roter DL, Katz NR. Task versus socioemotional behaviors in physicians. Med Care 1987;25(5):399-412. Gale EN, Carlsson SG, Eriksson A, Jontell M. Effects of dentists’ behavior on patients’ attitudes. J Am Dent Assoc 1984;109(3):444-6. Schouten BC, Eijkman MA, Hoogstraten J. Dentists’ and patients’ communicative behavior and their satisfaction with the dental encounter. Community Dent Health 2003;20(1):11-5. Lepper HS, Martin LR, DiMatteo MR. A model of nonverbal exchange in physician-patient expectations for patient involvement. J Nonverb Behav 1995;19:207-22.
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reference
12. Reichard A, Turnbull HR, Turnbull AP. Perspectives of dentists, families, and case managers on dental care for individuals with developmental disabilities in Kansas. Ment Retard 2001;39(4):268-85. 13. Lester GW, Smith SG. Listening and talking to patients: A remedy for malpractice suits. West J Med 1993;158(3): 268-72. 14. Beckman HB, Markakis KM, Suchman AL, Frankel RM. The doctor-patient relationship and malpractice. Lessons from plaintiff depositions. Arch Intern Med 1994;154 (12):1365-70. 15. Weinstein P, Getz T, Raetener P, Domoto P. The effect of dentists’ behavior on fear-related behaviors in children. J Am Dent Assoc 1982;104(1):32-8. 16. ten Berge M, Veerkamp J, Hoogstraten J. Dentists’ behavior in response to child dental fear. ASDC J Dent Child 1999;66(1):36-40. 17. Sarnat H, Arad P, Hanauer D, Shohami E. Communication strategies used during pediatric dental treatment: A pilot study. Pediatr Dent 2001;23(4):337-42. 18. Chambers DW. Communicating with the young dental patient. J Am Dent Assoc 1976;93(4):793-9. 19. Pinkham JR. The roles of requests and promises in child patient management. J Dent Child 1993;60(3):169-74. 20. Abushal MS, Adenubi JO. Attitudes of Saudi parents toward behavior management techniques in pediatric dentistry. J Dent Child 2003;70(2):104-10. 21. Chambers DW. Behavior management techniques for pediatric dentists: An embarrassment of riches. ASDC J Dent Child 1977;44(1):30-4, 12. 22. Klingberg G, Broberg AG. Temperament and child dental fear. Pediatr Dent 1998;20(4):237-43. 23. Arnup K, Broberg AG, Berggren U, Bodin L. Lack of cooperation in pediatric dentistry: The role of child personality characteristics. Pediatr Dent 2002;24(2):119-28. 24. Baier K, Milgrom P, Russell S, Mancl L, Yoshida T. Children’s fear and behavior in private pediatric dentistry practices. Pediatr Dent 2004;26(4):316-21.
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25. Rud B, Kisling E. The influence of mental development on children’s acceptance of dental treatment. Scand J Dent Res 1973;81(5):343-52. 26. Brill WA. The effect of restorative treatment on children’s behavior at the first recall visit in a private pediatric dental practice. J Clin Pediatr Dent 2002;26(4):389-94. 27. Allen KD, Hutfless S, Larzelere R. Evaluation of two predictors of child disruptive behavior during restorative dental treatment. J Dent Child 2003;70(3):221-5. 28. Cunha RF, Delbem ACB, Percinoto C, Melhado FL. Behavioral evaluation during dental care in children ages 0 to 3 years. J Dent Child 2003;70(2):100-3. 29. Radis FG, Wilson S, Griffen AL, Coury DL. Temperament as a predictor of behavior during initial dental examination in children. Pediatr Dent 1994;16(2):121-7. 30. Lochary ME, Wilson S, Griffen AL, Coury DL. Temperament as a predictor of behavior for conscious sedation in dentistry. Pediatr Dent 1993;15(5):348-52. 31. Jensen B, Stjernqvist K. Temperament and acceptance of dental treatment under sedation in preschool children. Acta Odontol Scand 2002;60(4):231-6. 32. Arnup K, Broberg AG, Berggren U, Bodin L. Treatment outcome in subgroups of uncooperative child dental patients: An exploratory study. Int J Paediatr Dent 2003;13(5):304-19. 33. Holst A, Hallonsten AL, Schroder U, Ek L, Edlund K. Prediction of behavior-management problems in 3-year-old children. Scand J Dent Res 1993;101(2):110-4. 34. Klingberg G, Berggen U, Carlsson SG, Noren JG. Child dental fear: Cause related factors and clinical effects. Eur J Oral Sci 1995;103(6):405-12. 35. Johnson R, Baldwin DC. Maternal anxiety and child behavior. J Dent Child 1969;36(2):87-92. 36. Peretz B, Nazarian Y, Bimstein E. Dental anxiety in a students’ pediatric dental clinic: Children, parents and students. Int J Paediatr Dent 2004;14(3):192-8. 37. Fullard W, McDevitt SC, Carey WB. Assessing temperament in one- to three-year-old children. J Pediatr Psychol 1984;9(2):205-17. 38. McDevitt SC, Carey WB. The measurement of temperament in 3- to 7-year-old children. J Child Psychol Psychiatry 1978;19(3):245-53. 39. Eyberg S, Pincus D. Child Behavior Inventory. Odessa, Fla: Professional Manual Psychological Assessment Resources, Inc; 1999. 40. Buchanan H, Niven N. Validation of a facial image scale to assess child dental anxiety. Int J Paediatr Dent 2002;12 (1):47-52. 41. Klingberg G, Vannas Löfqvist L, Hwang CP. Validity of the children’s dental fear picture test (CDFP). Eur J Oral Sci 1995;103(1):55-60. 42. Cuthbert MI, Melamed BG. A screening device: Children at risk for dental fears and management problems. ASDC J Dent Child 1982;49(6):432-6. 43. Gerard AB. Parent-Child Relationship Inventory (PCRI) Manual. Los Angeles, Calif: Western Psychological Services; 1994. 44. Corah NL. Development of a dental anxiety scale. J Dent Res 1969;48(4):596.
45. American Academy of Pediatric Dentistry. Guideline on pediatric restorative dentistry. Pediatr Dent 2006;28 (suppl):136-43. 46. American Academy of Pediatric Dentistry. Policy on alternative restorative treatment (ART). Pediatr Dent 2006;28 (suppl):33. 47. American Academy of Pediatric Dentistry. Policy on use of a caries-risk assessment tool (CAT) for infants, children and adolescents. Pediatr Dent 2006:28(suppl):24-28. 48. American Academy of Pediatric Dentistry. Guideline on fluoride therapy. Pediatr Dent 2006;28(suppl):95-6. 49. American Academy of Pediatric Dentistry. Guideline on informed consent. Pediatr Dent 2006;28(suppl):198-9. 50. Long N. The changing nature of parenting in America. Pediatr Dent 2004;26(2):121-4. 51. Sheller B. Challenges of managing child behavior in the 21st century dental setting. Pediatr Dent 2004;26(2):111-3. 52. Seale NS, Casamassimo PS. US predoctoral education in pediatric dentistry: Its impact on access to dental care. J Dent Educ 2003;67(1):23-30. 53. Connick C, Palat M, Puagliese S. The appropriate use of physical restraint: Considerations. ASDC J Dent Child 2000;67(4):231, 256-62. 54. Crossley ML, Joshi G. An investigation of pediatric dentists’ attitudes towards parent accompaniment and behavioral management techniques in the UK. Br Dent J 2002;192 (9):517-21. 55. Peretz B, Zadik D. Parents’ attitudes toward behavior management techniques during dental treatment. Pediatr Dent 1999;2(3):201-4. 56. Peretz B, Gluck GM. The use of restraint in the treatment of pediatric dental patients: Old and new insights. Int J Paediatr Dent 2002;12(6):392-7. 57. Brill WA. Parents’ assessment and children’s reactions to a passive restraint device used for behavior control in a private pediatric dental practice. ASDC J Dent Child 2002; 69(3):236, 310-3. 58. Law CS, Blain S. Approaching the pediatric dental patient: A review of nonpharmacologic behavior management strategies. J Calif Dent Assoc 2003;31(9):703-13. 59. Kupietzky A. Strap him down or knock him out: Is conscious sedation with restraint an alternative to general anesthesia? Br Dent J 2004;196(3):133-8. 60. Manley MCG. A UK perspective. Br Dent J 2004;196 (3): 138-9. 61. Morris CDN. A commentary on the legal issues. Br. Dent J 2004;196(3):139-40. 62. Joint Commission on Accreditation of Healthcare Organizations (JCAHO). Comprehensive Accreditation Manual for Hospitals 2004-2005. Oakbrook Terrace, Ill: Joint Commission on Accreditation of Healthcare Organizations; 2004:pc25-pc40. 63. American Academy of Pediatrics Committee on Pediatric Emergency Medicine. The use of physical restraint interventions for children and adolescents in the acute care setting. Pediatrics 1997;99(3):497-8.
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Guideline on Use of Local Anesthesia for Pediatric Dental Patients Originating Council Council on Clinical Affairs
Review Council Council on Clinical Affairs
Adopted 2005
Revised 2009
Purpose The American Academy of Pediatric Dentistry (AAPD) intends this guideline to help practitioners make decisions when using local anesthesia to control pain in infants, children, adolescents, and individuals with special health care needs during the delivery of oral health care.
Methods This revision included a new systematic literature search of the MEDLINE/Pubmed electronic database using the following parameters: Terms: dental anesthesia, dental local anesthesia, and topical anesthesia; Field: all fields; Limits: within the last 10 years, humans, English, and clinical trials. One thousand one hundred thirty articles matched these criteria. Papers for review were chosen from this list and from references within selected articles. When data did not appear sufficient or were inconclusive, recommendations were based upon expert and/or consensus opinion by experienced researchers and clinicians.
Background Local anesthesia is the temporary loss of sensation including pain in one part of the body produced by a topically-applied or injected agent without depressing the level of consciousness. Prevention of pain during dental procedures can nurture the relationship of the patient and dentist, building trust, allaying fear and anxiety, and promoting a positive dental attitude. The technique of local anesthetic administration is an important consideration in the behavior guidance of a pediatric patient. Age-appropriate “nonthreatening” terminology, distraction, topical anesthetics, proper injection technique, and nitrous oxide/oxygen analgesia/ anxiolysis can help the patient have a positive experience during administration of local anesthesia.1,2 In pediatric dentistry, the dental professional should be aware of proper dosage (based on weight) to minimize the chance of toxicity and the prolonged duration of anesthesia, which can lead to accidental lip or tongue trauma. Knowledge of the gross and neuroanatomy of the head and neck allows for proper placement of the anesthetic solu-
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tion and helps minimize complications (eg, hematoma, trismus, intravascular injection). Familiarity with the patient’s medical history is essential to decrease the risk of aggravating a medical condition while rendering dental care. Appropriate medical consultation should be obtained when needed. Many local anesthetic agents are available to facilitate management of pain in the dental patient. There are 2 general types of local anesthetic chemical formulations: (1) esters (eg, procaine, benzocaine, tetracaine); and (2) amides (eg, lidocaine, mepivacaine, prilocaine, articaine).3 Local anesthetics are vasodilators; they eventually are absorbed into the circulation, where their systemic effect is related directly to their blood plasma level.4 Vasoconstrictors are added to local anesthetics to constrict blood vessels in the area of injection. This lowers the rate of absorption of the local anesthetic into the blood stream, thereby lowering the risk of toxicity and prolonging the anesthetic action in the area.4 Epinephrine is contraindicated in patients with hyperthyroidism.5 Its dose should be kept to a minimum in patients receiving tricylic antidepressants since dysrhythmias may occur. Levonordefrin and norepinephrine are absolutely contraindicated in these patients.6 Patients with significant cardiovascular disease, thyroid dysfunction, diabetes, or sulfite sensitivity and those receiving monoamine oxidase inhibitors, tricyclic antidepressants, or phenothiazines may require a medical consultation to determine the need for a local anesthetic without vasoconstrictor.6,7 When halogenated gases (eg, halothane) are used for general anesthesia, the myocardium is sensitized to epinephrine. Such situations dictate caution with use of a local anesthetic.6 Amide-type local anesthetics no longer are contraindicated in patients with a family history of malignant hyperthermia, an abnormal elevation in body temperature during general anesthesia with inhalation anesthetics or succinylcholine.7,8 If a local anesthetic is injected into an area of infection, its onset will be delayed or even prevented.3 The inflammatory process in an area of infection lowers the pH of the extracellular tissue from its normal value (7.4) to 5 to 6 or lower. This low pH inhibits anesthetic action because little of the free base form of the anesthetic
American academy of pediatric dentistry
is allowed to cross into the nerve sheath to prevent conduction of nerve impulses.9 Inserting a needle into an active site of infection also could lead to possible spread of the infection.
Recommendations Topical anesthetics The application of topical anesthetic may help minimize discomfort caused during administration of local anesthesia. Topical anesthetic is effective on surface tissues (2-3 mm in depth) to reduce painful needle penetration of the oral mucosa.10,11 A variety of topical anesthetic agents are available in gel, liquid, ointment, patch, and aerosol forms. The topical anesthetic benzocaine is manufactured in concentrations up to 20%; lidocaine is available as a solution or ointment up to 5% and as a spray up to a 10% concentration.3 Benzocaine has a rapid onset. Benzocaine toxic (overdose) reactions are virtually unknown. Localized allergic reactions, however, may occur after prolonged or repeated use.12 Topical lidocaine has an exceptionally low incidence of allergic reactions but is absorbed systemically and can combine with an injected amide local anesthetic to increase the risk of overdose.13 Compounded topical anesthetics also are available.14,15 Two of the more common formulations contain 20% lidocaine, 4% tetracaine, and 2% phenylephrine or 10% lidocaine, 10% prilocaine, 4% tetracaine, and 2% phenylephrine.15 Compounded topical anesthetics have been used in orthodontic procedures for placement of mini-screw implants to aid tooth movement,14,16 as well as in pediatric dentistry to anesthetize palatal tissues prior to injection and for extraction of loose primary teeth without the need for an injection. They contain high doses of both
amide and ester agents and are at risk for side effects.15 The US Food and Drug Administration does not regulate compounded topical anesthetics and recently issued warning about their use.17,18 Recommendations: 1. Topical anesthetic may be used prior to the injection of a local anesthetic to reduce discomfort associated with needle penetration. 2. The pharmacological properties of the topical agent should be understood. 3. A metered spray is suggested if an aerosol preparation is selected. 4. Systemic absorption of the drugs in topical anesthetics must be considered when calculating the total amount of anesthetic administered. The AAPD recommends further investigation regarding the safety and efficacy of compounded topical anesthetics and their applications for pediatric dental patients. Selection of syringes and needles The American Dental Association (ADA) has established standards for aspirating syringes for use in the administration of local anesthesia.19,20 Needle selection should allow for profound local anesthesia and adequate aspiration. Larger gauge needles provide for less deflection as the needle passes through soft tissues and for more reliable aspiration.21 The depth of insertion varies not only by injection technique, but also by the age and size of the patient. Dental needles are available in 3 lengths: long (32 mm), short (20 mm), and ultrashort (10 mm).
Table 1. injectable Local Anesthetics Duration in minutes3,23 Maxillary infiltration Anesthetic
Pulp
Soft tissue
Mandibular block Pulp
Soft tissue
Lidocaine 2% plain
5
2%+1:50,000 epinephrine
60
170
85
190
2%+1:100,000 epinephrine
60
170
85
190
3% plain
25
90
40
165
2%+1:100,000 epinephrine
60
170
85
190
2%+1:20,000 levonordefrin
50
130
75
185
Articaine 60
190
90
230
4% plain
20
105
55
190
4%+1:200,000 epinephrine
40
140
60
220
40
340
240
440
Prilocaine
Bupivacaine 0.5%+1:200,000 epinephrine
Maximum total dosage23*
mg/kg
mg/lb
(mg)
4.4
2.0
300
4.4
2.0
300
7.0
3.2
500
6.0
2.7
400
1.3
0.6
90
5-10
Mepivacaine
4%+1:100,000 epinephrine
Maximum dosage23
* Total dosage should be based on child’s weight and should never exceed maximum total dosage.
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Injectable local anesthetic agents
Table 2. Dosage per Dental Cartridge 3
Local amide anesthetics available for dental usage include lidocaine, mepivacaine, articaine, prilocaine, and bupivacaine (Tables 1 and 2). Absolute contraindications for local anesthetics include a docuLidocaine mented local anesthetic allergy.23 True allergy to 2% plain 34 or 36 N/A an amide is exceedingly rare. Allergy to one amide 34 µg or 0.034 mg or 2%+1:50,000 epinephrine 34 or 36 does not rule out the use of another amide, but 36 µg or 0.036 mg allergy to one ester rules out use of another ester.3 17 µg or 0.017 mg or 2%+1:100,000 epinephrine 34 or 36 18 µg or 0.018 mg A bisulfate preservative is used in local anesthetics containing epinephrine. For patients having an alMepivacaine lergy to bisulfates, use of a local anesthetic without 3% plain 51 or 54 N/A a vasoconstrictor is indicated.12 Local anesthetics 17 µg or 0.017 mg or 2%+1:100,000 epinephrine 34 or 36 without vasoconstrictors should be used with cau18 µg or 0.018 mg tion due to rapid systemic absorption which may 85 µg or 0.085 mg or 2%+1:20,000 levonordefrin 34 or 36 result in overdose.12 90 µg or 0.090 mg A long-acting local anesthetic (ie, bupivacaine) Articaine is not recommended for the child or the physically 17 µg or 0.017 mg or or mentally disabled patient due to its prolonged 4%+1:100,000 epinephrine 68 or 72 18 µg or 0.018 mg effect, which increases the risk of soft tissue inPrilocaine jury.23 Claims have been made that articaine can 4% plain 68 or 72 N/A diffuse through hard and soft tissue from a buccal infiltration to provide lingual or palatal soft tissue 8.5 µg or 0.0085 mg or 4%+1:200,000 epinephrine 68 or 72 9 µg or 0.009 mg anesthesia.23 Studies using articaine, lidocaine, and prilocaine, however, did not substantiate these Bupivacaine claims.23,24 8.5 µg or 0.0085 mg or 0.5%+1:200,000 epinephrine 8.5 or 9 Epinephrine decreases bleeding in the area of in9 µg or 0.009 mg jection. Epinephrine concentrations of 1:50,000 may be indicated for infiltration in small doses into a surgical site to achieve hemostasis but are not indicated in children to control pain.12 Local anNeedle gauges range from size 23 to 30. Needle breakage is a rare occurrence. The primary cause of needle breakage is esthetics that contain vasopressors help reduce toxicity weakening the needle due to bending it before insertion into by slowing the rate of absorption of the anesthetic and/or the soft tissues; another cause is patient movement after the vasopressor into the cardiovascular system.12 A vasopressorneedle is already inserted.22 containing local anesthetic should be used when treatment Recommendations: extends to 2 or more quadrants in a single visit.12 1. For the administration of local dental anesthesia, den- An end product of prilocaine metabolism can induce tists should select aspirating syringes that meet ADA formation of methemoglobin, reducing the blood’s oxygen standards. carrying capacity. In patients with subclinical methemoglo 2. Short needles may be used for any injection in which binemia25 or with toxic doses (>6 mg/kg), prilocaine can the thickness of soft tissue is less than 20 mm. A long induce methemoglobinemia symptoms26 (eg, gray or slate needle may be used for a deeper injection into soft blue cyanosis of the lips, mucous membranes, and nails; tissue.21 Any 23- through 30-gauge needle may be used respiratory and circulatory distress).6 Prilocaine may be con for intraoral injections, since blood can be aspirated traindicated in patients with methemoglobinemia, sickle cell through all of them. Aspiration can be more difficult, anemia, anemia, or symptoms of hypoxia or in patients re21 however, when smaller gauge needles are used. An since both medica extra-short, 30-gauge is appropriate for infiltration ceiving acetaminophen or phenacetin, 23 tions elevate methemoglobin levels. 21 injections. Recommendations: 3. Needles should not be bent if they are to be inserted 1. Selection of local anesthetic agents should be based into soft tissue to a depth of >5 mm or inserted to upon: their hub for injections to avoid needle breakage.21 a. the patient’s medical history and mental/develop mental status; Anesthetic
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mg/1.7 ml or 1.8 ml cartridge
Vasoconstrictor/1.7 ml or 1.8 ml cartridge
American academy of pediatric dentistry
b. the anticipated duration of the dental procedure; c. the need for hemorrhage control; d. the planned administration of other agents (eg, nitrous oxide, sedative agents, general anesthesia); e. the practitioner’s knowledge of the anesthetic agent. 2. Use of vasoconstrictors in local anesthetics is recom mended to decrease the risk of toxicity of the anesthetic agent, especially when treatment extends to 2 or
more quadrants in a single visit. 3.
In cases of bisulfate allergy, use of a local anesthetic without a vasoconstrictor is indicated. A local anesthetic without a vasoconstrictor also can be used for shorter treatment needs but should be used with caution to minimize the risk of toxicity of the anesthetic agents. 4. The established maximum dosage for any anesthetic should not be exceeded. Documentation of local anesthesia
The patient record is an essential component of the delivery of competent and quality oral health care.27 Following each appointment, an entry is made in the record that accurately and objectively summarizes that visit. Appropriate documentation includes specific information relative to the administration of local anesthesia. Recommendations: 1. Documentation must include the type and dosage of local anesthetic. Dosage of vasoconstrictors, if any, must be noted. (For example, 34 mg lido with 0.017 mg epi or 34 mg lido with 1:100,000 epi).2 2. Documentation may include the type of injection(s) given (eg, infiltration, block, intraosseous), needle se lection, and patient’s reaction to the injection. 3. If the local anesthetic was administered in conjunc tion with sedative drugs, the doses of all agents must be noted on a time-based record. 4. In patients for whom the maximum dosage of local anesthetic may be a concern, the weight should be documented preoperatively. 5. Documentation should include that post-injection in structions were reviewed with the patient and parent. Local anesthetic complications Toxicity (overdose) Most adverse drug reactions develop either during the injection or within 5 to 10 minutes.12 Overdose of local anesthetic can result from high blood levels caused by a single inadvertent intravascular injection or repeated injections.3 Local anesthetic causes a biphasic reaction (eg, excitation followed by depression) in the central nervous system (CNS). Early subjective indications of toxicity involve the CNS and include dizziness, anxiety, and confusion. This may be followed by diplopia, tinnitis, drowsiness, and circumoral numbness or tingling. Objective signs may include muscle twitching, tremors, talkativeness, slowed speech,
and shivering, followed by overt seizure activity. Unconsciousness and respiratory arrest may occur.3 The cardiovascular system (CVS) response to local anesthetic toxicity also is biphasic. The CVS is more resistant to local anesthetics than the CNS.28 Initially, during CVS stimulation, heart rate and blood pressure may increase. As plasma levels of the anesthetic increase, however, vasodilatation occurs followed by depression of the myocardium with subsequent fall in blood pressure. Bradycardia and cardiac arrest may follow. The cardiodepressant effects of local anesthetics are not seen until there is a significantly elevated local anesthetic blood level.12 Local anesthetic toxicity can be prevented by careful injection technique, watchful observation of the patient, and knowledge of the maximum dosage based on weight. Practitioners should aspirate before every injection and inject slowly.12 After the injection, the doctor, hygienist, or assistant should remain with the patient while the anesthetic begins to take effect. Early recognition of a toxic response is critical for effective management. When signs or symptoms of toxicity are noted, administration of the local anesthetic agent should be discontinued. Additional emergency management is based on the severity of the reaction.3,12 Allergy to local anesthesia Allergic reactions are not dose dependant but are due to the patient’s heightened capacity to react to even a small dose. Allergies can manifest in a variety of ways, some of which include urticaria, dermatitis, angioedema, fever, photosensitivity, or anaphylaxis.12 Emergency management is dependent on the rate and severity of the reaction. Paresthesia Paresthesia is persistent anesthesia beyond the expected duration. Trauma to the nerve can produce paresthesia and, among other etiologies, trauma can be caused by the needle during the injection.29 The patient may experience an “electric shock” in the involved nerve distribution area. Paresthesia also can be caused by hemorrhage in or around the nerve.30 Risk of permanent paresthesia is 1:1,200,000 for 0.5%, 2%, and 3% local anesthetics and 1:500,000 for 4% local anesthetics.29 Reports of paresthesia are more common with articaine and prilocaine than expected from their frequency of use. Paresthesia unrelated to surgery most often involves the tongue, followed by the lip, and is more common with 4% solutions of articaine or prilocaine.30 Most cases resolve in 8 weeks.31 Postoperative soft tissue injury Self-induced soft tissue trauma is an unfortunate clinical complication of local anesthetic use in the oral cavity. Most lip- and cheek-biting lesions of this nature are self-limiting and heal without complications, although bleeding and infection possibly may result. The use of bilateral mandibular blocks does not increase the risk of soft tissue trauma when compared to unilateral mandibular blocks or ipsilateral maxillary infiltration.32 In fact, the frequency of soft tissue trauma was much
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higher than expected when only 1 side was anesthetized. Using mandibular infiltration vs blocks is not of great value in prevention of these injuries, since the duration of soft tissue anesthesia may not be reduced significantly. In addition, for some procedures, infiltration is not as effective as the mandibular block.33 Caregivers responsible for postoperative supervision should be given a realistic time for duration of numbness and informed of the possibility of soft tissue trauma. Visual examples may help stress the importance of observation during the period of numbness. For all local anesthetics, the duration of soft tissue anesthesia is greater than dentinal or osseous anesthesia. Use of phentolamine mesylate injections in patients over age 6 years or at least 15 kg has been shown to reduce the duration of effects of local anesthetic by about 47% in the maxilla and 67% in the mandible.34,35 However, there is no research demonstrating a relationship between reduction in soft tissue trauma and the use of shorter acting local anesthetics.36 Recommendations to reduce local anesthetic complications: 1. Practitioners who utilize any type of local anesthetic in a pediatric dental patient shall possess appropriate training and skills and have available the proper facilities, personnel, and equipment to manage any reasonably foreseeable emergency. 2. Care should be taken to ensure proper needle place ment during the intraoral administration of local anesthetics. Practitioners should aspirate before every injection and inject slowly. 3. After the injection, the doctor, hygienist, or assistant should remain with the patient while the anesthetic begins to take effect. 4. Residual soft tissue anesthesia should be minimized in pediatric and special health care needs patients to de crease risk of self-inflicted postoperative injuries. 5. Practitioners should advise patients and their care givers regarding behavioral precautions (eg, do not bite or suck on lip/cheek, do not ingest hot substances) and the possibility of soft tissue trauma while anesthe sia persists. Placing a cotton roll in the mucobuccal fold may help prevent injury, and lubricating the lips with petroleum jelly helps prevent drying.36 Practi tioners who use pheytolamine mesylate injections to reduce the duration of local anesthesia still should follow these recommendations. Supplemental injections to obtain local anesthesia The majority of local anesthesia procedures in pediatric dentistry involve traditional methods of infiltration or nerve block techniques with a dental syringe, disposable cartridges, and needles as described so far. Several alternative techniques, however, are available. These include computer-controlled local anesthetic delivery, periodontal injection techniques (ie, periodontal ligament [PDL], intraligamentary, and peridental injection), “needleless” systems, and intraseptal or intrapulpal injection. These techniques may improve comfort of injection by better
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control of the administration rate, pressure, and location of anesthetic solutions and/or result in successful and more controlled anesthesia. Endocarditis prophylaxis is recommended for intraligamentary local anesthetic injections in patients at risk.37 Intraseptal injection for lingual anesthesia is a variation in technique after the buccal tissue is anesthetized. The needle is inserted through the buccal tissue to anesthetize the lingual/ palatal soft tissues. It can be used with the PDL injection to gain lingual anesthesia when postoperative soft tissue trauma is a concern.38 During pulpal therapy, administering local anesthetic directly into the pulp may be indicated when other methods fail to anesthetize the tooth.38 As with traditional methods of obtaining oral local anesthesia, the alternative methods generally are safe if the practitioner understands the principles for their use. Some of these techniques are desirable, especially in infants, children, adolescents, and special health care needs patients, since specific teeth may be anesthetized with less residual anesthesia (ie, avoid discomfort and potential self-mutilation of block anesthesia).38 The mandibular bone of a child usually is less dense than that of an adult, permitting more rapid and complete diffusion of the anesthetic.9 Mandibular buccal infiltration anesthesia is as effective as inferior nerve block anesthesia for some operative procedures.9,33 In patients with bleeding disorders, the PDL injection minimizes the potential for postoperative bleeding of soft tissue vessels.6 Intraosseus techniques may be contraindicated with primary teeth due to potential for damage to developing permanent teeth.30 Also, the use of the PDL injection or intraosseus methods is contraindicated in the presence of inflammation or infection at the injection site.38
Recommendation: Alternative techniques for the delivery of local anesthesia may be considered to minimize the dose of anesthetic used, improve patient comfort, and/or improve successful dental anesthesia. Local anesthesia with sedation, general anesthesia, and/or nitrous oxide/oxygen analgesia/anxiolysis Drugs that have the same mechanism of action often will have additive effects when used together. Local anesthetics and sedative agents both depress the CNS. An increase in toxic reactions of local anesthetics when combined with opioids has been demonstrated.39 Narcotics may decrease the amount of protein binding of local anesthetics and also elevate arterial carbon dioxide, both of which will increase CNS sensitivity to convulsions. In addition, narcotics such as meperidine have convulsant properties when excessive doses are administered. It has been suggested that the dose of local anesthesia be adjusted downward when sedating children with opioids.39 Using local anesthesia has been found to reduce the dosage of inhalation anesthetics for patients undergoing general anesthesia.40 The anesthesia care provider needs to be aware of the concomitant use of a local anesthetic containing epinephrine, as epinephrine can produce dysrhythmias when used with halogenated hydrocarbons (eg, halothane).41 Local anesthesia
American academy of pediatric dentistry
also has been reported to reduce pain in the postoperative recovery period after general anesthesia.42 Recommendations: 1. Particular attention should be paid to local anesthetic doses used in children. To avoid excessive doses for the patient who is going to be sedated, a maximum re commended dose based upon weight should be cal culated. 2. The dosage of local anesthetic should not be altered if nitrous oxide/oxygen analgesia/anxiolysis is admi nistered. 3. When general anesthesia is employed, local anesthesia may be used to reduce the maintenance dosage of the anesthetic drugs. The anesthesiologist should be in formed of the type and dosage of the local anesthetic used. Recovery room personnel also should be in formed.
References 1. Nathan JE, Venham LL, West MS, Werboff J. The ef-
2. 3. 4. 5.
6. 7.
8.
9. 10.
fects of nitrous oxide on anxious young pediatric patients across sequential visits: A double-blind study. ASDC J Dent Child 1988;55(3):220-30. Malamed SF. Basic injection technique in local anesthesia. In: Handbook of Local Anesthesia. 5th ed. St. Louis, Mo: Mosby; 2004:159-69. Haas DA. An update on local anesthetics in dentistry. J Can Dent Assoc 2002;68(9):546-51. Malamed SF. Pharmacology of vasoconstrictors. In: Handbook of Local Anesthesia. 5 th ed. St. Louis, Mo: Mosby; 2004:41-54. Pérusse R, Goulet JP, Turcotte JY. Contraindications to vasoconstrictors in dentistry: Part II. Hyperthyroidism, diabetes, sulfite sensitivity, cortico-dependant asthma, and pheochromocytoma. Oral Surg Oral Med Oral Pathol 1992;74(5):687-91. Malamed SF. Physical and psychological evaluation. In: Handbook of Local Anesthesia. 5 th ed. St. Louis, Mo: Mosby; 2004:141-56. Goulet JP, Perusse R, Turcotte JY. Contraindications to vasoconstrictors in dentistry: Part III. Pharmacologic interactions. Oral Surg Oral Med Oral Pathol 1992;74(5): 692-7. Gielen M, Viering W. 3-in-1 lumbar plexus block for muscle biopsy in malignant hyperthermia patients: Amide local anesthetics may be used safely. Acta Anaesthesiol Scand 1986;30(7):581-3. Malamed SF. Local anesthetic considerations in dental specialties. In: Handbook of Local Anesthesia. 5th ed. St. Louis, Mo: Mosby; 2004:269, 274-5. Jeske AH, Blanton PL. Misconceptions involving dental local anesthesia. Part 2: Pharmacology. Tex Dent J 2002; 119(4):310-4.
11. Rosivack RG, Koenigsberg SR, Maxwell KC. An analysis of the effectiveness of two topical anesthetics. Anesth Prog 1990;37(6):290-2. 12. Malamed SF. Systemic complications. In: Handbook of Local Anesthesia. 5 th ed. St. Louis, Mo: Mosby; 2004: 311-25. 13. Malamed SF. Additional armamentarium. In: Handbook of Local Anesthesia. 5th ed. St. Louis, Mo: Mosby; 2004:120. 14. Graham JW. Profound, needle-free anesthesia in orthodontics. Clin Ortho 2006;40(12):723-4. 15. Kravitz ND. The use of compound topical anesthetics: A review. J Am Dent Assoc 2007;138(10)1333-9. 16. Kravits ND, Kusnoto B, Tsay TP, Hohlt WF. The use of temporary anchorage devices for molar intrusion. J Am Dent Assoc 2007;138(1):56-64. 17. US Food and Drug Administration. FDA public health advisory: Life-threatening side effect with the use of skin products containing numbing ingredients for cosmetic procedures. Available at: “http://www.fda.gov/cder/drug/ advisory/topical_anesthetics.htm”. Accessed November 15, 2008. 18. US Dept for Health and Human Services, Food and Drug Administration, Center for Drug Evaluation and Research. Guidance for FDA staff and industry: Marketed unapproved drugs–Compliance policy guide. Sec 440.100 Marketed new drugs without approved NDAs or ANDAs. Available at “http://www.fda.gov/cder/guidance/6911fnl. pdf ”. Accessed November 15, 2008. 19. American Dental Association Council on Dental Materials and Devices. New American National Standards Institute/American Dental Association specification no. 34 for dental aspirating syringes. J Am Dent Assoc 1978;97(2): 236-8. 20. American Dental Association Council on Dental Materials, Instruments, and Equipment. Addendum to American National Standards Institute/American Dental Association specification no. 34 for dental aspirating syringes. J Am Dent Assoc 1982;104(1):69-70. 21. Malamed SF. The needle. In: Handbook of Local Anesthesia. 5th ed. St. Louis, Mo: Mosby; 2004:99-107. 22. Malamed SF. Local complications. In: Handbook of Local Anesthesia. 5 th ed. St. Louis, Mo: Mosby; 2004: 285-7. 23. Malamed SF. Clinical action of specific agents. In: Handbook of Local Anesthesia. 5th ed. St Louis, Mo: Mosby; 2004:55-81. 24. Haas DA, Harper DG, Saso MA, Young ER. Lack of differential effect by Ultracaine (articaine) and Citanest (prilocaine) in infiltration anaesthesia. J Can Dent Assoc 1991;57(3):217-23. 25. Bellamy MC, Hopkins PM, Hallsall PJ, Ellis FR. A study into the incidence of methaemoglobinaemia after “threein-one” block with procaine. Anaesthesia 1992;47(12): 1084-5.
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26. Hardwick FK, Beaudreau RW. Methemoglobinemia in renal transplant patient: Case report. Pediatr Dent 1995; 17(7):460-3. 27. American Academy of Pediatric Dentistry. Guideline on record-keeping. Pediatr Dent 2008;30(suppl):226-33. 28. Scott DB. Toxicity caused by local anesthetic drugs. Br J Anaesth 1981;53(6):553-4. 29. Haas DA. Local complications. In: Malamed SF, ed. Handbook of Local Anesthesia. 5th ed. St Louis, Mo: Mosby; 2004:288-9. 30. Haas DA, Lennon D. A 21-year retrospective study of reports of paresthesia following local anesthetic administration. J Can Dent Assoc 1995;61(4):319-20, 323-6, 329-30. 31. Nickel AA. A retrospective study of reports of paresthesia following local anesthetic administration. Anesth Prog 1990;37(1):42-5. 32. College C, Feigal R, Wandera A, Strange M. Bilateral vs unilateral mandibular block anesthesia in a pediatric population. Pediatr Dent 2000;22(6):453-7. 33. Oulis C, Vadiakas G, Vasilopoulou A, The effectiveness of mandibular infiltration compared to mandibular block anesthesia in treating primary molars in children. Pediatr Dent 1996;18(4):301-5. 34. Tavares M, Goodson MJ, Studen-Pavlovich D, et al. Reversal of soft-tissue local anesthesia with phentolamine mesylate in pediatric patients. J Am Dent Assoc 2008; 139(8):1095-104. 35. Hersh EV, Moore PA, Papas AS, et al. Reversal of softtissue local anesthesia with phentolamine mesylate in adolescents and adults. J Am Dent Assoc 2008;139(8): 1080-93.
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36. Malamed SF. Anatomical considerations. In: Handbook of Local Anesthesia. 5th ed. St. Louis, Mo: Mosby; 2004; 173-4 37. Wilson W, Taubert KA, Gevitz P, et al. Prevention of infective endocarditis: Guidelines from the American Heart Association. Circulation e-published April 19, 2007. Available at: “http://circ.ahajournals.org/cgi/ reprint/CIRCULATIONAHA.106.183095)”. Accessed March 30, 2008. Correction Circulation. 2007;116: e376-e377. Available at: “htttp://circ.ahajournals.org/cgi/ content/full/116/15/1736”. Accessed May 23, 2008. 38. Malamed SF. Supplemental injection techniques. In: Handbook of Local Anesthesia. 5th ed. St Louis, Mo: Mosby; 2004:256-68. 39. Moore PA. Adverse drug reactions in dental practice: Interactions associated with local anesthetics, sedatives, and anxiolytics. J Am Dent Assoc 1999;130(4):541-4. 40. Barash PG, Cullen BF, Stoelting RK. Clinical Anesthesia. 2nd ed. Philadelphia, Pa: JB Lippincott Co; 1992:531. 41. Dionne RA, Phero JC, Becker DE. Management of Pain and Anxiety in the Dental Office. Philadelphia, Pa: WB Saunders; 2002:274-5. 42. Nick D, Thompson L, Anderson D, Trapp L. The use of general anesthesia to facilitate dental treatment. Gen Dent 2003;51(5):464-8.
american academy of pediatric dentistry
Guideline on Use of Nitrous Oxide for Pediatric Dental Patients Originating Council Council on Clinical Affairs
Review Council Council on Clinical Affairs
Adopted 2005
Revised 2009
Purpose The American Academy of Pediatric Dentistry (AAPD) recognizes nitrous oxide/oxygen inhalation as a safe and effective technique to reduce anxiety, produce analgesia, and enhance effective communication between a patient and health care provider. The need to diagnose and treat, as well as the safety of the patient and practitioner, should be considered before using nitrous oxide. By producing this guideline, the AAPD intends to assist the dental profession in developing appropriate practices in the use of nitrous oxide/oxygen analgesia/anxiolysis for pediatric patients.
Methods This guideline is based on a review of the current dental and medical literature related to nitrous oxide/oxygen analgesia/ anxiolysis in pediatric patients. A MEDLINE search was conducted using the terms “nitrous oxide”, “analgesia”, “anxiolysis”, “behavior management”, and “dental treatment”.
Background Dentists have expertise in providing anxiety and pain control for their patients. While anxiety and pain can be modified by psychological techniques, in many instances pharmacological approaches are required.1 Analgesia/anxiolysis is defined as diminution or elimination of pain and anxiety in a conscious patient.2 The patient responds normally to verbal commands. All vital signs are stable, there is no significant risk of losing protective reflexes, and the patient is able to return to preprocedure mobility. In children, analgesia/anxiolysis may expedite the delivery of procedures that are not particularly uncomfortable, but require that the patient not move.2 It also may allow the patient to tolerate unpleasant procedures by reducing or relieving anxiety, discomfort, or pain. The outcome of pharmacological approaches is variable and depends upon each patient’s response to various drugs. The clinical effect of nitrous oxide/oxygen inhalation, however, is more predictable among the majority of the population.
Nitrous oxide is a colorless and virtually odorless gas with a faint, sweet smell. It is an effective analgesic/anxiolytic agent causing central nervous system (CNS) depression and euphoria with little effect on the respiratory system.3 Nitrous oxide has multiple mechanisms of action. The analgesic effect of nitrous oxide appears to be initiated by neuronal release of endogeneous opioid peptides with subsequent activation of opioid receptors and descending Gamma-aminobutyric acid type A (GABAA) receptors and noradrenergic pathways that modulate nociceptive processing at the spinal level. The anxiolytic effect involves activation of the GABAA receptor either directly or indirectly through the benzodiazepine binding site.4 Nitrous oxide has rapid uptake, being absorbed quickly from the alveoli and held in a simple solution in the serum. It is relatively insoluble, passing down a gradient into other tissues and cells in the body, such as the CNS. It is excreted quickly from the lungs. As nitrous oxide is 34 times more soluble than nitrogen in blood, diffusion hypoxia may occur. Studies5-7 have shown that children desaturate more rapidly than adolescents, and administering 100% oxygen to the patient for 3 to 5 minutes once the nitrous oxide in a closed system has been terminated is important.5 Nitrous oxide causes minor depression in cardiac output while peripheral resistance is slightly increased, thereby maintaining the blood pressure.3 This is of particular advantage in treating patients with cerebrovascular system disorders. Nitrous oxide is absorbed rapidly, allowing for both rapid onset and recovery (2-3 minutes). It causes minimal impairment of any reflexes, thus protecting the cough reflex.3 Although rare, silent regurgitation and subsequent aspiration need to be considered with nitrous oxide/oxygen sedation. The concern lies in whether pharyneal-laryngeal reflexes remain intact. This problem can be avoided by not allowing the patient to go into an unconscious state.8 It generally is acceptable to children and can be titrated easily. Most children are enthusiastic about the administration of nitrous oxide/oxygen; many children report dreaming or being on a “space-ride”.8 For some patients, however, the feeling of “losing control” may be troubling and
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claustrophobic patients may find the nasal hood confining and unpleasant.9 The decision to use nitrous oxide/oxygen analgesia/anxiolysis must take into consideration alternative behavioral guidance modalities, the patient’s dental needs, the effect on the quality of dental care, the patient’s emotional development, and the patient’s physical considerations. The objectives of nitrous oxide/oxygen inhalation include: 1. reduce or eliminate anxiety; 2. reduce untoward movement and reaction to dental treatment; 3. enhance communication and patient cooperation; 4. raise the pain reaction threshold; 5. increase tolerance for longer appointments; 6. aid in treatment of the mentally/physically disabled or medically compromised patient; 7. reduce gagging; 8. potentiate the effect of sedatives. Disadvantages of nitrous oxide/oxygen inhalation may include:3 1. lack of potency; 2. dependant largely on psychological reassurance; 3. interference of the nasal hood with injection to ante rior maxillary region; 4. patient must be able to breathe through the nose; 5. nitrous oxide pollution and potential occupational exposure health hazards.
Recommendations Patient selection Indications for use of nitrous oxide/oxygen analgesia/anxiolysis include: 1. a fearful, anxious, or obstreperous patient; 2. certain patients with special health care needs; 3. a patient whose gag reflex interferes with dental care; 4. a patient for whom profound local anesthesia cannot be obtained; 5. a cooperative child undergoing a lengthy dental pro cedure. Review of the patient’s medical history should be performed prior to the decision to use nitrous oxide/oxygen analgesia/ anxiolysis. This assessment should include: 1. allergies and previous allergic or adverse drug reac tions; 2. current medications including dose, time, route, and site of administration; 3. diseases, disorders, or physical abnormalities and pregnancy status; 4. previous hospitalization to include the date and purpose. Contraindications for use of nitrous oxide/oxygen inhalation may include: 1. some chronic obstructive pulmonary diseases; 2. severe emotional disturbances or drug-related depen dencies10; 3. first trimester of pregnancy11;
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4. treatment with bleomycin sulfate12; 5. methylenetetrahydrofolate reductase deficiency.13 Whenever possible, appropriate medical specialists should be consulted before administering analgesic/anxiolytic agents to patients with significant underlying medical conditions (eg, severe obstructive pulmonary disease, congestive heart failure, sickle cell disease,14 acute otitis media, recent tympanic membrane graft15, acute severe head injury16). Technique of nitrous oxide/oxygen administration Nitrous oxide/oxygen must be administered only by appropriately licensed individuals, or under the direct supervision thereof, according to state law. The practitioner responsible for the treatment of the patient and/or the administration of analgesic/ anxiolytic agents must be trained in the use of such agents and techniques and appropriate emergency response. Selection of an appropriately sized nasal hood should be made. A flow rate of 5 to 6 L/min generally is acceptable to most patients. The flow rate can be adjusted after observation of the reservoir bag. The bag should pulsate gently with each breath and should not be either over- or underinflated. Introduction of 100% oxygen for 1 to 2 minutes followed by titration of nitrous oxide in 10% intervals is recommended. During nitrous oxide/ oxygen analgesia/anxiolysis, the concentration of nitrous oxide should not routinely exceed 50%. Nitrous oxide concentration may be decreased during easier procedures (eg, restorations) and increased during more stimulating ones (eg, extraction, injection of local anesthetic). During treatment, it is important to continue the visual monitoring of the patient’s respiratory rate and level of consciousness. The effects of nitrous oxide largely are dependent on psychological reassurance. Therefore, it is important to continue traditional behavior guidance techniques during treatment. Once the nitrous oxide flow is terminated, 100% oxygen should be delivered for 3 to 5 minutes.3 The patient must return to pretreatment responsiveness before discharge. Monitoring The response of patients to commands during procedures performed with anxiolysis/analgesia serves as a guide to their level of consciousness. Clinical observation of the patient must be done during any dental procedure. During nitrous oxide/oxygen analgesia/anxiolysis, continual clinical observation of the patient’s responsiveness, color, and respiratory rate and rhythm must be performed. Spoken responses provide an indication that the patient is breathing.2 If any other pharmacologic agent is used in addition to nitrous oxide/oxygen and a local anesthetic, monitoring guidelines for the appropriate level of sedation must be followed.17 Adverse effects of nitrous oxide/oxygen inhalation Nitrous oxide/oxygen analgesia/anxiolysis has an excellent safety record. When administered by trained personnel on carefully selected patients with appropriate equipment and technique, nitrous oxide is a safe and effective agent for providing pharmacological guidance of behavior in children. Acute and
american academy of pediatric dentistry
chronic adverse effects of nitrous oxide on the patient are rare.18 Nausea and vomiting are the most common adverse effects, occurring in 0.5% of patients.19 A higher incidence is noted with longer administration of nitrous oxide/oxygen, fluctuations in nitrous oxide levels, and increased concentrations of nitrous oxide.3 Fasting is not required for patients undergoing nitrous oxide analgesia/anxiolysis. The practitioner, however, may recommend that only a light meal be consumed in the 2 hours prior to the administration of nitrous oxide.20 Diffusion hypoxia can occur as a result of rapid release of nitrous oxide from the blood stream into the alveoli, thereby diluting the concentration of oxygen. This may lead to headache and disorientation and can be avoided by administering 100% oxygen after nitrous oxide has been discontinued.3 Documentation Informed consent must be obtained from the parent and documented in the patient’s record prior to administration of nitrous oxide/oxygen. The practitioner should provide instructions to the parent regarding pretreatment dietary precautions, if indicated. In addition, the patient’s record should include indication for use of nitrous oxide/oxygen inhalation, nitrous oxide dosage (ie, percent nitrous oxide/oxygen and/or flow rate), duration of the procedure, and post treatment oxygenation procedure. Facilities/personnel/equipment All newly installed facilities for delivering nitrous oxide/ oxygen must be checked for proper gas delivery and fail-safe function prior to use. Inhalation equipment must have the capacity for delivering 100%, and never less than 30%, oxygen concentration at a flow rate appropriate to the child’s size. Additionally, inhalation equipment must have a fail-safe system that is checked and calibrated regularly according to the practitioner’s state laws and regulations.17 If nitrous oxide/ oxygen delivery equipment capable of delivering more than 70% nitrous oxide and less than 30% oxygen is used, an inline oxygen analyzer must be used. The equipment must have an appropriate scavenging system. The practitioner who utilizes nitrous oxide/oxygen analgesia/anxiolysis for a pediatric dental patient shall possess appropriate training and skills and have available the proper facilities, personnel, and equipment to manage any reasonably foreseeable emergency. Training and certification in basic life support are required for all clinical personnel. These individuals should participate in periodic review of the office’s emergency protocol, the emergency drug cart, and simulated exercises to assure proper emergency management response. An emergency cart (kit) must be readily accessible. Emergency equipment must be able to accommodate children of all ages and sizes. It should include equipment to resuscitate a nonbreathing, unconscious patient and provide continuous support until trained emergency personnel arrive. A positivepressure oxygen delivery system capable of administering >90% oxygen at a 10 L/min flow for at least 60 minutes (650 L, “E” cylinder) must be available. When a self-inflating
bag valvemask device is used for delivering positive pressure oxygen, a 15 L/min flow is recommended. There should be documentation that all emergency equipment and drugs are checked and maintained on a regularly scheduled basis.17 Where state law mandates equipment and facilities, such statutes should supersede this guideline.17 Occupational safety In an effort to reduce occupational health hazards associated with nitrous oxide, the AAPD recommends exposure to ambient nitrous oxide be minimized through the use of effective scavenging systems and periodic evaluation and maintenance of the delivery and scavenging systems.21
References 1. American Dental Association. Position statement: The use of conscious sedation, deep sedation and general anesthesia in dentistry. Available at: “http://ada.org/prof/ resources/positions/statements/useof.asp”. Accessed November 24, 2008. 2. American Society of Anesthesiologists. Practice guidelines for sedation and analgesia by nonanesthesiologists: An updated report by the American Society of Anesthesiologists task force on sedation and analgesia by nonanesthesiologists. Anesthesiology 2002;96:1004-17. 3. Paterson SA, Tahmassebi JF. Pediatric dentistry in the new millennium: Use of inhalation sedation in pediatric dentistry. Dent Update 2003;30(7):350-6, 358. 4. Emmanouil DE, Quock RM. Advances in understanding the actions of nitrous oxide. Anesth Prog 2007;54(1):9-18. 5. Patel R, Lenczyk M, Hannallah RS, McGill WA. Age and onset of desaturation in apnoeic children. Can J Anaesth 1994;41(9):771-4. 6. Patel R, Norden J, Hannallah RS. Oxygen administration prevents hypoxemia during post-anesthesia transport in children. Anesthesiology 1988;69(4):616-8. 7. Kinouci K, Tanigami H, Tashiro C, Nishimura M, Fukumitsu K, Takauchi Y. Duration of apnea in anesthetized infants and children required for desaturation of hemoglobin to 95%. Anesthesiology 1992;77(6):1105-7. 8. Hogue D, Ternisky M, Iranour B. The response to nitrous oxide analgesia in children. ASDC J Dent Child 1971;38 (2):129-33. 9. Stach DJ. Nitrous oxide sedation: Understanding the benefit and risks. Am J Dent 1995;8(1):47-50. 10. Clark MS, Brunkick AL. Nitrous Oxide and Oxygen Sedation. 3rd ed. St Louis, Mo; Mosby; 2008:94. 11. Rowland AS, Baird DD, Shore DL, Weinberg CR, Savitz DA, Wilcox AJ. Nitrous oxide and spontaneous abortion in female dental assistants. Am J Epidemiol 1995;141(6): 531-7. 12. Fleming P, Walker PO, Priest JR. Bleomycin therapy: A contraindication to the use of nitrous oxide-oxygen psychosedation in the dental office. Pediatr Dent 1988;10 (4):345-6.
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13. Selzer R, Rosenblatt D, Laxova R, Hogan K. Adverse effect of nitrous oxide in a child with 5,10- methylenetetrahydrofolate reductase deficiency. N Engl J Med 2003; 349(1):45-50. 14. Ogundipe O, Pearson MW, Slater NG, Adepegba T, Westerdale N. Sickle cell disease and nitrous oxide-induced neuropathy. Clin Lab Haematol 1999;21(6):409-12. 15. Fish BM, Banerjee AR, Jennings CR, et al. Effect of anaesthetic agents on tympanometry and middle-ear effusions. J Laryngol Otol 2000;114(5):336-8. 16. Moss E, McDowall DG. ICP increase with 50% nitrous oxide in oxygen in severe head injuries during controlled ventilation. Br J Anaest 1979;51(8):757-61. 17. American Academy of Pediatrics, American Academy of Pediatric Dentistry. Guidelines for monitoring and management of pediatric patients during and after sedation for diagnostic and therapeutic procedures: An update. Pediatr Dent 2008;30(suppl):143-59.
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18. Donaldson D, Meechan JG. The hazards of chronic exposure to nitrous oxide: An update. Br Dent J 1995;178(3): 95-100. 19. Kupietzky A, Tal E, Shapira J, Ram D. Fasting state and episodes of vomiting in children receiving nitrous oxide for dental treatment. Pediatr Dent 2008;30(5):414-9. 20. Hosey MT. UK National Clinical Guidelines in Paediatric Dentistry. Managing anxious children: The use of conscious sedation in paediatric dentistry. Int J Paediatr Dent 2002;12(5):359-72. 21. American Academy of Pediatric Dentistry. Policy on minimizing occupational health hazards associated with nitrous oxide. Pediatr Dent 2008;30(suppl):64-5.
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Guideline for Monitoring and Management of Pediatric Patients During and After Sedation for Diagnostic and Therapeutic Procedures Developed and Endorsed by
American Academy of Pediatrics and the American Academy of Pediatric Dentistry Adopted 2006
Abstract The safe sedation of children for procedures requires a systematic approach that includes the following: no administration of sedating medication without the safety net of medical supervision, careful presedation evaluation for underlying medical or surgical conditions that would place the child at increased risk from sedating medications, appropriate fasting for elective procedures and a balance between depth of sedation and risk for those who are unable to fast because of the urgent nature of the procedure, a focused airway examination for large tonsils or anatomic airway abnormalities that might increase the potential for airway obstruction, a clear understanding of the pharmacokinetic and pharmacodynamic effects of the medications used for sedation as well as an appreciation for drug interactions, appropriate training and skills in airway management to allow rescue of the patient, age- and size-appropriate equipment for airway management and venous access, appropriate medications and reversal agents, sufficient numbers of people to both carry out the procedure and monitor the patient, appropriate physiologic monitoring during and after the procedure, a properly equipped and staffed recovery area, recovery to presedation level of consciousness before discharge from medical supervision, and appropriate discharge instructions.
Introduction Invasive diagnostic and minor surgical procedures on pediatric patients outside the traditional operating room setting have increased in the last decade. As a consequence of this change and the increased awareness of the importance of providing analgesia and anxiolysis, the need for sedation for procedures in physician offices, dental offices, subspecialty procedure suites, imaging facilities, emergency departments, and ambulatory surgery centers also has markedly increased.1-37 In recognition of this need for both elective and emergency use of sedation in nontraditional settings, the American Academy of Pediatrics (AAP) and American Academy of Pediatric Dentistry (AAPD) have published a series of guidelines for the monitoring and management of pediatric patients during and after sedation for a procedure.38-42 The purpose of this updated statement is
to unify the guidelines for sedation used by medical and dental practitioners, add clarifications regarding monitoring modalities, provide new information from medical and dental literature, and suggest methods for further improvement in safety and outcomes. With the revision of this document, the Joint Commission on Accreditation of Healthcare Organizations, the American Society of Anesthesiologists (ASA), the AAP, and the AAPD will use similar language to define sedation categories and the expected physiologic responses.41-44 This revised statement reflects the current understanding of appropriate monitoring needs both during and after sedation for a procedure.4,5,12,19,21,22,26,45-53 The monitoring and care outlined in this guideline may be exceeded at any time, based on the judgment of the responsible practitioner. Although intended to encourage high-quality patient care, adherence to this guideline cannot guarantee a specific patient outcome. However, structured sedation protocols designed to incorporate the principles in this document have been widely implemented and shown to reduce morbidity.29,32-34,37,54,55 This guideline is proffered with the awareness that, regardless of the intended level of sedation or route of administration, the sedation of a pediatric patient represents a continuum and may result in respiratory depression and the loss of the patient’s protective reflexes.43,57-60 Sedation of pediatric patients has serious associated risks, such as hypoventilation, apnea, airway obstruction, laryngospasm, and cardiopulmonary impairment.2,6,22,45,46,54,60-69 These adverse responses during and after sedation for a diagnostic or therapeutic procedure may be minimized, but not completely eliminated, by a careful preprocedure review of the patient’s underlying medical conditions and consideration of how the sedation process might affect or be affected by these conditions.54 Appropriate drug selection for the intended procedure as well as the presence of an individual with the skills needed to rescue a patient from an adverse response are essential. Appropriate physiologic monitoring and continuous observation by personnel not directly involved with the procedure allow for accurate and rapid diagnosis of complications and initiation of appropriate rescue interventions.46,51,54
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The sedation of children is different from the sedation of adults. Sedation in children often is administered to control behavior to allow the safe completion of a procedure. A child’s ability to control his or her own behavior to cooperate for a procedure depends both on his or her chronologic and developmental age. Often, children younger than 6 years and those with developmental delay require deep levels of sedation to gain control of their behavior.57 Therefore, the need for deep sedation should be anticipated. Children in this age group are particularly vulnerable to the sedating medication’s effects on respiratory drive, patency of the airway, and protective reflexes.46 Studies have shown that it is common for children to pass from the intended level of sedation to a deeper, unintended level of sedation.56,59,70 For older and cooperative children, other modalities, such as parental presence, hypnosis, distraction, topical local anesthetics, and guided imagery, may reduce the need for or the needed depth of pharmacologic sedation.31,71-81 The concept of rescue is essential to safe sedation. Practitioners of sedation must have the skills to rescue the patient from a deeper level than that intended for the procedure. For example, if the intended level of sedation is “minimal,” practitioners must be able to rescue from “moderate sedation”; if the intended level of sedation is “moderate,” practitioners must have the skills to rescue from “deep sedation”; if the intended level of sedation is “deep,” practitioners must have the skills to rescue from a state of “general anesthesia.” The ability to rescue means that practitioners must be able to recognize the various levels of sedation and have the skills necessary to provide appropriate cardiopulmonary support if needed. Sedation and anesthesia in a nonhospital environment (private physician or dental office or freestanding imaging facility) may be associated with an increased incidence of “failure to rescue” the patient should an adverse event occur, because the only backup in this venue may be to activate emergency medical services (EMS).46,82 Rescue therapies require specific training and skills.46,54,83,84 Maintenance of the skills needed to perform successful bagvalve-mask ventilation is essential to successfully rescue a child who has become apneic or developed airway obstruction. Familiarity with emergency airway management procedure algorithms is essential.83-87 Practitioners should have an in-depth knowledge of the agents they intend to use and their potential complications. A number of reviews and handbooks for sedating pediatric patients are available.32,48,55,88-93 This guideline is intended for all venues in which sedation for a procedure might be performed (hospital, surgical center, freestanding imaging facility, dental facility, or private office). There are other guidelines for specific situations and personnel that are beyond the scope of this document. Specifically, guidelines for the delivery of general anesthesia and monitored anesthesia care (sedation or analgesia), outside or within the operating room by anesthesiologists or other practitioners functioning within a department of anesthesiology, are addressed by policies developed by the ASA and by individual departments of anesthesiology.94 Also, guidelines for the sedation
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of patients undergoing mechanical ventilation in a critical care environment or for providing analgesia for patients postoperatively, patients with chronic painful conditions, and hospice care are beyond the scope of this document. Definitions of Terms for This Report • “Pediatric patients”: all patients through 21 years of age, as defined by the AAP. • “Must” or “shall”: an imperative need or duty that is essential, indispensable, or mandatory. • “Should”: the recommended need and/or duty. • “May” or “could”: freedom or liberty to follow a suggested or reasonable alternative. • “Medical supervision” or “medical personnel”: a current, licensed practitioner in medicine, surgery, or dentistry trained in the administration of medications used for procedural sedation and the management of complications associated with these medications. • “Are encouraged”: a suggested or reasonable action to be taken. • “ASA Physical Status Classification”: guidelines for classifying the baseline health status according to the ASA (see Appendix B). • “Minimal sedation” (old terminology “anxiolysis”): a druginduced state during which patients respond normally to verbal commands. Although cognitive function and coordination may be impaired, ventilatory and cardiovascular functions are unaffected. • “Moderate sedation” (old terminology “conscious sedation”or “sedation/analgesia”): a drug-induced depression of consciousness during which patients respond purposefully to verbal commands (eg,“open your eyes” either alone or accompanied by light tactile stimulation—a light tap on the shoulder or face, not a sternal rub). For older patients, this level of sedation implies an interactive state; for younger patients, age-appropriate behaviors (eg, crying) occur and are expected. Reflex withdrawal, although a normal response to a painful stimulus, is not considered as the only ageappropriate purposeful response (eg, it must be accompanied by another response, such as pushing away the painful stimulus so as to confirm a higher cognitive function). With moderate sedation, no intervention is required to maintain a patent airway, and spontaneous ventilation is adequate. Cardiovascular function is usually maintained. However, in the case of procedures that may themselves cause airway obstruction (eg, dental or endoscopic), the practitioner must recognize an obstruction and assist the patient in opening the airway. If the patient is not making spontaneous efforts to open his/her airway so as to relieve the obstruction, then the patient should be considered to be deeply sedated. • “Deep sedation” (“deep sedation/analgesia”): a drug-induced depression of consciousness during which patients cannot be easily aroused but respond purposefully (see discussion of reflex withdrawal above) after repeated verbal or painful stimulation
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(eg, purposefully pushing away the noxious stimuli). The ability to independently maintain ventilatory function may be impaired. Patients may require assistance in maintaining a patent airway, and spontaneous ventilation may be inadequate. Cardiovascular function is usually maintained. A state of deep sedation may be accompanied by partial or complete loss of protective airway reflexes. • “General anesthesia”: a drug-induced loss of consciousness during which patients are not arousable, even by painful stimulation. The ability to independently maintain ventilatory function is often impaired. Patients often require assistance in maintaining a patent airway, and positive-pressure ventilation may be required because of depressed spontaneous ventilation or drug-induced depression of neuromuscular function. Cardiovascular function may be impaired.
Goals of Sedation The goals of sedation in the pediatric patient for diagnostic and therapeutic procedures are: 1) to guard the patient’s safety and welfare; 2) to minimize physical discomfort and pain; 3) to control anxiety, minimize psychological trauma, and maximize the potential for amnesia; 4) to control behavior and/or movement so as to allow the safe completion of the procedure; and 5) to return the patient to a state in which safe discharge from medical supervision, as determined by recognized criteria, is possible (Appendix A). These goals can best be achieved by selecting the lowest dose of drug with the highest therapeutic index for the procedure. It is beyond the scope of this document to specify which drugs are appropriate for which procedures; however, the selection of the fewest number of drugs and matching drug selection to the type and goal of the procedure are essential for safe practice.53,88,91-93,95-97 For example, analgesic medications such as opioids are indicated for painful procedures. For nonpainful procedures, such as computed tomography or magnetic resonance imaging (MRI), sedatives/hypnotics are preferred. When both sedation and analgesia are desirable (eg, fracture reduction), either single agents with analgesic/sedative properties or combination regimens commonly are used. Anxiolysis and amnesia are additional goals that should be considered in selection of agents for particular patients. However, the potential for an adverse outcome may be increased when 3 or more sedating medications are administered.44,98 Knowledge of each drug’s time of onset, peak response, and duration of action is essential. Although the concept of titration of drug to effect is critical, one must know whether the previous dose has taken full effect before administering additional drug. Such management will improve safety and outcomes. Drugs with long durations of action (eg, chloral hydrate, intramuscular pentobarbital, phenothiazines) will require longer periods of observation even after the child achieves currently used recovery and discharge criteria.45,99,100 This concept is particularly important for infants and toddlers transported in car safety seats who are at risk of resedation after discharge because of residual prolonged drug effects with the potential for airway obstruction.45,46
General Guidelines Candidates Patients who are in ASA classes I and II are frequently considered appropriate candidates for minimal, moderate, or deep sedation (Appendix B). Children in ASA classes III and IV, children with special needs, and those with anatomic airway abnormalities or extreme tonsillar hypertrophy present issues that require additional and individual consideration, particularly for moderate and deep sedation.51 Practitioners are encouraged to consult with appropriate subspecialists and/or an anesthesiologist for patients at increased risk of experiencing adverse sedation events because of their underlying medical/surgical conditions. Responsible Person The pediatric patient shall be accompanied to and from the treatment facility by a parent, legal guardian, or other responsible person. It is preferable to have 2 or more adults accompany children who are still in car safety seats if transportation to and from a treatment facility is provided by 1 of the adults.101 Facilities The practitioner who uses sedation must have immediately available facilities, personnel, and equipment to manage emergency and rescue situations. The most common serious complications of sedation involve compromise of the airway or depressed respirations resulting in airway obstruction, hypoventilation, hypoxemia, and apnea. Hypotension and cardiopulmonary arrest may occur, usually from inadequate recognition and treatment of respiratory compromise. Other rare complications may also include seizures and allergic reactions. Facilities providing pediatric sedation should monitor for, and be prepared to treat, such complications. Back-up Emergency Services A protocol for access to back-up emergency services shall be clearly identified, with an outline of the procedures necessary for immediate use. For nonhospital facilities, a protocol for ready access to ambulance service and immediate activation of the EMS system for life-threatening complications must be established and maintained. It should be understood that the availability of EMS services does not replace the practitioner’s responsibility to provide initial rescue in managing life-threatening complications. On-Site Monitoring and Rescue Equipment An emergency cart or kit must be immediately accessible. This cart or kit must contain equipment to provide the necessary age- and size-appropriate drugs and equipment to resuscitate a nonbreathing and unconscious child. The contents of the kit must allow for the provision of continuous life support while the patient is being transported to a medical facility or to another area within a medical facility. All equipment and drugs must be checked and maintained on a scheduled basis (see Appendices C and D for suggested drugs and emergency life support equipment to consider before the need for rescue
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occurs). Monitoring devices, such as electrocardiography (ECG) machines, pulse oximeters (with size-appropriate oximeter probes), end-tidal carbon dioxide monitors, and defibrillators (with size-appropriate defibrillator paddles), must have a safety and function check on a regular basis as required by local or state regulation. Documentation Before Sedation Documentation shall include, but not be limited to, the guidelines that follow: 1. Informed consent. The patient record shall document that appropriate informed consent was obtained according to local, state, and institutional requirements.102 2. Instructions and information provided to the responsible person. The practitioner shall provide verbal and/or written instructions to the responsible person. Information shall include objectives of the sedation and anticipated changes in behavior during and after sedation. Special instructions shall be given to the adult responsible for infants and toddlers who will be transported home in a car safety seat regarding the need to carefully observe the child’s head position so as to avoid airway obstruction. Transportation by car safety seat poses a particular risk for infants who have received medications known to have a long half-life, such as chloral hydrate, intramuscular pentobarbital, or phenothiazine. 45,46,100,103 Consideration for a longer period of observation shall be given if the responsible person’s ability to observe the child is limited (eg, only 1 adult who also has to drive). Another indication for prolonged observation would be a child with an anatomic airway problem or a severe underlying medical condition. A 24-hour telephone number for the practitioner or his or her associates shall be provided to all patients and their families. Instructions shall include limitations of activities and appropriate dietary precautions. Dietary Precautions Agents used for sedation have the potential to impair protective airway reflexes, particularly during deep sedation. Although a rare occurrence, pulmonary aspiration may occur if the child regurgitates and cannot protect his or her airway. Therefore, it is prudent that before sedation, the practitioner evaluate preceding food and fluid intake. It is likely that the risk of aspiration during procedural sedation differs from that during general anesthesia involving tracheal intubation or other airway manipulation.104,105 However, because the absolute risk of aspiration during procedural sedation is not yet known, guidelines for fasting periods before elective sedation generally should follow those used for elective general anesthesia. For emergency procedures in children who have not fasted, the risks of sedation and the possibility of aspiration must be balanced against the benefits of performing the procedure promptly (see below). Further research is needed to better elucidate the relationships between various fasting intervals and sedation complications.
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Before Elective Sedation Children receiving sedation for elective procedures should generally follow the same fasting guidelines as before general anesthesia (Table 1). It is permissible for routine necessary medications to be taken with a sip of water on the day of the procedure. For the Emergency Patient The practitioner must always balance the possible risks of sedating nonfasted patients with the benefits and necessity for completing the procedure. In this circumstance, the use of sedation must be preceded by an evaluation of food and fluid intake. There are few published studies with adequate statistical power to provide guidance to the practitioner regarding safety or risk of pulmonary aspiration of gastric contents during procedural sedation.104-109 When protective airway reflexes are lost, gastric contents may be regurgitated into the airway. Therefore, patients with a history of recent oral intake or with other known risk factors, such as trauma, decreased level of consciousness, extreme obesity, pregnancy, or bowel motility dysfunction, require careful evaluation before administration of sedatives. When proper fasting has not been ensured, the increased risks of sedation must be carefully weighed against its benefits, and the lightest effective sedation should be used. The use of agents with less risk of depressing protective airway reflexes may be preferred.110 Some emergency patients requiring deep sedation may require protection of the airway before sedation. Use of Immobilization Devices Immobilization devices, such as papoose boards, must be applied in such a way as to avoid airway obstruction or chest restriction. The child’s head position and respiratory excursions should be checked frequently to ensure airway patency. If an immobilization device is used, a hand or foot should be kept exposed, and the child should never be left unattended. If sedating medications are administered in conjunction with an immobilization device, monitoring must be used at a level consistent with the level of sedation achieved. Documentation at the Time of Sedation 1. Health evaluation. Before sedation, a health evaluation shall be performed by an appropriately-licensed practitioner and reviewed by the sedation team at the time of treatment for possible interval changes. The purpose of this evaluation is not only to document baseline status but also to determine whether patients present specific risk factors that may warrant additional consultation before sedation. This evaluation will also screen out patients whose sedation will require more advanced airway or cardiovascular management skills or alterations in the doses or types of medications used for procedural sedation. A new concern for the practitioner is the widespread use of medications that may interfere with drug absorption or metabolism and, therefore, enhance or shorten the effect time of sedating medications. Herbal medicines (eg, St. John’s
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wort, echinacea) may alter drug pharmacokinetics through inhibition of the cytochrome P450 system, resulting in prolonged drug effect and altered (increased or decreased) blood drug concentrations.111-116 Kava may increase the effects of sedatives by potentiating gamma-aminobutyric acid inhibitory neurotransmission, and valerian may itself produce sedation that apparently is mediated through modulation of gamma-aminobutyric acid neurotransmission and receptor function.117,118 Drugs such as erythromycin, cimetidine, and others also may inhibit the cytochrome P450 system, resulting in prolonged sedation with midazolam as well as other medications competing for the same enzyme systems. 119-122 Medications used to treat human immunodeficiency virus infection, some anticonvulsants, and some psychotropic medications also may produce clinically important drug-drug interactions.123-125 Therefore, a careful drug history is a vital part of the safe sedation of children. The clinician should consult various sources (a pharmacist, textbooks, online services, or handheld databases) for specific information on drug interactions.126 The health evaluation should include: • Age and weight • Health history, including: 1) allergies and previous allergic or adverse drug reactions; 2) medication/drug history, including dosage, time, route, and site of admi nistration for prescription, over-the-counter, herbal, or illicit drugs; 3) relevant diseases, physical abnormali ties, and neurologic impairment that might increase the potential for airway obstruction, such as a history of snoring or obstructive sleep apnea;127,128 4) preg nancy status; 5) a summary of previous relevant hospi talizations; 6) history of sedation or general anesthesia and any complications or unexpected responses; and 7) relevant family history, particularly related to anesthesia • Review of systems with a special focus on abnormali ties of cardiac, pulmonary, renal, or hepatic function that might alter the child’s expected responses to se dating/analgesic medications • Vital signs, including heart rate, blood pressure, res spiratory rate, and temperature (for some children who are very upset or noncooperative, this may not be possible and a note should be written to document this occurrence) • Physical examination, including a focused evaluation of the airway (tonsillar hypertrophy, abnormal anato my—eg, mandibular hypoplasia) to determine whether there is an increased risk of airway obstruction54,129,130 • Physical status evaluation (ASA classification [see Ap pendix B]) • Name, address, and telephone number of the child’s medical home For hospitalized patients, the current hospital record may suffice for adequate documentation of presedation health;
however, a brief note shall be written documenting that the chart was reviewed, positive findings were noted, and a management plan was formulated. If the clinical or emer gency condition of the patient precludes acquiring com plete information before sedation, this health evaluation should be obtained as soon as feasible. 2. Prescriptions. When prescriptions are used for sedation, a copy of the prescription or a note describing the content of the prescription should be in the patient’s chart along with a description of the instructions that were given to the responsible person. Prescription medications intended to accomplish procedural sedation must not be administered without the benefit of direct supervision by trained medical personnel. Administration of sedating medications at home poses an unacceptable risk, particularly for infants and preschool-aged children traveling in car safety seats.46 Documentation During Treatment The patient’s chart shall contain a time-based record that includes the name, route, site, time, dosage, and patient effect of administered drugs. Before sedation, a “time out” should be performed to confirm the patient’s name, procedure to be performed, and site of the procedure.43 During administration, the inspired concentrations of oxygen and inhalation sedation agents and the duration of their administration shall be documented. Before drug administrations, special attention must be paid to calculation of dosage (ie, mg/kg). The patient’s chart shall contain documentation at the time of treatment that the patient’s level of consciousness and responsiveness, heart rate, blood pressure, respiratory rate, and oxygen saturation were monitored until the patient attained predetermined discharge criteria (see Appendix A). A variety of sedation scoring systems are available and may aid this process.70,100 Adverse events and their treatment shall be documented. Documentation After Treatment The time and condition of the child at discharge from the treatment area or facility shall be documented; this should include documentation that the child’s level of consciousness and oxygen saturation in room air have returned to a state that is safe for discharge by recognized criteria (see Appendix A). Patients receiving supplemental oxygen before the procedure should have a similar oxygen need after the procedure. Because some sedation medications are known to have a long half-life and may delay a patient’s complete return to baseline or pose the risk of resedation,45,103,131,132 some patients might benefit from a longer period of less-intense observation (eg, a stepdown observation area) before discharge from medical supervision.133 Several scales to evaluate recovery have been devised and validated.70,134,135 A recently described and simple evaluation tool may be the ability of the infant or child to remain awake for at least 20 minutes when placed in a quiet environment.100
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Continuous Quality Improvement The essence of medical error reduction is a careful examination of index events and root cause analysis of how the event could be avoided in the future.137-141 Therefore, each facility should maintain records that track adverse events, such as desaturation, apnea, laryngospasm, the need for airway interventions including jaw thrust, positive pressure ventilation, prolonged sedation, unanticipated use of reversal agents, unintended or prolonged hospital admission, and unsatisfactory sedation/ analgesia/anxiolysis. Such events can then be examined for assessment of risk reduction and improvement in patient satisfaction.
Preparation and Setting up for Sedation Procedures Part of the safety net of sedation is to use a systematic approach so as to not overlook having an important drug, piece of equipment, or monitor immediately available at the time of a developing emergency. To avoid this problem, it is helpful to use an acronym that allows the same setup and checklist for every procedure. A commonly used acronym useful in planning and preparation for a procedure is SOAPME: S = Size-appropriate suction catheters and a functioning suction apparatus (eg, Yankauer-type suction) O = An adequate oxygen supply and functioning flow meters/ other devices to allow its delivery A = Airway: size-appropriate airway equipment (nasopharyngeal and oropharyngeal airways, laryngoscope blades [checked and functioning], endotracheal tubes, stylets, face mask, bag-valve-mask or equivalent device [functioning]) P = Pharmacy: all the basic drugs needed to support life during an emergency, including antagonists as indicated M = Monitors: functioning pulse oximeter with sizeappropriate oximeter probes141,142 and other monitors as appropriate for the procedure (eg, noninvasive blood pressure, end-tidal carbon dioxide, ECG, stethoscope) E = Special equipment or drugs for a particular case (eg, defibrillator)
Specific Guidelines for Intended Level of Sedation Minimal Sedation Minimal sedation (old terminology “anxiolysis”) is a druginduced state during which patients respond normally to verbal commands. Although cognitive function and coordination may be impaired, ventilatory and cardiovascular functions are unaffected. Children who have received minimal sedation generally will not require more than observation and intermittent assessment of their level of sedation. Some children will become moderately sedated despite the intended level of minimal sedation; should this occur, then the guidelines for moderate sedation apply.57 Moderate Sedation “Moderate sedation” (old terminology “conscious sedation” or “sedation/analgesia”) is a drug-induced depression of consciousness during which patients respond purposefully to verbal
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commands or following light tactile stimulation (see Definition of Terms for This Report). No interventions are required to maintain a patent airway, and spontaneous ventilation is adequate. Cardiovascular function usually is maintained. The caveat that loss of consciousness should be unlikely is a particularly important aspect of the definition of moderate sedation. The drugs and techniques used should carry a margin of safety wide enough to render unintended loss of consciousness highly unlikely. Because the patient who receives moderate sedation may progress into a state of deep sedation and obtundation, the practitioner should be prepared to increase the level of vigilance corresponding to what is necessary for deep sedation.57 Personnel The Practitioner The practitioner responsible for the treatment of the patient and/or the administration of drugs for sedation must be competent to use such techniques, to provide the level of monitoring provided in this guideline, and to manage complications of these techniques (ie, to be able to rescue the patient). Because the level of intended sedation may be exceeded, the practitioner must be sufficiently skilled to provide rescue should the child progress to a level of deep sedation. The practitioner must be trained in, and capable of providing, at the minimum, bagvalve-mask ventilation so as to be able to oxygenate a child who develops airway obstruction or apnea. Training in, and maintenance of, advanced pediatric airway skills is required; regular skills reinforcement is strongly encouraged. Support Personnel The use of moderate sedation shall include provision of a person, in addition to the practitioner, whose responsibility is to monitor appropriate physiologic parameters and to assist in any supportive or resuscitation measures, if required. This individual may also be responsible for assisting with interruptible patientrelated tasks of short duration.44 This individual must be trained in and capable of providing pediatric basic life support. The support person shall have specific assignments in the event of an emergency and current knowledge of the emergency cart inventory. The practitioner and all ancillary personnel should participate in periodic reviews and practice drills of the facility’s emergency protocol to ensure proper function of the equipment and coordination of staff roles in such emergencies. Monitoring and Documentation Baseline Before administration of sedative medications, a baseline determination of vital signs shall be documented. For some children who are very upset or noncooperative, this may not be possible and a note should be written to document this happenstance. During the Procedure The practitioner shall document the name, route, site, time of administration, and dosage of all drugs administered. There shall be continuous monitoring of oxygen saturation and heart
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rate and intermittent recording of respiratory rate and blood pressure; these should be recorded in a time-based record. Restraining devices should be checked to prevent airway obstruction or chest restriction. If a restraint device is used, a hand or foot should be kept exposed. The child’s head position should be checked frequently to ensure airway patency. A functioning suction apparatus must be present. After the procedure The child who has received moderate sedation must be observed in a suitably equipped recovery facility (eg, the facility must have functioning suction apparatus as well as the capacity to deliver more than 90% oxygen and positive-pressure ventilation—eg, bag and mask with oxygen capacity as described previously). The patient’s vital signs should be recorded at specific intervals. If the patient is not fully alert, oxygen saturation and heart rate monitoring shall be used continuously until appropriate discharge criteria are met (see Appendix A). Because sedation medications with a long half-life may delay the patient’s complete return to baseline or pose the risk of resedation, some patients might benefit from a longer period of less-intense observation (eg, a step-down observation area where multiple patients can be observed simultaneously) before discharge from medical supervision (see also Documentation Before Sedation for instructions to families).45,103,131,132 A recently described and simple evaluation tool may be the ability of the infant or child to remain awake for at least 20 minutes when placed in a quiet environment.100 Patients who have received reversal agents, such as flumazenil or naloxone, will also require a longer period of observation, because the duration of the drugs administered may exceed the duration of the antagonist, which can lead to resedation. Deep Sedation Deep sedation is a drug-induced depression of consciousness during which patients cannot be easily aroused but respond purposefully after repeated verbal or painful stimulation (see Definition of Terms for This Report). The state and risks of deep sedation may be indistinguishable from those of general anesthesia.
Vascular Access Patients receiving deep sedation should have an intravenous line placed at the start of the procedure or have a person skilled in establishing vascular access in pediatric patients immediately available. Monitoring and Documentation A competent individual shall observe the patient continuously. The monitoring shall include all parameters described for moderate sedation. Vital signs, including oxygen saturation and heart rate, must be documented at least every 5 minutes in a timebased record. The use of a precordial stethoscope or capnograph for patients difficult to observe (eg, during MRI, in a darkened room) to aid in monitoring adequacy of ventilation is encouraged.143 The practitioner shall document the name, route, site, time of administration, and dosage of all drugs administered. The inspired concentrations of inhalation sedation agents and oxygen and the duration of administration shall be documented. Postsedation Care The facility and procedures followed for postsedation care shall conform to those described under “Moderate Sedation.”
Special Considerations Local Anesthetic Agents All local anesthetic agents are cardiac depressants and may cause central nervous system excitation or depression. Particular attention should be paid to dosage in small children.64,66 To ensure that the patient will not receive an excessive dose, the maximum allowable safe dosage (ie, mg/kg) should be calculated before administration. There may be enhanced sedative effects when the highest recommended doses of local anesthetic drugs are used in combination with other sedatives or narcotics (see Tables 2 and 3 for limits and conversion tables of commonly used local anesthetics).64,144-157 In general, when administering local anesthetic drugs, the practitioner should aspirate frequently so as to minimize the likelihood that the needle is in a blood vessel; lower doses should be used when injecting into vascular tissues.158
Personnel There must be 1 person available whose only responsibility is to constantly observe the patient’s vital signs, airway patency, and adequacy of ventilation and to either administer drugs or direct their administration. At least 1 individual must be present who is trained in, and capable of, providing advanced pediatric life support, and who is skilled in airway management and cardiopulmonary resuscitation; training in pediatric advanced life support is required.
Pulse Oximetry The new generation of pulse oximeters is less susceptible to motion artifacts and may be more useful than older oximeters that do not contain the updated software.159-163 Oximeters that change tone with changes in hemoglobin saturation provide immediate aural warning to everyone within hearing distance. It is essential that any oximeter probe is positioned properly; clip-on devices are prone to easy displacement, which may produce artifactual data (eg, under- or overestimation of oxygen saturation).141,142
Equipment In addition to the equipment previously cited for moderate sedation, an electrocardiographic monitor and a defibrillator for use in pediatric patients should be readily available.
Capnography Expired carbon dioxide monitoring is valuable to diagnose the simple presence or absence of respirations, airway obstruction, or respiratory depression, particularly in patients sedated in
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less-accessible locations, such as magnetic resonance imaging or computerized axial tomography devices or darkened rooms.47,49, 50,143,164-173 The use of expired carbon dioxide monitoring devices is encouraged for sedated children, particularly in situations where other means of assessing the adequacy of ventilation are limited. Several manufacturers have produced nasal cannulae that allow simultaneous delivery of oxygen and measurement of expired carbon dioxide values.164,165 Although these devices can have a high degree of false-positive alarms, they are also very accurate for the detection of complete airway obstruction or apnea.166,168,173 Adjuncts to Airway Management and Resuscitation The vast majority of sedation complications can be managed with simple maneuvers, such as supplemental oxygen, opening the airway, suctioning, and bag-mask-valve ventilation. Occasionally, endotracheal intubation is required for more prolonged ventilatory support. In addition to standard endotracheal intubation techniques, a number of new devices are available for the management of patients with abnormal airway anatomy or airway obstruction. Examples include the laryngeal mask airway (LMA), the cuffed oropharyngeal airway, and a variety of kits to perform an emergency cricothyrotomy. The largest clinical experience in pediatrics is with the LMA, which is available in a variety of sizes and can even be used in neonates. Use of the LMA is now being introduced into advanced airway training courses, and familiarity with insertion techniques can be life saving.174,175 The LMA also can serve as a bridge to secure airway management in children with anatomic airway abnormalities.176,177 Practitioners are encouraged to gain experience with these techniques as they become incorporated into pediatric advanced life support courses. An additional emergency device with which to become familiar is the intraosseous needle. Intraosseous needles also are available in several sizes and can be life saving in the rare situation when rapid establishment of intravenous access is not possible. Familiarity with the use of these adjuncts for the management of emergencies can be obtained by keeping current with resuscitation courses, such as Pediatric Advanced Life Support and Advanced Pediatric Life Support or other approved programs. Patient Simulators Advances in technology, particularly patient simulators that allow a variety of programmed adverse events (eg, apnea, bronchospasm, laryngospasm), response to medical interventions, and printouts of physiologic parameters, are now available. The use of such devices is encouraged to better train medical professionals to respond more appropriately and effectively to rare events.178-180
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Monitoring During MRI The powerful magnetic field and the generation of radiofrequency emissions necessitate the use of special equipment to provide continuous patient monitoring throughout the MRI scanning procedure. Pulse oximeters capable of continuous function during scanning should be used in any sedated or restrained pediatric patient. Thermal injuries can result if appropriate precautions are not taken; avoid coiling the oximeter wire and place the probe as far from the magnetic coil as possible to diminish the possibility of injury. Electrocardiogram monitoring during magnetic resonance imaging has been associated with thermal injury; special MRI-compatible ECG pads are essential to allow safe monitoring.181-184 Expired carbon dioxide monitoring is strongly encouraged in this setting. Nitrous Oxide Inhalation sedation/analgesia equipment that delivers nitrous oxide must have the capacity of delivering 100% and never less than 25% oxygen concentration at a flow rate appropriate to the size of the patient. Equipment that delivers variable ratios of nitrous oxide to oxygen and that has a delivery system that covers the mouth and nose must be used in conjunction with a calibrated and functional oxygen analyzer. All nitrous oxideto-oxygen inhalation devices should be calibrated in accordance with appropriate state and local requirements. Consideration should be given to the National Institute of Occupational Safety and Health standards for the scavenging of waste gases.185 Newly constructed or reconstructed treatment facilities, especially those with piped-in nitrous oxide and oxygen, must have appropriate state or local inspections to certify proper function of inhalation sedation/analgesia systems before any delivery of patient care. Nitrous oxide in oxygen with varying concentrations has been successfully used for many years to provide analgesia for a variety of painful procedures in children.15,186-210 The use of nitrous oxide for minimal sedation is defined as the administration of nitrous oxide (50% or less) with the balance as oxygen, without any other sedative, narcotic, or other depressant drug before or concurrent with the nitrous oxide to an otherwise healthy patient in ASA class I or II. The patient is able to maintain verbal communication throughout the procedure. It should be noted that although local anesthetics have sedative properties, for purposes of this guideline, they are not considered sedatives in this circumstance. If nitrous oxide in oxygen is combined with other sedating medications, such as chloral hydrate, midazolam, or an opioid, or if nitrous oxide is used in concentrations greater than 50%, the likelihood for moderate or deep sedation increases.211,212 In this situation, the clinician must be prepared to institute the guidelines for moderate or deep sedation as indicated by the patient’s response.213
american academy of pediatric dentistry
Table 1. Appropriate Intake of Food and Liquids Before Elective Sedation* Ingested Material
Minimum Fasting Period (h)
Clear liquids: water, fruit juices without pulp, carbonated beverages, clear tea, black coffee
2
Breast milk
4
Infant formula
6
Nonhuman milk: because nonhuman milk is similar to solids in gastric emptying time, the amount ingested must be considered when determining an appropriate fasting period
6
Light meal: a light meal typically consists of toast and clear liquids. Meals that include fried or fatty foods or meat may prolong gastric emptying time. Both the amount and type of foods ingested must be considered when determining an appropriate fasting period.
6
* American Society of Anesthesiologists. Practice Guidelines for Preoperative Fasting and the Use of Pharmacologic Agents to Reduce the Risk of Pulmonary Aspiration: Application to Healthy Patients Undergoing Elective Procedures. A Report of the American Society of Anesthesiologists. Available at: “http://www.asahq.org/publicationsAndServices/npoguide.html”.
Table 2. Commonly Used Local Anesthetic Agents: Doses, Duration, and Calculations* Maximum Dose with Epinephrine (mg/Kg)† Local Anesthetic
Duration of Action (min) ‡
Medical
Dental
Procaine
10.0
6
Chloroprocaine
20.0
12
30-60
1.5
1
180-600
Lidocaine
7.0
4.4
90-200
Mepivacaine
7.0
4.4
120-240
Bupivacaine
3.0
1.3
180-600
Levobupivacaine
3.0
2
180-600
Ropivacaine
3.0
2
180-600
7
60-230
Esters
Tetracaine
60-90
Amides
Articaine
* Maximum recommended doses and duration of action. Note that lower doses should be used in very vascular areas. † These are maximum doses of local anesthetics combined with epinephrine; lower doses are recommended when used without epinephrine. Doses of amides should be decreased by 30% in infants younger than 6 months. When lidocaine is being administered intravascularly (eg, during intravenous regional anesthesia), the dose should be decreased to 3 to 5 mg/kg; long-acting local anesthetic agents should not be used for intravenous regional anesthesia. ‡ Duration of action is dependent on concentration, total dose, and site of administration; use of epinephrine; and the patient’s age.
Table 3. Local Anesthetic Percent Concentration: Conversion to mg/mL Concentration (%)
mg/mL
3.0
30.0
2.5
25.0
2.0
20.0
1.0
10.0
0.5
5.0
025
2.5
0.125
1.25
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Appendix A. Recommended Discharge Criteria 1. 2. 3. 4. 5. 6.
Cardiovascular function and airway patency are satisfactory and stable. The patient is easily arousable, and protective reflexes are intact. The patient can talk (if age appropriate). The patient can sit up unaided (if age appropriate). For a very young or handicapped child incapable of the usually expected responses, the presedation level of responsiveness or a level as close as possible to the normal level for that child should be achieved. The state of hydration is adequate.
Appendix B. ASA Physical Status Classification Class I Class II Class III Class IV Class V
A normally healthy patient. A patient with mild systemic disease (eg, controlled reactive airway disease). A patient with severe systemic disease (eg, a child who is actively wheezing). A patient with severe systemic disease that is a constant threat to life (eg, a child with status asthmaticus). A moribund patient who is not expected to survive without the operation (eg, a patient with severe cardiomyopathy requiring heart transplantation).
Appendix C. Drugs* That May Be Needed to Rescue a Sedated Patient44 Albuterol for inhalation Ammonia spirits Atropine Diphenhydramine Diazepam Epinephrine (1:1000, 1:10 000) Flumazenil Glucose (25% or 50%) Lidocaine (cardiac lidocaine, local infiltration) Lorazepam Methylprednisolone Naloxone Oxygen Fosphenytoin Racemic epinephrine Rocuronium Sodium bicarbonate Succinylcholine * The choice of emergency drugs may vary according to individual or procedural needs.
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Appendix D. Emergency Equipment † That May Be Needed to Rescue a Sedated Patient ‡ Intravenous Equipment Assorted IV catheters (eg, 24-, 22-, 20-, 18-, 16-gauge) Tourniquets Alcohol wipes Adhesive tape Assorted syringes (eg, 1-, 3-, 5-, 10-mL) IV tubing Pediatric drip (60 drops/mL) Pediatric burette Adult drip (10 drops/mL) Extension tubing 3-way stopcocks IV fluid Lactated Ringer solution Normal saline solution D5 0.25 normal saline solution Pediatric IV boards Assorted IV needles (eg, 25-, 22-, 20-, and 18-gauge) Intraosseous bone marrow needle Sterile gauze pads Airway Management Equipment Face masks (infant, child, small adult, medium adult, large adult) Breathing bag and valve set Oropharyngeal airways (infant, child, small adult, medium adult, large adult) Nasopharyngeal airways (small, medium, large) Laryngeal mask airways (1, 1.5, 2, 2.5, 3, 4, and 5) Laryngoscope handles (with extra batteries) Laryngoscope blades (with extra light bulbs) Straight (Miller) No. 1, 2, and 3 Curved (Macintosh) No. 2 and 3 Endotracheal tubes (2.5, 3.0, 3.5, 4.0, 4.5, 5.0, 5.5, and 6.0 uncuffed and 6.0, 7.0, and 8.0 cuffed) Stylettes (appropriate sizes for endotracheal tubes) Surgical lubricant Suction catheters (appropriate sizes for endotracheal tubes) Yankauer-type suction Nasogastric tubes Nebulizer with medication kits Gloves (sterile and nonsterile, latex free) † The choice of emergency equipment may vary according to individual or procedural needs. ‡ The practitioner is referred to the SOAPME acronym described in the text in preparation for sedating a child for a procedure.
american academy of pediatric dentistry
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118. Abebe W. Herbal medication: Potential for adverse interactions with analgesic drugs. J Clin Pharm Ther 2002; 27:391-401. 119. von Rosensteil NA, Adam D. Macrolide antibacterials. Drug interactions of clinical significance. Drug Saf 1995; 13:105-22. 120. Hiller A, Olkkola KT, Isohanni P, Saarnivaara L. Unconsciousness associated with midazolam and erythromycin. Br J Anaesth 1990;65:826-8. 121. Mattila MJ, Idanpaan-Heikkila JJ, Tornwall M, Vanakoski J. Oral single doses of erythromycin and roxithromycin may increase the effects of midazolam on human performance. Pharmacol Toxicol 1993;73:180-5. 122. Olkkola KT, Aranko K, Luurila H, et al. A potentially hazardous interaction between erythromycin and midazolam. Clin Pharmacol Ther 1993;53:298-05. 123. Flockhart DA, Oesterheld JR. Cytochrome P450-mediated drug interactions. Child Adolesc Psychiatr Clin N Am 2000;9:43-76. 124. Yuan R, Flockhart DA, Balian JD. Pharmacokinetic and pharmacodynamic consequences of metabolism-based drug interactions with alprazolam, midazolam, and triazolam. J Clin Pharmacol 1999;39:1109-25. 125. Young B. Review: Mixing new cocktails: Drug interactions in antiretroviral regimens. AIDS Patient Care STDS 2005;19:286-97. 126. Wilkinson GR. Drug metabolism and variability among patients in drug response. N Engl J Med 2005;352:2211-21. 127. American Academy of Pediatrics, Section on Pediatric Pulmonology, Subcommittee on Obstructive Sleep Apnea Syndrome. Clinical practice guideline: Diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics 2002;109:704-12. 128. Schechter MS. Technical report: Diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics 2002;109(4):e69. 129. Litman RS, Kottra JA, Berkowitz RJ, Ward DS. Upper airway obstruction during midazolam/nitrous oxide sedation in children with enlarged tonsils. Pediatr Dent 1998; 20:318-20. 130. Fishbaugh DF, Wilson S, Preisch JW, Weaver JM II. Relationship of tonsil size on an airway blockage maneuver in children during sedation. Pediatr Dent 1997;19:277-81. 131. Mayers DJ, Hindmarsh KW, Sankaran K, Gorecki DK, Kasian GF. Chloral hydrate disposition following singledose administration to critically ill neonates and children. Dev Pharm & Ther 1991;16:71-7. 132. Terndrup TE, Dire DJ, Madden CM, Davis H, Cantor RM, Gavula DP. A prospective analysis of intramuscular meperidine, promethazine, and chlorpromazine in pediatric emergency department patients. Ann Emerg Med 1991;20:31-5. 133. Coté CJ. Discharge criteria for children sedated by nonanesthesiologists: Is “safe” really safe enough?” Anesthesiology 2004;100:207-9.
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134. Macnab AJ, Levine M, Glick N, Susak L, Baker-Brown G. A research tool for measurement of recovery from sedation: The Vancouver Sedative Recovery Scale. J Pediatr Surg 1991;26:1263-7. 135. Chernik DA, Gillings D, Laine H, et al. Validity and reliability of the Observer’s Assessment of Alertness/ Sedation Scale: Study with intravenous midazolam. J Clin Psychopharmacol 1990;10:244-51. 136. Bagian JP, Lee C, Gosbee J, et al. Developing and deploying a patient safety program in a large health care delivery system: You can’t fix what you don’t know about. Jt Comm J Qual Improv 2001;27:522-32. 137. May T, Aulisio MP. Medical malpractice, mistake prevention, and compensation. Kennedy Inst Ethics J 2001; 11:135-46. 138. Kazandjian VA. When you hear hoofs, think horses, not zebras: An evidence-based model of health care accountability. J Eval Clin Pract 2002;8:205-13. 139. Connor M, Ponte PR, Conway J. Multidisciplinary approaches to reducing error and risk in a patient care setting. Crit Care Nurs Clin North Am 2002;14:359-67. 140. Gosbee J. Human factors engineering and patient safety. Qual Saf Health Care 2002;11:352-4. 141. Barker SJ, Hyatt J, Shah NK, Kao YJ. The effect of sensor malpositioning on pulse oximeter accuracy during hypoxemia. Anesthesiology 1993;79:248-54. 142. Kelleher JF, Ruff RH. The penumbra effect: Vasomotiondependent pulse oximeter artifact due to probe malposition. Anesthesiology 1989;71:787-91. 143. Hart LS, Berns SD, Houck CS, Boenning DA. The value of end-tidal CO2 monitoring when comparing three methods of conscious sedation for children undergoing painful procedures in the emergency department. Pediatr Emerg Care 1997;13:189-93. 144. Aubuchon RW. Sedation liabilities in pedodontics (abstr). Pediatr Dent 1982;4:171-80. 145. Fitzmaurice LS, Wasserman GS, Knapp JF, Roberts DK, Waeckerle JF, Fox M. TAC use and absorption of cocaine in a pediatric emergency department. Ann Emerg Med 1990;19:515-8. 146. Tipton GA, DeWitt GW, Eisenstein SJ. Topical TAC (tetracaine, adrenaline, cocaine) solution for local anesthesia in children: Prescribing inconsistency and acute toxicity. South Med J 1989;82:1344-6. 147. Gunter JB. Benefit and risks of local anesthetics in infants and children. Paediatr Drugs 2002;4:649-72. 148. Resar LM, Helfaer MA. Recurrent seizures in a neonate after lidocaine administration. J Perinatol 1998;18:193-5. 149. Yagiela JA, Neidle EA, Dowd FJ. Local anesthetics. In: Pharmaclogy and Therapeutics for Dentistry. Elsevier Health Sciences 2004;251-70. 150. Haas DA. An update on local anesthetics in dentistry. J Can Dent Assoc 2002;68:546-51.
151. Malamed SF. Local anesthetic considerations in dental specialties. In: Handbook of Local Anesthesia, 5 th ed. St. Louis, Mo: Mosby; 2004:269, 274-5. 152. Malamed SF. The needle. In: Handbook of Local Anesthesia, 5th ed. St. Louis, Mo: Mosby; 2004:99-107. 153. Malamed SF. Clinical action of specific agents. In: Handbook of Local Anesthesia, 5th ed. St. Louis, Mo: Mosby; 2004:55-81. 154. Ram D, Amir E. Comparison of articaine 4% and lidocaine 2% in pediatric dental patients. Intl J Pediatric Dent 2006;16:252-6. 155. Jakobs W, Ladwig B, Cichon P, Ortel R, Kirch W. Serum levels of articaine 2% and 4% in children. Anesth Prog 1995;42:113-5. 156. Wright GZ, Weinberger SJ, Friedman CS, Plotzke OB. Use of articaine local anesthesia in children under 4 years of age–A retrospective report. Anesth Report 1989;36:268-71. 157. Malamed SF, Gagnon S, Leblanc D. A comparison between articaine HCl and lidocaine HCl in pediatric dental patients. Pediatr Dent 2000;22:307-11. 158. American Academy of Pediatric Dentistry. Guideline on appropiate use of local anesthesia for pediatric dental patients. Pediatr Dent 2005;27(suppl):101-6. 159. Next-generation pulse oximetry. Health Devices 2003;32: 49-103. 160. Barker SJ. “Motion-resistant” pulse oximetry: A comparison of new and old models. Anesth Analg 2002;95:967-72. 161. Malviya S, Reynolds PI, Voepel-Lewis T, et al. False alarms and sensitivity of conventional pulse oximetry versus the Masimo SET technology in the pediatric postanesthesia care unit. Anesth Analg 2000;90:1336-40. 162. Barker SJ, Shah NK. Effects of motion on the performance of pulse oximeters in volunteers. Anesthesiology 1996;85:774-81. 163. Barker SJ, Shah NK. The effects of motion on the performance of pulse oximeters in volunteers (revised publication). Anesthesiology 1997;86:101-8. 164. Colman Y, Krauss B. Microstream capnograpy technology: A new approach to an old problem. J Clin Monit Comput 1999;15:403-9. 165. Wright SW. Conscious sedation in the emergency department: The value of capnography and pulse oximetry. Ann Emerg Med 1992;21:551-5. 166. Croswell RJ, Dilley DC, Lucas WJ, Vann WF Jr. A comparison of conventional versus electronic monitoring of sedated pediatric dental patients. Pediatr Dent 1995;17: 332-9. 167. Tobias JD. End-tidal carbon dioxide monitoring during sedation with a combination of midazolam and ketamine for children undergoing painful, invasive procedures. Pediatr Emerg Care 1999;15:173-5. 168. Primosch RE, Buzzi IM, Jerrell G. Monitoring pediatric dental patients with nasal mask capnography. Pediatr Dent 2000;22:120-4.
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169. Roelofse J. Conscious sedation: Making our treatment options safe and sound. SADJ 2000;55:273-6. 170. Wilson S, Creedon RL, George M, Troutman K. A history of sedation guidelines: Where we are headed in the future. Pediatr Dent 1996;18:194-9. 171. Miner JR, Heegaard W, Plummer D. End-tidal carbon dioxide monitoring during procedural sedation. Acad Emerg Med 2002;9:275-80. 172. Vascello LA, Bowe EA. A case for capnographic monitoring as a standard of care. J Oral Maxillofac Surg 1999;57: 1342-7. 173. Iwasaki J, Vann WF Jr, Dilley DC, Anderson JA. An investigation of capnography and pulse oximetry as monitors of pediatric patients sedated for dental treatment. Pediatr Dent 1989;11:111-7. 174. Berry AM, Brimacombe JR, Verghese C. The laryngeal mask airway in emergency medicine, neonatal resuscitation, and intensive care medicine. Int Anesthesiol Clin 1998;36: 91-109. 175. Patterson MD. Resuscitation update for the pediatrician. Pediatr Clin North Am 1999;46:1285-303. 176. Selim M, Mowafi H, Al Ghamdi A, Adu-Gyamfi Y. Intubation via LMA in pediatric patients with difficult airways. Can J Anaesth 1999;46:891-3. 177. Munro HM, Butler PJ, Washington EJ. Freeman-Sheldon (whistling face) syndrome. Anaesthetic and airway management. Paediatr Anaesth 1997;7:345-8. 178. Rowe R, Cohen RA. An evaluation of a virtual reality airway simulator. Anesth Analg 2002;95:62-6. 179. Medina LS, Racadio JM, Schwid HA. Computers in radiology. The sedation, analgesia, and contrast media computerized simulator: A new approach to train and evaluate radiologists’ responses to critical incidents. Pediatr Radiol 2000;30:299-305. 180. Blike G, Cravero J, Nelson E. Same patients, same critical events-different systems of care, different outcomes: Description of a human factors approach aimed at improving the efficacy and safety of sedation/analgesia care. Qual Manag Health Care 2001;10:17-36. 181. Kanal E, Shellock FG, Talagala L. Safety considerations in MR imaging. Radiology 1990;176:593-606. 182. Shellock FG, Kanal E. Burns associated with the use of monitoring equipment during MR procedures. J Magn Reson Imaging 1996;6:271-2. 183. Shellock FG. Magnetic resonance safety update 2002: Implants and devices. J Magn Reson Imaging 2002;16: 485-96. 184. Dempsey MF, Condon B, Hadley DM. MRI safety review. Semin Ultrasound CT MR. 2002;23:392-401 185. National Institute for Occupational Safety and Health (NIOSH). Criteria for a Recommended Standard: Occupational Exposure to Waste Anesthetic Gases and Vapors. Cinncinnati, Oh. Publication 77-140. 1977. Ref Type: Statute.
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186. O’Sullivan I, Benger J. Nitrous oxide in emergency medicine. Emerg Med J 2003;20:214-7. 187. Kennedy RM, Luhmann JD, Luhmann SJ. Emergency department management of pain and anxiety related to orthopedic fracture care: A guide to analgesic techniques and procedural sedation in children. Paediatr Drugs 2004; 6:11-31. 188. Frampton A, Browne GJ, Lam LT, Cooper MG, Lane LG. Nurse administered relative analgesia using high concentration nitrous oxide to facilitate minor procedures in children in an emergency department. Emerg Med J 2003;20:410-3. 189. Everitt I, Younge P, Barnett P. Paediatric sedation in emergency department: What is our practice? Emerg Med (Fremantle) 2002;14:62-6. 190. Krauss B. Continuous-flow nitrous oxide: Searching for the ideal procedural anxiolytic for toddlers. Ann Emerg Med 2001;37:61-2. 191. Otley CC, Nguyen TH. Conscious sedation of pediatric patients with combination oral benzodiazepines and inhaled nitrous oxide. Dermatol Surg 2000;26:1041-4. 192. Luhmann JD, Kennedy RM, Jaffe DM, McAllister JD. Continuous-flow delivery of nitrous oxide and oxygen: A safe and cost-effective technique for inhalation analgesia and sedation of pediatric patients. Pediatr Emerg Care 1999;15:388-92. 193. Burton JH, Auble TE, Fuchs SM. Effectiveness of 50% nitrous oxide/50% oxygen during laceration repair in children. Acad Emerg Med 1998;5:112-7. 194. Gregory PR, Sullivan JA. Nitrous oxide compared with intravenous regional anesthesia in pediatric forearm fracture manipulation. J Pediatr Orthop 1996;16:187-91. 195. Hennrikus WL, Shin AY, Klingelberger CE. Selfadministered nitrous oxide and a hematoma block for analgesia in the outpatient reduction of fractures in children. J Bone Joint Surg Am 1995;77:335-9. 196. Hennrikus WL, Simpson RB, Klingelberger CE, Reis MT. Self-administered nitrous oxide analgesia for pediatric fracture reductions. J Pediatr Orthop 1994;14:538-42. 197. Wattenmaker I, Kasser JR, McGravey A. Self-administered nitrous oxide for fracture reduction in children in an emergency room setting. J Orthop Trauma 1990;4:35-8. 198. Gamis AS, Knapp JF, Glenski JA. Nitrous oxide analgesia in a pediatric emergency department. Ann Emerg Med 1989;18:177-81. 199. Kalach N, Barbier C, el Kohen R, et al. [Tolerance of nitrous oxide-oxygen sedation for painful procedures in emergency pediatrics: Report of 600 cases] [article in French]. Arch Pediatr 2002;9:1213-5. 200. Michaud L, Gottrand F, Ganga-Zandzou PS, et al. Nitrous oxide sedation in pediatric patients undergoing gastrointestinal endoscopy. J Pediatr Gastroenterol Nutr 1999; 28:310-4.
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201. Baskett PJ. Analgesia for the dressing of burns in children: A method using neuroleptanalgesia and Entonox. Postgrad Med J 1972;48:138-42. 202. Veerkamp JS, van Amerongen WE, Hoogstraten J, Groen HJ. Dental treatment of fearful children, using nitrous oxide. Part 1: Treatment times. ASDC J Dent Child 1991; 58:453-7. 203. Veerkamp JS, Gruythuysen RJ, van Amerongen WE, Hoogstraten J. Dental treatment of fearful children using nitrous oxide. Part 3: Anxiety during sequential visits. ASDC J Dent Child 1993;60:175-82. 204. Veerkamp JS, Gruythuysen RJ, van Amerongen WE, Hoogstraten J. Dental treatment of fearful children using nitrous oxide. Part 2: The parent’s point of view. ASDC J Dent Child 1992;59:115-9. 205. Veerkamp JS, Gruythuysen RJ, Hoogstraten J, van Amerongen WE. Dental treatment of fearful children using nitrous oxide. Part 4: Anxiety after two years. ASDC J Dent Child 1993;60:372-6. 206. Houpt MI, Limb R, Livingston RL. Clinical effects of nitrous oxide conscious sedation in children. Pediatr Dent 2004;26:29-36. 207. Shapira J, Holan G, Guelmann M, Cahan S. Evaluation of the effect of nitrous oxide and hydroxyzine in controlling the behavior of the pediatric dental patient. Pediatr Dent 1992;14:167-70.
208. Primosch RE, Buzzi IM, Jerrell G. Effect of nitrous oxideoxygen inhalation with scavenging on behavioral and physiological parameters during routine pediatric dental treatment. Pediatr Dent 1999;21:417-20. 209. McCann W, Wilson S, Larsen P, Stehle B. The effects of nitrous oxide on behavior and physiological parameters during conscious sedation with a moderate dose of chloral hydrate and hydroxyzine. Pediatr Dent 1996;18: 35-41. 210. Wilson S, Matusak A, Casamassimo PS, Larsen P. The effects of nitrous oxide on pediatric dental patients sedated with chloral hydrate and hydroxyzine. Pediatr Dent 1998;20:253-8. 211. Litman RS, Kottra JA, Berkowitz RJ, Ward DS. Breathing patterns and levels of consciousness in children during administration of nitrous oxide after oral midazolam premedication. J Oral Maxillofac Surg 1997;55:1372-7. 212. Litman RS, Kottra JA, Verga KA, Berkowitz RJ, Ward DS. Chloral hydrate sedation: The additive sedative and respiratory depressant effects of nitrous oxide. Anesth Analg 1998;86:724-8. 213. American Academy of Pediatric Dentistry. Guideline on appropiate use of nitrous oxide for pediatric dental patients. Pediatr Dent 2005;27(suppl ):107-9.
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Guideline on Use of Anesthesia Personnel in the Administration of Office-based Deep Sedation/ General Anesthesia to the Pediatric Dental Patient Originating Committee
Clinical Affairs Committee – Sedation and General Anesthesia Subcommittee Review Council Council on Clinical Affairs
Adopted 2001
Revised 2005, 2007, 2009
Purpose The American Academy of Pediatric Dentistry (AAPD) recognizes that there are pediatric dental patients for whom routine dental care using nonpharmacologic behavior guidance techniques is not a viable approach.1 The AAPD intends this guideline to assist the dental practitioner who elects to use anesthesia personnel for the administration of deep sedation/ general anesthesia for pediatric dental patients in a dental office or other facility outside of an accredited hospital or surgicenter. This document discusses personnel, facilities, documentation, and quality assurance mechanisms necessary to provide optimal and responsible patient care.
Methods The revision of this guideline is based upon a review of current dental and medical literature pertaining to deep sedation/general anesthesia of dental patients, including the 2006 guideline on pediatric sedation co-authored by the American Academy of Pediatrics (AAP) and the AAPD.2 A MEDLINE search was performed using the terms “office-based anesthesia”, “pediatric sedation”, and “dental sedation”.
Background Pediatric dentists seek to provide oral health care to infants, children, adolescents, and persons with special health care needs in a manner that promotes excellence in quality of care and concurrently induces a positive patient attitude toward dental treatment. Behavior guidance techniques have allowed many pediatric dental patients to receive treatment in the office with minimal discomfort and without expressed fear. Minimal or moderate sedation has allowed others who are less compliant to receive treatment. There are some children and special needs patients with extensive treatment needs, acute situational anxiety, uncooperative age-appropriate behavior, immature
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cognitive functioning, disabilities, or medical conditions that require deep sedation/general anesthesia to receive dental treatment in a safe and humane fashion. Access to hospital-based anesthesia services may be limited for a variety of reasons, including restriction of coverage of by third party payors. Pediatric dentists and others who treat children can provide for the administration of deep sedation/general anesthesia by properly trained individuals in their offices or other facilities outside of the traditional surgical setting. Deep sedation/general anesthesia in the dental office can provide benefits for the patient and the dental team. Access to care may be improved. The treatment may be scheduled more easily and efficiently. Facility charges and administrative procedures may be less than those associated with a surgical center. Complex or lengthy treatment can be provided comfortably while minimizing patient memory of the dental procedure. Movement by the patient is decreased, and the quality of care may be improved. The dentist can use his/her customary inoffice delivery system with access to supplemental equipment, instrumentation, or supplies should the need arise. The use of anesthesia personnel to administer deep sedation/general anesthesia in the pediatric dental population is an accepted treatment modality.2-6 The AAPD supports the provision of deep sedation/general anesthesia when clinical indications have been met and additional properly-trained and credentialed personnel and appropriate facilities are used.1,2,6 In many cases, the patient may be treated in an appropriate out-patient facility (including the dental office) because the extensive medical resources of a hospital are not necessary. This guideline does not supercede, nor is it to be used in deference to, federal, state, and local credentialing and licensure laws, regulations, and codes. It cannot and does not predict nor guarantee a specific patient outcome.
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Recommendations Personnel Office-based deep sedation/general anesthesia techniques require at least 3 individuals. The anesthesia care provider’s responsibilities are to administer drugs or direct their administration and to observe constantly the patient’s vital signs, airway patency, cardiovascular and neurological status, and adequacy of ventilation.2 In addition to the anesthesia care provider, the operating dentist and other staff shall be trained in emergency procedures. It is the obligation of treating practitioners, when employing anesthesia personnel to administer deep sedation/general anesthesia, to verify their credentials and experience. 1. The anesthesia care provider must be a licensed dental and/or medical practitioner with appropriate and current state certification for deep sedation/general anesthesia. 2. The anesthesia care provider must have completed a 1- or 2-year dental anesthesia residency or its equivalent, as approved by the American Dental Association (ADA), and/ or medical anesthesia residency, as approved by the American Medical Association (AMA). 3. The anesthesia care provider currently must be licensed by and in compliance with the laws of the state in which he/ she practices. Laws vary from state to state and may supercede any portion of this document. 4. If state law permits a certified registered nurse anesthetist or anesthesia assistant to function under the supervision of a dentist, the dentist is required to have completed training in deep sedation/general anesthesia and be licensed or permitted, as appropriate to state law. The dentist and anesthesia care provider must be compliant with the AAP/AAPD’s Guideline on Monitoring and Management of Pediatric Patients During and After Sedation for Diagnostic and Therapeutic Procedures2 or other appropriate guideline(s) of the ADA, AMA, and their recognized specialties. The recommendations in this document may be exceeded at any time if the change involves improved safety and is supported by currently-accepted practice and/or is evidence-based. The dentist and anesthesia personnel must work together to enhance patient safety. Effective communication is essential. The dentist introduces the concept of deep sedation/general anesthesia to the parent and provides appropriate preoperative instructions and informational materials. The dentist or his/her designee coordinates medical consultations when necessary. The anesthesia care provider explains potential risks and obtains informed consent for sedation/anesthesia. Office staff should understand their additional responsibilities and special considerations (eg, loss of protective reflexes) associated with office-based deep sedation/general anesthesia. Advanced training in recognition and management of pediatric emergencies is critical in providing safe sedation and anesthetic care. Although it is appropriate for the most experienced professional (ie, the anesthesia provider) to assume responsibility in managing anesthesia-related emergencies, the operating dentist and clinical staff need to maintain current
expertise in basic life support. An individual experienced in recovery care must be in attendance in the recovery facility until the patient, through continual monitoring, exhibits respiratory and cardiovascular stability and appropriate discharge criteria2 have been met. In addition, the staff of the treating dentist must be well-versed in rescue and emergency protocols (including cardiopulmonary resuscitation) and have contact numbers for emergency medical services and ambulance services. Emergency preparedness must be updated and practiced on a regular basis. Facilities A continuum exists that extends from wakefulness across all levels of sedation. Often these levels are not easily differentiated, and patients may drift through them. When anesthesia care providers are utilized for office-based administration of deep sedation or general anesthesia, the facilities in which the dentist practices must meet the guidelines and appropriate local, state, and federal codes for administration of the deepest possible level of sedation/anesthesia. Facilities also should comply with applicable laws, codes, and regulations pertaining to controlled drug storage, fire prevention, building construction and occupancy, accommodations for the disabled, occupational safety and health, and disposal of medical waste and hazardous waste.3 The treatment room must accommodate the dentist and auxiliaries, the patient, the anesthesia care provider, the dental equipment, and all necessary anesthesia delivery equipment along with appropriate monitors and emergency equipment. Expeditious access to the patient, anesthesia machine (if present), and monitoring equipment should be available at all times. It is beyond the scope of this document to dictate equipment necessary for the provision of deep sedation/general anesthesia, but equipment must be appropriate for the technique used and consistent with the guidelines for anesthesia providers, in accordance with governmental rules and regulations. Because laws and codes vary from state to state, the Guideline on Monitoring and Management of Pediatric Patients During and After Sedation for Diagnostic and Therapeutic Procedures2 should be followed as the minimum requirements. For deep sedation, there shall be continuous monitoring of oxygen saturation and heart rate and intermittent time-based recording of respiratory rate and blood pressure. When adequacy of ventilation is difficult to observe, use of a precordial stethoscope or capnograph is encouraged.2 An electrocardiographic monitor should be readily available for patients undergoing deep sedation. In addition to the monitors previously mentioned, a temperature monitor and pediatric defibrillator are required for general anesthesia.2 Emergency equipment must be readily accessible and should include suction, drugs necessary for rescue and resuscitation (including 100% oxygen capable of being delivered by positive pressure at appropriate flow rates for up to 1 hour), and age-/ size-appropriate equipment to resuscitate and rescue a nonbreathing and/or unconscious pediatric dental patient and provide continuous support while the patient is being transported to a medical facility.2,7 The treatment facility should
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have medications, equipment, and protocols available to treat malignant hyperthermia when triggering agents are used.3 Recovery facilities must be available and suitably equipped. Back up power sufficient to ensure patient safety should be available in case of an emergency.3 Documentation Prior to delivery of deep sedation/general anesthesia, patient safety requires that appropriate documentation shall address rationale for sedation/general anesthesia, informed consent, instructions to parent, dietary precautions, preoperative health evaluation, and any prescriptions along with the instructions given for their use.2 Because laws and codes vary from state to state, the Guideline on Monitoring and Management of Pediatric Patients During and After Sedation for Diagnostic and Therapeutic Procedures2 should be followed as minimum requirements for a time-based anesthesia record. 1. Vital signs: Pulse and respiratory rates, blood pressure, and oxygen saturation must be monitored and recorded at least every 5 minutes2 throughout the procedure and at specific intervals until the patient has met documented discharge criteria. 2. Drugs: Name, dose, route, site, time of administration, and patient effect of all drugs, including local anesthesia, must be documented. When anesthetic gases are administered, inspired concentration and duration of inhalation agents and oxygen shall be documented. 3. Recovery: The condition of the patient, that discharge criteria have been met, time of discharge, and into whose care the discharge occurred must be documented. Requiring the signature of the responsible adult to whom the child has been discharged, verifying that he/she has received and understands the post-operative instructions, is encouraged. Various business/legal arrangements may exist between the treating dentist and the anesthesia provider. Regardless, because services were provided in the dental facility, the dental staff must maintain all patient records, including time-based anesthesia records, so that they may be readily available for emergency or other needs. The dentist must assure that the anesthesia provider also maintains patient records and that they are readily available. Risk management and quality assurance Dentists who utilize in-office anesthesia care providers must take all necessary measures to minimize risk to patients. The dentist must be familiar with the American Society of Anesthesiologists (ASA) physical status classification. Knowledge, preparation, and communication between professionals are essential.8 Prior to subjecting a patient to deep sedation/general
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anesthesia, the patient must undergo a preoperative health evaluation.2,9 High-risk patients should be treated in a facility properly equipped to provide for their care.2,9 The dentist and anesthesia care provider must communicate during treatment to share concerns about the airway or other details of patient safety. Furthermore, they must work together to develop and document mechanisms of quality assurance. Untoward and unexpected outcomes must be reviewed to monitor the quality of services provided. This will decrease risk, allow for open and frank discussions, document risk analysis and intervention, and improve the quality of care for the pediatric dental patient.
References 1. American Academy of Pediatric Dentistry. Guideline on behavior guidance for the pediatric dental patient. Pediatr Dent 2008;30(suppl):125-33. 2. American Academy of Pediatrics, American Academy of Pediatric Dentistry. Guideline for monitoring and management of pediatric patients during and after sedation for diagnostic and therapeutic procedures. Pediatr Dent 2008;30(suppl):143-59. 3. A merican Society of Anesthesiologists. Guidelines for office-based anesthesia. 2004. Available at: “http://www. asahq.org/publicationsAndServices/standards/12.pdf ”. Accessed April 20, 2009. 4. American Dental Association. Policy statement: The use of conscious sedation, deep sedation, and general anesthesia in dentistry. 2005. Available at: “http://www.ada.org/ prof/resources/positions/statements/useof.asp”. Accessed April 20, 2009. 5. Nick D, Thompson L, Anderson D, Trapp L. The use of general anesthesia to facilitate dental treatment. Gen Dent 2003;51:464-8. 6. Wilson S. Pharmacologic behavior management for pediatric dental treatment. Pediatr Clinic North Am 2000;47 (5):1159-73. 7. American Society of Anesthesiologists. Guidelines for ambulatory anesthesia and surgery. 2003. Available at: “http://www.asahq.org/publicationsAndServices/standards/ 04.pdf ”. Accessed April 20, 2009. 8. American Society of Anesthesiologists. ASA physical status classification system. Available at: “http://www.asahq. org/clinical/physicalstatus.htm”. Accessed June 24, 2009. 9. American Dental Association. Guidelines for the use of conscious sedation, deep sedation, and general anesthesia for dentists. 2005. Available at: “http://www.ada.org/ prof/resources/positions/statements/anesthesia_guidelines. pdf ”. Accessed April 20, 2009.
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Guideline on Pediatric Restorative Dentistry Originating Committee
Clinical Affairs Committee – Restorative Dentistry Subcommittee Review Council Council on Clinical Affairs
Adopted 1991
Revised 1998, 2001, 2004, 2008
Purpose The American Academy of Pediatric Dentistry (AAPD) presents this guideline to assist the practitioner in the restorative care of infants, children, adolescents, and persons with special health care needs. The objectives of restorative treatment are to repair or limit the damage from caries, protect and preserve the tooth structure, reestablish adequate function, restore esthetics (where applicable), and provide ease in maintaining good oral hygiene. Pulp vitality should be maintained whenever possible.
Methods The AAPD convened a consensus conference on pediatric restorative dentistry in April, 2002. Consensus statements resulted from the expert literature review and science-based position papers presented.1 Results of the conference, updated literature review, MEDLINE searches using the terms “dental amalgam”, “dental composites”, “stainless steel crowns”, “glass ionomer cements”, and “dental sealants”, and expert opinion were used to revise these guidelines.
Background Restorative treatment is based upon the results of an appropriate clinical examination and is ideally part of a comprehensive treatment plan. The treatment plan shall take into consideration: 1. developmental status of the dentition; 2. caries-risk assessment2,3; 3. patient’s oral hygiene; 4. anticipated parental compliance and likelihood of timely recall; 5. patient’s ability to cooperate for treatment. The restorative treatment plan must be prepared in conjunction with an individually-tailored preventive program. Caries risk is greater for children who are poor, rural, or minority or who have limited access to care.4 Factors for high caries risk include decayed/missing/filled surfaces greater than the child’s age, numerous white spot lesions, high levels of mutans streptococci, low socioeconomic status, high caries rate in siblings/parents, diet high in sugar, and/or presence of dental appliances.5 Studies
have reported that maxillary primary anterior caries has a direct relationship with caries in primary molars6-8, and caries in the primary dentition is highly predictive of caries occurring in the permanent dentition.5 Restoration of primary teeth differs from restoration of permanent teeth, due in part to the differences in tooth morphology. The mesiodistal diameter of a primary molar crown is greater than the cervicoocclusal dimension. The buccal and lingual surfaces converge toward the occlusal. The enamel and dentin are thinner. The cervical enamel rods slope occlusally, ending abruptly at the cervix instead of being oriented gingivally, gradually becoming thinner as in permanent teeth. The pulp chambers of primary teeth are proportionately larger and closer to the surface. Primary teeth contact areas are broad and flattened rather than being a small distinct circular contact point, as in permanent teeth. Shorter clinical crown heights of primary teeth also affect the ability of these teeth to adequately support and retain intracoronal restorations. Young permanent teeth also exhibit characteristics that need to be considered in restorative procedures, such as large pulp chambers and broad contact areas that are proximal to primary teeth. Tooth preparation should include the removal of caries or improperly developed tooth structure to establish appropriate outline, resistance, retention, and convenience form compatible with the restorative material to be utilized. Rubber-dam isolation should be utilized when possible during the preparation and placement of restorative materials. As with all guidelines, it is expected that there will be exceptions to the recommendations based upon individual clinical findings. For example, stainless steel crowns (SSCs) are recommended for teeth having received pulp therapy. However, an amalgam or resin restoration could be utilized in a tooth having conversative pulpal access, sound lateral walls, and less than 2 years to exfoliation. 9 Likewise, a conservative Class II restoration for a primary tooth could be expanded to include more surface area when the tooth is expected to exfoliate within 1 to 2 years.
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Recommendations Dentin/enamel adhesives Dentin/enamel adhesives allow bonding of resin-based composites and compomers to primary and permanent teeth. Adhesives have been developed with reported dentin bond strengths exceeding that of enamel.10-12 In vitro studies have shown that enamel and dentin bond strength is similar for primary and permanent teeth.7-14 The clinical success of adhesives allows for more conservative preparation when using composite restorative materials. Adhesive systems currently follow either a “total-etch” or a “self-etch” technique. Total etch technique requires 3 steps. It involves use of an etchant to prepare the enamel while opening the dentinal tubules, removing the smear layer, and decalcifying the dentin. After rinsing the etchant, a primer is applied that penetrates the dentin, preparing it for the bonding agent. The enamel can be dried before placing the primer, but the dentin should remain moist. A bonding agent then is applied to the primed dentin. A simplified adhesive system that combines the primer and the adhesive is available. Because the adhesive systems require multiple steps, errors in any step can affect clinical success. Attention to proper technique for the specific adhesive system is critical to success.15 Recommendations: The dental literature supports the use of tooth bonding adhesives, when used according to the manufacturer’s instruction unique for each product, as being effective in primary and permanent teeth in enhancing retention of restorations, minimizing microleakage, and reducing sensitivity.16 Pit and fissure sealants Sealant has been described as a material placed into the pits and fissures of caries-susceptible teeth that micromechanically bonds to the tooth preventing access by cariogenic bacteria to their source of nutrients.17 Pit and fissure caries account for approximately 80-90% of all caries in permanent posterior teeth and 44% in primary teeth.18,19 Sealants reduce the risk of caries in those susceptible pits and fissures. Placement of resin-based sealants in children and adolescents have shown a reduction of caries incidence of 86% after 1 year and 58% after 4 years.20,21 Before sealants are placed, a tooth’s caries risk should be determined.22 Any primary or permanent tooth judged at risk would benefit from sealant application.22 The best evaluation of caries risk is done by an experienced clinician using indicators of tooth morphology, clinical diagnostics, caries history, fluoride history, and oral hygiene.22 Sealant placement on teeth with the highest risk will give the greatest benefit.22 High-risk pits and fissures should be sealed as soon as possible. Low-risk pits and fissures may not require sealants. Caries risk, however, may increase due to changes in patient habits, oral microflora, or physical condition, and unsealed teeth subsequently might benefit from sealant application.22 With appropriate diagnosis and monitoring, sealants can be placed on teeth exhibiting incipient pit and fissure caries.23 Studies have shown arrested caries and elimination of viable organisms under sealants or restorations with sealed margins.24-26 Surveys
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have shown that pediatric dentists often incorporate enameloplasty into the sealant technique.27 In vitro studies have shown enameloplasty may enhance retention of sealants.28-31 However, short-term clinical studies show enameloplasty as equal to but not better than sealant placement without enameloplasty.32,33 Isolation is a key factor in a sealant’s clinical success.34 Contamination with saliva results in decreased bond strength of the sealant to enamel.34 In vitro and in vivo studies report that use of a bonding agent will improve the bond strength and minimize microleakage.35,36 Fluoride application immediately prior to etching for sealant placement does not appear to affect bond strength adversely.37,38 Sealants must be retained on the tooth and should be monitored to be most effective. Studies have shown glass ionomer sealant to have a poor retention rate.39,40 Studies incorporating recall and maintenance have reported sealant success levels of 80% to 90% after 10 or more years.41,42 Recommendations: 1. Sealants should be placed into pits and fissures of teeth based upon the patient’s caries risk, not the patient’s age or time lapsed since tooth eruption. 2. Sealants should be placed on surfaces judged to be at high risk or surfaces that already exhibit incipient carious lesions to inhibit lesion progression. Follow up care, as with all dental treatment, is recommended.22 3. Sealant placement methods should include careful cleaning of the pits and fissures without removal of any appreciable enamel. Some circumstances may indicate use of a minimal enameloplasty technique.22 4. A low-viscosity hydrophilic material bonding layer, as part of or under the actual sealant, is recommended for long-term retention and effectiveness.22 5. Glass ionomer materials could be used as transitional sealants.22 Glass ionomer cements Glass ionomers have been used as restorative cements, cavity liner/ base, and luting cement. The initial glass ionomer materials were difficult to handle, exhibited poor wear resistance, and were brittle. Advancements in glass ionomer formulation led to better properties, including the formation of resin-modified glass ionomers. These products showed improvement in handling characteristics, decreased setting time, increased strength, and improved wear resistance.43,44 Glass ionomers have several properties that make them favorable to use in children: 1. chemical bonding to both enamel and dentin; 2. thermal expansion similar to that of tooth structure; 3. biocompatibility; 4. uptake and release of fluoride; 5. decreased moisture sensitivity when compared to resins. Glass ionomers are hydrophilic and tolerate a moist, not wet, environment, whereas resins and adhesives are affected adversely by water. Because of their ability to adhere, seal, and protect, glass ionomers often are used as dentin replacement materials.45-47
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Glass ionomer has a coefficient of thermal expansion similar to dentin. Resin-modified glass ionomers have improved wear resistance compared to the original glass ionomers and are appropriate restorative materials for primary teeth.48-52 In permanent teeth, resin-based composites provide better esthetics and wear resistance than glass ionomers. Glass ionomer and resin “sandwich technique” was developed on the basis of the best physical properties of each.53 A glass ionomer is used as dentin replacement for its ability to seal and adhere while covered with a surface resin because of its better wear resistance and esthetics. Fluoride is released from glass ionomer and taken up by the surrounding enamel and dentin, resulting in a tooth that is less susceptible to acid challenge.54-56 Studies have shown that fluoride release can occur for at least 5 years.57,58 Glass ionomers can act as a reservoir of fluoride, as uptake can occur from dentifrices, mouthrinses, and topical fluoride applications.59,60 This fluoride protection, useful in patients at high risk for caries, has led to the use of glass ionomers as a luting cement for SSCs, space maintainers, and orthodontic bands.61,62 Other applications of glass ionomers where fluoride release has advantages are for interim therapeutic restorations (ITR) and the alternative (atraumatic) restorative technique (ART). These procedures have similar techniques but different therapeutic goals. ITR may be used in very young patients63, uncooperative patients, or patients with special health care needs64 for whom traditional cavity preparation and/or placement of traditional dental restorations are not feasible or need to be postponed. Additionally, ITR may be used for caries control in children with multiple open carious lesions, prior to definitive restoration of the teeth.65 ART, endorsed by the World Health Organization and the International Association for Dental Research, is a means of restoring and preventing caries in populations that have little access to traditional dental care and necessarily functions as definitive treatment. These procedures involve the removal of soft tooth tissue using hand or slow-speed rotary instruments with caution to not expose the pulp when caries is deep. Leakage of the restoration can be minimized if unsound tooth structure is removed from the periphery of the preparation. Following preparation, the tooth is restored with an adhesive restorative material, such as selfsetting or resin-modified glass ionomer cement.64,65 This technique has been shown to reduce the levels of oral bacteria (eg, mutans streptococci, lactobacilli) in the oral cavity.62,64 Success is greatest when the technique is applied to single- or small 2-surface restorations.52,66 Inadequate cavity preparation with subsequent lack of retention and insufficient bulk can lead to failure.64 Recommendations: Glass ionomers can be recommended67 as: 1. luting cements; 2. cavity base and liner; 3. Class I, II, III, and V restorations in primary teeth; 4. Class III and V restorations in permanent teeth in high risk patients or teeth that cannot be isolated;
5.
caries control with: a. high-risk patients; b. restoration repair; c. ITR; d. ART.
Resin-based composites Resin-based composite is an esthetic restorative material used for posterior and anterior teeth. There are a variety of resin products on the market, with each having different physical properties and handling characteristics based upon their composition. “Resinbased composites are classified according to their filler size, because filler size affects polishability/esthetics, polymerization depth, polymerization shrinkage, and physical properties.”68 Microfilled resins have filler sizes less than 0.1 micron. Minifilled particle sizes range from 0.1 to 1 microns. Midsize resin particles range from 1 to 10 microns. Macrofilled particles range from 10 to 100 microns. The smaller filler particle size allows greater polishability and esthetics, while larger size provides strength. Hybrid resins combine a mixture of particle sizes for improved strength while retaining esthetics. Flowable resins have a lower volumetric filler percentage than hybrid resins. Highly-filled, small particle resins have been shown to have better wear characteristics.69-71 Resin-based composites allow the practitioner to be conservative in tooth preparation. With minimal pit and fissure caries, the carious tooth structure can be removed and restored while avoiding the traditional “extension for prevention” removal of healthy tooth structure. This technique of restoration with preventive sealing of the remaining tooth has been described as a preventive resin restoration.72 Resins require longer time for placement and are more technique sensitive than amalgams. In cases where isolation or patient cooperation is compromised, resin-based composite may not be the restorative material of choice. Recommendations73: Indications: Resin-based composites are indicated for: 1. Class I pit-and-fissure caries where conservative pre ventive resin restorations are appropriate; 2. Class I caries extending into dentin; 3. Class II restorations in primary teeth that do not ex tend beyond the proximal line angles; 4. Class II restorations in permanent teeth that extend approximately one third to one half the buccolingual intercuspal width of the tooth; 5. Class III, IV, V restorations in primary and permanent teeth; 6. strip crowns in the primary and permanent dentitions. Contraindications: Resin-based composites are not the restorations of choice in the following situations: 1. where a tooth cannot be isolated to obtain moisture control; 2. in individuals needing large multiple surface restora tions in the posterior primary dentition; clinical guidelines
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in high-risk patients who have multiple caries and/or tooth demineralization and who exhibit poor oral hygiene and compliance with daily oral hygiene, and when maintenance is considered unlikely.
Amalgam restorations Dental amalgam has been used for restoring teeth since the 1880s. Amalgam’s properties (eg, ease of manipulation, durability, relatively low cost, reduced technique sensitivity compared to other restorative materials) have contributed to its popularity. Esthetics and improved tooth-color restorative materials, however, have led to a decrease in its use. The durability of amalgam restorations has been shown in numerous studies.74-76 Studies of defective restorations have indicated that operator error plays a significant role the restoration’s durability.77,78 For example, in Class II restorations where the proximal box is large and the intercuspal isthmus is narrow, the restoration is stressed and can result in fracture. In primary teeth, studies have shown that 3-surface mesial-occlusal-distal (MOD) restorations can be placed but that SSCs are more durable.79-80 In primary molars, the patient’s age can affect the restoration’s longevity. 72-76 In children age 4 or younger, SSCs had a success rate twice that of amalgams. 74 The decision to use amalgam should be based upon the needs of each individual patient. Amalgam restorations often require removal of healthy tooth structure to achieve adequate resistance and retention. Glass ionomer or resin restorative materials might be a better choice for conservative restorations, thereby retain-ing healthier tooth structure. SSCs are recommended for primary teeth with pulpotomies. Yet, a Class I amalgam could be appropriate if enamel walls can withstand occlusal forces and the tooth is expected to exfoliate within 2 years.9 SSCs may be the better choice in patients with poor compliance and questionable long-term follow-up.81 Recommendations: Dental amalgam is recommended82 for: 1. Class I restorations in primary and permanent teeth; 2. Class II restorations in primary molars where the pre paration does not extend beyond the proximal line angles; 3. Class II restorations in permanent molars and pre molars; 4. Class V restorations in primary and permanent poste rior teeth. Stainless steel crown restorations Stainless steel crowns are prefabricated crown forms that are adapted to individual teeth and cemented with a biocompatible luting agent. “The SSC is extremely durable, relatively inexpensive, subject to minimal technique sensitivity during placement, and offers the advantage of full coronal coverage.”83 SSCs have been indicated for the restoration of primary and permanent teeth with caries, cervical decalcification, and/or developmental defects (eg, hypoplasia, hypocalcification), when failure of other available restorative materials is likely (eg, interproximal
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caries extending beyond line angles, patients with bruxism), following pulpotomy or pulpectomy, for restoring a primary tooth that is to be used as an abutment for a space maintainer, or for the intermediate restoration of fractured teeth. In high caries-risk children, definitive treatment of primary teeth with SSCs is better over time than multisurface intracoronal restorations. Review of the literature comparing SSCs and Class II amalgams concluded that, for multisurface restorations in primary teeth, SSCs are superior to amalgams.84 SSCs have a success rate greater than that of amalgams in children under age 4.76 The use of SSCs also should be considered in patients with increased caries risk whose cooperation is affected by age, behavior, or medical history. These patients often receive treatment under sedation or general anesthesia. For patients whose developmental or medical problems will not improve with age, SSCs are likely to last longer and possibly decrease the frequency for sedation or general anesthesia with its increased costs and its inherent risks. SSCs can be indicated to restore anterior teeth in cases where multiple surfaces are carious, where there is incisal edge involvement, following pulp therapy, when hypoplasia is present, and when there is poor moisture control.85 Where esthetics are a concern, the facing can be removed and replaced with a resinbased composite (open-faced technique). Several brands of primary SSCs are available with preformed tooth-colored veneers. These veneered SSCs can be more difficult to adapt and are subject to fracture or loss of the facing. Recommendations: 1. “Children at high risk exhibiting anterior tooth caries and/or molar caries may be treated with SSCs to pro tect the remaining at-risk tooth surfaces. 2. Children with extensive decay, large lesions, or multiple-surface lesions in primary molars should be treated with SSCs. 3. Strong consideration should be given to the use of SSCs in children who require general anesthesia.”83 Labial resin or porcelain veneer restorations A resin or porcelain veneer restoration is a thin layer of restorative material bonded over the facial or buccal surface of a tooth. Veneer restorations are considered conservative in that minimal, if any, tooth preparation is required. Porcelain veneers usually are placed on permanent teeth. Recommendations: Veneers may be indicated for the restoration of anterior teeth with fractures, developmental defects, intrinsic discoloration, and/or other esthetic conditions.86 Full-cast or porcelain-fused-to-metal crown restorations A cast or porcelain-fused-to-metal crown is a fixed restoration that employs metal formed to a desired anatomic shape or a metal substructure onto which a ceramic porcelain veneer is fused. The crown is cemented with a biocompatible luting cement.
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Recommendations: Full-cast metal crowns or porcelain-fused-to-metal crown restorations may be utilized in permanent teeth that are fully erupted and the gingival margin is at the adult position for: 1. teeth having developmental defects, extensive carious or traumatic loss of structure, or endodontic treatment; 2. as an abutment for fixed prostheses; or 3. for restoration of single-tooth implants.87-89 Fixed prosthetic restorations for missing teeth A fixed prosthetic restoration replaces 1 or more missing teeth in the primary, transitional, or permanent dentition. This restoration attaches to natural teeth, tooth roots, or implants and is not removable by the patient. Growth must be considered when using fixed restorations in the developing dentition. Recommendations: Fixed prosthetic restorations to replace 1 or more missing teeth may be indicated to: 1. establish esthetics; 2. maintain arch space or integrity in the developing dentition; 3. prevent or correct harmful habits; or 4. improve function.90,91 Removable prosthetic appliances A removable prosthetic appliance is indicated for the replacement of 1 or more teeth in the dental arch to restore masticatory efficiency, prevent or correct harmful habits or speech abnormalities, maintain arch space in the developing dentition, or obturate congenital or acquired defects of the orofacial structures. Recommendations: Removable prosthetic appliances may be indicated in the primary, mixed, or permanent dentition when teeth are missing. Removable prosthetic appliances may be utilized to: 1. maintain space; 2. obturate congenital or acquired defects; 3. establish esthetics or occlusal function; or 4. facilitate infant speech development or feeding.92-94
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41. Simonsen RJ. Retention and effectiveness of dental sealant after 15 years. J Am Dent Assoc 1991;122(10):34-42. 42. Romcke RG, Lewis, DW Maze BD, Vickerson RA. Retention and maintenance of fissure sealants over 10 years. J Can Dent Assoc 1990;56(3):235-7. 43. Mitra SB, Kedrowski BL. Long-term mechanical properties of glass ionomers. Dent Mater 1994:10(2):78-82. 44. Douglas WH, Lin CP. Strength of the new systems. In: Hunt PR, ed. Glass Ionomers: The Next Generation. Philadelphia, Pa: International Symposia in Dentistry, PC; 1994:209-16. 45. Quackenbush BM, Donly KJ, Croll TP. Solubility of a resin-modified glass ionomer cement. ASDC J Dent Child 1998;65(5):310-2, 354. 46. Kerby RE, Knobloch L, Thakur A. Strength properties of visible light-cured, resin-modified glass ionomer cements. Oper Dent 1997;22(2):79-83. 47. Croll TP. Visible light-hardened glass-ionomer cement base/liner as an interim restorative material. Quintessence Int 1991;22(2):137-41. 48. Welbury RR, Shaw AJ, Murray JJ, Gordon PH, McCabe JF. Clinical evaluation of paired compomer and glass ionomer restorations in primary molars: Final results after 42 months. Br Dent J 2000;189(2):93-7. 49. Vilkinis V, Hörsted-Bindslev P, Baelum V. Two-year evaluation of Class II resin-modified glass ionomer cement/ composite open sandwich and composite restorations. Clin Oral Investig 2000;4(3):133-9. 50. Rutar J, McAllan L, Tyas MJ. Three-year clinical performance of glass ionomer cement in primary molars. Int J Paediatr Dent 2002;12(2):146-7. 51. Donly KJ, Segura A, Kanellis M, Erickson RL. Clinical performance and caries inhibition of resin-modified glass ionomer cement and amalgam restorations. J Am Dent Assoc 1999;130(10):1459-66. 52. Croll TP, Bar-Xion Y, Segura A, Donly KJ. Clinical performance of resin-modified glass ionomer cement restorations in primary teeth. A retrospective evaluation. J Am Dent Assoc 2001;132(8):1110-6. 53. Wilson AD, McLean JW. Laminate restorations. In: Glass Ionomer Cement. Chicago, Ill: Quintessence Publishing Co; 1988:159-78. 54. Tam LE, Chan GP, Yim D. In vitro caries inhibition effects by conventional and resin-modified glass ionomer restorations. Oper Dent 1997;22(1):4-14. 55. Scherer W, Lippman N, Kalm J, LoPresti J. Antimicrobial properties of VLC liners. J Esthet Dent 1990;2(2):31-2. 56. Tyas MJ. Cariostatic effect of glass ionomer cements: A 5year clinical study. Aust Dent J 1991;36(3):236-9. 57. Forsten L. Fluoride release from a glass ionomer cement. Scand J Dent Res 1977;85(6):503-4. 58. Swartz ML, Phillips RW, Clark HE. Long-term fluoride release from glass ionomer cements. J Dent Res 1984;63 (2):158-60. 59. Forsten L. Fluoride release and uptake by glass ionomers and related materials and its clinical effect. Biomaterials 1998;19(6):503-8.
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60. Donly KJ, Nelson JJ. Fluoride release of restorative materials exposed to a fluoridated dentifrice. ASDC J Dent Child 1997;64(4):249-50. 61. Donly KJ, Istre S, Istre T. In vitro enamel remineralization at orthodontic band margins cemented with glass ionomer cement. Am J Orthod Dentofacial Orthop 1995;107(5): 461-4. 62. Vorhies AB, Donly KJ, Staley RN, Wefel JS. Enamel demineralization adjacent to orthodontic brackets bonded with hybrid glass ionomer cements: An in vitro study. Am J Orthod Dentofacial Orthop 1998;114(6):668-74. 63. Wambier DS, dos Santos FA, Guedes-Pinto AC, Jaeger RG, Simionato MR. Ultrastructural and microbiological analysis of the dentin layers affected by caries lesions in primary molars treated by minimal intervention. Pediatr Dent 2007;29(3):228-34. 64. Mandari GJ, Frencken JE, van’ t Hof MA. Six year success rates of occlusal amalgam and glass ionomer restorations placed using three minimal intervention approaches. Caries Res 2003;37(4):246-53. 65. Dulgergil DT, Soyman M, Civelek A. Atraumatic restorative treatment with resin-modified glass ionomer material: Short-term results of a pilot study. Med Princ Pract 2005;14(3):277-80. 66. Ersin NK, Candan U, Aykut A, Oncag O, Eronat E, Kose T. A clinical evaluation of resin-based composite and glass ionomer cement restorations placed in primary teeth using the ART approach: Results at 24 months. J Am Dent Assoc 2006;137(11):1529-36. 67. Berg JH. Glass ionomer cements. Pediatr Dent 2002;24 (5):430-8. 68. Burgess JO, Walker R, Davidson JM. Posterior resin-based composite: Review of the literature. Pediatr Dent 2002; 24(5):465-79. 69. Pallav P, de Gee AJ, Davidson CL. The influence of admixing microfiller to small-particle composite resins on wear, tensil strength, hardness and surface roughness. J Dent Res 1989;68(3):489-90. 70. Robertson TM, Bayne SC, Taylor DF, Sturdevant JR. Five-year clinical wear analysis of 19 posterior composites [abstract No. 63]. J Dent Res 1988;67:120. 71. Bayne SC, Taylor DF, Wilder AD, Heymann HO, Tangen CM. Clinical longevity of 10 posterior composite materials based on wear [abstract No. 630]. J Dent Res 1991; 70:344. 72. Simonsen RJ. Preventive resin restorations: Three-year results. J Am Dent Assoc 1980;100(4):535-9. 73. Donly KJ, García-Godoy F. The use of resin-based composite in children. Pediatr Dent 2002;24(5):480-8. 74. Levering NJ, Messer LB. The durability of primary molar restorations: I. Observations and predictions of success of amalgams. Pediatr Dent 1988;10(2):74-80. 75. Hunter B. Survival of dental restorations in young patients. Community Dent Oral Epidemiol 1985;18(5): 285-7.
76. Holland IS, Walls AW, Wallwork MA, Murray JJ. The longevity of amalgam restorations in deciduous molars. Br Dent J 1986;161(7):255-8. 77. Dahl DE, Ericksen HM. Reasons for replacement amalgam dental restorations. Scand J Dent Res 1978;86(5):404-7. 78. Roberts JF, Sheriff M. The fate on survival of amalgam and preformed crown molar restorations placed in a specialist paediatric dental practice. Br Dent J 1990;169(8):237-44. Erratum in Br Dent J 1990;169(9):285. 79. Waggoner WF. Restorative dentistry for the primary dentition. In: Pinkham J, Casamassimo PS, Fields HW Jr, McTigue DJ, Nowak AJ, eds. Pediatric Dentistry: Infancy Through Adolescence. 4th ed. St. Louis: Elsevier/Saunders; 2005:341-74. 80. Randall RC, Vrijhoef MA, Wilson NH. Efficacy of preformed metal crowns vs amalgam restorations in primary molars: A systematic review. J Am Dent Assoc 2000;131 (3):337-43. 81. Seale NS. Stainless steel crowns in pediatric dentistry. In: Pinkham J, Casamassimo PS, Fields HW Jr, McTigue DJ, Nowak AJ, eds. Pediatric Dentistry: Infancy Through Adolescence. 4th ed. St. Louis: Elsevier/Saunders; 2005:361-2. 82. Fuks AB. The use of amalgam in pediatric dentistry. Pediatr Dent 2002;24(5):448-55. 83. Seale NS. The use of stainless steel crowns. Pediatr Dent 2002;24(5):501-5. 84. Randall RC. Preformed metal crowns for primary and permanent molar teeth: Review of the literature. Pediatr Dent 2002;24(5):489-500. 85. Waggoner WF. Restoring primary anterior teeth. Pediatr Dent 2002;24(5):511-6. 86. Horn HR. Porcelain laminate veneers bonded to etched enamel. Dent Clin North Am 1983;27(4):671-84. 87. Simonsen R, Thompson V, Barrack G. Etched Cast Restorations: Clinical and Laboratory Techniques. Quintessence Publishing: Chicago Ill; 1983. 88. Creugers NHJ, van’t Hof MA, Vrijhoef MMA. A clinical comparison of 3 types of resin-retained cast metal prostheses. J Prosthet Dent 1986;56(3):297-300. 89. McLaughlin G. Porcelain fused to tooth: A new esthetic and reconstructive modality. Compend Contin Educ Dent 1984;5(5):430-5. 90. Thompson VP, Livaditis GJ. Etched casting acid etch composite bonded posterior bridges. Pediatr Dent 1982;4 (1):38-43. 91. Wood M, Thompson VP. Anterior etched cast resin-bonded retainer: An overview of design, fabrication, and clinical use. Compend Contin Educ Dent 1983;4(3):247-56, 258. 92. Winstanley RB. Prosthodontic treatment of patients with hypodontia. J Prosthet Dent 1984;52(5):687-91. 93. Abadi BJ, Kimmel NA, Falace DA. Modified overdentures for the management of oligodontia and developmental defects. ASDC J Dent Child 1982;49(2):123-6. 94. Nayar AK, Latta JB, Soni NN. Treatment of dentinogenesis imperfecta in a child: Report of a case. ASDC J Dent Child 1981;48(6):453-5. clinical guidelines
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Guideline on Pulp Therapy for Primary and Immature Permanent Teeth Originating Committee
Clinical Affairs Committee – Pulp Therapy Subcommittee Review Council Council on Clinical Affairs
Adopted 1991
Revised 1998, 2001, 2004, 2009
Purpose The American Academy of Pediatric Dentistry (AAPD) intends this guideline to aid in the diagnosis of pulp health versus pathosis and to set forth the indications, objectives, and therapeutic interventions for pulp therapy in primary and immature permanent teeth.
Methods This revision included a new systematic literature search of the MEDLINE/Pubmed electronic data base using the following parameters: Terms: “pulpotomy”, “pulpectomy”, “indirect pulp treatment”, “stepwise excavation”, “pulp therapy”, “pulp capping”, “pulp exposure”, “bases”, “liners”, “calcium hydroxide”, “formocresol”, “ferric sulfate”, “gluteraldehyde pulpotomies”, “glass ionomer”, “mineral trioxide aggregate” (MTA), “bacterial microleakage under restorations”, “dentin bonding agents”, “resin modifies glass ionomers” (RMGI’s), and “endodontic irrigants”; Fields: all fields, Limits: within the last 10 years, humans, English, and clinical trials. Papers for review were chosen from the resultant lists and from hand searches. When data did not appear sufficient or were inconclusive, recommendations were based upon expert and/or consensus opinion including those from the 2007 joint symposium of the AAPD and the American Association of Endodontists (AAE) titled “Emerging Science in Pulp Therapy: New Insights into Dilemmas and Controversies” (Chicago, Ill).
Background The primary objective of pulp therapy is to maintain the integrity and health of the teeth and their supporting tissues. It is a treatment objective to maintain the vitality of the pulp of a tooth affected by caries, traumatic injury, or other causes. Especially in young permanent teeth with immature roots, the pulp is integral to continue apexogenesis. Long term retention of a permanent tooth requires a root with a favorable crown/root ratio and dentinal walls that are thick enough to withstand normal function. Therefore, pulp preservation is a primary goal for
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treatment of the young permanent dentition. A tooth without a vital pulp, however, can remain clinically functional.1 The indications, objectives, and type of pulpal therapy depend on whether the pulp is vital or nonvital, based on the clinical diagnosis of normal pulp (symptom free and normally responsive to vitality testing), reversible pulpitis (pulp is capable of healing), symptomatic or asymptomatic irreversible pulpitis (vital inflamed pulp is incapable of healing), or necrotic pulp.2 The clinical diagnosis3 is derived from a: 1. comprehensive medical history; 2. review of past and present dental history and treatment, including current symptoms and chief complaint; 3. subjective evaluation of the area associated with the current symptoms/chief complaint by questioning the child and parent on the location, intensity, duration, stimulus, relief, and spontaneity; 4. objective extraoral examination as well as examination of the intraoral soft and hard tissues; 5. if obtainable, radiograph(s) to diagnose pulpitis or ne crosis showing the involved tooth, furcation, periapical area, and the surrounding bone; and 6. clinical tests such as palpation, percussion, and mobility.1,4 In permanent teeth, electric pulp tests and thermal tests may be helpful.3 Teeth exhibiting signs and/or symptoms such as a history of spontaneous unprovoked toothache, a sinus tract, soft tissue inflammation not resulting from gingivitis or periodontitis, excessive mobility not associated with trauma or exfoliation, furcation/apical radiolucency, or radiographic evidence of internal/external resorption have a clinical diagnosis of irreversible pulpitis or necrosis. These teeth are candidates for nonvital pulp treatment.5,6 Teeth exhibiting provoked pain of short duration relieved with over-the-counter analgesics, by brushing, or upon the removal of the stimulus and without signs or symptoms of irreversible pulpitis, have a clinical diagnosis of reversible pulpitis and are candidates for vital pulp therapy. Teeth diag-
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nosed with a normal pulp requiring pulp therapy or with reversible pulpitis should be treated with vital pulp procedures.7-10
Recommendations All relevant diagnostic information, treatment, and treatment follow-up shall be documented in the patient’s record. Any planned treatment should include consideration of: 1. the patient’s medical history; 2. the value of each involved tooth in relation to the child’s overall development; 3. alternatives to pulp treatment; and 4. restorability of the tooth. When the infectious process cannot be arrested by the treatment methods included in this section, bony support cannot be regained, inadequate tooth structure remains for a restoration, or excessive pathologic root resorption exists, extraction should be considered.1,5,6 It is recommended that all pulp therapy be performed with rubber-dam or other equally effective isolation to minimize bacterial contamination of the treatment site. This guideline is intended to recommend the best currently-available clinical care for pulp treatment, but the AAPD encourages additional research for consistently successful and predictable techniques using biologically-compatible medicaments for vital and nonvital primary and immature permanent teeth. Pulp therapy requires periodic clinical and radiographic assessment of the treated tooth and the supporting structures. Post-operative clinical assessment generally should be performed every 6 months and could occur as part of a patient’s periodic comprehensive oral examinations. Patients treated for an acute dental infection initially may require more frequent clinical reevaluation. A radiograph of a primary tooth pulpectomy should be obtained immediately following the procedure to document the quality of the fill and to help determine the tooth’s prognosis. This image also would serve as a comparative baseline for future films (the type and frequency of which are at the clinician’s discretion). Radiographic evaluation of primary tooth pulpotomies should occur at least annually because the success rate of pulpotomies diminishes over time.11 Since failure of a primary molar pulpotomy may be evidenced in the furcation, posterior tooth pulpotomies should be monitored by radiographs that clearly demonstrate the interradicular area. Bitewing radiographs obtained as part of the patient’s periodic comprehensive examinations may suffice. If a bitewing radiograph does not display the interradicular area, a periapical image is indicated. Pulp therapy for immature permanent teeth should be reevaluate radiographically 6 and 12 months after treatment and then periodically at the discretion of the clinician. For any tooth that has undergone pulpal therapy, clinical signs and/or symptoms may prompt a clinician to select a more frequent periodicity of reassessment. Apexification, reimplantation of avulsions, and placement of prefabricated post and cores are not indicated for primary teeth. For endodontic procedures not included in this section, the AAPD supports the AAE’s Guide to Clinical Endodontics.12
Primary teeth Vital pulp therapy for primary teeth diagnosed with a normal pulp or reversible pulpitis Protective liner A protective liner is a thinly-applied liquid placed on the pulpal surface of a deep cavity preparation, covering exposed dentin tubules, to act as a protective barrier between the restorative material or cement and the pulp. Placement of a thin protective liner such as calcium hydroxide, dentin bonding agent, or glass ionomer cement is at the discretion of the clinician.13,14 • Indications: In a tooth with a normal pulp, when all caries is removed for a restoration, a protective liner may be placed in the deep areas of the preparation to minimize injury to the pulp, promote pulp tissue healing, and/or minimize postoperative sensitivity.15,16 • Objectives: The placement of a liner in a deep area of the preparation is utilized to preserve the tooth’s vitality, promote pulp tissue healing and tertiary dentin formation, and minimize bacterial microleakage.17,18 Adverse post-treatment clinical signs or symptoms such as sensitivity, pain, or swelling should not occur. Indirect pulp treatment Indirect pulp treatment is a procedure performed in a tooth with a deep carious lesion approximating the pulp but without signs or symptoms of pulp degeneration.1 The caries surrounding the pulp is left in place to avoid pulp exposure and is covered with a biocompatible material.19 A radiopaque liner such as a dentin bonding agent,20 resin modified glass ionomer,21,22 calcium hydroxide,23,24 zinc oxide/eugenol,24 or glass ionomer cement7,9,25-27 is placed over the remaining carious dentin to stimulate healing and repair. If calcium hydroxide is use, a glass ionomer or reinforced zinc oxide/eugenol material should be placed over it to provide a seal against microleakage since calcium hydroxide has a high solubility, poor seal, and low compressive strength.28-31 The use of glass ionomer cements or reinforced zinc oxide/eugenol restorative materials has the additional advantage of inhibitory activity against cariogenic bacteria.32,33 The tooth then is restored with a material that seals the tooth from microleakage. Interim therapeutic restorations (ITR) with glass ionomers can used for caries control in teeth with carious lesions that exhibit signs of reversible pulpitis. The ITR can be removed once the pulp’s vitality is determined and, if the pulp is vital, an indirect pulp cap can be performed.34,35 Current literature indicates that there is inconclusive evidence that it is necessary to reenter the tooth to remove the residual caries.36,37 As long as the tooth remains sealed from bacterial contamination, the prognosis is good for caries to arrest and reparative dentin to form to protect the pulp.32,33,36-40 Indirect pulp capping has been shown to have a higher success rate than pulpotomy in long term studies.7,9,20,22-27,35 It also allows for a normal exfoliation time. Therefore, indirect pulp treatment is preferable to a pulpotomy when the pulp is normal or has a diagnosis of reversible pulpitis.
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• Indications: Indirect pulp treatment is indicated in a primary tooth with no pulpitis18 or with reversible pulpitis when the deepest carious dentin is not removed to avoid a pulp exposure.8 The pulp is judged by clinical and radiographic criteria to be vital and able to heal from the carious insult.8,9 • Objectives: The restorative material should seal completely the involved dentin from the oral environment. The tooth’s vitality should be preserved. No post-treatment signs or symptoms such as sensitivity, pain, or swelling should be evident. There should be no radiographic evidence of pathologic external or internal root resorption or other pathologic changes. There should be no harm to the succedaneous tooth. Direct pulp cap When a pinpoint mechanical exposure of the pulp is encountered during cavity preparation or following a traumatic injury, a biocompatible radiopaque base such as mineral trioxide aggregate (MTA)41-44 or calcium hydroxide45 may be placed in contact with the exposed pulp tissue. The tooth is restored with a material that seals the tooth from microleakage.7 • Indications: This procedure is indicated in a primary tooth with a normal pulp following a small mechanical or traumatic exposure when conditions for a favorable response are optimal.41-45 Direct pulp capping of a carious pulp exposure in a primary tooth is not recommended.1 • Objectives: The tooth’s vitality should be maintained. No post-treatment signs or symptoms such as sensitivity, pain, or swelling should be evident. Pulp healing and reparative dentin formation should result. There should be no radiographic signs of pathologic external or progressive internal root resorption or furcation/apical radiolucency. There should be no harm to the succedaneous tooth. Pulpotomy A pulpotomy is performed in a primary tooth with extensive caries but without evidence of radicular pathology when caries removal results in a carious or mechanical pulp exposure. The coronal pulp is amputated, and the remaining vital radicular pulp tissue surface is treated with a long-term clinicallysuccessful medicament such as Buckley’s Solution of formocresol or ferric sulfate.46-52 Electrosurgery also has demonstrated success.53 Gluteraldehyde54,55 and calcium hydroxide50,52,56 have been used but with less long-term success. MTA is a more recent material used for pulpotomies with a high rate of success. Clinical trials show that MTA performs equal to or better than formocresol or ferric sulfate8,11,57-61 and may be the preferred pulpotomy agent in the future.61,62 After the coronal pulp chamber is filled with zinc/oxide eugenol or other suitable base, the tooth is restored with a restoration that seals the tooth from microleakage. The most effective long-term restoration has been shown to be a stainless steel crown. However, if there is sufficient supporting enamel remaining, amalgam or composite resin can provide a functional alternative when the primary tooth has a life span of 2 years or less.63-65
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• Indications: The pulpotomy procedure is indicated when caries removal results in pulp exposure in a primary tooth with a normal pulp or reversible pulpitis or after a traumatic pulp exposure.6 The coronal tissue is amputated, and the remaining radicular tissue is judged to be vital without suppuration, purulence, necrosis, or excessive hemorrhage that cannot be controlled by a damp cotton pellet after several minutes, and there are no radiographic signs of infection or pathologic resorption. • Objectives: The radicular pulp should remain asymptomatic without adverse clinical signs or symptoms such as sensitivity, pain, or swelling. There should be no postoperative radiographic evidence of pathologic external root resorption. Internal root resorption can be self limiting and stable. The clinician should monitor the internal resorption, removing the affected tooth if perforation causes loss of supportive bone and/or clinical signs of infection and inflammation.52,55,66-68 There should be no harm to the succedaneous tooth. Nonvital pulp treatment for primary teeth diagnosed with irreversible pulpitis or necrotic pulp Pulpectomy Pulpectomy is a root canal procedure for pulp tissue that is irreversibly infected or necrotic due to caries or trauma. The root canals are debrided and shaped with hand or rotary files. 21 Since instrumentation and irrigation with an inert solution alone cannot adequately reduce the microbial population in a root canal system, disinfection with irrigants such as 1% sodium hypochlorite and/or chlorhexidine is an important step in assuring optimal bacterial decontamination of the canals.68-70 Because it is a potent tissue irritant, sodium hypochlorite must not be extruded beyond the apex.71 After the canals are dried, a resorbable material such as nonreinforced zinc/oxideeugenol,5,72 iodoform-based paste (KRI),73 or a combination paste of iodoform and calcium hydroxide (Vitapex®, Endoflax®)74-76 is used to fill the canals. The tooth then is restored with a restoration that seals the tooth from microleakage. • Indications: A pulpectomy is indicated in a primary tooth with irreversible pulpitis or necrosis or a tooth treatment planned for pulpotomy in which the radicular pulp exhibits clinical signs of irreversible pulpitis (eg, excessive hemorrhage that is not controlled with a damp cotton pellet applied for several minutes) or pulp necrosis (eg, suppration, purulence). The roots should exhibit minimal or no resorption. • Objectives: Following treatment, the radiographic infectious process should resolve in 6 months, as evidenced by bone deposition in the pretreatment radiolucent areas, and pretreatment clinical signs and symptoms should resolve within a few weeks. There should be radiographic evidence of successful filling without gross overextension or underfilling.72,74,76 The treatment should permit resorption of the primary tooth root and filling material to permit normal eruption of the succedaneous tooth. There should be no pathologic root resorption or furcation/apical radiolucency.
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Young permanent teeth Vital pulp therapy for teeth diagnosed with a normal pulp or reversible pulpitis Protective liner A protective liner is a thinly-applied liquid placed on the pulpal surface of a deep cavity preparation, covering exposed dentin tubules, to act as a protective barrier between the restorative material or cement and the pulp. Placement of a thin protective liner such as calcium hydroxide, dentin bonding agent, or glass ionomer cement is at the discretion of the clinician.13,14 The liner must be followed by a well-sealed restoration to minimize bacterial leakage from the restoration-dentin interface.17,18 • Indications: In a tooth with a normal pulp, when caries is removed for a restoration, a protective liner may be placed in the deep areas of the preparation to minimize pulp injury, promote pulp tissue healing, and/or minimize postoperative sensitivity. • Objectives: The placement of a liner in a deep area of the preparation is utilized to preserve the tooth’s vitality, promote pulp tissue healing, and facilitate tertiary dentin formation. This liner must be followed by a well-sealed restoration to minimize bacterial leakage from the restoration-dentin interface.17,18 Adverse post-treatment signs or symptoms such as sensitivity, pain, or swelling should not occur. Indirect pulp treatment Indirect pulp treatment is a procedure performed in a tooth with a diagnosis of reversible pulpitis and deep caries that might otherwise need endodontic therapy if the decay was completely removed.6 In recent years, rather than complete the caries removal in 2 appointments, the focus has been to excavate as close as possible to the pulp, place a protective liner, and restore the tooth without a subsequent reentry to remove any remaining affected dentin.77-79 The risk of this approach is either an unintentional pulp exposure or irreversible pulpitis.78 More recently, the stepwise excavation of deep caries has been revisited70-82 and shown to be successful in managing reversible pulpitis without pulpal perforation and/or endodontic therapy.83 This approach involves a 2-step process. The first step is the removal of carious dentin along the dentin-enamel junction (DEJ) and excavation of only the outermost infected dentin, leaving a carious mass over the pulp. The objective is to change the cariogenic environment in order to decrease the number of bacteria, close the remaining caries from the biofilm of the oral cavity, and slow or arrest the caries development.83-85 The second step is the removal of the remaining caries and placement of a final restoration. The most common recommendation for the interval between steps is 3-6 months, allowing sufficient time for the formation of tertiary dentin and a definitive pulpal diagnosis. Critical to both steps of excavation is the placement of a well-sealed restoration.17,18 The decision to use a one-appointment caries excavation or a step-wise technique should be based on the individual patient circumstances since the research available is inconclusive on which approach is the most successful over time.36,37 • Indications: Indirect pulp treatment is indicated in a permanent tooth diagnosed with a normal pulp with no symptoms of pulpitis or with a diagnosis of reversible pulpitis. The pulp is
judged by clinical and radiographic criteria to be vital and able to heal from the carious insult.6 • Objectives: The intermediate and/or final restoration should seal completely the involved dentin from the oral environment. The vitality of the tooth should be preserved. No post-treatment signs or symptoms such as sensitivity, pain, or swelling should be evident. There should be no radiographic evidence of internal or external root resorption or other pathologic changes. Teeth with immature roots should show continued root development and apexogenesis. Partial pulpotomy for carious exposures The partial pulpotomy for carious exposures is a procedure in which the inflamed pulp tissue beneath an exposure is removed to a depth of 1 to 3 mm or deeper to reach healthy pulp tissue. Pulpal bleeding must be controlled by irrigation with a bacteriocidal agent such as sodium hypochlorite or chlorhexidine68-70 before the site is covered with calcium hydroxide6,91,92 or MTA.9395 While calcium hydroxide has been demonstrated to have longterm success, MTA results in more predictable dentin bridging and pulp health.96 MTA (at least 1.5 mm thick) should cover the exposure and surrounding dentin followed by a layer of light cured resin-modified glass ionomer.90 A restoration that seals the tooth from microleakage is placed. • Indications: A partial pulpotomy is indicated in a young permanent tooth for a carious pulp exposure in which the pulpal bleeding is controlled within several minutes. The tooth must be vital, with a diagnosis of normal pulp or reversible pulpitis.6 • Objectives: The remaining pulp should continue to be vital after partial pulpotomy. There should be no adverse clinical signs or symptoms such as sensitivity, pain, or swelling. There should be no radiographic sign of internal or external resorption, abnormal canal calcification, or periapical radiolucency postoperatively. Teeth having immature roots should continue normal root development and apexogenesis. Partial pulpotomy for traumatic exposures (Cvek pulpotomy) The partial pulpotomy for traumatic exposures is a procedure in which the inflamed pulp tissue beneath an exposure is removed to a depth of 1 to 3 mm or more to reach the deeper healthy tissue. Pulpal bleeding is controlled using bacteriodical irrigants such as sodium hypochlorite or chlorhexidine69,70, and the site then is covered with calcium hydroxide97-100 or MTA.6,101 White, rather than gray, MTA is recommended in anterior teeth to decrease the chance of discoloration. The 2 versions have been shown to have similar properties.102,103 While calcium hydroxide has been demonstrated to have longterm success, MTA results in more predictable dentin bridging and pulp health.96 MTA (at least 1.5 mm thick) should cover the exposure and surrounding dentin, followed by a layer of light-cured resin-modified glass ionomer.101 A restoration that seals the tooth from microleakage is placed. • Indications: This pulpotomy is indicated for a vital, traumatically-exposed, young permanent tooth, especially one with an incompletely formed apex. Pulpal bleeding after removal of inflamed pulpal tissue must be controlled. Neither CLINICAL GUIDELINES
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time between the accident and treatment nor size of exposure is critical if the inflamed superficial pulp tissue is amputated to healthy pulp.104 • Objectives: The remaining pulp should continue to be vital after partial pulpotomy. There should be no adverse clinical signs or symptoms of sensitivity, pain, or swelling. There should be no radiographic signs of internal or external resorption, abnormal canal calcification, or periapical radiolucency postoperatively. Teeth with immature roots should show continued normal root development and apexogenesis. Apexogenesis (root formation) Apexogenesis is a histological term used to describe the continued physiologic development and formation of the root’s apex. Formation of the apex in vital, young, permanent teeth can be accomplished by implementing the appropriate vital pulp therapy previously described in this section (ie, indirect pulp treatment, direct pulp capping, partial pulpotomy for carious exposures and traumatic exposures). Nonvital pulp treatment Pulpectomy (conventional root canal treatment) Pulpectomy in apexified permanent teeth is conventional root canal (endodontic) treatment for exposed, infected, and/or necrotic teeth to eliminate pulpal and periradicular infection. In all cases, the entire roof of the pulp chamber is removed to gain access to the canals and eliminate all coronal pulp tissue. Following debridement, disinfection, and shaping of the root canal system, obturation of the entire root canal is accomplished with a biologically-acceptable, nonresorbable filling material. Obturation as close as possible to the cementodentinal junction should be accomplished with gutta percha or other filling material acceptable as described in the Guide to Clinical Endodontics.14 • Indications: Pulpectomy or conventional root canal treatment is indicated for a restorable permanent tooth with irreversible pulpitis or a necrotic pulp in which the root is apexified. For root canal-treated teeth with unresolved periradicular lesions, root canals that are not accessible from the conventional coronal approach, or calcification of the root canal space, endodontic treatment of a more specialized nature may be indicated. • Objectives: There should be evidence of a successful filling without gross overextension or underfilling in the presence of a patent canal. There should be no adverse post-treatment signs or symptoms such as prolonged sensitivity, pain, or swelling, and there should be evidence of resolution of pretreatment pathology with no further breakdown of periradicular supporting tissues clinically or radiographically. Apexification (root end closure) Apexification is a method of inducing root end closure of an incompletely formed nonvital permanent tooth by removing the coronal and nonvital radicular tissue just short of the root end and placing a biocompatible agent such as calcium hydroxide in the canals for 2-4 weeks to disinfect the canal space. Root end closure is accomplished with an apical barrier such as MTA.105 In instances when complete closure cannot be accomplish 198
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by MTA, an absorbable collagen wound dressing (eg, CollaCote®)106 can be placed at the root end to allow MTA to be packed within the confines of the canal space. Gutta percha is used to fill the remaining canal space. If the canal walls are thin, the canal space can be filled with MTA or composite resin instead of gutta percha to strengthen the tooth against fracture.107 • Indications: This procedure is indicated for nonvital permanent teeth with incompletely formed roots. • Objectives: This procedure should induce root end closure (apexification) at the apices of immature roots or result in an apical barrier as confirmed by clinical and radiographic evaluation. Adverse post-treatment clinical signs or symptoms of sensitivity, pain, or swelling should not be evident. There should be no radiographic evidence of external root resorption, lateral root pathosis, root fracture, or breakdown of periradicular supporting tissues during or following therapy. The tooth should continue to erupt, and the alveolus should continue to grow in conjunction with the adjacent teeth.
References 1. Fuks AB. Pulp therapy for the primary dentition. In: Pinkham JR, Casamassimo PS, Fields HW Jr, McTigue DJ, Nowak A, eds. Pediatric Dentistry: Infancy Through Adolescence. 4th ed. St. Louis, Mo: Elsevier Saunders Co; 2005:375-93. 2. American Association of Endodontists. Glossary of Endodontic Terms. 7th ed. Chicago, Ill: American Association of Endodontists; 2003. 3. American Association of Endodontists. Systematic endodontic diagnosis. Insert to the Fall/Winter edition of Endodontics: Colleagues for Excellence; 1996. 4. McDonald RE, Avery DR, Dean JA. Management of trauma to the teeth and supporting tissues. In: Dentistry for the Child and Adolescent. 8 th ed. St Louis, Mo: Mosby Inc; 2004:455-502. 5. Coll JA, Sadrian R. Predicting pulpectomy success and its relationship to exfoliation and succedaneous dentition. Pediatr Dent 1996;18(1):57-63. 6. Camp JH, Fuks AB. Pediatric endodontics: Endodontic treatment for the primary and young permanent dentition. In: Cohen S, Hargreaves KM, eds. Pathways of the Pulp. 9th ed. St. Louis, Mo: Mosby Elsevier; 2006:834-59. 7. Farooq NS, Coll JA, Kuwabara A, Shelton P. Success rates of formocresol pulpotomy and indirect pulp therapy in the treatment of deep dentinal caries in primary teeth. Pediatr Dent 2000;22(4):278-86. 8. Fuks AB. Current concepts in vital pulp therapy. Eur J Pediatr Dent 2002;3(3):115-20. 9. Vij R, Coll JA, Shelton P, Farooq NS. Caries control and other variables associated with success of primary molar vital pulp therapy. Pediatr Dent 2004;26(3):214-20. 10. Murray PE, About I, Franquin JC, Remusat M, Smith AJ. Restorative pulpal and repair responses. J Am Dent Assoc 2001;132(4):482-91. 11. Holan G, Eidelman E, Fuks AB. Long-term evaluation of pulpotomy in primary molars using mineral trioxide aggregate or formocresol. Pediatr Dent 2005;27(2):129-36.
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12. American Association of Endodontists. Guide to Clinical Endodontics. 4th ed. Chicago, Ill: American Association of Endodontists; 2004. 13. Itota T, Nakabo S, Torii Y, Narukami T, Doi J, Yoshiyama M. Effect of fluoride-releasing liner on demineralized dentin. Quintessence Int 2006;37(4):297-303. 14. Weiner RS, Weiner LK, Kugel G. Teaching the use of bases and liners: A survey of North American dental schools. J Am Dent Assoc 1996;127(11):1640-5. 15. Wisithphrom K, Murray PE, About I, Windsor LJ. Interactions between cavity preparation and restoration events and their effects on pulp vitality. Int J Periodontics Restorative Dent 2006;26(6):596-605. 16. de Souza Costa CA, Teixeira HM, Lopes do Nascimento AB, Hebling J. Biocompatibility of resin-based dental materials applied as liners in deep cavities prepared in human teeth. J Biomed Mater Res B Appl Biomater 2007; 81(1):175-84. 17. Murray PE, Hafez AA, Smith AJ, Cox CF. Bacterial microleakage and pulp inflammation associated with various restorative materials. Dent Mater 2002;18(6):470-8. 18. Rabchinsky J, Donly KJ. A comparison of glass-ionomer cement and calcium hydroxide liners in amalgam restorations. Int J Periodontics Restorative Dent 1993;13(4): 378-83. 19. Büyükgüral B, Cehreli ZC. Effect of different adhesive protocols vs calcium hydroxide on primary tooth pulp with different remaining dentin thicknesses: 24 month results. Clin Oral Investig 2008;12(1):91-6. 20. Falster CA, Araújo FB, Straffon LH, Nör JE. Indirect pulp treatment: in vivo outcomes of an adhesive resin system vs calcium hydroxide for protection of the dentin-pulp complex. Pediatr Dent 2002;24(3):241-8. 21. Lo EC, Holmgren CJ, Hu D, Van Palenstein Helderman W. Six-year follow up of atraumatic restorative treatment restorations placed in Chinese school children. Community Dent Oral Epidemiol 2007;35(5):387-92. 22. de Souza EM, Cefaly DF, Terada RS, Rodrigues CC, de Lima Navarro MF. Clinical evaluation of the ART technique using high density and resin-modified glass ionomer cements. Oral Health Prev Dent 2003;1(3):201-7. 23. Pinto AS, de Araújo FB, Franzon R, et al. Clinical and microbiological effect of calcium hydroxide protection in indirect pulp capping in primary teeth. Am J Dent 2006;19(6):382-6. 24. Al-Zayer MA, Straffon LH, Feigal RJ, Welch KB. Indirect pulp treatment of primary posterior teeth: A retrospective study. Pediatr Dent 2003:25(1):29-36. 25. Davidovich E, Weiss E, Fuks AB, Beyth N. Surface antibacterial properties of glass ionomer cements used in a traumatic restorative treatment. J Am Dent Assoc 2007; 138(10):1347-52. 26. M archi JJ, de Araújo FB, Froner AM, Straffon LH, Nör JE. Indirect pulp capping in the primary dentition: A 4 year follow-up study. J Clin Pediatr Dent 2006;31 (2):68-71.
27. Menezes JP, Rosenblatt A, Medeiros E. Clinical evaluation of atraumatic restorations in primary molars: A comparison between 2 glass ionomer cements. J Dent Child 2006;73(2):91-7. 28. Brännström M. Communication between the oral cavity and the dental pulp associated with restorative treatment. Oper Dent 1984;9(2):57-68. 29. Pereira JC, Manfio AP, Franco EB, Lopes ES. Clinical evaluation of Dycal under amalgam restorations. Am J Dent 1990;3:67-70. 30. Tam LE, Pulver E, McComb D, Smith DC. Physical properties of calcium hydroxide and glass-ionomer base and lining materials. Dent Mater 1989;5:145-9. 31. Lewis BA, Burgess JO, Gray SE. Mechanical properties of dental base materials. Am J Dent 1992;5:69-72. 32. Duque C, Negrini Tde C, Hebling J, Spolidorio DM. Inhibitory activity of glass-ionomer cements on cariogenic bacteria. Oper Dent 2005;30(5):636-40. 33. Loyola-Rodriguez JP, García-Godoy F, Linquist R. Growth inhibition of glass ionomer cements on mutans streptococci. Pediatr Dent 1994;16(5):346-9. 34. Wambier DS, dos Santos FA, Guedes-Pinto AC, Jaeger RG, Simionato MR. Ultrastructural and microbiological analysis of the dentin layers affected by carious lesions in primary molars treated by minimal intervention. Pediatr Dent 2007;29(3):228-35. 35. Coll JA. Indirect pulp capping and primary teeth: Is the primary tooth pulpotomy out of date? Pediatr Dent 2008;30(3):230-6. 36. Ricketts DNJ, Kidd EAM, Innes N, Clarkson J. Complete or ultraconservative removal of decayed tissue in unfilled teeth. Cochrane Database of Systematic Reviews 2006, Issue 3. Art. No.: CD003808. DOI:10.1002/14651858. CD003808.pub2. 37. Thompson V, Craig RG, Curro FA, Green WS, Ship JA. Treatment of deep carious lesions by complete excavation or partial removal: A critical review. J Am Dent Assoc 2008;139(6):705-12. 38. Ribeiro CC, Baratieri LN, Perdigao J, Baratieri NM, Ritter AV. A clinical, radiographic, and scanning electron microscopic evaluation of adhesive restorations on carious dentin in primary teeth. Quintessence Int 1999;30 (9):591-9. 39. Foley J, Evans D, Blackwell A. Partial caries removal and cariostatic materials in carious primary molar teeth: A randomized controlled clinical trail. Br Dent J 2004;197(11):697-701. 40. Oliveira EF, Carminatti G, Fontanella V, Maltz M. The monitoring of deep caries lesions after incomplete dentin caries removal: Results after 14-18 months. Clin Oral Investig 2006;10(2):134-9. 41. Agamy HA, Bakry NS, Mounir MM, Avery DR. Comparison of mineral trioxide aggregate and formocresol as pulp-capping agents in pulpotomized primary teeth. Pediatr Dent 2004;26(4):302-9.
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42. Maroto M, Barbería E, Planells P, García-Godoy F. Dentin bridge formation after mineral trioxide aggregate (MTA) pulpotomies in primary teeth. Am J Dent 2005;18(3): 151-4. 43. Caicedo R, Abbott PV, Alongi DJ, Alarcon MY. Clinical, radiographic and histological analysis of the effects of mineral trioxide aggregate used in direct pulp capping and pulpotomies of primary teeth. Aust Dent J 2006;51 (4):297-305. 44. Tuna D, Olmez A. Clinical long-term evaluation of MTA as a direct pulp capping material in primary teeth. Int Endod J 2008;41(4):273-8. 45. Kopel HM. The pulp capping procedure in primary teeth “revisited”. ASDC J Dent Child 1997;64(5):327-33. 46. Smith NL, Seale NS, Nunn ME. Ferric sulfate pulpotomy in primary molars: A retrospective study. Pediatr Dent 2000;22(3):192-9. 47. Burnett S, Walker J. Comparison of ferric sulfate, formocresol, and a combination of ferric sulfate/formocresol in primary tooth vital pulpotomies: A retrospective radiographic survey. ASDC J Dent Child 2002;69(1):44-8. 48. Ibricevic H, Al-Jame Q. Ferric sulphate and formocresol in pulpotomy of primary molars: Long term follow-up study. Eur J Paediatr Dent 2003;4(1):28-32. 49. Loh A, O’Hoy P, Tran X, et al. Evidence-based assessment: Evaluation of the formocresol versus ferric sulfate primary molar pulpotomy. Pediatr Dent 2004;26(5):401-9. 50. Markovic D, Zivojinovic V, Vucetic M. Evaluation of three pulpotomy medicaments in primary teeth. Eur J Paediatr Dent 2005;6(3):133-8. 51. Vargas KG, Packham B. Radiographic success of ferric sulfate and formocresol pulpotomies in relation to early exfoliation. Pediatr Dent 2005;27(3):233-7. 52. Huth KC, Paschos E, Hajek-Al-Khatar N, et al. Effectiveness of 4 pulpotomy techniques – Randomized controlled trial. J Dent Res 2005;84(12):1144-8. 53. Dean JA, Mack RB, Fulkerson BT, Sanders BJ. Comparison of electrical and formocresol pulpotomy procedures in children. Int J Pediatr Dent 2002;12(3):177-82. 54. Waterhouse PJ. Formocresol and alternative primary molar pulpotomy medicaments: A review. Endod Dent Traumatol 1995;11(4):157-62. 55. Shumayrikh NM, Adenubi JO. Clinical evaluation of gluteraldehyde with calcium hydroxide and gluteraldehyde with zinc oxide eugenol in pulpotomy of primary molars. Endod Dent Traumatol 1999;15(6):259-64. 56. Zurn D, Seale NS. Light-cured calcium hydroxide vs formocresol in human primary molar pulpotomies: A randomized controlled trial. Pediatr Dent 2008;30(1):34-41. 57. Farsi N, Alamoudi N, Balto K, Al Mushayt A. Success of mineral trioxide aggregate in pulpotomized primary molars. J Clin Pediatr Dent 2005;29(4):307-11. 58. Maroto M, Barbería E, Vera V, García-Godoy F. Mineral trioxide aggregate as pulp dressing agent in pulptomy treatment of primary molars: 42-month clinical study. Am J Dent 2007;20(5):283-6. 200
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59. Peng L, Ye L, Tan H, Zhou X. Better outcomes in pulpotomies on primary molars with MTA. Evidence-Based Dentistry 2007;8:11-12. 60. Fuks AB, Papagiannoulis L. Pulpotomy in primary teeth: Review of the literature according to standardized criteria. Eur Arch Paediatr Dent 2006;7(2):64-71. 61. Ng FK, Messer LB. Mineral trioxide aggregate as a pulpotomy medicament: A narrative review. Eur Arch Paediatr Dent 2008;9(1):4-11. 62. Seale NS, Glickman GN. Contemporary perspectives on vital pulp therapy: Views from the endodontists and pediatric dentists. Pediatr Dent 2008;30(3):261-7. 63. Guelmann M, Fair J, Bimstein E. Permanent versus temporary restorations after emergency pulpotomies in primary molars. Pediatr Dent 2005;27(6):478-81. 64. Holan G, Fuks AB, Keltz N. Success rate of formocresol pulpotomy in primary molars restored with stainless steel crown vs amalgam. Pediatr Dent 2002;24(3):212-6. 65. Guelmann M, McIlwain MF, Primosch RE. Radiographic assessment of primary molar pulpotomies restored with resin-based materials. Pediatr Dent 2005;27(1):24-7. 66. Thompson KS, Seale NS, Nunn ME, Huff G. Alternative method of hemorrhage control in full strength formocresol pulpotomy. Pediatr Dent 2001;23(3):217-222. 67. Strange DM, Seale NS, Nunn ME, Strange M. Outcome of formocresol/ZOE sub-base pulpotomies utilizing alternative radiographic success criteria. Pediatr Dent 2001;23 (3):331-6. 68. Siqueira JF Jr, Rôças IN, Paiva SS, Guimarães-Pinto T, Magalhaes KM, Lima KC. Bacteriologic investigation of the effects of sodium hypochlorite and chlorhexidine during the endodontic treatment of teeth with apical periodontitis. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2007;104(1):122-30. 69. Ercan E, Ozekinci T, Atakul F, Gül K. Antibacterial activity of 2% chlorhexidine gluconate and 5.25% sodium hypochlorite in infected root canal: in vivo study. J Endod 2004;30(2):84-7. 70. Zehnder M. Root canal irrigants. J Endod 2006;32(5): 389-98. 71. Mehdipour O, Kleier DJ, Averbach RE. Anatomy of sodium hypochlorite accidents. Compend Contin Educ Dent 2007;28(10):548-50. 72. Casas MJ, Kenny DJ, Johnston DH, Judd PL. Long-term outcomes of primary molar ferric sulfate pulpotomy and root canal therapy. Pediatr Dent 2004;26(1):44-8. 73. Holan G, Fuks AB. A comparison of pulpectomies using ZOE and KRI paste in primary molars: A retrospective study. Pediatr Dent 1993;15(6):403-7. 74. Ozalp N, Saroğlu, I, Sönmez H. Evaluation of various root canal filling materials in primary molar pulpectomies: An in vivo study. Am J Dent 2005;18(6):347-50. 75. Kubota K, Golden BE, Penugonda B. Root canal filling materials for primary teeth: A review of the literature. ASDC J Dent Child 1992;59(3):225-7.
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76. Primosch RE, Ahmadi A, Setzer B, Guelmann M. A retrospective assessment of zinc oxide-eugenol pulpectomies in vital maxillary primary incisors successfully restored with composite resin crowns. Pediatr Dent 2005;27(6): 470-7. 77. Oen KT, Thompson VP, Vena D, et al. Attitudes and expectations of treating deep caries: A PEARL Network survey. Gen Dent 2007;55(3):197-203. 78. Maltz M, de Oliveira EF, Fontanella V, Bianchi R. A clinical, microbiologic, and radiographic study of deep caries lesions after incomplete caries removal. Quintessence Int 2002;33(2):151-9. 79. Fairbourn DR, Charbeneau GT, Loesche WJ. Effect of improved Dycal and IRM on bacteria in deep carious lesions. J Am Dent Assoc 1980;100(4):547-52. 80. Leksell E, Ridell K, Cvek M, Mejàre I. Pulp exposure after stepwise versus direct complete excavation of deep carious lesions in young posterior permanent teeth. Endod Dent Traumatol 1996;12(4):192-6. 81. Massler M. Treatment of profound caries to prevent pulpal damage. J Pedod 1978;2(2):99-105. 82. B jørndal L, Thylstrup A. A practice-based study on stepwise excavation of deep carious lesions in permanent teeth: A 1-year follow-up study. Community Dent Oral Epidemiol 1998;26(2):122-8. 83. Bjørndal L, Larsen T, Thylstrup A. A clinical and microbiological study of deep carious lesions during stepwise excavation using long treatment intervals. Caries Res 1997;31(6):411-7. 84. Bjørndal L, Larsen T. Changes in the cultivable flora in deep carious lesions following a stepwise excavation procedure. Caries Res 2000;34(6):502-8. 85. Bjørndal L, Mjör IA. Pulp-dentin biology in restorative dentistry. Part 4: Dental caries-characteristics of lesions and pulpal reactions. Quintessence Int 2001;32(9):717-36. 86. Horsted P, Sondergaard B, Thylstrup A, El Attar K, Fejerskov O. A retrospective study of direct pulp capping with calcium hydroxide compounds. Endod Dent Traumatol 1985;1(1):29-34. 87. Baume LJ, Holz J. Long term clinical assessment of direct pulp capping. Int Dent J 1981;31(4):251-60. 88. Barthel CR, Rosenkranz B, Leuenberg A, Roulet JF. Pulp capping of carious exposures: Treatment outcome after 5 and 10 years–A retrospective study. J Endod 2000;26(9): 525-8. 89. Matsuo T, Nakanishi T, Shimizu H, Ebisu S. A clinical study of direct pulp capping applied to carious-exposed pulps. J Endod 1996;22(10):551-6. 90. Bogen G, Kim JS, Bakland LK. Direct pulp capping with mineral trioxide aggregate: An observational study. J Am Dent Assoc 2008;139(3):305-15. 91. Mejàre I, Cvek M. Partial pulpotomy in young permanent teeth with deep carious lesions. Endod Dent Traumatol 1993;9(6):238-42.
92. Nosrat IV, Nosrat CA. Reparative hard tissue formation following calcium hydroxide application after partial pulpotomy in cariously exposed pulps of permanent teeth. Int Endod J 1998;31(3):221-6. 93. El-Meligy OAS, Avery DR. Comparison of mineral trioxide aggregate and calcium hydroxide as pulpotomy agents in young permanent teeth (apexogenesis). Pediatr Dent 2006;28(5):399-404. 94. Qudeimat MA, Barrieshi-Nusair KM, Owais AI. Calcium hydroxide vs mineral trioxide aggregates for partial pulpotomy of permanent molars with deep caries. Eur Arch Paediatr Dent 2007;8(2):99-104. 95. Witherspoon DE, Small JC, Harris GZ. Mineral trioxide aggregate pulpotomies: A series outcomes assessment. J Am Dent Assoc 2006;137(9):610-8. 96. Chacko V, Kurikose S. Human pulpal response to mineral trioxide aggregate (MTA): A histological study. J Clin Pediatr Dent 2006;30(3):203-10. 97. Fuks AB, Gavra S, Chosack A. Long-term followup of traumatized incisors treated by partial pulpotomy. Pediatr Dent 1993;15(5):334-6. 98. de Blanco LP. Treatment of crown fractures with pulp exposure. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1996;82(5):564-8. 99. Blanco L, Cohen S. Treatment of crown fractures with exposed pulps. J Calif Dent Assoc 2002;30(6):419-25. 100. Cvek M. Endodontic management and the use of calcium hydroxide in traumatized permanent teeth. In: Andreasen JO, Andreasen FM, Andersson L, eds. Textbook and Color Atlas of Traumatic Injuries to the Teeth. 4th ed. Ames, Iowa: Blackwell Munksgaard; 2007:598-657. 101. Bakland LK. New endodontic procedures using mineral trioxide aggregate (MTA) for teeth with traumatic injuries. In: Andreasen JO, Andreasen FM, Andersson L, eds. Textbook and Color Atlas of Traumatic Injuries to the Teeth. 4th ed. Ames, Iowa: Blackwell Munksgaard; 2007:658-68. 102. Ferris DM, Baumgartner JC. Perforation repair comparing two types of mineral trioxide aggregate. J Endod 2004;30(6):422-4. 103. Menezes R, Bramante CM, Letra A, Carvalho VG, Garcia RB. Histologic evaluation of pulpotomies in dog using two types of mineral trioxide aggregate and regular and white Portland cements as wound dressings. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2004;98(3):376-9. 104. Pereira JC, Stanley HR. Pulp capping: Influence of the exposure site on pulp healing: Histologic and radiographic study in dog’s pulp. J Endod 1981;7(5):213-23. 105. Torabinejad M, Chivian N. Clinical applications of mineral trioxide aggregate. J Endod 1999;25(3):197-205. 106. Patino MG, Neiders ME, Andreana S, Noble B, Cohen RE. Collagen as an implantable material in medicine and dentistry. J Oral Implantol 2002;28(5):220-5. 107. Katebzadeh N, Dalton BC, Trope M. Strengthening immature teeth during and after apexification. J Endod 1998;24(4):256-9.
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Guideline on Management of Acute Dental Trauma Originating Council
Council on Clinical Affairs Review Council Council on Clinical Affairs
Adopted 2001
Revised 2004, 2007, 2010
Purpose The American Academy of Pediatric Dentistry (AAPD) intends these guidelines to define, describe appearances, and set forth objectives for general management of acute traumatic dental injuries rather than recommend specific treatment procedures that have been presented in considerably more detail in text-books and the dental/medical literature. Methods This guideline is an update of the previous document revised in 2007. It is based on a review of the current dental and medical literature related to dental trauma. An electronic search was conducted using the following parameters: Terms: “teeth”, “trauma”, “permanent teeth”, and “primary teeth”; Field: all fields; Limits: within the last 10 years; humans; English. There were 5269 articles that matched these criteria. Papers for review were chosen from this list and from references within select articles. In addition, a review of the journal Dental Traumatology was conducted for the years 2000-2009. When data did not appear sufficient or were inconclusive, recommendations were based upon expert and/or consensus opinion including those from the 2008 AAPD “Symposium on Trauma: A Comprehensive Update on Permanent Tooth Trauma in Children” (Chicago, Ill). The recommendations are congruent with the 2007 guidelines developed by the International Association of Dental Traumatology.1-3 Background Facial trauma that results in fractured, displaced, or lost teeth can have significant negative functional, esthetic, and psychological effects on children.4,5 Dentists and physicians should collaborate to educate the public about prevention and treatment of traumatic injuries to the oral and maxillofacial region. The greatest incidence of trauma to the primary teeth occurs at 2 to 3 years of age, when motor coordination is developing.6 The most common injuries to permanent teeth occur secondary to falls, followed by traffic accidents,
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violence, and sports.7-10 All sporting activities have an associated risk of orofacial injuries due to falls, collisions, and contact with hard surfaces.11 The AAPD encourages the use of protective gear, including mouthguards, which help distribute forces of impact, thereby reducing the risk of severe injury.13,14 Dental injuries could have improved outcomes if the public were aware of first-aid measures and the need to seek immediate treatment.14-17 Because optimal treatment results follow immediate assessment and care,18 dentists have an ethical obligation to ensure that reasonable arrangements for emergency dental care are available.19 The history, circumstances of the injury, pattern of trauma, and behavior of the child and/or caregiver are important in distinguishing nonabusive injuries from abuse.20 Practitioners have the responsibility to recognize, differentiate, and either appropriately manage or refer children with acute oral traumatic injuries, as dictated by the complexity of the injury and the individual clinician’s training, knowledge, and experience. Compromised airway, neurological manifestations such as altered orientation, hemorrhage, nausea/vomiting, or suspected loss of consciousness requires further evaluation by a physician. To efficiently determine the extent of injury and correctly diagnose injuries to the teeth, periodontium, and associated structures, a systematic approach to the traumatized child is essential.21,22 Assessment includes a thorough medical and dental history, clinical and radiographic examination, and additional tests such as palpation, percussion, sensitivity, and mobility evaluation. Intraoral radiography is useful for the evaluation of dentoalveolar trauma. If the area of concern extends beyond the dentoalveolar complex, extraoral imaging may be indicated. Treatment planning takes into consideration the patient’s health status and developmental status, as well as extent of injuries. Advanced behavior guidance techniques or an appropriate referral may be necessary to ensure that proper diagnosis and care are given.
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All relevant diagnostic information, treatment, and recommended follow-up care are documented in the patient’s record. Appendix I is a sample document for recording assessment of acute traumatic injuries. This sample form, developed by the AAPD, is provided as a practice tool for pediatric dentists and other dentists treating children. It was developed by pediatric dentistry experts and offered to facilitate excellence in practice. This form, however, does not establish or evidence a standard of care. In issuing this form, the AAPD is not engaged in rendering legal or other professional advice. If such services are required, competent legal or other professional counsel should be sought. Welldesigned follow-up procedures are essential to diagnose complications. After a primary tooth has been injured, the treatment strategy is dictated by the concern for the safety of the permanent dentition.6,21,23 If determined that the displaced primary tooth has encroached upon the developing permanent tooth germ, removal is indicated.3,6,24-28 In the primary dentition, the maxillary anterior region is at low risk for space loss unless the avulsion occurs prior to canine eruption or the dentition is crowded.23 Fixed or removable appliances, while not always necessary, can be fabricated to satisfy parental concerns for esthetics or to return a loss of oral or phonetic function.6 When an injury to a primary tooth occurs, informing parents about possible pulpal complications, appearance of a vestibular sinus tract, or color change of the crown associated with a sinus tract can help assure timely intervention, minimizing complications for the developing succedaneous teeth.3,6,29,30 Also, it is important to caution parents that the primary tooth’s displacement may result in any of several permanent tooth complications, including enamel hypoplasia, hypocalcification, crown/root dilacerations, or disruptions in eruption patterns or sequence.29 The risk of trauma-induced developmental disturbances in the permanent successors is greater in children whose enamel calcification is incomplete.23,31 The treatment strategy after injury to a permanent tooth is dictated by the concern for vitality of the periodontal ligament and pulp. Subsequent to the initial management of the dental injury, continued periodic monitoring is indicated to determine clinical and radiographic evidence of successful intervention (ie, asymptomatic, positive sensitivity to pulp testing, root continues to develop in immature teeth, no mobility, no periapical pathology).1,2,21,24,32 Initiation of endodontic treatment is indicated in cases of spontaneous pain, abnormal response to pulp sensitivity tests, lack of continued root formation or apexogenesis, or breakdown of periradicular supportive tissue.1,2,21,24,32 To restore a fractured tooth’s normal esthetics and function, reattachment of the crown fragment is an alternative that should be considered.21,24,33 To stabilize a tooth following traumatic injury, a splint may be necessary.24,34-38 Flexible splinting assists in heal-
ing.21,39 Characteristics of the ideal splint include: 1. easily fabricated in the mouth without additional trauma; 2. passive unless orthodontic forces are intended; 3. allows physiologic mobility; 4. nonirritating to soft tissues; 5. does not interfere with occlusion; 6. allows endodontic access and vitality testing; 7. easily cleansed; 8. easily removed. Instructions to patients having a splint placed include to: 1. consume a soft diet; 2. avoid biting on splinted teeth; 3. maintain meticulous oral hygiene; 4. use chlorhexidine/antibiotics if prescribed; 5. call immediately if splint breaks/loosens.
Recommendations Infraction Definition: incomplete fracture (crack) of the enamel without loss of tooth structure. Diagnosis: normal gross anatomic and radiographic appearance; craze lines apparent, especially with transillumination. Treatment objectives: to maintain structural integrity and pulp vitality.24,40,41 General prognosis: Complications are unusual.42 Crown fracture–uncomplicated Definition: an enamel fracture or an enamel-dentin fracture that does not involve the pulp. Diagnosis: clinical and/or radiographic findings reveal a loss of tooth structure confined to the enamel or to both the enamel and dentin.1,3,6,18-21,23,26,30,32,39,41,43,44 Treatment objectives: to maintain pulp vitality and restore normal esthetics and function. Injured lips, tongue, and gingiva should be examined for tooth fragments. When looking for fragments in soft tissue lacerations, radiographs are recommended.1 For small fractures, rough margins and edges can be smoothed. For larger fractures, the lost tooth structure can be restored.1,3,6,21,23,26,29,30,32,41-44 General prognosis: The prognosis of uncomplicated crown fractures depends primarily upon the concomitant injury to the periodontal ligament and secondarily upon the extent of dentin exposed.22 Optimal treatment results follow timely assessment and care. Crown fracture–complicated Definition: an enamel-dentin fracture with pulp exposure. Diagnosis: clinical and radiographic findings reveal a loss of tooth structure with pulp exposure.1,3,6,21 Treatment objectives: to maintain pulp vitality and restore normal esthetics and function.29 Injured lips, tongue, and gingiva should be examined for tooth fragments. When looking for fragments in soft tissue lacerations, radiographs are recommended.1
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• Primary teeth: Decisions often are based on life expectancy of the traumatized primary tooth and vitality of the pulpal tissue. Pulpal treatment alter natives are pulpotomy, pulpectomy, and extrac tion.3,6,23,26,30 • Permanent teeth: Pulpal treatment alternatives are direct pulp capping, partial pulpotomy, full pulpotomy, and pulpectomy (start of root canal therapy).1,21,42,43 There is increasing evidence to suggest that utilizing conservative vital pulp therapies for mature teeth with closed apices is as appropriate a management technique as when used for immature teeth with open apices.45 General prognosis: The prognosis of crown fractures appears to depend primarily upon a concomitant injury to the periodontal ligament.21 The age of the pulp exposure, extent of dentin exposed, and stage of root development at the time of injury secondarily affect the tooth’s prognosis.21 Optimal treatment results follow timely assessment and care. Crown/root fracture Definition: an enamel, dentin, and cementum fracture with or without pulp exposure. Diagnosis: Clinical findings usually reveal a mobile coronal fragment attached to the gingiva with or without a pulp exposure. Radiographic findings may reveal a radiolucent oblique line that comprises crown and root in a vertical direction in primary teeth and in a direction usually perpendicular to the central radiographic beam in permanent teeth. While radiographic demonstration often is difficult, root fractures can only be diagnosed radiographically.1,3,6,21,30 Treatment objectives: to maintain pulp vitality and restore normal esthetics and function.11 • Primary teeth: When the primary tooth cannot or should not be restored, the entire tooth should be removed unless retrieval of apical fragments may result in damage to the succedaneous tooth.3,6 • Permanent teeth: The emergency treatment objec tive is to stabilize the coronal fragment. Definitive treatment alternatives are: to remove the coronal fragment followed by a supragingival restoration or necessary gingivectomy; osteotomy; or surgical or orthodontic extrusion to prepare for restoration. If the pulp is exposed, pulpal treatment alternatives are pulp capping, pulpotomy, and root canal treatment.1,21,42 General prognosis: Although the treatment of crown-root fractures can be complex and laborious, most fractured permanent teeth can be saved.21 Fractures extending significantly below the gingival margin may not be restorable. Root fracture Definition: a dentin and cementum fracture involving the pulp.
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Diagnosis: Clinical findings reveal a mobile coronal fragment attached to the gingiva that may be displaced. Radiographic findings may reveal 1 or more radiolucent lines that separate the tooth fragments in horizontal fractures. Multiple radiographic exposures at different angulations may be required for diagnosis. A root fracture in a primary tooth may be obscured by a succedaneous tooth.1,3,6,21 Treatment objectives: • Primary teeth: Treatment alternatives include ex traction of coronal fragment without insisting on removing apical fragment or observation.3,6,23 It is not recommended to reposition and stabilize the coronal fragment.3 • Permanent teeth: Reposition and stabilize the co ronal fragment.1,21 in its anatomically correct posi tion as soon as possible to optimize healing of the periodontal ligament and neurovascular supply while maintaining esthetic and functional integrity.24 General prognosis: Pulp necrosis in root-fractured teeth is attributed to displacement of the coronal fragment and mature root development.21,47 In permanent teeth, the location of the root fracture has not been shown to affect pulp survival after injury.21,47 Therefore, preservation of teeth with root fractures occurring in the tooth’s cervical third should be attempted.21,47 Young age, immature root formation, positive pulp sensitivity at time of injury, and approximating the dislocation within 1 mm have been found to be advantageous to both pulpal healing and hard tissue repair of the fracture.39,47,48 Concussion Definition: injury to the tooth-supporting structures without abnormal loosening or displacement of the tooth. Diagnosis: Because the periodontal ligament absorbs the injury and is inflamed, clinical findings reveal a tooth tender to pressure and percussion without mobility, displacement, or sulcular bleeding. Radiographic abnormalities are not expected.1,3,6,21,23,32 Treatment objectives: to optimize healing of the periodontal ligament and maintain pulp vitality.1,3,6,21,23,24,32,49 General prognosis: For primary teeth, unless associated infection exists, no pulpal therapy is indicated.6 Although there is a minimal risk for pulp necrosis, mature permanent teeth with closed apices may undergo pulpal necrosis due to associated injuries to the blood vessels at the apex and, therefore, must be followed carefully.21 Subluxation Definition: injury to tooth-supporting structures with abnormal loosening but without tooth displacement. Diagnosis: Because the periodontal ligament attempts to absorb the injury, clinical findings reveal a mobile tooth without displacement that may or may not have sulcular bleeding. Radiographic abnormalities are not expected.1,3,6,21
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Treatment objectives: to optimize healing of the periodontal ligament and neurovascular supply.1,3,6,21,23,24,26-28,30,32,49 • Primary teeth: The tooth should be followed for pathology. • Permanent teeth: Stabilize the tooth and relieve any occlusal interferences. For comfort, a flexible splint can be used. Splint for no more than 2 weeks. General prognosis: Prognosis is usually favorable.23,32 The primary tooth should return to normal within 2 weeks.6 Mature permanent teeth with closed apices may undergo pulpal necrosis due to associated injuries to the blood vessels at the apex and, therefore, must be followed carefully.21 Lateral luxation Definition: displacement of the tooth in a direction other than axially. The periodontal ligament is torn and contusion or fracture of the supporting alveolar bone occurs.23,32,50 Diagnosis: Clinical findings reveal that a tooth is displaced laterally with the crown usually in a palatal or lingual direction and may be locked firmly into this new position. The tooth usually is not mobile or tender to touch. Radiographic findings reveal an increase in periodontal ligament space and displacement of apex toward or though the labial bone plate.1,3,6,21,50 Treatment objectives: • Primary teeth: to allow passive or spontaneous re positiong if there is no occlusal interference.3 When there is occlusal interference, the tooth can be gently repositioned or slightly reduced if the interference is minor.3 When the injury is severe or the tooth is nearing exfoliation, extraction is the treatment of choice.3,6,24,26-28,30 • Permanent teeth: to reposition as soon as possible and then to stabilize the tooth in its anatomically correct position to optimize healing of the peri odontal ligament and neurovascular supply while maintaining esthetic and functional integrity. Re positioning of the tooth is done with digital pressure and little force. A displaced tooth may need to be extruded to free itself from the apical lock in the cortical bone plate. Splinting an addi tional 2 to 4 weeks may be needed with breakdown of marginal bone.1,21,24,49,50 General prognosis: Primary teeth requiring repositioning have an increased risk of developing pulp necrosis compared to teeth that are left to spontaneously reposition.6 In mature permanent teeth with closed apices, pulp necrosis and pulp canal obliteration are common healing complications while progressive root resorption is less likely to occur.50 Intrusion Definition: apical displacement of tooth into the alveolar bone. The tooth is driven into the socket, compressing the periodontal ligament and commonly causes a crushing fracture of the alveolar socket.23,32,51
Diagnosis: Clinical findings reveal that the tooth appears to be shortened or, in severe cases, it may appear missing. The tooth’s apex usually is displaced labially toward or through the labial bone plate in primary teeth and driven into the alveolar process in permanent teeth. The tooth is not mobile or tender to touch. Radiographic findings reveal that the tooth appears displaced apically and the periodontal ligament space is not continuous. Determination of the relationship of an intruded primary tooth with the follicle of the succedaneous tooth is mandatory. If the apex is displaced labially, the apical tip can be seen radiographically with the tooth appearing shorter than its contra-lateral. If the apex is displaced palatally towards the permanent tooth germ, the apical tip cannot be seen radiographically and the tooth appears elongated. An extraoral lateral radiograph also can be used to detect displacement of the apex toward or though the labial bone plate. An intruded young permanent tooth may mimic an erupting tooth.1,3,6,21,51 Treatment objectives: • Primary teeth: to allow spontaneous reeruption ex cept when displaced into the developing successor. Extraction is indicated when the apex is displaced toward the permanent tooth germ.3,6,24,26-28,30 • Permanent teeth: to reposition passively (allowing re-eruption to its preinjury position), actively (repositioning with traction), or surgically and then to stabilize the tooth with a splint for up to 4 weeks in its anatomically correct position to optimize healing of the periodontal ligament and neurovascular supply while maintaining esthetic and functional integrity. For immature teeth with more eruptive potential (root ½ to ²/³ formed), the objective is to allow for spontaneous eruption. In mature teeth, the goal is to reposition the tooth with orthodontic or surgical extrusion and initiate endodontic treatment within the first 3 weeks of the traumatic incidence.1,21,24,49,51 General prognosis: In primary teeth, 90% of intruded teeth will reerupt spontaneously (either partially or completely) in 2 to 6 months.23,52 Even in cases of complete intrusion and displacement of primary teeth through the labial bone plate, a retrospective study showed the reeruption and survival of most teeth for more than 36 months.53 Ankylosis may occur, however, if the periodontal ligament of the affected tooth was severely damaged, thereby delaying or altering the eruption of the permanent successor.6 In mature permanent teeth with closed apices, there is considerable risk for pulp necrosis, pulp canal obliteration, and progressive root resorption.51 Immature permanent teeth that are allowed to reposition spontaneously demonstrate the lowest risk for healing complications.54,55 Extent of intrusion (7 mm or greater) and adjacent intruded teeth have a negative influence on healing.54
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Extrusion Definition: partial displacement of the tooth axially from the socket; partial avulsion. The periodontal ligament usually is torn.23,32,56 Diagnosis: Clinical findings reveal that the tooth appears elongated and is mobile. Radiographic findings reveal an increased periodontal ligament space apically.1,3,6,21,56 Treatment objectives: • Primary teeth: to allow tooth to reposition sponta neously or reposition and allow for healing for minor extrusion (<3 mm) in an immature devel oping tooth. Indications for an extraction include severe extrusion or mobility, the tooth is nearing exfoliation, the child’s inability to cope with the emergency situation, or the tooth is fully formed.6,23,24,26-28,30,37 • Permanent teeth: to reposition as soon as possible and then to stabilize the tooth in its anatomically correct position to optimize healing of the peri odontal ligament and neurovascular supply while maintaining esthetic and functional integrity. Re positioning may be accomplished with slow and steady apical pressure to gradually displace coagu lum formed between root apex and floor of the socket. Splint for up to 2 weeks.1,21,24,49,56 General prognosis: There is a lack of clinical studies evaluating repositioning of extruded primary teeth.6 In permanent mature teeth with closed apices, there is considerable risk for pulp necrosis and pulp canal obliteration.56 These teeth must be followed carefully.1,21 Avulsion Definition: complete displacement of tooth out of socket. The periodontal ligament is severed and fracture of the alveolus may occur.23,32 Diagnosis: Clinical and radiographic findings reveal that the tooth is not present in the socket or the tooth already has been replanted. Radiographic assessment will verify that the tooth is not intruded when the tooth was not found.1,3,6,21,23,32 Treatment objectives: • Primary teeth: to prevent further injury to the developing successor. Avulsed primary teeth should not be replanted because of the potential for sub sequent damage to developing permanent tooth germs.3,6,21,23,24,27 • Permanent teeth: to replant as soon as possible and then to stabilize the replanted tooth in its anatom ically correct location to optimize healing of the periodontal ligament and neurovascular supply while maintaining esthetic and functional inte grity except when replanting is contraindicated by: 1. the child’s stage of dental development (risk for ankylosis where considerable alveolar growth has to take place);
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2. compromising medical condition; or 3. compromised integrity of the avulsed tooth or supporting tissues. Flexible splinting for 2 weeks is indicated.2 Tetanus prophylaxis and antibiotic coverage should be consi dered.2,21,24,58,59 Treatment strategies are directed at avoiding inflammation that may occur as a result of the tooth’s at tachment damage and/or pulpal infection.60,61 General prognosis: Prognosis in the permanent dentition is primarily dependent upon formation of root development and extraoral dry time.2,21 The tooth has the best prognosis if replanted immediately.24,61 If the tooth cannot be replanted within 5 minutes, it should be stored in a medium that will help maintain vitality of the periodontal ligament fibers.29,62 The best (ie, physiologic) transportation media for avulsed teeth include (in order of preference) Viaspan™, Hank’s Balanced Salt Solution (tissue culture medium), and cold milk.58,59,63-65 Next best would be a non-physiologic medium such as saliva (buccal vestibule), physiologic saline, or water.58,59,63-65 Although water is detrimental to cell viability due to its low osmolality and long term storage (ie, more than 20 minutes) in water has an adverse effect on periodontal ligament healing, it is a better choice than dry storage.24 Limited tooth storage in a cell-compatible medium prior to replantation has produced similar healing results as compared with immediately-replanted teeth.66 The risk of ankylosis increases significantly with an extraoral dry time of 20 minutes.29,62,67,68 An extraoral dry time of 60 minutes is considered the point where survival of the root periodontal cells is unlikely.61 In permanent avulsed teeth, there is considerable risk for pulp necrosis, root resorption, and ankylosis.63,69,70 Additional considerations: Recent evidence suggests that success of replantation is dependent upon many factors, some of which the clinician can manipulate in a manner that favors more successful outcomes. Decision Trees for acute management of avulsed permanent incisors have been developed with up-to-date information in an easy to use flowchart format.60,71 Revascularization: An immature (ie, open apex) tooth has the potential to establish revascularization when there is a minimum of a 1.0 mm apical opening.72 Complete pulpal revascularization has been shown to occur at a rate of 18% among immature teeth.73 It appears that antibiotic treatment reduces contamination of the root surface and/or pulp space, thereby creating a biological environment that aids revascularization.74 On the other hand, a mature tooth (ie, closed apex or apical opening <1 mm) has little or no chance of revascularization. Researchers have demonstrated that immature teeth soaked in doxycycline solution have a greater rate of pulp revascularization.74,75 Periodontal ligament (PDL) management – transitional therapy: When a tooth has been out of the oral cavity and in a dry environment for greater than 60 minutes, the PDL has no chance of survival. If such a tooth is replanted, it is
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likely to undergo osseous replacement resorption and, over time, the tooth will become ankylosed and ultimately will be lost.76 Because pediatric dentists need to consider the growth and development of the child patient, the goal for a tooth that has been avulsed for greater than 60 minutes with dry storage is to delay the osseous replacement and, hence, ankylotic process as long as possible. To slow down this process, the remaining PDL should be removed because otherwise it becomes a stimulus for inflammation that accelerates infection-related resorption. The remaining PDL can be removed by several methods: gentle scaling and root planning, soft pumice prophylaxis, gauze, or soaking the tooth in 3% citric acid for 3 minutes.75,77 This should be followed by a sodium fluoride treatment for 20 minutes. The rationale for this fluoride soak is based upon evidence that this procedure will delay, but not prevent, ankylosis; fluoroapatite is more resistant to ankylosis than hydroxyapatite.78 When teeth are soaked in fluoride before replantation, it has been shown to reduce significantly the risk of resorption after a follow-up of 5 years.79 Despite these recommendations, teeth that have been out of the oral cavity for greater than 60 minutes with dry storage have a poor prognosis and will not survive long term. Possible contraindications to replantation: There are possible contraindications to tooth replantation. Examples are immunocompromised health, severe congenital cardiac anomalies, severe uncontrolled seizure disorder, severe mental disability, severe uncontrolled diabetes, and lack of alveolar integrity. Current research: Antiresorptive-regenerative therapies may have potential for enhancing the prognosis of avulsed teeth.66 Treatment strategies are directed at avoiding or minimizing inflammation, increasing revascularization, and producing hard barriers in teeth with open apices.2,61,74,80-88
New treatment strategies also are directed at specific clinical challenges that include decoronation as an approach to treat ankylosis in growing children and transplantation of premolars as an approach for replacing avulsed teeth.89,90 Dental practitioners should follow current literature and consider carefully evidence-based recommendations that may enhance periodontal healing and revascularization of avulsed permanent teeth. Orthodontic movement of traumatized teeth Teeth that have been traumatized must be evaluated carefully prior to beginning or continuing orthodontic movement. Even with more simple crown/root fractures without pulpal involvement, a 3 month wait is recommended before tooth movement should begin. Other minor trauma to the tooth and periodontium (eg, minor concussions, subluxations, and extrusions) also require a 3 month wait. When there has been moderate to severe trauma/damage to the periodontium, a minimum of 6 months wait is recommended.91,92 Teeth that have sustained root fractures cannot be moved for at least 1 year.91,92 Where there is radiographic evidence of healing, these teeth can be moved successfully.93 In teeth that require endodontics, movement can begin once healing is evident.91,92 Because teeth that have sustained severe periodontal injury have been found to undergo pulp necrosis when orthodontic movement was initiated even after a rest period,94,95 light intermittent forces are recommended along with avoidance of prolonged tipping forces and contact with the buccal or lingual cortical plates.92 The use of a mouthguard during fixed appliance therapy is recommended. Studies have found the most effective is a modified custom mouthguard.96,97 The newer stock ortho-channel mouthguards may be more convenient, but there are no studies to date on their effectiveness.96
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EXTRAORAL EXAM
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american academy of pediatric dentistry
This sample form, developed by the American Academy of Pediatric Dentistry, is provided as a practice tool for pediatric dentists and other dentists treating children. It was developed by experts in pediatric dentistry and is offered to facilitate excellence in practice. However, this form does not establish or evidence a standard of care. In issuing this form, the American Academy of Pediatric Dentistry is not engaged in rendering legal or other professional advice. If such services are required, competent legal or other professional counsel should be sought.
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References 1. Flores M, Andersson L, Andreasen J, et al. Guidelines for the management of traumatic dental injuries. I. Fractures and luxations of permanent teeth. Dental Traumatol 2007;23(2):66-71. 2. Flores M, Andersson L, Andreasen J, et al. Guidelines for the management of traumatic dental injuries. II. Avulsion of permanent teeth. Dental Traumatol 2007; 23(3):130-6. 3. Flores M, Malmgren B, Andersson L, et al. Guidelines for the management of traumatic dental injuries. III. Primary teeth. Dental Traumatol 2007;23(4):196-202. 4. Cortes MI, Marcenes W, Shelham A. Impact of traumatic injuries to the permanent teeth on the oral healthrelated quality of life in 12- to 14-year old children. Community Dent Oral Epidemiol 2002;30(3):193-8. 5. Lee J, Divaris K. Hidden consequences of dental trauma: The social and psychological effects. Pediatr Dent 2009;31(2):96-101. 6. Flores MT. Traumatic injuries in the primary dentition. Dental Traumatol 2002;18(6):287-98. 7. Rocha MJ, Cardoso M. Traumatized permanent teeth in Brazilian children assisted at the Federal University of Santa Catarina, Brazil. Dental Traumatol 2001; 17(6):245-9. 8. Caldas AF Jr, Burgos ME. A retrospective study of traumatic dental injuries in a Brazilian dental trauma clinic. Dental Traumatol 2001;17(6):250-3. 9. Skaare AB, Jacobsen I. Dental injuries in Norwegians aged 7-18 years. Dental Traumatol 2003;19(2):67-71. 10. Tapias MA, Jiménez-Garcia R, Lamas F, Gil AA. Prevalence of traumatic crown fractures to permanent incisors in a childhood population: Móstoles, Spain. Dental Traumatol 2003;19(3):119-22. 11. Gassner R, Bosch R, Tuli T, Emshoff R. Prevalence of dental trauma in 6000 patients with facial injuries: Implications for prevention. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1999;87(1):27-33. 12. Ranalli DN. Sports dentistry and dental traumatology. Dental Traumatol 2002;18(5):231-6. 13. American Academy of Pediatric Dentistry. Policy on prevention of sports-related orofacial injuries. Pediatr Dent 2010;32(special issue):55-8. 14. Saroğlu I, Sönmez H. The prevalence of traumatic injuries treated in the pedodontic clinic of Ankara University, Turkey, during 18 months. Dental Traumatol 2002;18(6): 299-303. 15. Sae-Lim V, Chulaluk K, Lim LP. Patient and parental awareness of the importance of immediate management of traumatized teeth. Endod Dent Traumatol 1999;15(1):37-41. 16. Pacheco L, Filho P, Letra A, Menezes R, Villoria G, Ferreira S. Evaluation of the knowledge of the treatment of avulsions in elementary school teachers in Rio de Janeiro, Brazil. Dental Traumatol 2003;19(2):76-8. 17. Lin S, Levin L, Emodi O, Fuss Z, Peled M. Physician and emergency medical technicians’ knowledge and experience regarding dental trauma. Dental Traumatol 2006;22(3):124-6. 210
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18. Andreasen JO, Andreasen FM, Skeie A, Hjørting-Hansen E, Schwartz O. Effect of treatment delay upon pulp and periodontal healing of traumatic dental injuries: A review article. Dental Traumatol 2002;18(3):116-28. 19. American Academy of Pediatric Dentistry. Policy on emergency oral care for infants, children, and adolescents. Pediatr Dent 2007;29(suppl):21. 20. DiScala C, Sege R, Guohua L, Reece RM. Child abuse and unintentional injuries. Arch Pediatr Adolesc Med 2000;154(1):16-22. 21. Andreasen JO, Andreasen FM. Essentials of Traumatic Injuries to the Teeth. 2nd ed. Copenhagen, Denmark: Munksgaard and Mosby; 2000:9-154. 22. Day P, Duggal M. A multicentre investigation into the role of structured histories for patients with tooth avulsion at their initial visit to a dental hospital. Dental Traumatol 2003;19(5):243-7. 23. Holan G, McTigue D. Introduction to dental trauma: Managing traumatic injuries in the primary dentition. In: Pinkham JR, Casamassimo PS, Fields HW Jr, McTigue DJ, Nowak A, eds. Pediatric Dentistry: Infancy through Adolescence. 4th ed. St. Louis, Mo: Elsevier Saunders; 2005:236-56. 24. Andreasen JO, Andreasen FM. Textbook and Color Atlas of Traumatic Injuries to the Teeth. 4th ed. Copenhagen, Denmark: Munksgaard; 2007:897. 25. Borum M, Andreasen JO. Sequelae of trauma to primary maxillary incisors. 1. Complications in the primary dentition. Endod Dent Traumatol 1998;14(1):31-44. 26. Fried I, Erickson P. Anterior tooth trauma in the primary dentition: Incidence, classification, treatment methods, and sequelae: A review of the literature. J Dent Child 1995(4):256-61. 27. Ravn JJ. Sequelae of acute mechanical trauma in the primary dentition. J Dent Child 1968;35(4):281-9. 28. Soporowski NJ, Allred EN, Needleman HL. Luxation injuries of primary anterior teeth: Prognosis and related correlates. Pediatr Dent 1994;16(2):96-101. 29. American Academy of Pediatric Dentistry. Pediatric Dental Trauma Card–Primary Teeth, Permanent Teeth. Chicago, Ill: American Academy of Pediatric Dentistry; 2002:2. 30. Borum M, Andreasen J. Sequelae of trauma to primary maxillary incisors. Complications in the primary dentition. Endod Dent Traumatol 1998;14(1):31-44. 31. Christophersen P, Freund M, Harild L. Avulsion of primary teeth and sequelae on the permanent successors. Dental Traumatol 2005;21(6):320-3. 32. McTigue DJ. Managing traumatic injuries in the young permanent dentition. In: Pinkham JR, Casamassimo PS, Fields HW Jr, McTigue DJ, Nowak A, eds. Pediatric Dentistry: Infancy through Adolescence. 4th ed. St. Louis, Mo: Elsevier Saunders; 2005:593-607. 33. Macedo G, Ritter A. Essentials of rebonding tooth fragments for the best functional and esthetic outcomes. Pediatr Dent 2009;31(2):110-6. 34. Cengiz SB, Atac AS, Cehreli ZC. Biomechanical effects of splint types on traumatized tooth: A photoelastic stress analysis. Dental Traumatol 2006;22(3):133-8.
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35. McDonald N, Strassler HE. Evaluation for tooth stabilization and treatment of traumatized teeth. Dent Clin North Am 1999;43(1):135-49. 36. Olikarinen K. Tooth splinting: Review of the literature and consideration of the versatility of a wire composite splint. Endod Dent Traumatol 1990;6(6):237-50. 37. Olikarinen K, Andreasen JO, Andreasen FM. Rigidity of various fixation methods used as dental splints. Endod Dent Traumatol 1992;8(3):113-9. 38. von Arx T, Filippi A, Lussi A. Comparison of a new dental trauma splint device (TTS) with three commonly used splinting techniques. Dental Traumatol 2001; 17(6):266-74. 39. Cvek M, Andreasen J, Borum M. Healing of 208 intra-alveolar root fractures in patients aged 7-17 years. Dental Traumatol 2001;17(2):53-62. 40. Ravn JJ. Follow-up study of permanent incisors with enamel cracks as a result of acute trauma. Scand J Dent Res 1981;89(2):117-23. 41. Robertson A. A retrospective evaluation of patients with uncomplicated crown fractures and luxation injuries. Endod Dent Traumatol 1998;14(6):245-56. 42. Olsburgh S, Jacoby T, Krejci I. Crown fractures in the permanent dentition: Pulpal and restorative considerations. Dental Traumatol 2002;18(3):103-15. 43. Ravn JJ. Follow-up study of permanent incisors with enamel fractures as a result of acute trauma. Scand J Dent Res 1981;89(3):213-7. 44. Ravn JJ. Follow-up study of permanent incisors with enamel-dentin fractures as a result of acute trauma. Scand J Dent Res 1981;89(5):355-65. 45. Jackson N, Waterhouse P, Maguire A. Factors affecting treatment outcomes following complicated crown fractures managed in primary and secondary care. Dental Traumatol 2006;22(4):179-85. 46. Freely L, Mackie IC, Macfarlane T. An investigation of root-fractured permanent incisor teeth in children. Dental Traumatol 2003;19(1):52-4. 47. Andreasen JO, Andreasen FM, Mejàre I, Cvek M. Healing of 400 intra-alveolar root fractures. 1. Effect of preinjury and injury factors such as sex, age, stage of root development, fracture type, location on fracture and severity of dislocation. Dental Traumatol 2004;20(4): 192-202. 48. Andreasen JO, Andreasen FM, Mejàre I, Cvek M. Healing of 400 intra-alveolar root fractures. 2. Effect of treatment factors such as treatment delay, repositioning, splinting type and period of antibiotics. Dental Traumatol 2004;20(4):203-11. 49. Crona-Larsson G, Bjarnason S, Norén J. Affect of luxation injuries on permanent teeth. Endod Dent Trau-matol 1991;7(5):199-206. 50. Nikoui M, Kenny D, Barrett E. Clinical outcomes for permanent incisor luxations in a pediatric population. III. Lateral luxations. Dental Traumatol 2003;19(5): 280-5.
51. Humphrey J, Kenny D, Barrett E. Clinical outcomes for permanent incisor luxations in a pediatric population. I. Intrusions. Dental Traumatol 2003;19(5): 266-73. 52. Gondim JO, Moreira Neto JJ. Evaluation of intruded primary incisors. Dental Traumatol 2005;21(3):131-3. 53. Holan G, Ram D. Sequelae and prognosis of intruded primary incisors: A retrospective study. Pediatr Dent 1999;21(4):242-7. 54. Andreasen JO, Bakland L, Andreasen FM. Traumatic intrusion of permanent teeth. Part 2. A clinical study of the effect of preinjury and injury factors, such as sex, age, stage of root development, tooth location, and extent of injury including number of intruded teeth on 140 intruded permanent teeth. Dental Traumatol 2006;22 (2):90-8. 55. Andreasen JO, Bakland L, Andreasen FM. Traumatic intrusion of permanent teeth. Part 3. A clinical study of the effect of treatment variables such as treatment delay, method of repositioning, type of splint, length of splinting and antibiotics on 140 teeth. Dental Traumatol 2006;22(2):99-111. 56. Lee R, Barrett E, Kenny D. Clinical outcomes for permanent incisor luxations in a pediatric population. Dental Traumatol 2003;19(5):274-9. 57. Flores MT, Andreasen JO, Bakland LK, et al. Guidelines for the evaluation and management of traumatic dental injuries (part 2 of the series). Dental Traumatol 2001;17(2):49-52. 58. American Association of Endodontists. Treatment of the avulsed permanent tooth. Recommended guidelines of the American Association of Endodontists. Dent Clin North Am 1995;39(1):221-5. 59. Barrett EJ, Kenny DJ. Avulsed permanent teeth: A review of the literature and treatment guidelines. Endod Dent Traumatol 1997;13(4):153-63. 60. McIntyre J, Lee J, Trope M, Vann WJ, Permanent tooth replantation following avulsion: Using a decision tree to achieve the best outcome. Pediatr Dent 2009; 31(2):137-44. 61. Trope M. Clinical management of the avulsed tooth: Present strategies and future directions. Dental Traumatol 2002;18(1):1-11. 62. Sigalas E, Regan J, Kramer P, Witherspoon D, Opperman L. Survival of human periodontal ligament cells in media proposed for transport of avulsed teeth. Dental Traumatol 2004;20(1):21-8. 63. Andreasen JO, Borum MK, Jacobsen HL, Andreasen FM. Replantation of 400 avulsed permanent incisors: 4. Factors related to periodontal ligament healing. Endod Dent Traumatol 1995;11(2):76-89. 64. Barrett EJ, Kenny DJ. Survival of avulsed permanent maxillary incisors in children following delayed replantation. Endod Dent Traumatol 1997;13(6):269-75. 65. Hiltz J, Trope M. Vitality of human lip fibroblasts in milk, Hank’s Balanced Salt Solution, and Viaspan storage media. Endod Dent Traumatol 1991;7(2):69-72. CLINICAL GUIDELINES
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66. Pohl Y, Filippi A, Kirschner H. Results after replantation of avulsed permanent teeth. II. Periodontal healing and the role of physiologic storage and antiresorptiveregenerative therapy. Dental Traumatol 2005;21(2): 93-101. 67. Chappuis V, von Arx T. Replantation of 45 avulsed permanent teeth: A 1-year follow-up study. Dental Traumatol 2005;21(5):289-96. 68. Donaldson M, Kinirons M. Factors affecting the time of onset of resorption in avulsed and replanted incisor teeth in children. Dental Traumatol 2005;21(5):205-9. 69. Barrett E, Kenny D, Tenenbaum H, Sigal M, Johnston D. Replantation of permanent incisors in children using Emdogain®. Dental Traumatol 2005;21(5): 269-75. 70. Malmgren B, Malmgren O. Rate of infraposition of reimplanted ankylosed incisors related to age and growth in children and adolescents. Dental Traumatol 2002; 18(1):28-36. 71. American Academy of Pediatric Dentistry. Clinical management of avulsed permanent incisors flowcharts. Available at: “http://www.aapd.org/media/Policies_Guidelines/ RS_TraumaFlowSheet.pdf ”. 72. Kling M, Cvek M, Mejare I. Rate of predictability of pulp revascularization in therapeutically reimplanted permanent incisors. Endod Dent Traumatol 1986;2(3): 83-9. 73. Cvek M, Cleaton-Jones P, Austin J, Lownie J, Kling M, Fatti P. Pulp revascularization in reimplanted immature monkey incisors – Predictability and the effect of antibiotic systemic prophylaxis. Endod Dent Traumatol 1990;6(4):157-69. 74. Cvek M, Cleaton-Jones P, Austin J, Lownie J, Kling M, Fatti P. Effect of topical application of doxycycline on pulp revascularization and periodontal healing in reimplanted monkey incisors. Endod Dent Traumatol 1990; 6(4):170-6. 75. Yanpiset K, Trope M. Pulp revascularization of replanted immature dog teeth after different treatment methods. Endod Dent Traumatol 2000;16(5):211-7. 76. Kinirons M, Boyd D, Gregg T. Inflammatory and replacement resorption in reimplanted permanent incisor teeth: A study of the characteristics of 84 teeth. Endod Dent Traumatol 1999;15(6):269-72. 77. Nyman S, Houston F, Sarhed G, Lidhe J, Karring T. Healing following reimplantation of teeth subjected to root planing and citric acid treatment. J Clin Periodontol 1985;12(4):294-305. 78. Selvig KA, Zander HA. Chemical analysis and microradiography of cementum and dentin from periodontally diseased human teeth. J Periodontol 1962;33: 303-10. 79. Coccia C. A clinical investigation of root resorption rates in reimplanted young permanent incisors: A fiveyear study. J Endod 1980;6(1):413-20. 80. Bryson E, Levin L, Banchs F, Trope M. Effect of minocycline on healing of replanted dog teeth after extended dry times. Dental Traumatol 2003;19(2):90-5. 212
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81. Filippi A, Pohl Y, von Arx T. Treatment of replacement resorption with Emdogain®—Preliminary results after 10 months. Dental Traumatol 2001;17(3):134-8. 82. Finucane D, Kinirons M. External inflammatory and replacement resorption of luxated and avulsed replanted permanent incisors: A review and case presentation. Dental Traumatol 2003;19(3):170-4. 83. Khin Ma M, Sae-Lim V. The effect of topical minocycline on replacement resorption of replanted monkeys’ teeth. Dental Traumatol 2003;19(2):96-102. 84. Maroto M, Barberia E, Planells P, Vera V. Treatment of a non-vital immature incisor with mineral trioxide aggregate (MTA). Dental Traumatol 2003;19(3):165-9. 85. Rafter M. Apexification: A review. Dental Traumatol 2005;21(1):1-8. 86. Schjøtt M, Andreasen JO. Emdogain® does not prevent progressive root resorption after replantation of avulsed teeth: A clinical study. Dental Traumatol 2005; 21(1):46-50. 87. Trope M. A futuristic look at dental trauma. New York, NY: Presentation at the American Academy of Pediatric Dentistry 56th Annual Session; 2003. 88. Villa P, Fernández R. Apexification of a replanted tooth using mineral trioxide aggregate. Dental Traumatol 2005;21(5):306-8. 89. Andreasen J, Schwartz O, Kofoed T, Daugaard-Jensen J. Transplantation of premolars as an approach for replacing avulsed teeth. Pediatr Dent 2009;31(2):129-32. 90. Sigurdsson A. Decoronation as an approach to treat ankylosis in growing children. Pediatr Dent 2009;21 (2):123-28. 91. Kindelan S, Day P, Kindelan J, Spencer J, Duggal M. Dental trauma: An overview of its influence on the management of orthodontic treatment. Part 1. J Orthod 2008;35(2):68-78. 92. Malmgren O, Malmgren B. Orthodontic management of the traumatized dentition. In: Andreasen J, Andreasen F, Andersson L, eds. Textbook and Color Atlas of Traumatic Injuries to the Teeth. 4 th ed. Ames, Iowa: Blackwell Munksgaard; 2007:669-716. 93. Duggan D, Quinn F, O'Sullivan M. A long-term follow up of spontaneously healed root fractures later subjected to orthodontic forces - Two case reports. Dental Traumatol 2008;24(2):231-4. 94. Bauss O, Rohling J, Rahman A, Kiliaridis S. The effect of pulp obliteration on pulpal vitality of orthodontically intruded traumatized teeth. J Endod 2008;34(4): 417-20. 95. Bauss O, Rohling J, Sadat-Khonsari R. Influence of orthodontic intrusion on pulpal vitality of previously traumatized maxillary permanent incisors. Am J Orthod Dentofacial Orthop 2008;134(1):12-17. 96. Salam S, Caldwell S. Mouthguards and orthodontic patients. J Orthod 2008;35(4):270-75. 97. Sigurdsson A. Prevention of dental and oral injuries. In: Andreasen J, Andreasen F, Andersson L, eds. Textbook and Color Atlas of Traumatic Injuries to the Teeth. 4th ed. Ames, Iowa: Blackwell Munksgaard; 2007:814-34.
American academy of pediatric Dentistry
Guideline on Management of the Developing Dentition and Occlusion in Pediatric Dentistry Originating Committee
Clinical Affairs Committee – Developing Dentition Subcommittee Review Council Council on Clinical Affairs
Adopted 1990
Revised 1991, 1998, 2001, 2005, 2009
Purpose The American Academy of Pediatric Dentistry (AAPD) recognizes the importance of managing the developing dentition and occlusion and its effect on the well-being of infants, children, and adolescents. Management includes the recognition, diagnosis, and appropriate treatment of dentofacial abnormalities. This guideline is intended to set forth objectives for management of the developing dentition and occlusion in pediatric dentistry.
Methods This revision is based upon a new MEDLINE search using the following parameters: Terms: ankylosis, anterior crossbite, Class II malocclusion, Class III malocclusion, dental crowding, ectopic eruption, impaction, obstruction sleep apnea syndrome (OSAS), occlusal development, oligodontia, oral habits, posterior crossbite, space maintenance, and tooth size/arch length discrepancy; Field: all fields; Limits: within the last 10 years, humans, English, and birth through age 18. Papers for review were chosen from this search and from references within selected articles. When data did not appear sufficient or were inconclusive, recommendations were based upon expert and/or consensus opinion by experienced researchers and clinicians.
Background Guidance of eruption and development of the primary, mixed, and permanent dentitions is an integral component of comprehensive oral health care for all pediatric dental patients. Such guidance should contribute to the development of a permanent dentition that is in a stable, functional, and esthetically acceptable occlusion. Early diagnosis and successful treatment of developing malocclusions can have both short-term and longterm benefits while achieving the goals of occlusal harmony and function and dentofacial esthetics.1-4 Dentists have the responsibility to recognize, diagnose, and either appropriately manage or refer abnormalities in the developing dentition as dictated by the complexity of the problem and the individual clinician’s training, knowledge, and experience.5
Many factors can affect the management of the developing dental arches and minimize the overall success of any treatment. The variables associated with the treatment of the developing dentition that will affect the degree to which treatment is successful include, but are not limited to: 1. chronological/mental/emotional age of the patient and the patient’s ability to understand and cooperate in the treatment; 2. intensity, frequency, and duration of an oral habit; 3. parental support for the treatment; 4. compliance with clinician’s instructions; 5. craniofacial configuration; 6. craniofacial growth; 7. concomitant systemic disease or condition; 8. accuracy of diagnosis; 9. appropriateness of treatment. A thorough clinical examination, appropriate pretreatment records, differential diagnosis, sequential treatment plan, and progress records are necessary to manage any condition affecting the developing dentition. Clinical examination should include: 1. facial analysis to: a. identify adverse transverse growth patterns includ ing asymmetries (maxillary and mandibular); b. identify adverse vertical growth patterns; c. identify adverse sagittal (anteroposterior) growth patterns and dental anteroposterior (AP) occlusal disharmonies; d. assess esthetics and identify orthopedic and ortho dontic interventions that may improve esthetics and resultant self-image and emotional development. 2. intraoral examination to: a. assess overall oral health status; b. determine the functional status of the patient’s occlusion. 3. functional analysis to: a. determine functional factors associated with the malocclusion; CLINICAL GUIDELINES
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b. detect deleterious habits; c. detect temporomandibular joint dysfunction, which may require additional diagnostic pro cedures. Diagnostic records may be needed to assist in the evaluation of the patient’s condition and for documentation purposes. Prudent judgment is exercised to decide the appropriate records required for diagnosis of the clinical condition.6 Diagnostic orthodontic records fall into 3 major categories of evaluation: (1) health of the teeth and oral structures, (2) alignment and occlusal relationships of the teeth, and (3) facial and jaw proportions which includes both cephalometric radiographs and facial photographs. Digital images rapidly are replacing film, but both are acceptable as records.6 Diagnostic records may include: 1. extraoral and intraoral photographs to: a. supplement clinical findings with oriented facial and intraoral photographs; b. establish a database for documenting facial changes during treatment. 2. diagnostic dental casts to: a. assess the occlusal relationship; b. determine arch length requirements for intraarch tooth size relationships; c. determine arch length requirements for interarch tooth size relationships; d. determine location and extent of arch asymmetry. 3. intraoral and panoramic radiographs to: a. establish dental age; b. assess eruption problems; c. estimate the size and presence of unerupted teeth; d. identify dental anomalies/pathology. 4. lateral and AP cephalograms to: a. produce a comprehensive cephalometric analysis of the relative dental and skeletal components in the anteroposterior, vertical, and transverse dimensions; b. establish a baseline growth record for longitudinal assessment of growth and displacement of the jaws. 5. other diagnostic views (eg, magnetic resonance ima ging, computed tomographic scans) for hard and soft tissue imaging as indicated by history and clinical examination. A differential diagnosis and diagnostic summary are completed to: 1. establish the relative contributions of the dental and skeletal structures to the patient’s malocclusion; 2. prioritize problems in terms of relative severity; 3. detect favorable and unfavorable interactions that may result from treatment options for each problem area; 4. establish short-term and long-term objectives; 5. summarize the prognosis of treatment for achieving stability, function, and esthetics. A sequential treatment plan will: 1. establish timing priorities for each phase of therapy;
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2. 3.
establish proper sequence of treatments to achieve short-term and long-term objectives; assess treatment progress and update the biomechanical protocol accordingly on a regular basis.
Stages of development of occlusion General considerations and principles of management: The stages of occlusal development include: 1. Primary dentition: Beginning in infancy with the eruption of the first tooth, usually about 6 months of age, and complete from approximately 3 to 6 years of age when all primary teeth are erupted. 2. Mixed dentition: From approximately age 6 to 13, primary and permanent teeth are present in the mouth. 3. Adolescent dentition: All primary teeth have exfoli ated, second permanent molars may be erupted or erupting, and third molars have not erupted. 4. Adult dentition: All permanent teeth are present and eruptive growth is complete.7-10 These stages may further be divided and referenced as “early” and “late” (eg, early primary, late primary, early mixed, late mixed).7-10 Evaluation and treatment of occlusal and skeletal disharmonies may be initiated at various stages of dental arch development, depending on the problems, growth, parental involvement, risks and benefits of treatment and of withholding treatment, and interest/ability of the practitioner.5 Historically, orthodontic treatment was provided mainly for adolescents. Interest continues to be expressed in early treatment as well as in adult treatment. Treatment and timing options for the growing patient, especially in the mixed dentition and early permanent dentition, have increased and continue to be evaluated by the research community.9,11-13 Many clinicians seek to modify skeletal, muscular, and dentoalveolar abnormalities before the eruption of the full permanent dentition.7 A thorough knowledge of craniofacial growth and development of the dentition, as well as orthodontic treatment, must be used in diagnosing and reviewing possible treatment options before recommendations are made to parents.9 Early treatment is beneficial for many children but may not be indicated for every patient. Treatment considerations: The developing dentition should be monitored throughout eruption. This monitoring at regular clinical examinations should include, but not be limited to, diagnosis of missing, supernumerary, developmentally defective, and fused or geminated teeth; ectopic eruption; and space and tooth loss secondary to caries. Radiographic examination, when appropriate14 and feasible, should accompany clinical examination. Diagnosis of anomalies of primary or permanent tooth development and eruption should be made to inform the patient’s parent and to plan and recommend appropriate intervention. This evaluation is ongoing throughout the developing dentition, at all stages.6-10
American academy of pediatric Dentistry
1. Primary dentition stage: Anomalies of primary teeth and eruption may not be evident/diagnosable prior to eruption, due to the child’s not presenting for dental examination or to a radiographic examination not being possible in a young child. Evaluation, however, should be accomplished when feasible. The objectives of evaluation include identification of: a. all anomalies of tooth number and size (as previously noted); b. anterior and posterior crossbites; c. presence of habits along with their dental and skeletal sequelae. Radiographs are taken with appropriate clinical indicators or based upon risk assessment/history. 2. Early mixed dentition stage: Palpation for unerupted teeth should be part of every examination. Panoramic, occlusal, and periapical radiographs, as indicated at the time of eruption of the lower incisors and first permanent molars, provide diagnostic information concerning: a. anomalies of tooth numbers (eg, missing, supernu merary, fused, geminated); b. tooth size and shape (eg, peg or small lateral incisors); c. positions (eg, ectopic first permanent molars). Space analysis can be used to evaluate arch length/crowding at the time of incisor eruption. 3. Mid-to-late mixed dentition stage: Ectopic tooth positions should be diagnosed, especially canines, bi cuspids, and second permanent molars. 4. Adolescent dentition stage: If not instituted earlier, orthodontic diagnosis and treatment should be planned for Class I crowded, Class II, and Class III malocclusions as well as posterior and anterior crossbites. Third molars should be monitored as to position and space, and parents should be informed. 5. Early adult dentition stage: Third molars should be evaluated. If orthodontic diagnosis has not been ac complished, recommendations should be made as necessary. Objectives: At each stage, the objectives of intervention/treatment include reducing adverse growth, preventing increasing dental and skeletal disharmonies, improving esthetics of the smile and the accompanying positive effects on self-image, and improving the occlusion. 1. Primary dentition stage: Habits and posterior crossbites should be diagnosed and addressed as early as feasible. Parents should be informed about findings of adverse growth and developing malocclusions. Interventions/ treatment can be recommended if diagnosis can be made, treatment is appropriate and possible, and parents are supportive and desire to have treatment done. 2. Early mixed stage: Treatment should address: (1) habits; (2) arch length shortage; (3) intervention for
3. 4. 5.
crowded incisors; (4) intervention for ectopic molars and incisors; (5) holding of leeway space; (6) crossbites; and (7) adverse skeletal growth. Treatment should take advantage of high rates of growth and prevent worsened adverse dental and skeletal growth. Mid-to-late mixed dentition stage: Intervention for ectopic teeth may include extractions and space maintenance to aid eruption and reduce the risk of need for surgical bracket placement and orthodontic traction. Intervention for treatment of skeletal disharmonies and crowding may be instituted at this stage. Adolescent dentition stage: In full permanent dentition, final orthodontic diagnosis and treatment can provide the most functional occlusion. Early adult dentition stage: Third molar position or space can be evaluated and, if indicated, the tooth removed. Full orthodontic treatment should be recommended if needed.
Recommendations Oral habits General considerations and principles of management: The habits of nonnutritive sucking, bruxing, tongue thrust swallow and abnormal tongue position, self-injurious/self-mutilating behavior, and airway obstruction (OSAS) are discussed in this guideline. Oral habits may apply forces to the teeth and dentoalveolar structures. The relationship between oral habits and unfavorable dental and facial development is associational rather than cause and effect.15-17 Habits of sufficient frequency, duration, and intensity may be associated with dentoalveolar or skeletal deformations such as increased overjet, reduced overbite, posterior crossbite, or long facial height. The duration of force is more important than its magnitude; the resting pressure from the lips, cheeks, and tongue has the greatest impact on tooth position, as these forces are maintained most of the time.18,19 Nonnutritive sucking behaviors are considered normal in infants and young children. Prolonged nonnutritive sucking habits have been associated with decreased maxillary arch width, increased overjet, decreased overbite, anterior open bite, and posterior crossbite.16,18,19 As preliminary evidence indicates that some changes resulting from sucking habits persist past the cessation of the habit, it has been suggested that early dental visits provide parents with anticipatory guidance to help their children stop sucking habits by age 36 months or younger.16,18,19 Bruxism, defined as the habitual nonfunctional and forceful contact between occlusal surfaces, can occur while awake or asleep. The etiology is multifactorial and has been reported to include central factors (eg, emotional stress,20 parasomnias,21 traumatic brain injury,22 neurologic disabilities 23) and morphologic factors (eg, malocclusion24, muscle recruitment25). Reported complications include dental attrition, headaches, temporomandibular dysfunction, and soreness of the masticatory muscles.20 Preliminary evidence suggests that juvenile
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bruxism is a self-limiting condition that does not progress to adult bruxism.26 The spectrum of bruxism management ranges from patient/parent education, occlusal splints, and psychological techniques to medications.20,22,27,28 Tongue thrusting, an abnormal tongue position and deviation from the normal swallowing pattern, may be associated with anterior open bite, abnormal speech, and anterior protrusion of the maxillary incisors.17 There is no evidence that intermittent short-duration pressures, created when the tongue and lips contact the teeth during swallowing or chewing, have significant impact on tooth position.17,18 If the resting tongue posture is forward of the normal position, incisor displacement is likely, but if resting tongue posture is normal, a tongue thrust swallow has no clinical significance.18 Self-injurious or self-mutilating behavior (ie, repetitive acts that result in physical damage to the individual) is extremely rare in the normal child.29 Such behavior, however, has been associated with mental retardation, psychiatric disorders, developmental disabilities, and some syndromes.30 The spectrum of treatment options for developmentally disabled individuals includes pharmacologic management, behavior modification, and physical restraint.31 Reported dental treatment modalities include, among others, lip-bumper and occlusal bite appliances, protective pad-ding, and extractions.29 Some habits, such as lip-licking and lip-pulling, are relatively benign in relation to an effect on the dentition.29 More severe lip- and tongue-biting habits may be associated with profound neurodisability due to severe brain damage.31 Management options include monitoring the lesion, odontoplasty, providing a bite-opening appliance, or extracting the teeth.31 Research on the relationship between malocclusion and mouth breathing suggests that impaired nasal respiration may contribute to the development of increased facial height, anterior open bite, increased overjet, and narrow palate, but it is not the sole or even the major cause of these conditions.32 OSAS may be associated with narrow maxilla, crossbite, low tongue position, vertical growth, and open bite. History associated with OSAS may include snoring, observed apnea, restless sleep, daytime neurobehavioral abnormalities or sleepiness, and bedwetting. Physical findings may include growth abnormalities, signs of nasal obstruction, adenoidal facies, and/or enlarged tonsils.32-34 The identification of an abnormal habit and the assessment of its potential immediate and long-term effects on the craniofacial complex and dentition should be made as early as possible. The dentist should evaluate habit frequency, duration, and intensity in all patients with habits. Intervention to terminate the habit should be initiated if indicated.17 Patients and their parents should be provided with information regarding consequences of a habit. Parents may play a negative role in the correction of an oral habit as nagging or punishment may result in an increase in habit behaviors; change in the home environment may be necessary before a habit can be overcome.16
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Treatment considerations: Management of an oral habit is indicated whenever the habit is associated with unfavorable dentofacial development or adverse effects on child health or when there is a reasonable indication that the oral habit will result in unfavorable sequelae in the developing permanent dentition. Any treatment must be appropriate for the child’s development, comprehension, and ability to cooperate. Habit treatment modalities include patient/parent counseling, behavior modification techniques, myofunctional therapy, appliance therapy, or referral to other providers including, but not limited to, orthodontists, psychologists, myofunctional therapists, or otolaryngologists. Use of an appliance to manage oral habits is indicated only when the child wants to stop the habit and would benefit from a reminder.17 Objectives: Treatment is directed toward decreasing or eliminating the habit and minimizing potential deleterious effects on the dentofacial complex. Disturbances in number Congenitally missing teeth General considerations and principles of management: Hypodontia, the congenital absence of 1 or more permanent teeth, has a prevalence of 3.5% to 6.5%.35,36 Excluding third molars, the most frequently missing permanent tooth is the mandibular second premolar followed by the maxillary lateral incisor.36,37 In the primary dentition, hypodontia occurs less (0.1% to 0.9% prevalence) and almost always affects the maxillary incisors and first primary molars.39 The chance of familial occurrence of 1 or 2 congenitally missing teeth is to be differentiated from missing lateral incisors in cleft lip/palate40 and multiple missing teeth (6 or more) due to ectodermal dysplasia or other syndromes41 as the treatment usually differs. A congenitally missing tooth should be suspected in patients with cleft lip/palate, certain syndromes, and a familial pattern of missing teeth. In addition, patients with asymmetric eruption sequence or ankylosis of a primary mandibular second molar may have a congenitally missing tooth. Treatment considerations: With congenitally missing permanent maxillary incisor(s) or mandibular second premolar(s), the decision to extract the primary tooth and close the space orthodontically versus opening the space orthodontically and placing a prosthesis or implant depends on many factors. For maxillary laterals, the dentist may move the maxillary canine mesially and use the canine as a lateral incisor or create space for a future lateral prosthesis or implant.17,41 Factors that influence the decision are: (1) patient age; (2) canine shape; (3) canine position; (4) child’s occlusion and amount of crowding; (5) bite depth; and (6) quality and quantity of bone in the edentulous area.42,43 Early extraction of the primary canine and/or lateral may be needed.42,43 Opening space for a prosthesis or implant requires less tooth movement, but the space needs to be maintained with an interim prosthesis, especially if an implant is planned.41,42 Moving the canine into the lateral position produces little facial change, but the resultant tooth size discrepancy often does not allow a canine guided occlusion.42,44
American academy of pediatric Dentistry
For a congenitally missing premolar, the primary molar either may be maintained or extracted with subsequent placement of a prosthesis or orthodontically closing the space. Maintaining the primary second molar may cause occlusal problems due to its larger mesiodistal diameter, compared to the second premolar. Reducing the width of the second primary molar is a consideration, but root resorption and subsequent exfoliation may occur.17 In crowded arches or with multiple missing premolars, extraction of the primary molar(s) can be considered, especially in mild Class III cases.17 For a single missing premolar, if maintaining the primary molar is not possible, placement of a prosthesis or implant should be considered.17,41 Consultation with an orthodontist and/or prosthodontist may be required. In addition, preserving the primary tooth may be indicated in certain cases. Objectives: Treatment is directed toward an esthetically pleasing occlusion that functions well for the patient. Supernumerary teeth (primary, permanent, and mesiodens) General considerations and principles of management: Supernumerary teeth, or hyperdontia, can occur in the primary or permanent dentition but are 5 times more common in the permanent.36 Prevalence is reported in the primary and mixed dentitions from 0.52% to 2%.36,38,46 Between 80% and 90% of all supernumeraries occur in the maxilla, with half in the anterior area and almost all in the palatal position.36,47 A supernumerary primary tooth is followed by a supernumerary permanent tooth in one third of the cases.48 During the early mixed dentition, 79% to 91% of anterior permanent supernumerary teeth are unerupted.46,49 While more erupt with age, only 25% of all mesiodens (a permanent supernumerary incisor located at the midline) erupt spontaneously.47 Mesiodens can prevent or cause ectopic eruption of a central incisor. Less frequently, a mesiodens can cause dilaceration or resorption of the permanent incisor’s root. Dentigerous cyst formation involving the mesiodens, in addition to eruption into the nasal cavity, has been reported.47,50 If there is an asymmetric eruption pattern of the maxillary incisors, delayed eruption, an overretained primary incisor, or ectopic eruption of an incisor, a supernumerary can be suspected.36,45 Panoramic, occlusal, and periapical radiographs all can reveal a supernumerary, but the best way to locate the supernumerary is 2 periapical or occlusal films reviewed by the parallax rule.47 Treatment considerations: Management and treatment of hyperdontia differs if the tooth is primary or permanent. Primary supernumerary teeth normally are accommodated into the arch and usually erupt and exfoliate without complications.48 Extraction of an unerupted supernumerary tooth during the primary dentition usually is not done to allow it to erupt; surgical extraction of unerupted supernumerary teeth can displace or damage the permanent incisor.47 Removal of a mesiodens or other permanent supernumerary incisor results in eruption of the permanent adjacent normal incisor in 75% of the cases.51 Extraction of an unerupted supernumerary during the early mixed dentition allows for a normal eruptive force and eruption
of the permanent adjacent normal incisor.52,53 Later removal of the mesiodens reduces the likelihood that the adjacent normal permanent incisor will erupt on its own, especially if the apex is completed.47 Inverted conical supernumeraries can be harder to remove if removal is delayed, as they can migrate deeper into the jaw.45 After removal of the supernumerary, clinical and radiographic follow-up is indicated in 6 months to determine if the normal incisor is erupting. If there is no eruption after 6 to 12 months and sufficient space exists, surgical exposure and orthodontic extrusion is needed.47 Objectives: Removal of supernumerary teeth should facilitate eruption of permanent teeth and encourage normal alignment. In cases where normal alignment or spontaneous eruption does not occur, further orthodontic treatment is indicated. Localized disturbances in eruption Ectopic eruption General considerations and principles of management: Ectopic eruption (EE) of permanent first molars occurs due to the molar’s abnormal mesioangular eruption path, resulting in an impaction at the distal prominence of the primary second molar’s crown. EE can be suspected if asymmetric eruption is observed or if the mesial marginal ridge is noted to be under the distal prominence of the second primary molar. EE of permanent molars can be diagnosed from bitewing or panoramic radiographs in the early mixed dentition. This condition occurs in up to 0.75% of the population,54 but is more common in children with cleft lip and palate.554 The maxillary canine appears in an impacted position in 1.5% to 2% of the population,56,57 while maxillary incisors can erupt ectopically or be impacted from supernumerary teeth in up to 2% of the population.47 Incisors also can have altered eruption due to pulp necrosis (following trauma or caries) or pulpal treatment of the primary incisor.58 EE of permanent molars is classified into 2 types. There are those that self correct or “jump” and others that remain impacted. In 66% of the cases, the molar jumps.59 A permanent molar that presents with part of its occlusal surface clinically visible and part under the distal of the primary second molar normally does not jump and is the impacted type.60 Nontreatment can result in early loss of the primary second molar and space loss. Maxillary canine impaction should be suspected when the canine bulge is not palpable or when asymmetric canine eruption is evident. Panoramic radiographs would show the canine has an abnormal inclination and/or overlaps the lateral incisor root. EE of permanent incisors can be suspected after trauma to primary incisors, with pulpally-treated primary incisors, with asymmetric eruption, or if a supernumerary incisor is diagnosed. Treatment considerations: Treatment depends on how severe the impaction appears clinically and radiographically. For mildly impacted first permanent molars, where little of the tooth is impacted under the primary second molar, elastic or metal orthodontic separators can be placed to wedge the permanent first molar distally.16 For more severe impactions, distal tipping of the permanent molar is required. Tipping action can be accomplished with brass wires, removable appliances using
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springs, fixed appliances such as sectional wires with open coil springs, sling shot-type appliances,60 a Halterman appliance,61 or surgical uprighting.62 Early diagnosis and treatment of impacted maxillary canines can lessen the severity of the impaction and may stimulate eruption of the canine. Extraction of the primary canine is indicated when the canine bulge cannot be palpated in the alveolar process and there is radiographic overlapping of the canine with the formed root of the lateral during the mixed dentition.63 Even when the impacted canine is diagnosed at a later age (11 to 16), if the canine is not horizontal, extraction of the primary canine lessens the severity of the permanent canine impaction and 75% will erupt.64 Extraction of the first primary molar also has been reported to allow eruption of first bicuspids and to assist in the eruption of the cuspids. This need can be determined from a panoramic radiograph.61,65 Bonded orthodontic treatment normally is required to create space or align the canine. Long-term periodontal health of impacted canines after orthodontic treatment is similar to nonimpacted canines.68 Treatment of ectopically erupting incisors depends on the etiology. Extraction of necrotic or over-retained pulpally-treated primary incisors is indicated in the early mixed dentition.58 Removal of supernumerary incisors in the early mixed dentition will lessen ectopic eruption of an adjacent permanent incisor.47 After incisor eruption, orthodontic treatment involving removable or banded therapy may be needed. Objectives: Management of ectopically erupting molars, canines, and incisors should result in improved eruptive positioning of the tooth. In cases where normal alignment does not occur, subsequent comprehensive orthodontic treatment may be necessary to achieve appropriate arch form and intercuspation. Ankylosis General considerations and principles of management: Ankylosis is a condition in which the cementum of a tooth’s root fuses directly to the surrounding bone. The periodontal ligament is replaced with osseous tissue, rendering the tooth immobile to eruptive change. Ankylosis can occur in the primary and permanent dentitions, with the most common incidence involving primary molars. The incidence is reported to be between 7% and 14% in the primary dentition.49 In the permanent dentition, ankylosis occurs most frequently following luxation injuries.67 Ankylosis is common in anterior teeth following trauma and is referred to as replacement resorption. Periodontal ligament cells are destroyed and the cells of the alveolar bone perform most of the healing. Over time, normal bony activity results in the replacement of root structure with osseous tissue.67 Ankylosis can occur rapidly or gradually over time, in some cases as long as 5 years post trauma. It also may be transient if only a small bony bridge forms that can be resorbed with subsequent osteoclastic activity.69 Ankylosis can be verified by clinical and radiographic means. Submergence of the tooth is the primary recognizable sign, but the diagnosis also can be made through percussion
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and palpation. Radiographic examination also may reveal the loss of the periodontal ligament and bony bridging. Treatment considerations: With ankylosis of a primary molar, exfoliation usually occurs normally. Extraction is recommended if prolonged retention of the primary molar is noted. If a severe marginal ridge discrepancy develops, extraction should be considered to prevent the adjacent teeth from tipping and producing space loss.3 Replacement resorption of permanent teeth usually results in the loss of the involved tooth.67 Mildly to moderately ankylosed primary molars without permanent successors may be retained and restored to function in arches without crowding. Extraction of these molars can assist in resolving crowded arches in complex orthodontic cases.65,70 Surgical luxation of ankylosed permanent teeth with forced eruption has been described as an alternative to premature extraction.71 Objectives: Treatment of ankylosis should result in the continuing normal development of the permanent dentition. Or, in the case of replacement resorption of a permanent tooth, appropriate prosthetic replacement should be planned. Tooth size/arch length discrepancy and crowding General considerations and principles of management: Arch length discrepancies include inadequate arch length and crowding of the dental arches, excess arch length and spacing, and tooth size discrepancy, often referred to as a Bolton discrepancy.72 These arch length discrepancies may be found in conjunction with complicating and other etiological factors including missing teeth, supernumerary teeth, and fused or geminated teeth. Inadequate arch length with resulting incisor crowding is a common occurrence with various negative sequelae and is particularly common in the early mixed dentition.73-76 Studies of arch length in today’s children compared to their parents and grandparents of 50 years ago indicate less arch length, more frequent incisor crowding, and stable tooth sizes.77-79 This implies that the problem of incisor crowding and ultimate arch length discrepancies may be increasing in numbers of patients and in amount of arch length shortage.77,78 Arch length and especially crowding must be considered in the context of the esthetic, dental, skeletal, and soft tissue relationships. Mandibular incisors have a high relapse rate in rotations and crowding.73,75 Growth of the aging skeleton causes further crowding and incisor rotations.82 Functional contacts are diminished where rotations of incisors, canines, and bicuspids exist.83 Occlusal harmony and temporomandibular joint health are impacted negatively by less functional contacts.83 Initial assessment may be done in early mixed dentition, when mandibular incisors begin to erupt.73 Evaluation of available space and consideration of making space for permanent incisors to erupt may be done initially utilizing appropriate radiographs to ascertain the presence of permanent successors. Comprehensive diagnostic analysis is suggested, with evaluation of maxillary and mandibular skeletal relationships, direc-
American academy of pediatric Dentistry
tion and pattern of growth, facial profile, facial width, muscle balance, and dental and occlusal findings including tooth positions, arch length analysis, and leeway space. Derotation of teeth just after emergence in the mouth implies correction before the transseptal fiber arrangement has been established. 73,83 It has been shown that the transseptal fibers do not develop until the cementoenamel junction of erupting teeth pass the bony border of the alveolar process.83 Long-term stability of aligned incisors may be increased.84 Treatment considerations: Treatment considerations may include, but are not limited to: 1. making space for permanent incisors to erupt and be come straight naturally through primary canine ex traction and space/arch length maintenance; 2. orthodontic alignment of permanent teeth as soon as erupted and feasible, expansion and correction of arch length as early as feasible; 3. utilizing holding arches in the mixed dentition until all permanent bicuspids and canines have erupted; 4. extractions of permanent teeth; 5. maintaining patient’s original arch form.83 Other treatment modalities may include, but are not limited to: (1) interproximal reduction; (2) restorative bonding; (3) veneers; (4) crowns; (5) implants; and (6) orthognathic surgery. Objectives: Well-timed intervention can: 1. prevent crowded incisors; 2. increase long-term stability of incisor positions; 3. decrease ectopic eruption and impaction of permanent canines; 4. reduce orthodontic treatment time and sequelae; 5. improve gingival health and overall dental health.73, 85,86 Space maintenance General considerations and principles of management: The premature loss of primary teeth due to caries, trauma, ectopic eruption, or other causes may lead to undesirable tooth movements of primary and/or permanent teeth including loss of arch length. Arch length deficiency can produce or increase the severity of malocclusions with crowding, rotations, ectopic eruption, crossbite, excessive overjet, excessive overbite, and unfavorable molar relationships.87 The dental profession has recommended the use of space maintainers to reduce the prevalence and severity of malocclusion following premature loss of primary teeth.17,88,89 Space maintenance may be a consideration in the primary dentition after early loss of a maxillary incisor when the child has an active digit habit. An intense habit may reduce the space for the erupting permanent incisor. Adverse effects associated with space maintainers include: (1) dislodged, broken, and lost appliances; (2) plaque accumulation; (3) caries; (4) interference with successor eruption; (5) undesirable tooth movement; (6) inhibition of alveolar growth; (7) soft tissue impingement; and (8) pain.87,90-92 Premature loss of a primary tooth of any type has the potential to cause loss of space available for the succeeding permanent tooth, but
there is a lack of consensus regarding the effectiveness of space maintainers in preventing or reducing the severity of malocclusion.87,93-95 Treatment considerations: It is prudent to consider space maintenance when primary teeth are lost prematurely. Factors to consider include: (1) specific tooth lost; (2) time elapsed since tooth loss; (3) pre-existing occlusion; (4) favorable space analysis; (5) presence and root development of permanent successor; (6) amount of alveolar bone covering permanent successor; (7) patient’s health status; (8) patient’s cooperative ability; (9) active oral habits; and (10) oral hygiene.17,87 If a space analysis is required prior to the placement of a space maintainer, appropriate radiographs and study models should be considered.96 The literature pertaining to the use of space maintainers specific to the loss of a particular primary tooth type include expert opinion, case reports, and details of appliance design.17,88,89 Treatment modalities may include, but are not limited to: 1. fixed appliances (eg, band and loop, crown and loop, passive lingual arch, distal shoe, Nance appliance, transpalatal arch); 2. removable appliances (eg, partial dentures, Hawley appliance).17,88,89 The placement and retention of space maintaining appliances requires ongoing compliant patient behavior. Follow-up of patients with space maintainers is necessary to assess integrity of cement and to evaluate and clean the abutment teeth.91 The appliance should function until the succedaneous teeth have erupted into the arch. Objectives: The goal of space maintenance is to prevent loss of arch length, width, and perimeter by maintaining the relative position of the existing dentition.17,88 The AAPD supports controlled randomized clinical trials to determine efficacy of space maintainers as well as analysis of costs and side effects of treatment. Space regaining General considerations and principles of management: Some of the more common causes of space loss within an arch are (1) primary teeth with interproximal caries; (2) ectopically erupting teeth; (3) alteration in the sequence of eruption; (4) ankylosis of a primary molar; (5) dental impaction; (6) transposition of teeth; (7) loss of primary molars without proper space management; (8) congenitally missing teeth; (9) abnormal resorption of primary molar roots; (10) premature and delayed eruption of permanent teeth; and (11) abnormal dental morphology.17,87,97 Loss of space in the dental arch that interferes with the desired eruption of the permanent teeth may require evaluation. Space loss may occur unilaterally or bilaterally and may result from teeth tipping, rotating, extruding, being ankylosed, or translating or from extrusion of teeth and the deepening of the curve of Spee.98 The degree to which space is affected varies according to the arch affected, site in the arch, and time elapsed since tooth loss. The quantity and incidence of space loss also are dependent upon which adjacent teeth are present in the dental arch
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and their status.17,87 The amount of crowding or spacing in the dental arch will determine the degree to which space loss has a significant consequence.1,98 Treatment considerations: Treatment modalities may include, but are not limited to, fixed appliances or removable appliances (eg, Hawley appliance, lip bumper, headgear). Space loss and dentofacial skeletal development may dictate that space regaining not be indicated. This should be determined as the result of a comprehensive analysis. The timing of clinical intervention subsequent to premature loss of a primary molar is critical.1 Objectives: The goal of space regaining intervention is the recovery of lost arch width and perimeter and/or improved eruptive position of succedaneous teeth. Space regained should be maintained until adjacent permanent teeth have erupted completely and/or until a subsequent comprehensive orthodontic treatment plan is initiated. Crossbites (dental, functional, and skeletal) General considerations and principles of management: Anterior and posterior crossbites are malocclusions which involve one or more teeth in which the maxillary teeth occlude lingually with the antagonistic mandibular teeth.99,100 If the midlines undergo a compensatory or habitual shift when the teeth occlude in crossbite, this is termed a functional shift.101 A crossbite can be of dental or skeletal origin or a combination of both.102 A simple anterior crossbite is of dental origin if the molar occlusion is Class I and the malocclusion is the result of an abnormal axial inclination of maxillary anterior teeth. This condition should be differentiated from a Class III skeletal malocclusion where the crossbite is the result of the basal bone position.100 Dental crossbites result from the tipping or rotation of a tooth or teeth. The condition is localized and does not involve the basal bone. Skeletal crossbites involve disharmony of the craniofacial skeleton. Aberrations in bony growth may give rise to crossbites in 2 ways: 1. adverse transverse growth of the maxilla and mandible; 2. disharmonious or adverse growth in the sagittal (AP) length of the maxilla and mandible.99,101 Such growth aberrations can be due to inherited growth patterns, trauma, or functional disturbances that alter normal growth. Treatment considerations: Crossbites should be considered in the context of the patient’s total treatment needs. Anterior cross-bite correction can: (1) reduce dental attrition; (2) improve dental esthetics; (3) redirect skeletal growth; (4) improve the tooth-toalveolus relationship; and (5) increase arch perimeter. A simple anterior crossbite can be aligned as soon as the condition is noted, if there is sufficient space; otherwise, space needs to be created first. Such appliances as acrylic incline planes, acrylic retainers with lingual springs, or fixed appliances all have been effective. If space is needed, an expansion appliance also is required.99 Posterior crossbite correction can accomplish the
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same objectives and can improve the eruptive position of the succedaneous teeth. Early correction of unilateral posterior crossbites has been shown to improve functional conditions significantly and largely eliminate morphological and positional asymmetries of the mandible.103,104 Functional shifts should be eliminated as soon as possible with early correction101 to avoid asymmetric growth. Treatment can be completed with: 1. equilibration; 2. appliance therapy (fixed or removable); 3. extractions; or 4. a combination of these treatment modalities to correct the palatal constriction. Fixed or removable palatal expanders can be utilized until midline suture fusion occurs.101,102 Treatment decisions depend on the: 1. amount and type of movement (tipping vs bodily movement, rotation, or dental vs orthopedic move ment); 2. space available; 3. AP, transverse, and vertical skeletal relationships; 4. growth status; 5. patient cooperation. Patients with crossbites and concomitant Class III skeletal patterns and/or skeletal asymmetry should receive comprehensive treatment as covered in the Class III malocclusion section. Objectives: Treatment of a crossbite should result in improved intramaxillary alignment and an acceptable interarch occlusion and function.103 Class II malocclusion General considerations and principles of management: Class II malocclusion (distocclusion) may be unilateral or bilateral and involves a distal relationship of the mandible to the maxilla or the mandibular teeth to maxillary teeth. This relationship may result from dental (malposition of the teeth in the arches), skeletal (mandibular retrusion and/or maxillary protrusion), or a combination of dental and skeletal factors.6 Results of randomized clinical trials indicate that Class II malocclusion can be corrected effectively with either a single or 2-phase regimen.105-108 Growth-modifying effects in some studies did not show an influence on the Class II skeletal pattern,107,109,110 while other studies dispute these findings.111,112 There is substantial variation in treatment response to growth modification treatments (headgear or functional appliance) and no reliable predictors for favorable growth response have been found.105,111 Some reports state early treatment does not reduce the need for either premolar extractions or orthognathic surgery,106,107 while others disagree with these findings.113 Two-phase treatment results in significantly longer treatment time.101,106,114 Clinicians may decide to provide early treatment based on other factors.106,111 Preliminary evidence suggests that, for some children, early Class II treatment improves self-esteem and decreases negative social experiences.115 Incisor injury that is more severe than simple enamel fractures has been associ-
American academy of pediatric Dentistry
ated positively with increased overjet and prognathic position of the maxilla.116 Some studies indicate early treatment for Class II malocclusions can be initiated, depending upon patient cooperation and management.117 Treatment considerations: Factors to consider when planning orthodontic intervention for Class II malocclusion are: (1) facial growth pattern; (2) amount of AP discrepancy; (3) patient age; (4) projected patient compliance; (5) space analysis; (6) anchorage requirements; and (7) patient and parent desires. Treatment modalities include: (1) extraoral appliances (headgear); (2) functional appliances; (3) fixed appliances; (4) tooth extraction and interarch elastics; and (5) orthodontics with orthognathic surgery.102 Objectives: Treatment of a developing Class II malocclusion should result in an improved overbite, overjet, and intercuspation of posterior teeth and an esthetic appearance and profile compatible with the patient’s skeletal morphology. Class III malocclusion General considerations and principles of management: Class III malocclusion (mesocclusion) may be unilateral or bilateral and involves a mesial relationship of the mandible to the maxilla or mandibular teeth to maxillary teeth. This relationship may result from dental factors (malposition of the teeth in the arches), skeletal factors (asymmetry, mandibular prognathism, and/or maxillary retrognathism), or a combination of these factors.118 The etiology of Class III malocclusions can be hereditary, environmental, or both. In a study of 320 orthodontic patients in 155 sibships, the hereditary effect on molar relationship was determined to be 56%.119 Hereditary factors include clefts of the alveolus and palate and other craniofacial anomalies that are part of a genetic syndrome. Some environmental factors are trauma, oral/digital habits, caries, and early childhood OSAS.120 Treatment considerations: Treatment of Class III malocclusions is indicated to provide psychosocial benefits for the child patient by reducing or eliminating facial disfigurement and to reduce the severity of malocclusion by promoting compensating growth. Early Class III treatment has been proposed for several years and has been advocated as a necessary tool in contemporary orthodontics.121-126 Factors to consider when planning orthodontic intervention for Class III malocclusion are: (1) facial growth pattern; (2) amount of AP discrepancy; (3) patient age; (4) projected patient compliance; (5) space analysis; (6) anchorage (headgear); (7) functional appliances; (8) fixed appliances; (9) tooth extraction; (10) interarch elastics; and (11) orthodontics with orthognathic surgery.127 Objectives: Early Class III treatment may provide a more fa-vorable environment for growth and may improve occlusion, function, and esthetics.128 Although early treatment can mini-mize the malocclusion and potentially eliminate future orthognathic surgery, this is not always possible. Typically, Class III patients tend to grow longer and more unpredictably and, therefore, surgery combined with orthodontics is the best alternative to achieve a satisfactory result for some patients.102
Treatment of a Class III malocclusion in a growing patient should result in improved overbite, overjet, and intercuspation of posterior teeth and an esthetic appearance and profile compatible with the patient’s skeletal morphology.
References 1. Kanellis MJ. Orthodontic treatment in the primary dentition. In: Bishara SE, ed. Textbook of Orthodontics. Philadelphia, Pa: WB Saunders Co; 2001:248-56. 2. Woodside DG. The significance of late developmental crowding to early treatment planning for incisor crowding. Am J Orthod Dentofacial Orthop 2000;117(5):559-61. 3. Kurol J. Early treatment of tooth-eruption disturbances. Am J Orthod Dentofacial Orthop 2002;121(6):588-91. 4. Sankey WL, Buschang PH, English J, Owen AH III. Early treatment of vertical skeletal dysplasia: The hyperdivergent phenotype. Am J Orthod Dentofacial Orthop 2000;118(3):317-27. 5. American Academy of Pediatric Dentistry. Policy on ethical responsibility to treat or refer. Pediatr Dent 2008; 30(suppl):83. 6. Profitt WR, Sarver DM, Ackerman JL. Orthodontic diagnosis: The development of a problem list. In: Proffit WR, Fields HW Jr, Sarver DM, eds. Contemporary Orthodontics. 4th ed. St. Louis, Mo: Mosby; 2007:167-233. 7. Dale JG, Dale HC. Interceptive guidance of occlusion with emphasis on diagnosis. In: Graber TM, Vanarsdall RL Jr, Vig KWL, eds. Orthodontics: Current Principals and Techniques. 4th ed. St. Louis, Mo: Mosby; 2005:422-39. 8. Ferguson DJ. Growth of the face and dental arches. In: McDonald RE, Avery DR, Dean JA, eds. Dentistry for the Child and Adolescent. 8th ed. St. Louis, Mo: Mosby; 2004:590-6. 9. McNamara JA, Brudon WL. Dentitional development. In: Orthodontics and Dentofacial Orthopedics. Ann Arbor, Mich: Needham Press, Inc; 2001:31-8. 10. Profitt WR The later stages of development. In: Proffit WR, Fields HW Jr, Sarver DM, eds. Contemporary Orthodontics. 4th ed. St. Louis, Mo: Mosby; 2007:107-29. 11. Hunt O, Hepper P, Johnston C, Stevenson M, Burden D. Professional perceptions of the benefits of orthodontic treatment. Eur J Orthod 2001;23(3):315-23. 12. International Symposium on Early Orthodontic Treatment. Am J Orthod Dentofacial Orthop 2002;121(6):552-95. 13. Ackerman M. Evidenced-based orthodontics for the 21 st century. J Am Dent Assoc 2004;135(2):162-7. 14. American Dental Association, US Dept of Health and Human Services. The selection of patients for dental radiographic examinations—2004. Available at: “http:// www.ada.org/prof/resources/topics/radiography.asp”. Accessed May 26, 2008. 15. Proffit WR. The etiology and development of orthodontic problems. In: Proffit WR, Fields HW Jr, Sarver DM, eds. Contemporary Orthodontics. 4th ed. St. Louis, Mo: Mosby; 2007:130-61.
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16. Warren JJ, Bishara SE, Steinbock KL, Yonezu T, Nowak AJ. Effects of oral habits’ duration on dental characteristics in the primary dentition. J Am Dent Assoc 2001;132 (12):1685-93. 17. Dean JA. Management of the developing occlusion. In: McDonald RE, Avery DR, Dean JA, eds. Dentistry for the Child and Adolescent. 8th ed. St. Louis, Mo: Mosby; 2004:631-68. 18. Ogaard B, Larsson E, Lindsten R. The effect of sucking habits, cohort, sex, intercanine arch widths, and breast or bottle feeding on posterior crossbite in Norwegian and Swedish 3-year-old children. Am J Orthod Dentofacial Orthop 1994;106(2):161-6. 19. Warren JJ, Bishara SE. Duration of nutritive and nonnutritive sucking behaviors and their effects on the dental arches in the primary dentition. Am J Orthod Dentofacial Orthop 2002;121:347-56. 20. Monaco A, Ciammella NM, Marci MC, Pirro P, Giannoni M. The anxiety in bruxer child: A case-control study. Minverva Stomatol 2002;51(6):247-50. 21. Weideman CL, Bush DL, Yan-Go FL, Clark GT, Gornbein JA. The incidence of parasomnias in child bruxers vs nonbruxers. Pediatr Dent 1996;18(7):456-60. 22. Ivanhoe CB, Lai JM, Francisco GE. Bruxism after brain injury: Successful treatment with botulinum toxin-A. Arch Phys Med Rehabil 1997;78(11):1272-3. 23. Rugh JD, Harlan J. Nocturnal bruxism and temporomandibular disorders. Adv Neurol 1988;49:329-41. 24. Sari S, Sonmez H. The relationship between occlusal factors and bruxism in permanent and mixed dentition in Turkish children. J Clin Pediatr Dent 2001;25(3):191-4. 25. Negoro T, Briggs J, Plesh O, Nielsen I, McNeill C, Miller AJ. Bruxing patterns in children compared to intercuspal clenching and chewing as assessed with dental models, electromyography, and incisor jaw tracing: Preliminary study. ASDC J Dent Child 1998;65(6):449-58. 26. Kiesser JA, Groeneveld HT. Relationship between juvenile bruxing and craniomandibular dysfunction. J Oral Rehabil 1998;25(9):662-5. 27. Restrepo CC, Alvarez E, Jaramillo C, Velez C, Valencia I. Effects of psychological techniques on bruxism in children with primary teeth. J Oral Rehabil 2001;28(9):354-60. 28. Nissani M. A bibliographical survey of bruxism with special emphasis on nontraditional treatment modalities. J Oral Sci 2001;43(2):73-83. 29. Christensen J, Fields HW Jr, Adair S. Oral habits. In: Pinkham JR, Casamassimo PS, McTigue DJ, Fields HW Jr, Nowak AJ, eds. Pediatric Dentistry: Infancy Through Adolescence. 4th ed. St. Louis, Mo: Elsvier Saunders; 2005: 431-9. 30. Saemundsson SR, Roberts MW. Oral self-injurious behavior in the developmentally disabled: Review and a case. ASDC J Dent Child 1997;64(3):205-9. 31. Milwood J, Fiske J. Lip biting in patients with profound neurodisability. Dent Update 2001;28(2):105-8.
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32. Fields HW Jr, Warren DW, Black BK, Phillips C. Relationship between vertical dentofacial morphology and respiration in adolescents. Am J Orthod Dentofacial Orthop 1991;99(2):147-54. 33. American Academy of Pediatrics. Clinical practice guideline: Diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics 2002;109(4):704-12. 34. Ward T, Mason TB II. Sleep disorders in children. Nurs Clin North Am 2002;37(4):693-706. 35. Brook AH. Dental anomalies of number, form, and size: Their prevalence in British school children. J Int Assoc Dent Child 1974;5(2):37-53. 36. Byrd ED. Incidence of supernumerary and congenitally missing teeth. ASDC J Dent Child 1943;10:84-6. 37. Rose JS. A survey of congenitally missing teeth, excluding third molars, in 6,000 orthodontic patients. Dent Pract Dent Rec 1966;17(3):107-14. 38. Clayton JM. Congenital dental anomalies occurring in 3,552 children. J Dent Child 1956;23:206-86. 39. Brabant H. Comparison of the characteristics and anomalies of the deciduous and permanent dentitions. J Dent Res 1967;46(5):897-902. 40. Graber LW. Congenital absence of teeth: A review with emphasis on inheritance patterns. J Am Dent Assoc 1978;96(2):266-75. 41. Hobkirk JA, Brook AH. The management of patients with severe hypodontia. J Oral Rehabil 1980;7(4):289-98. 42. Riolo ML, Avery DR. Preadolescent orthodontic treatment and orthodontic treatment during active stages of growth and development. In: Essentials for Orthodontic Practice. Ann Arbor & Grand Haven, Mich: ESOP Press; 2003:48-9. 43. Woodworth DA, Sinclair PM, Alexander RG. Bilateral congenital absence of maxillary lateral incisors: A craniofacial and dental cast analysis. Am J Orthod 1985;87(4):280-93. 44. Robertson S, Mohlin B. The congenitally missing upper lateral incisor. A retrospective study of orthodontic space closure vs restorative treatment. Eur J Orthod 2000;22 (6):697-710. 45. Primosch RE. Anterior supernumerary teeth: Assessment and surgical intervention in children. Pediatr Dent 1981;3(2):204-15. 46. Luten JR. The prevalence of supernumerary teeth in primary and mixed dentitions. ASDC J Dent Child 1967; 34(5):346-53. 47. Russell KA, Folwarczna MA. Mesiodens: Diagnosis and management of a common supernumerary tooth. J Can Dent Assoc 2003;69(6):362-6. 48. Taylor GS. Characteristics of supernumerary teeth in the primary and permanent dentition. Dent Pract Dent Rec 1972;22(5):203-8. 49. McKibben DR, Brearley LJ. Radiographic determination of the prevalence of selected dental anomalies in children. J Dent Child 1971;28(6):390-8.
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50. Humerfelt D, Hurlen B, Humerfelt S. Hyperdontia in children below four years of age: A radiographic study. ASDC J Dent Child 1985;52(2):121-4. 51. Howard RD. The unerupted incisor. A study of the postoperative eruptive history of incisors delayed in their eruption by supernumerary teeth. Dent Pract Dent Rec 1967;17(9):332-41. 52. Tay F, Pang A, Yuen S. Unerupted maxillary anterior supernumerary teeth: A report of 204 cases. ASDC J Dent Child 1984;51(4):289-94. 53. Witsenburg B, Boering G. Eruption of impacted permanent upper incisors after removal of supernumerary teeth. Int J Oral Surg 1981;10(6):423-31. 54. Chintakanon K, Boonpinon P. Ectopic eruption of the first permanent molars: Prevalence and etiology factors. Angle Orthod 1998;68(2):153-60. 55. Carr GE, Mink JR. Ectopic eruption of the first permanent maxillary molar in cleft lip and palate children. ASDC J Dent Child 1965;32:179-88. 56. Grover P, Lorton L. The incidence of unerupted permanent teeth and related clinical cases. Oral Surg Oral Med Oral Pathol 1985;59(4):420-5. 57. Ericson S, Kurol J. Radiographic examination of ectopically erupting maxillary canines. Am J Orthod Dentofacial Orthop 1987;91(6):483-92. 58. Coll JA, Sadrian R. Predicting pulpectomy success and its relationship to exfoliation and succedaneous dentition. Pediatr Dent 1996;18(1):57-63. 59. Young DH. Ectopic eruption of the first permanent molar. ASDC J Dent Child 1957;24:153-62. 60. Gehm S, Crespi PV. Management of ectopic eruption of permanent molars. Compend Cont Educ Dent 1997;18 (6):561-9. 61. Halterman CW. A simple technique for the treatment of ectopically erupting first permanent molars. J Am Dent Assoc 1982;105(6):1031-3. 62. Terry BC, Hegtvedt AK. Self-stabilizing approach to surgical uplifting of the mandibular second molar. Oral Surg Oral Med Oral Pathol 1993;75(6):674-6. 63. Fernandez E, Bravo LA, Canteras M. Eruption of the permanent upper canine: A radiographic study. Am J Orthod Dentofacial Orthop 1998;113(4):414-20. 64. Olive RJ. Orthodontic treatment of palatally impacted maxillary canines. Aust Orthod J 2002;18(2):64-70. 65. D’Amico RM, Bjerklin K, Kurol J, Falahat B. Long-term results of orthodontic treatment of impacted maxillary canines. Angle Orthod 2003;73(3):231-8. 66. McTigue DJ. Managing traumatic injuries in the young permanent dentition. In: Pinkham JR, Casamassimo PS, McTigue DJ, Fields HW Jr, Nowak AJ, eds. Pediatric Dentistry: Infancy Through Adolescence. 4th ed. St Louis, Mo: Elsevier Saunders; 2005:593-607. 67. Andreasen JO, Andreasen FM. Intrusion, general prognosis. In: Essentials of Traumatic Injuries to the Teeth. Copenhagen, Denmark: Munksgaard; 1994:111.
68. Andreasen JO, Andreasen FM. Avulsion injuries: Pattern of injury and diagnosis. In: Essentials of Traumatic Injuries to the Teeth. Copenhagen, Denmark: Munksgaard; 1994: 115-20. 69. Kokich VO. Congenitally missing teeth: Orthodontic management in the adolescent patient. Am J Orthod Dentofacial Orthop 2002;121(6):594-5. 70. Sabri R. Management of congenitally missing second premolars with orthodontics and single-tooth implants. Am J Orthod Dentofacial Orthop 2004;125(5):634-42. 71. Geiger AM, Brunsky MJ. Orthodontic management of ankylosed permanent posterior teeth: A clinical report of three cases. Am J Orthod Dentofacial Orthop 1994; 106(5):543-8. 72. Bolton WA. The clinical application of a tooth-size analysis. Am J Orthod 1962;48:504-29. 73. Dugoni SA, Lee JS, Varela J, Dugoni AA. Early mixed dentition treatment: Postretention evaluation of stability and relapse. Angle Orthod 1995;65(5):311-20. 74. Foster H, Wiley W. Arch length deficiency in the mixed dentition. Am J Orthod 1958;68:61-8. 75. Little RM, Riedel RA, Stein A.. Mandibular arch length increase during the mixed dentition: Postretention evaluation of stability and relapse. Am J Orthod Dentofacial Orthop 1990;97(5):393-404. 76. Little RM. Stability and relapse of mandibular anterior alignment: University of Washington studies. Semin Orthod 1999;5(3):191-204. 77. Warren JJ, Bishara SE, Yonezu T. Tooth size-arch length relationships in the deciduous dentition: A comparison between contemporary and historical samples. Am J Orthod Dentofacial Orthop 2003;123(6):614-9. 78. Warren JJ, Bishara SE. Comparison of dental arch measurements in the primary dentition between contemporary and historic samples. Am J Orthod Dentofacial Orthop 2001;119(3):211-5. 79. Moorrees CF. Register of longitudinal growth studies of facial and dental development. J Dent Res 1967;46(6): 1206-7. 80. Moorrees CF, Burstone CJ, Christiansen RL, Hixon EH, Weinstein S. Research related to malocclusion. A “state-ofthe-art” workshop conducted by the Oral-Facial Growth and Development Program, The National Institute of Dental Research. Am J Orthod 1971;59(1):1-18. 81. Turpin DL. Where has all the arch length gone? (editorial) Am J Orthod Dentofacial Orthop 2001;119(3):201. 82. Behrents, RG. Growth in the aging craniofacial skeleton. Monograph 17. Craniofacial Growth Series. Ann Arbor, Mich: University of Michigan, Center for Human Growth and Development; 1985. 83. Zachrisson BU. Important aspects of long-term stability. J Clin Orthod 1997;31(9):562-83. 84. Kusters ST, Kuijpers-Jagman AM, Maltha JC. An experimental study in dogs of transseptal fiber arrangement between teeth which have emerged in rotated and nonrotated positions. J Dent Res 1991;70(3):192-7. CLINICAL GUIDELINES
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85. Ericson S, Kurol J. Radiographic assessment of maxillary canine eruption in children with clinical signs of eruption disturbances. Eur J Orthod 1986;8(3):133-40. 86. Ericson S, Kurol J. Early treatment of palatally erupting maxillary canines by extraction of the primary canines. Eur J Orthod 1988;10(4):283-95. 87. Brothwell DJ. Guidelines on the use of space maintainers following premature loss of primary teeth. J Can Dent Assoc 1997;63(10):753-66. 88. Ngan P, Alkire RG, Fields HW Jr. Management of space problems in the primary and mixed dentitions. J Am Dent Assoc 1999;130(9):1330-9. 89. Terlaje RD, Donly KJ. Treatment planning for space maintenance in the primary and mixed dentition. J Dent Child 2001;68(2):109-14. 90. Dincer M, Haydar S, Unsal B, Turk T. Space maintainer effects on intercanine arch width and length. J Clin Pediatr Dent 1996;21(1):47-50. 91. Qudeimat MA, Fayle SA. The longevity of space maintainers: A retrospective study. Pediatr Dent 1998;20(4): 267-72. 92. Cuoghi OA, Bertoz FA, de Mendonca MR, Santos EC. Loss of space and dental arch length after the loss of the lower first primary molar: A longitudinal study. J Clin Pediatr Dent 1998;22(2):117-20. 93. Rajab LD. Clinical performance and survival of space maintainers: Evaluation over a period of 5 years. ASDC J Dent Child 2002;69(2):156-60. 94. Owen DG. The incidence and nature of space closure following the premature extraction of deciduous teeth: A literature survey study. Am J Orthod Dentofacial Orthop 1971;59(1):37-49. 95. Kisling E, Hoffding J. Premature loss of primary teeth. Part IV, a clinical control of Sannerud’s space maintainer, type I. ASDC J Dent Child 1979;46(2):109-13. 96. Qudeimat MA, Fayle SA. The use of space maintainers at a UK pediatric dentistry department. ASDC J Dent Child 1999;66(6):383-6. 97. Christensen JR, Fields HW Jr. Space maintenance in the primary dentition. In: Pinkham JR, Casamassimo PS, McTigue DJ, Fields HW Jr, Nowak AJ, eds. Pediatric Dentistry Infancy Through Adolescence. 4th ed. St Louis, Mo: Elsevier Saunders; 2005:423-30. 98. Profitt WR, Fields HW Jr, Sarver DM. Orthodontic treatment planning: From problem list to specific plan. In: Contemporary Orthodontics. 4th ed. St. Louis, Mo: Mosby; 2007:234-67. 99. Richards B. An approach to the diagnosis of different malocclusions. In: Bishara SE, ed. Textbook of Orthodontics. Philadelphia, Pa: Saunders Co; 2001:157-8. 100. Bishara SE, Staley RN. Maxillary expansion: Clinical implications. Am J Orthod Dentofacial Orthop 1987;91 (1):3-14.
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101. Kluemper GT, Beeman CS, Hicks, EP. Early orthodontic treatment: What are the imperatives? J Am Dent Assoc 2000;131(5):613-20. 102. Proffit WR, Fields HW Jr, Sarver DM. Orthodontic treatment planning: Limitations, controversies, and special problems. In: Contemporary Orthodontics. 4 th ed. St. Louis, Mo: Mosby; 2007:268-327. 103. Sonnesen L, Bakke M, Solow B. Bite force in preorthodontic children with unilateral crossbite. Eur J Orthod 2001; 23(6):741-9. 104. Pinto AS, Bushang PH, Throckmorton GS, Chen P. Morphological and positional asymmetries of young children with functional unilateral posterior crossbites. Am J Orthod Dentofacial Orthop 2001;120(5):513-20. 105. Ghafari J, Shofur FS, Jacobsson-Hunt U, Markowitz DL, Laster LL. Headgear vs functional regulator in the early treatment of Class II, division 1 malocclusion: A randomized clinical trial. Am J Orthod Dentofacial Orthop 1998;113(1):51-61. 106. Tulloch JF, Proffit WR, Phillips C. Benefit of early Class II treatment: Progress report of a two-phase randomized clinical trial. Am J Orthod Dentofacial Orthop 1998;113 (1):62-72. 107. Keeling SD, Wheeler TT, King GJ, et al. Anteroposterior skeletal and dental changes after early Class II treatment with bionators and headgear. Am J Orthod Dentofacial Orthop 1998;113(1):40-50. 108. Tulloch JF, Phillips C, Proffit WR. Outcomes in a 2-phase randomized clinical trial of early Class II treatment. Am J Orthod Dentofacial Orthop 2004;125(6):657-67. 109. Chen JY, Will LA, Niederman R. Analysis of efficacy of functional appliances on mandibular growth. Am J Orthod Dentofacial Orthop 2002;122(5):470-6. 110. O’Brien K, Wright J, Conboy F, et al. Effectiveness of early orthodontic treatment with the twin-block appliance: A multicenter, randomized, controlled trial. Part 1: Dental and skeletal effects. Am J Orthod Dentofacial Orthop 2003;124(3):234-43. 111. McNamara JA, Brookstein FL, Shaughnessy TG. Skeletal and dental changes following regulatory therapy on Class II patients. Am J Orthod Dentofacial Orthop 1985;88(2); 91-110. 112. Toth LR, McNamara JA Jr. Treatment effects produced by the twin-block appliance and the FR-2 appliance of Frankel compared with untreated Class II sample. Am J Orthod Dentofacial Orthop 1999;116(6):597-609. 113. Carapezza L. Early treatment vs late treatment Class II closed bite malocclusion. Gen Dent 2003;51(5):430-4. 114. Von Bremen J, Pancherz H. Efficiency of early and late Class II division 1 treatment. Am J Orthod Dentofacial Orthop 2002;121(1):31-7.
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115. O’Brien K, Wright J, Conboy F, et al. Effectiveness of early orthodontic treatment with the twin-block appliance: A multicenter, randomized, controlled trial. Part 2: Psychosocial effects. Am J Orthod Dentofacial Orthop 2003;124(5):488-95. 116. Kania MJ, Keeling SD, McGorray SP, Wheeler TT, King GJ. Risk factors associated with incisor injury in elementary school children. Angle Orthod 1996;66(6): 423-31. 117. Baccetti T, Franchi L, McNamara JA Jr, Tollaro I. Early dentofacial features of Class II malocclusion: A longitudinal study from the deciduous through the mixed dentition. Am J Orthod Dentofacial Orthop 1997;111 (5):502-9. 118. Staley RN. Orthodontic diagnosis and treatment planning: Angle’s classification system. In: Bishara SE, ed. Textbook of Orthodontics. Philadelphia, Pa: Saunders Co; 2001:102-3. 119. Cassidy KM, Harris EF, Tolley EA Keim RG. Genetic influences on dental arch in orthodontic patients. Angle Orthod 1998;68(5):445-54. 120. Staley RN. Etiology and prevalence of malocclusion. In: Bishara SE, ed. Textbook of Orthodontics. Philadelphia, Pa:Saunders Co; 2001:84.
121. Campbell PM. The dilemma of Class III treatment. Early or late? Angle Orthod 1983;53(3):175-91. 122. Kim JH, Viana MA, Graber TM, Omerza FF, BeGole EA. The effectiveness of protraction face mask therapy: A meta-analysis. Am J Orthod Dentofacial Orthop 1999; 115(6):675-85. 123. Jager A, Braumann B, Kim C, Wahner S. Skeletal and dental effects of maxillary protraction in patients with Angle class III malocclusions. A meta-analysis. 2001;62 (4):275-84. 124. Page DC. Early orthodontics: 5 new steps to better care. Dent Today 2004;23(2):1-7. 125. Stahl F, Grabowski R. Orthodontic findings in the deciduous and early mixed dentition: Inferences for a preventive strategy. J Orofac Orthop 2003;64(6):401-16. 126. Ricketts RM. A statement regarding early treatment. Am J Orthod Dentofacial Orthop 2000;117(5):556-8. 127. Profitt WR, Sarver DM. Combined surgical and orthodontic treatment. In: Profitt WR, Fields HW Jr, Sarver DM, eds. Contemporary Orthodontics. 4th ed. St. Louis, Mo: Mosby; 2007:686-718. 128. Toffol LD, Pavoni C, Baccetti T, Franchi L, Cozza P. Orthopedic treatment outcomes in Class III malocclusion. Angle Orthod 2008;78(3)561-73.
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Guideline on Oral Health Care/Dental Management of Heritable Dental Developmental Anomalies Originating Council Council on Clinical Affairs
Adopted 2008
Purpose The American Academy of Pediatric Dentistry (AAPD) recognizes that pediatric dentists are uniquely qualified to manage the oral health care needs of children with heritable dental developmental anomalies. These children have multiple, complex problems as their dental conditions affect both form and function and can have significant psychological impact. These conditions may present early in life and require both immediate intervention and management of a protracted nature, including coordination of multi-disciplinary care. The AAPD’s Guideline on Management of Dental Patients with Special Health Care Needs1 alludes to this patient population but does not make specific treatment recommendations for the oral manifestations of such diagnoses. This guideline is intended to address the diagnosis, principles of management, and objectives of therapy of children with heritable dental developmental anomalies rather than provide specific treatment recommendations. This guideline will focus on the following heritable dental developmental anomalies: amelogenesis imperfecta (AI), dentinogenesis imperfecta (DI), and dentin dysplasia (DD). Ectodermal dysplasia has been thoroughly studied and reported in the National Foundation for Ectodermal Dysplasia’s “Parameters of Oral Health Care for Individuals Affected by Ectodermal Dysplasia Syndromes.”2 Refer to that document for care of children with ectodermal dysplasia.
Methods This guideline is based on a review of the current dental and medical literature related to heritable dental developmental anomalies. A MEDLINE search was conducted using the terms “amelogenesis imperfecta”, “dentinogenesis imperfecta”, “dentinal dysplasia”, “dentin dysplasia”, “enamel hypoplasia”, “enamel hypocalcification”, “amelogenin”, and “enamelin”.
Background Anomalies of tooth development are relatively common and may occur as an isolated condition or in association with other anomalies. Developmental dental anomalies often exhibit patterns that reflect the stage of development during which the malformation occurs. For example, disruptions in tooth initiation result in hypodontia or supernumerary teeth, whereas
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disruptions during morphodifferentiation lead to anomalies of size and shape (eg, macrodontia, microdontia, taurodontism, dens invaginatus).3 Disruptions occurring during histodifferentiation, apposition, and mineralization result in enamel hypoplasia, AI, DI, and DD.3 Heritable dental developmental anomalies can have profound negative consequences for the affected individual and the family. The problems range from esthetic concerns that impact self-esteem to masticatory difficulties, tooth sensitivity, financial burdens, and protracted, complex dental treatment. These emotional and physical strains have been demonstrated in a recent study showing that persons with AI have fewer long-term relationships and children than nonaffected people.4 Amelogenesis Imperfecta Amelogenesis imperfecta is a developmental disturbance that interferes with normal enamel formation in the absence of a systemic disorder.5,6 In general, it affects all or nearly all of the teeth in both the primary and permanent dentitions. 3,5-7 The estimated frequency of AI in the US population is 1:7,000.8,9 Genetic etiology: AI may be inherited by x-linked, autosomal dominant or recessive, or sporadic inheritance. The different clinical manifestations of AI have a specific gene anomaly associated with each phenotype.10-12 Clinical manifestation: The most widely accepted classification of AI includes 4 types: hypocalcified, hypoplastic pitted, hypoplastic generalized and hypomaturation (See Figure 1). Each type has subtypes differentiated by mode of inheritance. The variability of the appearance of the different types of AI makes identification difficult.13 Some dentitions will appear normal to the untrained eye while other types of AI will be disfiguring. Children with AI can exhibit accelerated tooth eruption compared to the normal population or have late eruption.15,16 Pathologies associated with AI are enlarged follicles, impacted permanent teeth, and ectopic eruption.16 Agenesis of second molars also has been observed.17 Although uncommon in AI, enamel resorption and ankylosis have been reported.16 In addition, the incidence of anterior open bite is 50% in hypoplastic AI, 31% in hypomaturation AI, and 60% of hypocalcified AI.15,18
American academy of pediatric Dentistry
Figure 1. Amelogenesis imperfecta. Diagram of enamel defects of basic types. Hypocalcified - normal thickness, smooth surface, less hardness. Hypoplastic, pitted - normal thickness, pitted surface, normal hardness. Hypoplastic, generalized - reduced thickness, smooth surface, normal hardness. Hypomaturation - normal thickness, chipped surface, less hardness, opaque white coloration.
This figure was published in Contemporary Oral and Maxillofacial Pathology, Sapp J, Eversole L, Wysocki G; Developmental Disturbances of the Oral Region, page 19; Mosby, Inc. 2004.14
Differential diagnosis: Other forms of enamel dysmineralization will exhibit a pattern based upon the time of insult, thus affecting the enamel forming at the time. In contrast, AI will affect all teeth similarly and can have a familial history. Fluorosis can mimic AI, but usually the teeth are not affected uniformly, often sparing the premolars and second permanent molars. A history of fluoride intake can aid in the diagnosis. Dentinogenesis Imperfecta Dentinogenesis imperfecta is a hereditary developmental disturbance of the dentin originating during the histodifferentiation stage of tooth development. DI may be seen alone or in conjunction with the systemic hereditary disorder of the bone, osteogenesis imperfecta. Children with unexplained bone fracturing should be evaluated for DI as a possible indicator of an undiagnosed case of OI. This is important in helping delineate child abuse from mild or undiagnosed OI.19 The incidence of DI is about 1 in 8000.20 Two systems, one by Witkop 20and the other by Shields 21, are well accepted classification systems of DI (See Table 1). Genetic etiology: Type I collagen (product of COL1A1 and COL1A2 genes) is the most abundant dentin protein.22 The diverse mutations associated with the COL1A1 and COL1A2 genes can cause the DI phenotype in association with osteogenesis imperfecta (DI type I). DI Type II and Type III are
autosomal dominant conditions that have been linked to chromosome 4q12-21, suggesting these may be allelic mutations of the DSPP gene encoding dentin phosphoprotein and dentin sialoprotein.23,24 Clinical manifestation: In all 3 DI types, the teeth have a variable blue-gray to yellow-brown discoloration that appears opalescent due to the defective, abnormally-colored dentin shining through the translucent enamel. Due to the lack of support of the poorly mineralized dentin, enamel frequently fractures from the teeth leading to rapid wear and attrition of the teeth. The severity of discoloration and enamel fracturing in all DI types is highly variable, even within the same family. If left untreated, it is not uncommon to see the entire DI-affected dentition worn to the gingiva. Shields Type I occurs with osteogenesis imperfecta. All teeth in both dentitions are affected. Primary teeth are affected most severely, followed by the permanent incisors and first molars, with the second and third molars being the least altered. Radiographically, the teeth have bulbous crowns, cervical constriction, thin roots, and early obliteration of the root canal and pulp chambers due to excessive dentin production. Periapical radiolucencies and root fractures are evident. An amber translucent tooth color is common. Shields Type II is also known as hereditary opalescent dentin.
Table 1. Dentinogenesis imperfecta* Shields
Clinical Presentation
Witkop
Dentinogenesis Imperfecta I
Osteogenesis Imperfecta with opalescent teeth
Dentinogenesis Imperfecta
Dentinogenesis Imperfecta II
Isolated Dentinogenesis Imperfecta
Hereditary Opalescent Dentin
Dentinogenesis Imperfecta III
Isolated Dentinogenesis Imperfecta
Brandywine Isolate
* This table was published in Oral and Maxillofacial Pathology, 2nd ed, Neville BW, Damm DD, Allen CM, Bouquot JE, Abnormalities of Teeth, page 94, Copyright WB Saunders Company, 2002.6
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Both primary and permanent dentitions are equally affected, and the characteristics previously described for Type I are the same. Radiographically, pulp chamber obliteration can begin prior to tooth eruption. Shields Type III is rare; its predominant characteristic is bellshaped crowns, especially in the permanent dentition. Unlike Types I and II, Type III involves teeth with shell-like appearance and multiple pulp exposures. Shell teeth demonstrate normalthickness enamel in association with extremely thin dentin and dramatically enlarged pulps. The thin dentin may involve the entire tooth or be isolated to the root. Differential diagnosis: OI, other collagen disorders, and numerous syndromes have DI-like phenotypes associated with them. DD Type I clinically has normal appearing crowns, but radiographically the teeth have pulpal obliterations and short blunted roots. DD Type II has the same phenotype as DI Type II in the primary dentition but normal to slight blue-gray discoloration in permanent dentition. Dentin Dysplasia Dentin dysplasia represents another group of inherited dentin disorders resulting in characteristic features involving the dentin and root morphology. DD is rarer than DI, affecting 1:100,000.5 Genetic etiology: DD exhibits an autosomal dominant pattern of inheritance.5-7 Clinical manifestation: In 1973, Shields and colleagues proposed a classification system of dentinal dysplasia.21 Dentin Dysplasia Type I (Radicular Dentin Dysplasia; Rootless Teeth):5-7,25 The crowns in DD Type I appear mostly normal in color and shape in both the primary and permanent dentitions. Occasionally, an amber translucency is apparent. The roots tend to be short and sharply constricted. DD Type I has been referred to as “rootless teeth” because of the shortened root length due to a loss of organization of root dentin. Wide variation of root formation and pulp formation exists due to the timing of dentinal disorganization. With early disorganization, the roots are extremely short or absent and no pulp can be detected. With later disorganization, the roots are shortened with crescent or chevron-shaped pulp chambers. With late disorganization, typical root lengths exist with pulp stones present in a normal shaped pulp chambers. This variability is most profound in the permanent dentition and can vary for each person and from tooth to tooth in a single individual. Radiographically, the roots of all teeth in the primary and permanent dentitions are either short or abnormally shaped. The primary teeth have obliterated pulps that completely fill in before eruption. The extent of pulp canal and chamber obliteration in the permanent dentition is variable. Both the primary and permanent teeth demonstrate multiple periapical radiolucencies. They represent chronic abscesses, granulomas, or cysts. The inflammatory lesions appear secondary to caries or spontaneous coronal exposure of microscopic threads of pulpal remnants present within the defective dentin.
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Dentin Dysplasia Type II (Coronal Dentin Dysplasia):5-7,25 DD Type II demonstrates numerous features of DI. In contrast to DD Type I, root lengths are normal in both dentitions. The primary teeth are amber-colored closely resembling DI. Radiographically, the primary teeth exhibit bulbous crowns, cervical constrictions, thin roots, and early pulp obliteration. The permanent teeth are normal in coloration. Radiographically, they exhibit thistle-tube shaped pulp chambers with multiple pulp stones; periapical radiolucencies are not present. Differential diagnosis: The first differential diagnosis for DD Type II is DI. The differentiation between DD and DI can be challenging because these 2 developmental anomalies form a continuum.5 Both DD and DI have amber tooth coloration and obliterated or occluded pulp chambers. However, the pulp chambers do not fill in before eruption in DD Type II. A finding of a thistle-tube shaped pulp chamber in a single-rooted tooth increases the likelihood of DD diagnosis. The crowns in DD usually are normal in size, shape, and proportion while the crowns in DI typically are bell-shaped with a cervical constriction. The roots in DD usually are not present or appear normal while the roots in DI typically are short and narrow. Association of periapical radiolucencies with non-carious teeth and without obvious cause is an important characteristic of DD Type I.5,6 An unrelated disorder with pulpal findings similar to DD Type II is pulpal dysplasia.6 This process occurs in teeth that appear clinically normal. Radiographically, pulpal dysplasia exhibits thistle-tube shaped pulp chambers and multiple pulp stones in the both the primary and permanent dentitions.
Recommendations Amelogenesis Imperfecta General considerations and principles of management: A primary goal for treatment is to address each concern as it presents but with an overall comprehensive plan that outlines anticipated future treatment needs. Clinicians treating children and adolescents with AI must address the clinical and emotional demands of these disorders with sensitivity. It is important to establish good rapport with the child and family early. Timely intervention is critical to spare the patient from the psychosocial consequences of these potentially disfiguring conditions. A comprehensive and timely approach is reassuring to the patient and family and may help decrease their anxiety. Preventive care: Early identification and preventive interventions are critical for infants and children with AI in order to avoid the negative social and functional consequences of the disorder. Regular periodic examinations can identify teeth needing care as they erupt. Meticulous oral hygiene, calculus removal, and oral rinses can improve periodontal health. Fluoride applications and desensitizing agents may diminish tooth sensitivity.26,27 Restorative care: The appearance, quality, and amount of affected enamel and dentin will dictate the type of restorations necessary to achieve esthetic, masticatory, and functional health. 26,28,29
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When the enamel is intact but discolored, bleaching and/or microabrasion may be used to enhance the appearance.30,31 If the enamel is hypocalcified, composite resin or porcelain veneers may be able to be retained with bonding.32 If the enamel or dentin cannot be bonded, full coverage restorations will be required.17,3338 In order to facilitate veneer or crown placement, periodontal therapy may be necessary when acute/chronic marginal gingivitis along with hyperplastic tissue exists 34,39-42 During the primary dentition, it is important to restore the teeth for adequate function and to maintain adequate arch parameters. Primary teeth may require composite or veneered anterior crowns with posterior full coverage steel or veneered crowns.35,43,44 The permanent dentition usually involves a complex treatment plan with specialists from multiple disciplines.38,41,45 Periodontics, endodontics, and orthodontics may be necessary and treatment could include orthognathic surgery.34,38,42,46,47 The prosthetic treatment may require veneers, full coverage crowns, implants, and fixed or removable prostheses.28,33,36,37,48-50 The fabrication of an occlusal splint is advocated to reestablish vertical dimension when full mouth rehabilitation is necessary.17,40,45 Therapy will need to be planned carefully in phases as teeth erupt and the need arises. Behavior guidance, as well as the psychological health of the patient, will need to be addressed in each phase. Counseling for the child or adolescent and his/her family should be recommended when negative psychosocial consequences of the disorder are recognized. Due to extensive treatment needs, a patient may require sedation or general anesthesia for restorative care.37 Dentinogenesis Imperfecta General considerations and principles of management: Providing optimal oral health treatment for DI frequently includes preventing severe attrition associated with enamel loss and rapid wear of the poorly mineralized dentin, rehabilitating dentitions that have undergone severe wear, optimizing esthetics, and preventing caries and periodontal disease. The dental approach for managing DI will vary depending on the severity of the clinical expression. The clinician must be cautious in treating individuals with OI if performing surgical procedures or other treatment that could transmit forces to the jaws, increasing the risk of bone fracture. Some types of protective stabilization may be contraindicated in the patients with OI. Preventive care: Early identification and preventive interventions are critical for individuals with DI in order to avoid the negative social and functional consequences of the disorder. Regular periodic examinations can identify teeth needing care as they erupt. Meticulous oral hygiene, calculus removal, and oral rinses can improve periodontal health. Fluoride applications and desensitizing agents may diminish tooth sensitivity.26,27 Restorative care: Routine restorative techniques often can be used effectively to treat mild to moderate DI. These treatments more commonly are applied to the permanent teeth, as the permanent dentition frequently is less severely affected than the primary
dentition. In more severe cases with significant enamel fracturing and rapid dental wear, the treatment of choice is full coverage restorations in both the primary and permanent dentitions.50 The success of full coverage is greatest in teeth with crowns and roots that exhibit close to a normal shape and size, minimizing the risk of cervical fracture. Ideally, restorative stabilization of the dentition will be completed before excessive wear and loss of vertical dimension occur.51 Cases with significant loss of vertical dimension will benefit from reestablishing a more normal vertical dimension during dental rehabilitation. Cases having severe loss of coronal tooth structure and vertical dimension maybe considered candidates for overdenture therapy. Overlay dentures placed on teeth that are covered with fluoride-releasing glass ionomer cement have been used with success.6 Bleaching has been reported to lighten the color of DI teeth with some success; however, because the discoloration is caused primarily by the underlying yellow-brown dentin, bleaching alone is unlikely to produce normal appearance in cases of significant discoloration. Different types of veneers can be used to improve the esthetics and mask the opalescent blue-gray discoloration of the anterior teeth. Endodontic considerations: Some patients with dentinogenesis imperfecta will suffer from multiple periapical abscesses apparently resulting from pulpal strangulation secondary to pulpal obliteration or from pulp exposure due to extensive coronal wear. The potential for periapical abscesses is an indication for periodic radiographic surveys on individuals with DI. Because of pulpal obliteration, apical surgery may be required to maintain the abscessed teeth. Attempting to negotiate and instrument obliterated canals in DI teeth can result in lateral perforation due to the poorly mineralized dentin. Occlusion: Class III malocclussion with high incidences of posterior crossbites and openbites occur in DI Type I and should be evaluated.52 Multidisciplinary approaches are essential in addressing the complex needs of the individuals affected with DI. Dentin Dysplasia General considerations and principles of management7: The goal of treatment is to retain the teeth for as long as possible. However, due to shortened roots and periapical lesions, the prognosis for prolonged tooth retention is poor. Prosthetic replacement including dentures, overdentures, partial dentures, and/or dental implants may be required. Preventive care6: Preventive care is of foremost importance. Meticulous oral hygiene must be established and maintained. As a result of shortened roots with DD Type I, early tooth loss from periodontitis is frequent. Restorative care: Teeth with DD Type I have such poor crown to root ratios that prosthetic replacement including dentures, overdentures, partial dentures, and/or dental implants are the only practical courses for dental rehabilitation.5 Teeth with DD Type II that are of normal shape, size, and support can be restored with
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full coverage restorations if necessary. For esthetics, discolored anterior teeth can be improved with resin bonding, veneering, or full coverage esthetic restorations. Clinicians should be aware that even shallow occlusal restorations may result in pulpal necrosis due to the pulpal vascular channels that extend close to the dentin-enamel junction. 6 If periapical inflammatory lesions develop, the treatment plan is guided by the root length.6 Endodontic considerations 6: Endodontic therapy, negotiating around pulp stones and through whorls of tubular dentin, has been successful in teeth without extremely short roots. Periapical curettage and retrograde amalgam seals have demonstrated short-term success in teeth with short roots. Ectodermal Dysplasia The AAPD endorses the National Foundation for Ectodermal Dysplasia’s “Parameters of Oral Health Care for Individuals Affected by Ectodermal Dysplasia Syndromes.”2
References 1. American Academy of Pediatric Dentistry. Guideline on management of dental patients with special health care needs. Pediatr Dent 2008;30(suppl):107-11. 2. National Foundation for Ectodermal Dysplasias. Parameters of oral health care for individuals affected by ectodermal dysplasias. National Foundation for Ectodermal Dysplasias. Mascoutah, Ill; 2003. Available at: “http:// www.nfed.org”. Accessed June 7, 2008. 3. Slayton RL. Congenital genetic disorders and syndromes. In: Pinkham JR, Casamassimo PS, Fields HW Jr, McTigue DJ, Nowak AJ, eds. Pediatric Dentistry: Infancy through Adolescence. 4 th ed. St. Louis, Mo: Elsevier Saunders; 2005:257-74. 4. Coffield K, Philips C, Brady M, Roberts M, Strauss R, Wright J. The psychosocial impact of developmental dental defects in people with hereditary amelogenesis imperfecta. J Am Dent Assoc 2005;136(5):620-30. 5. White SC, Pharoah MJ. Dental anomalies. In: Oral Radiology: Principles and Interpretation. 5th ed. St. Louis, Mo: Mosby; 2004:344-9. 6. Neville BW, Damm DD, Allen CM, Bouquot JE. Abnormalities of Teeth. In: Oral & Maxillofacial Pathology. 2nd ed. Philadelphia, Pa: WB Saunders Company; 2002: 89-99. 7. Regezi JA, Sciubba JJ, Jordan RCK. Abnormalities of teeth. In: Oral Pathology: Clinical-Pathologic Correlations. 4th ed. St. Louis, Mo: WB Saunders; 2003:376-80. 8. Bäckman B, Holmgren G. Amelogenesis imperfecta: A genetic study. Human Heredity 1988;38(4):189-206. 9. Witkop CJ. Amelogenesis imperfecta, dentinogenesis imperfecta and dentin dysplasia revisited: Problems in classification. J Oral Pathol 1988;17(9-10):547-53. 10. Hu J, Simmer J. Developmental biology and genetics of dental malformations. Orthod Craniofac Res 2007;10(2): 45-52.
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11. Stephanopoulos G, Garefalaki M, Lyroudia K. Genes and related proteins involved in amelogenesis imperfecta. J Dent Res 2005;84(12):1117-26. 12. Aldred M, Savarirayan R, Crawford P. Amelogenesis imperfecta: A classification and catalogue for the 21st century. Oral Dis 2003;9(1):19-23. 13. Kim J, Simmer J, Lin B, Seymen F, Bartlett J, Hu J. Mutational analysis of candidate genes in 24 amelogenesis imperfecta families. Eur J Oral Sci 2006;114(suppl 1):3-12, 39-41. 14. Sapp J, Eversole L, Wysocki G. Developmental disturbances of the oral region. In: Contemporary Oral and Maxillofacial Pathology. 2nd ed. St. Louis, Mo: Mosby Inc; 2004:17-20. 15. Aren G, Ozdemir D, Firatli S, Uygur C, Sepet E, Firatli E. Evaluation of oral and systemic manifestations in an amelogenesis imperfecta population. J Dent Res 2003; 31(8):585-91. 16. Seow W. Dental development in amelogenesis imperfecta: A controlled study. Pediatr Dent 1995;17(1):26-30. 17. Yip H, Smales R. Oral rehabilitation of young adults with amelogenesis imperfecta. Int J Prosth 2003;16(4):345-9. 18. Crawford P, Aldred M, Bloch-Zupan A. Amelogenesis imperfecta. Orphanet J Rare Dis 2007;4(2):17. 19. Wright J, Thornton J. Osteogenesis imperfecta with dentinogenesis imperfecta: A mistaken case of child abuse. Pediatr Dent 1983;5(3):207-9. 20. Witkop CJ. Hereditary defects in enamel and dentin. Acta Genet Stat Med 1957;7(1):236-9. 21. Shields ED, Bixler D, el-kafrawy AM. A proposed classification for heritable human dentine defects with a description of a new entity. Arch Oral Biol 1973;18(4):543-53. 22. Linde A, Goldberg M. Dentinogenesis. Crit Rev Oral Biol Med 1993;4(5):679-728. 23. Takagi Y, Sasaki S. A probable common disturbance in the early stage of odontoblast differentiation in dentinogenesis imperfecta type I and type II. J Oral Pathol 1988; 17(5):208-12. 24. MacDougall M, Jeffords L, Gu T, et al. Genetic linkage of the dentinogenesis imperfecta type III locus to chromosome 4q. J Dent Res 1999;78(6):1277-82. 25. Dummett CO Jr. Anomalies of the developing dentition. In: Pinkham JR, Casamassimo PS, Fields HW Jr, McTigue DJ, Nowak AJ, eds. Pediatric Dentistry: Infancy through Adolescence. 4th ed. St. Louis, Mo: Elsevier Saunders; 2005:61-73. 26. Sapir S, Shapira J. Clinical solutions for developmental defects of enamel and dentin in children. Pediatr Dent 2007;29(4):330-6. 27. Hicks J, Flaitz C. Role of remineralizing fluid in in vitro enamel caries formation and progression. Quintessence Int 2007;38(4):313-24. 28. Lindunger A, Smedberg J. A retrospective study of the prosthodontic management of patients with amelogenesis imperfecta. Int J Prosth 2005;18(3):189-94.
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29. Seymen F, Kiziltan B. Amelogenesis imperfecta: A scanning electron microscopic and histopathologic study. J Clin Pediatr Dent 2002;26(4):327-35. 30. Ashkenazi M, Sarnat H. Microabrasion of teeth with discoloration resembling hypomaturation enamel defects: Four-year follow up. J Clin Pediatr Dent 2000;25(1):29-34. 31. Dale B. Bleaching and related agents. In: Esthetic Dentistry: A Clinical Approach to Techniques and Materials. St. Louis, Mo: Mosby Inc; 2001:245-55. 32. Sengun A, Ozer F. Restoring function and esthetics in a patient with amelogenesis imperfecta: A case report. Quintessence Int 2002;33(3):199-204. 33. Akin H, Tasveren S, Yeler D. Interdisciplinary approach to treating a patient with amelogenesis imperfecta: A clinical report. J Esthet Restor Dent 2007;19(3):131-6. 34. Williams W, Becker L. Amelogenesis imperfecta: Functional and esthetic restoration of a severely compromised dentition. Quintessence Int 2000;31(6):397-403. 35. Rosenblum S. Restorative and orthodontic treatment of an adolescent patient with amelogenesis imperfecta. Pediatr Dent 1999;21(4):289-92. 36. Robinson F, Haubenreich J. Oral rehabilitation of a young adult with hypoplastic amelogenesis imperfecta: A clinical report. J Prosth Dent 2006;95(1):10-3. 37. Quiñonez R, Hoover R, Wright JT. Transitional anterior esthetic restorations for patients with enamel defects. Pediatr Dent 2000;22(1):65-7. 38. Encinas R, Garcia-Espona I, Mondelo J. Amelogenesis imperfecta: Diagnosis and resolution of a case with hypoplasia and hypocalcification of enamel, dental agenesis, and skeletal open bite. Quintessence Int 2001;32(3):183-9. 39. Brennan M, O’Connell B, Rams T, O’Connell A. Management of gingival overgrowth associated with generalized enamel defects in a child. J Clin Pediatr Dent 1999; 23(2):97-101. 40. Kostoulas I, Kourtis S, Andritsakis D, Doukoudakis A. Functional and esthetic rehabilitation in amelogenesis imperfecta with all-ceramic restorations: A case report. Quintessence Int 2005;36(5):329-38.
41. Turkün L. Conservative restoration with resin composites of a case of amelogenesis imperfecta. Int Dent J 2005;55 (1):38-41. 42. Ayna E, Celenk S, Kadirogulu E. Restoring function and esthetics in 2 patients with amelogenesis imperfecta: Case report. Quintessence Int 2007;38(1):51-3. 43. Kwok-Tung L, King N. The restorative management of amelogenesis imperfecta in the mixed dentition. J Clin Pediatr Dent 2006;31(2):130-5. 44. Vitkov L, Hannig M, Krautgartner W. Restorative therapy of primary teeth severely affected by amelogenesis imperfecta. Quintessence Int 2006;37(3):219-24. 45. O zturk N, Sari Z, Ozturk B. An interdisciplinary approach for restoring function and esthetics in a patient with amelogenesis imperfecta and malocclusion: A clinical report. J Prosth Dent 2004;92(2):112-5. 46. Bäckman B, Adolfsson U. Craniofacial structure related to inheritance pattern in amelogenesis imperfecta. Am J Orthod Dentofac Orthop 1994;105(6):575-82. 47. Hoppenreijs T, Voorsmic R, Freihofer H, van ’t Hof M. Open bite deformity in amelogenesis imperfecta Part 2: Le Fort 1 osteotomies and treatment results. J Craniomaxillofacial Surg 1998;26(5):286-93. 48. Ayers K, Drummond B, Harding W, Salis S, Liston P. Amelogenesis imperfecta – Multidisciplinary management from eruption to adulthood. Review and case report. N Z Dent J 2004;100(4):101-4. 49. Yamaguti P, Acevedo A, de Paula L. Rehabilitation of an adolescent with autosomal dominant amelogenesis imperfecta: Case report. Op Dent 2006;31(2):266-72. 50. Bouvier D, Duprez J, Bois D. Rehabilitation of young patients with amelogenesis imperfecta: A report of two cases. ASDC J Dent Child 1996;63(6):443-7. 51. Sapir S, Shapira J. Dentinogenesis imperfecta: An early treatment strategy. Pediatr Dent 2001;23(3):232-7. 52. O’Connell A, Marini J. Evaluation of oral problems in an osteogenesis imperfecta population. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1999;87(2):189-96.
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Guideline on Acquired Temporomandibular Disorders in Infants, Children, and Adolescents Originating Committee
Clinical Affairs Committee – Temporomandibular Joint Problems in Children Subcommittee Review Council Council on Clinical Affairs
Adopted 1990
Revised 1999, 2002, 2006, 2010
Purpose The American Academy of Pediatric Dentistry (AAPD) recognizes that disorders of the temporomandibular joint (TMJ) occasionally occur in infants, children, and adolescents. This guideline is intended to assist the practitioner in the recognition and diagnosis of temporomandibular disorders (TMD) and to identify possible treatment options. It is beyond the scope of this document to recommend the use of specific treatment modalities.
Methods This document is an update of the previous document, revised in 2006. The update included an electronic search using the following parameters: Terms: “temporomandibular disorder”, “TMJ dysfunction”, “TMD AND adolescents”, “TMD AND gender differences”, “TMD AND occlusion”, TMD AND treatment”; Fields: all fields; Limits: within the last 15 years; humans; English; clinical trials. The reviewers agreed upon the inclusion of 69 references to support this guideline. When data did not appear sufficient or were inconclusive, recommendations were based upon expert and/or consensus opinion by experienced researchers and clinicians.
Background Development of the TMJ Function influences form as development and growth of the TMJ proceeds. The TMJ is comprised of 3 major components: the mandibular condyle, the mandibular fossa, and the associated connective tissue (including the articular disk).1 The first evidence of development of the TMJ in humans is seen 8 weeks after conception.2 During the first decade of life, the mandibular condyle becomes less vascularized and most of the major morphological changes are completed. During the second decade of life, there is continued but progressive slowing of growth. The shape of the mandibular condyle may change significantly during growth with approximately 5% of condyles undergoing radiographic changes in shape between
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12 and 16 years of age.3 From adolescence to adulthood, the condyle changes to a form that is greater in width than length. Although the TMJ experiences active growth in the first 2 decades, it undergoes adaptive remodeling changes throughout life. Definition of TMD Temporomandibular disorder is a term adopted by the American Dental Association in 1983 to facilitate coordination of research and communication.4 While TMD has been defined as “functional disturbances of the masticatory system”5, others include masticatory muscle disorders6, degenerative and inflammatory TMJ disorders7, and TMJ disk displacements8 under the umbrella of TMD. Certain medical conditions are reported to occasionally mimic TMD. Among them are trigeminal neuralgia, central nervous system lesions, odontogenic pain, sinus pain, otological pain, developmental abnormalities, neoplasias, parotid diseases, vascular diseases, myofascial pain, cervical muscle dysfunction, and Eagle’s syndrome. Other common medical conditions (eg, otitis media, allergies, airway congestion, rheumatoid arthritis) can cause symptoms similar to TMD.9 Etiology of TMD Temporomandibular disorders have multiple etiological factors.10 Many studies show a poor correlation between any single etiological factor and resulting signs (findings identified by the dentist during the examination) and symptoms (findings reported by the child or parent).10 In fact, the TMJ and masticatory system is complex and, thus, requires a thorough understanding of the anatomy and physiology of the structural, vascular, and neurological components in order to manage TMD. Alterations in any one or a combination of teeth, periodontal ligament, the TMJ, or the muscles of mastication eventually can lead to TMD.11 Research is insufficient to predict reliably which patient will or will not develop TMD. Etiologic factors suggested as contributing to the development of TMD are:
American academy of pediatric Dentistry
1. Trauma: This would include impact injuries such as trauma to the chin. A common occurrence in childhood because of falling, chin trauma is reported to be a factor in the development of TMD in pediatric patients.12-14 Unilateral and bilateral intracapsular or subcondylar fractures are the most common mandibular fractures in children.15 Closed reduction and prolonged immobilization can result in ankylosis.16,17 2. Occlusal factors: There is a relatively low association of occlusal factors and the development of temporomandibular disorders.18,19 However, several features characterize malocclusions associated with TMD: • skeletal anterior open bite;20 • overjet greater than 6 to 7 mm;20-23 • retrocuspal position (centric relation) to intercuspal po sition (centric occlusion) slides greater than 4 mm;24 • unilateral lingual cross bite;20-25 • 5 or more missing posterior teeth;26,27 • Class III malocclusion.28 3. Parafunctional habits (eg, bruxism, clenching, hyperextension, other repetitive habitual behavior): Bruxism is thought to contribute to the development of TMD by joint overloading that leads to cartilage breakdown, synovial fluid alterations, and other changes within the joint. These parafunctional habits may occur while the patient is asleep or awake. A study of 854 patients younger than 17 years old found the prevalence of bruxism to be 38%.29 The literature on the association between parafunction and TMD in pediatric patients is contradictory.30-32 However, childhood parafunction was found to be a predictor of the same parafunction 20 years later.33 Other studies found correlations between reported bruxism and TMD34 with a 3.4 odds ratio.35 Children who grind their teeth were found to complain more often of pain and muscle tenderness when eating.36 4. Posture: Craniocervical posture has been associated with occlusion and with dysfunction of the TMJ, including abnormalities of the mandibular fossa, condyle, ramus, and disc.37-39 5. Changes in “free-way” dimension of the rest position: Normally 2-4 mm, this may be impinged by occlusal changes, disease, muscle spasms, nervous tension, and/or restorative prosthetics.11 6. Orthodontic treatment: Current literature does not support that the development of TMD is caused by orthodontic treatment,21,40-43 regardless of whether premolars were extracted prior to treatment.44 Prevalence of TMD in children and adolescents The reported prevalence of TMD in infants, children, and adolescents varies widely in the literature.44-47 Prevalence of signs and symptoms increases with age. One study of the primary dentition reported 34% of patients with signs and/or symptoms of TMD.48 An epidemiological study of 4724 children aged 5-17 years reported 25% with symptoms. Clicking was
seen in 2.7% of children in the primary dentition and 10.1% in late mixed dentition and further increased to 16.6% in patients with permanent dentition.20 A similar study in preschool children found TMJ sounds and clicking in 16.6% of patients.49 A study of 217 adolescents found that over 20% had signs and/or symptoms of dysfunction, with TMJ sounds and tenderness in the lateral pterygoid muscle as the most common findings.50 Clicking is seen more frequently than either locking or luxation and affects girls more than boys. In general, the prevalence of signs and symptoms of TMD is lower in children compared to adults and is even less the younger the child but increases with increasing age.25 Recent surveys have indicated a significantly higher prevalence of symptoms and greater need for treatment in girls than boys45 with the development of symptomatic TMD correlated with the onset of puberty in girls.51,52 Controversy surrounds the significance of signs and symptoms in this age group, the value of certain diagnostic procedures, and what constitutes appropriate therapy. It is not clear whether these signs and symptoms constitute normal variation, preclinical features, or manifestations of a disease state. Whether these signs and symptoms warrant treatment as predictors of TMD in adulthood is questionable.33 Diagnosing TMD All comprehensive dental examinations should include a screening evaluation of the TMJ and surrounding area.53-55 Diagnosis of TMD is based upon a combination of historical information, clinical examination, and/or craniocervical and TMJ imaging.56,57 The findings are classified as symptoms and signs.53 For a diagnosis of TMD, patients must have a history of facial pain combined with physical findings, supplemented by radiographic or imaging data when indicated.58 A screening history, as part of the health history, may include questions such as:59 • Do you have difficulty opening your mouth? • Do you hear noises within your jaw joint? • Do you have pain in or around your ears or your cheeks? • Do you have pain when chewing? • Do you have pain when opening your mouth wide or when yawning? • Has your “bite” felt uncomfortable or unusual? • Does your jaw ever “lock” or “go out”? • Have you ever had an injury to your jaw, head, or neck? If so, when? How was it treated? • Have you previously been treated for a temporomandibular disorder? If so, when? How was it treated? Clinical and physical assessment of the TMJ may include:23 • Manual palpation of the muscles and TMJ to evaluate for tenderness of intraoral and extraoral jaw muscles, neck muscles, and TMJ capsule; • Evaluation of jaw movements including assessment of mandibular range of motion using a millimeter ruler (ie, maximum unassisted opening, maximum assisted
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opening, maximum lateral excursion, maximum protrusive excursion) and mandibular opening pattern (ie, is it symmetrical?). Restricted mandibular opening with or without pain on mandibular movement may be interpreted as signs of TMJ internal derangement.60 • Determination of TMJ sounds by palpation and auscultation with a stethoscope; • Radiographs (panoramic, full mouth periapicals, lateral cephalometric), TMJ tomography, and magnetic resonance imaging to examine for TMJ pathology and/or dental pathology. TMJ arthography is not recommended as a routine diagnostic procedure.4,59 As some mental disorders can greatly influence a patient’s pain experience, psychosocial factors related to temporomandibular symptoms should be considered; this would include mood disorders, anxiety disorders, musculoskeletal problems, migraine headaches, tension headaches, emotional factors, ulcers, coliltis, occupational factors, and developmental/acquired craniofacial anomalies.11 There is a need for improved classification of TMDs; however, they largely can be grouped into 3 classes: 1. Disorders of the muscles of mastication (including protective muscle splinting, muscle spasm, and muscle inflammation); 2. Disorders of the TMJ (including internal disk derangement, disk displacement with reduction accompanied by clicking, and anterior disk displacement without reduction seen as mechanical restriction or closed lock); and 3. Disorders in other related areas that may mimic TMD (eg, chronic mandibular hypomobility, inflammatory joint disorders such as juvenile rheumatoid arthritis, degenerative joint disease, extrinsic trauma such as fracture).4 Treatment of TMD Few studies document success or failure of specific treatment modalities for TMD in infants, children, and adolescents on a long-term basis. These suggest that simple, conservative, and reversible types of therapy are effective in reducing most TMD symptoms in children.61 The focus of treatment should be to find a balance between active and passive treatment modalities. Active modalities include participation of the patient whereas passive modalities may include wearing a stabilization splint. The most common form of treatment of TMD in children was information combined with occlusal appliance therapy.62 It has been shown that combined approaches are more successful in treating TMD than single treatment modalities.62,63 Treatment of TMD can be divided into reversible and irreversible treatment. Reversible therapies may include: • Patient education (eg, relaxation training, developing behavior coping strategies, modifying inadequate perceptions about TMD, patient awareness of clenching and bruxing habits, if present).59 • Physical therapy [eg, jaw exercises or transcutaneous elec-
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trical nerve stimulation (TENS), ultrasound, iontophoresis, massage, thermotherapy, coolant therapy)].5,64,65 • Behavioral therapy (eg, avoiding excessive chewing of hard foods or gum, voluntary avoidance of stressors, habit reversal, decreasing stress, anxiety, and/or depression).66 • Prescription medication (eg, non-steroidal antiinflammatory drugs, anxiolytic agents, muscle relaxers). While antidepressants have proved to be beneficial, they should be prescribed by a physician.67 • Occlusal splints. The goal of an occlusal appliance is to provide orthopedic stability to the TMJ. These alter the patient’s occlusion temporarily and may be used to decrease parafunctional activity.62,68,69 Irreversible therapies can include: • Occlusal adjustment (ie, permanently altering the occlusion or mandibular position by selective grinding or full mouth restorative dentistry); • Mandibular repositioning [designed to alter the growth or permanently reposition the mandible (eg, headgear, functional appliances]; • Orthodontics. Referral should be made to other health care providers, including those with expertise in TMD, oral surgery, or pain management, when the diagnostic and/or treatment needs are beyond the treating dentist’s scope of practice.
Recommendations Every comprehensive dental history and examination should include a TMJ history and assessment. The history should include questions concerning the presence of head and neck pain and mandibular dysfunction, previous orofacial trauma, and history of present illness with an account of current symptoms. In the presence of a positive history and/or signs and symptoms of TMD, additional information is suggested and a referral may be considered. A more comprehensive examination should be performed and include palpation of masticatory and associated muscles and the TMJ’s, documentation of joint sounds, occlusal analysis, and assessment of range of mandibular movements including maximum opening, protrusion, and lateral excursions. Joint imaging may be recommended by other specialists to investigate joint sounds in the absence of other TMD signs and symptoms. For example, the presence of crepitus may indicate degenerative change that is not yet painful. Therapeutic modalities to prevent TMD in the pediatric population are yet to be supported by controlled studies. For children and adolescents with signs and symptoms of TMD, reversible therapies should be considered. Because of inadequate data regarding their usefulness, irreversible therapies should be avoided.61,69 Referral to a medical specialist may be indicated when otitis media, allergies, abnormal posture, airway congestion, rheumatoid arthritis, or other medical conditions are suspected.59
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References 1. Carlson DS. Growth of the temporomandibular joint. In: Zarb GAC, Carlsson GE, Sessle BJ, Mohl ND, eds. Temporomandibular Joint and Masticatory Muscle Disorders. 2nd ed. Copenhagen: Munksgaard; 1994:128-50. 2. Dixon Ad. Formation of the cranial base. In: Dixon AD, Howyte DAN, Rönning O, eds. Fundamentals of Craniofacial Growth. Boca Raton, Fl: CRC press; 1997:100-29. 3. Dibbets JM, Van der Weele LT. Prevalence of structural bony change in the mandibular condyle. J Craniomand Dis Fac Oral Pain 1992;6(4):254-9. 4. Griffiths R. Report of the President’s conference on the examination, diagnosis, and management of temporomandibular disorders and occlusion. J Am Dent Assoc 1983;106(1):75-7. 5. Okeson J. Etiology of functional disturbances in the masticatory system. In: Management of Temporomandibular Disorders and Occlusion. 6 th ed. St Louis, Mo: Mosby Year Book Publication, Inc; 2008:130-63. 6. Stohler CS. Clinical perspectives on masticatory and related muscle disorders. In: Sessle BJ, Bryant PS, Dionne RA, eds. Temporomandibular Disorders and Related Pain Conditions. Vol 4. Seattle, Wash: IASP Press; 1995:3-30. 7. Kopp S. Degenerative and inflammatory temporomandibular joint disorders. In: Sessle BJ, Bryant PS, Dionne RA, eds. Temporomandibular Disorders and Related Pain Conditions. Vol 4. Seattle, Wash: IASP Press; 1995: 119-32. 8. Dolwich MF. Temporomandibular joint disk displacement. In: Sessle BJ, Bryant PS, Dionne RA, eds. Temporomandibular Disorders and Related Pain Conditions. Volume 4. Seattle, Wash: IASP Press; 1995:79-113. 9. Loos PJ, Aaron GA. Standards for management of the pediatric patient with acute pain in the temporomandibular joint or muscles of mastication. Pediatr Dent 1989; 11(4):331. 10. Greene CS. The etiology of temporomandibular disorders: Implications for treatment. J Orofac Pain 2001;15(2):93105. 11. Hiatt JL, Gartner LP. Temporomandibular joint. In: Textbook of Head and Neck Anatomy. 2 nd ed. Baltimore, Md; Williams and Wilkins; 1987:223. 12. Greco CM, Rudy TE, Turk DC, Herlich A, Zaki HH. Traumatic onset of temporomandibular disorders: Positive effects of a standardized conservative treatment program. Clin J Pain 1997;13(4):337-47. 13. Fischer DJ, Mueller BA, Critchlow CW, LeResche L. The association of temporomandibular disorder pain with history of head and neck injury in adolescents. J Orofac Pain 2006;20(3):191-8. 14. Imahara SD, Hopper RA, Wang J, Rivara FP, Klein MB. Patterns and outcomes of pediatric facial fractures in the United States: A survey of the National Trauma Data Bank. J Am Col of Surg 2008;207(5):710-6.
15. Posnick JC, Wells M, Pron GE. Pediatric facial fractures: Evolving patterns of treatment. J Oral Maxillofac Surg 1993;51(5):836-44; discussion 844-5. 16. Kaban L. Acquired abnormalities of the temporomandibular joint. In: Kaban LB, Troulis MJ, eds. Pediatric Oral and Maxillofacial Surgery. Philadelphia, Pa; WB Saunders; 2004:340-76. 17. Güven O. A clinical study on temporomandibular joint ankylosis in children. J Craniofac Surg 2008;19(5): 1263-9. 18. De Boever JA, Carlsson GE, Klineberg IJ. Need for occlusal therapy and prosthodontic treatment in the management of temporomandibular disorders. Part I. Occlusal interference and occlusal adjustment. J Oral Rehabil 2000;27(5):367-79. 19. Taskaya-Yilmaz N, Öğütcen-Toller M, Saraç YŞ. Relationship between the TMJ disc and condyle position on MRI and occlusal contacts on lateral excursions in TMD patients. J Oral Rehab 2004;31(8):754-8. 20. Thilander B, Rubio G, Pena L, De Mayorga C. Prevalence of temporomandibular dysfunction and its association with malocclusion in children and adolescents: An epidemiologic study related to specified stages of dental development. Angle Orthod 2002;72(2):146-54. 21. Henrikson T, Nilner M. Temporomandibular disorders, occlusion and orthodontic treatment. J Orthod 2003;30 (2):129-37; discussion 27. 22. Phillips JT. What skeletal and dental characteristics do TMD patients have in common? Funct Orthod 2007;24 (1):24-6,28,30. 23. Pahkala R, Qvarnström M. Can temporomandibular dysfunction signs be predicted by early morphological or functional variables? Euro J Orthod 2004;26(4):367-73. 24. Pullinger AG, Seligman DA. Quantification and validation of predictive values of occlusal variables in temporomandibular disorders using a multifactorial analysis. J Prosthet Dent 2000;83(1):66-75. 25. Seligman DA, Pullinger AG. Analysis of occlusal variables, dental attrition, and age for distinguishing healthy controls from female patients with intracapsular temporomandibular disorders. J Prosthet Dent 2000;83(1): 76-82. 26. Ciancaglini R, Gherlone EF, Radaelli G. Association between loss of occlusal support and symptoms of functional disturbances of the masticatory system. J Oral Rehabil 1999;26(3):248-53. 27. Tallents RH, Macher DJ, Kyrkanides S, Katzberg RW, Moss ME. Prevalence of missing posterior teeth and intraarticular temporomandibular disorders. J Prosthet Dent 2002;87(1):45-50. 28. Rey D, Oberti G, Baccetti T. Evaluation of temporomandibular disorders in Class III patients treated with mandibular cervical headgear and fixed appliances. Am J Orthod Dentofac Orthop 2008;133(3):379-81.
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29. Cheifetz AT, Osganian SK, Allred EN, Needleman HL. Prevalence of bruxism and associated correlates in children as reported by parents. J Dent Child 2005;72(2): 67-73. 30. Barbosa Tde S, Miyakoda LS, Pocztaruk Rde L, Rocha CP, Gavião MBD. Temporomandibular disorders and bruxism in childhood and adolescence: Review of the literature. Int J Pediatr Otorhinolaryngol 2008;72(3): 299-314. 31. Castelo PM, Gavião MB, Pereira LJ, Bonjardim LR, Gavião MBD. Relationship between oral parafunctional/ nutritive sucking habits and temporomandibular joint dysfunction in primary dentition. Int J Paediatr Dent 2005;15(1):29-36. 32. Winocur E, Gavish A, Finkelshtein T, Halachmi M, Gazit E. Oral habits among adolescent girls and their association with symptoms of temporomandibular disorders. J Oral Rehabil 2001;28(7):624-9. 33. Carlsson GE, Egermark I, Magnusson T. Predictors of signs and symptoms of temporomandibular disorders: A 20-year follow-up study from childhood to adulthood. Acta Odontol Scand 2002;60(3):180-5. 34. Magnusson T, Egermarki I, Carlsson GE, Magnusson T, Egermarki I, Carlsson GE. A prospective investigation over two decades on signs and symptoms of temporomandibular disorders and associated variables. A final summary. Acta Odontol Scand 2005;63(2):99-109. 35. Gesch D, Bernhardt O, Mack F, John U, Kocher T, Dietrich A. Association of malocclusion and functional occlusion with subjective symptoms of TMD in adults: Results of the Study of Health in Pomerania (SHIP). Angle Orthod 2005;75(2):183-90. 36. Alamoudi N. Correlation between oral parafunction and temporomandibular disorders and emotional status among Saudi children. J Clin Pediatr Dent 2001;26(1): 71-80. 37. Sonnesen L, Bakke B, Solow B. Temporomandibular disorder in relation to craniofacial dimensions, head posture and bite force in children selected for orthodontic treatment. Eur J Orthod 2001;20(2):179-92. 38. Kondo E, Nakahara R, Ono M, et al. Cervical spine problems in patients with temporomandibular disorder symptoms: An investigation of the orthodontic treatment effects for growing and nongrowing patients. World J Orthod 2002;3(4):295-312. 39. Motoyshi M, Shimazaki T, Namura S. Biomechanical influences of head posture on occlusion: An experimental study using finite element analysis. Eur J Orthod 2002; 24(4):319-26. 40. Egermark I, Carlsson GE, Magnusson T. A prospective long-term study of signs and symptoms of temporomandibular disorders in patients who received orthodontic treatment in childhood. Angle Orthod 2005;75(4): 645-50.
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41. Henrikson T, Nilner M, Kurol J. Symptoms and signs of temporomandibular disorders before, during and after orthodontic treatment. Swed Dent J 1999;23(5-6): 193-207. 42. Henrikson T, Nilner M, Kurol J. Signs of temporomandibular disorders in girls receiving orthodontic treatment. A prospective and longitudinal comparison with untreated Class II malocclusions and normal occlusion subjects. Eur J Orthod 2000;22(3):271-81. 43. Kim MR, Graber TM, Viana MA. Orthodontics and temporomandibular disorder: A meta-analysis. Am J Orthod Dentofac Orthop 2002;121(5):438-46. 44. Alamoudi N, Farsi N, Salako N, Feteih R. Temporomandibular disorders among school children. J Clin Pediatr Dent 1998;22(4):323-9. 45. List T, Wahlund K, Wenneberg B, Dworkin SF. TMD in children and adolescents: Prevalence of pain, gender differences, and perceived treatment need. J Orofac Pain 1999;13(1):9-20. 46. Stockstill JW, Bowley JF, Dunning D, Spalding P, Stafford K, Erickson L. Prevalence of temporomandibular disorders in children based on physical signs. J Dent Child 1998;65(6):459-67, 438. 47. Paesani D, Salas E, Martinez A, Isberg A. Prevalence of temporomandibular joint disk displacement in infants and young children. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1999;87(1):15-9. 48. Bonjardim LR, Baviao MB, Carmagnani FG, Pereira LF, Castelo PM. Signs and symptoms of temporomandibular joint dysfunction in children with primary dentition. J Clin Pediatr Dent 2003;28(1):53-8. 49. Widmalm SE, Christiansen RL, Gunn SM. Oral parafunctions as temporomandibular disorder risk factors in children. Cranio 1995;13(4):242-6. 50. Bonjardim LR, Gavião MB, Pereira LJ, Castelo PM, Garcia RC. Signs and symptoms of temporomandibular disorders in adolescents. Braz Oral Res 2005;19(2):93-8. 51. LeResche L, Mancl LA, Drangsholt MT, Saunders K, Von Korff M. Relationship of pain and symptoms to pubertal development in adolescents. Pain 2005;118(1-2):201-9. 52. LeResche L, Mancl LA, Drangsholt MT, Huang G, von Korff MV. Predictors of onset of facial pain and temporomandibular disorders in early adolescence. Pain 2007; 129(3):269-78. 53. McDonald RE, Avery DR, Dean JA. Examination of the mouth and other relevant structures. In: Dean JA, Avery DR, McDonald RE, eds. McDonald and Avery’s Dentistry for the Child and Adolescent. 9th ed. Maryland Heights Mo: Mosby Elsevier; 2011:1-18. 54. Casamassimo PS, Christensen JR, Fields HW Jr, Ganzberg S. Examination, diagnosis, and treatment planning for general and orthodontic problems. In: Pinkham JR, Casamassimo PS, McTigue DJ, Fields HW Jr, Nowak AJ, eds. Pediatric Dentistry: Infancy through Adolescence. 4th ed. St. Louis, Mo; Elsevier Saunders 2005:661-89.
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55. American Academy of Pediatric Dentistry. Guideline on recordkeeping. Pediatr Dent 2009;31(special issue): 239-46. 56. American Academy of Orofacial Pain. General assessment of the orofacial pain patient. In: de Leeuw R, ed. Orofacial Pain: Guidelines for Assessment, Diagnosis, and Management. Carol Stream, Ill: Quintessence Publishing Co Inc; 2008:25-47. 57. Wahlund K, List T, Dworkin SF. Temporomandibular disorders in children and adolescents: Reliability of a questionnaire, clinical examination, and diagnosis. J Orofac Pain 1998;12(1):42-51. 58. De Boever JA, Nilner M, Orthlieb JD, Steenks MH, Educational Committee of the European Academy of Craniomandibular Disorders. Recommendations by the EACD for examination, diagnosis, and management of patients with temporomandibular disorders and orofacial pain by the general dental practitioner. J Orofac Pain 2008;22(3):268-78. 59. Brooks, SL, Brand JW, Gibbs SJ, et al. Imaging of the tempromandibular joint: A position paper of the American Academy of Oral and Maxillofacial Radiology. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1997;83(5):609-18. 60. Hu YS, Schneiderman ED, Harper RP. The temporomandibular joint in juvenile rheumatoid arthritis: Part II. Relationship between computed tomographic and clinical findings. Pediatr Dent 1996;18(4):312-9. 61. Bodner L, Miller VJ. Temporomandibular joint dysfunction in children: Evaluation of treatment. Int J Pediatr Otorhinolaryngol 1998;44(2):133-7. 62. Wahlund K, List T, Larsson B. Treatment of temporomandibular disorders among adolescents: A comparison between occlusal appliance, relaxation training, and brief information. Acta Odontol Scand 2003;61(4):203-11.
63. Kurita H, Kurashina K, Kotani A. Clinical effect of full coverage occlusal splint therapy for specific temporomandibular disorder conditions and symptoms. J Prosthet Dent 1997;78(5):506-10. 64. Michelotti A, Steenks MH, Farella M, Parisini F, Cimino R, Martina R. The additional value of a home physical therapy regimen versus patient education only for the treatment of myofascial pain of the jaw muscles: Shortterm results of a randomized clinical trial. J Orofac Pain 2004;18(2):114-25. [Erratum in J Orofac Pain 2006;20 (2):106]. 65. Medlicott, MS, Harris SR. A systematic review of the effectiveness of exercise, manual therapy, electrotherapy, relaxation training, and biofeedback in the management of temporomandibular disorder. Phys Ther 2006;86(7): 955-73. 66. Crider, AB, Glaros AG. A meta-analysis of EMG biofeedback treatment of temporomandibular disorders.J Orofac Pain 1999;13(1):29-37. 67. List T, Axelsson S, Leijon G. Pharmacologic interventions in the treatment of temporomandibular disorders, atypical facial pain, and burning mouth syndrome. A qualitative systematic review. J Orofac Pain 2003;17(4):301-10. 68. Fujii T, Torisu T, Nakamura S. A change of occlusal conditions after splint therapy for bruxers with and without pain in the masticatory muscles. Cranio 2005;23 (2):113-8. 69. Koh H, Robinson PG. Occlusal adjustment for treating and preventing temporomandibular joint disorders. The Cochrane Database of Systematic Reviews 2003;1:Art. No. CD003812. DOP: 10.1002/146751858.CD003812.
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Guideline on Pediatric Oral Surgery Originating Council Council on Clinical Affairs
Adopted 2005
Revised 2010
Purpose The American Academy of Pediatric Dentistry (AAPD) intends this guideline to define, describe clinical presentation, and set forth general criteria and therapeutic goals for common pediatric oral surgery procedures that have been presented in considerably more detail in textbooks and the dental/medical literature.
Methods This guideline is an update of the previous document adopted in 2005. It is based on a review of the current dental and medical literature related to pediatric oral surgery, including a systematic literature search of the MEDLINE/Pubmed electronic database with the following parameters: Terms: “pediatric”, “oral surgery”, “extraction”, “odontogenic infections”, “impacted canines”, “third molars”, “supernumerary teeth”, “mesiodens”, “mucocele”, “eruption cyst”, “eruption hematoma”, “attached frenum”, “ankyloglossia”, “gingival keratin cysts”, “Epstein pearls”, “Bohn’s nodules”, “congenital epulis of newborn”, “dental lamina cysts”, “natal teeth”, and “neonatal teeth” Fields: all fields; Limits: within the last 10 years; humans; English; clinical trials. There were 7761 articles that matched these criteria. Papers for review were chosen from this list and from references with selected articles. When data did not appear sufficient or were inconclusive, recommendations were based upon expert and/or consensus opinion by experience researchers and clinicians. In addition, the manual Parameters of Care: Clinical Practice Guidelines for Oral and Maxillofacial Surgery,1 developed by the American Association of Oral and Maxillofacial Surgeons (AAOMS), was consulted.
Background Surgery performed on pediatric patients involves a number of special considerations unique to this population. Several critical issues deserve to be addressed. These include: 1. preoperative evaluation; a. medical, b. dental. 2. behavioral considerations; 3. growth and development; 4. developing dentition;
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5. pathology; 6. perioperative care.
Preoperative evaluation Medical Important considerations in treating a pediatric patient include obtaining a thorough medical history, obtaining appropriate medical and dental consultations, anticipating and preventing emergency situations, and being prepared to treat emergency situations.2 Dental It is important to perform a thorough clinical and radiographic preoperative evaluation of the dentition as well as extraoral and intraoral soft tissues.2-4 Radiographs can include intraoral films and extraoral imaging if the area of interest extends beyond the dentoalveolar complex. Behavioral considerations Behavioral guidance of children in the operative and perioperative periods presents a special challenge. Many children benefit from modalities beyond local anesthesia and nitrous oxide/oxygen inhalation to control their anxiety.2,5 Management of children under sedation or general anesthesia requires extensive training and expertise.2,6 Special attention should be given to the assessment of the social, emotional, and psychological status of the pediatric patient prior to surgery.7 Children have many unvoiced fears concerning the surgical experience, and their psychological management requires that the dentist be cognizant of their emotional status. Answering questions concerning the surgery is important and should be done in the presence of the parent. The dentist also should obtain informed consent8 prior to the procedure. Growth and development The potential for adverse effects on growth from injuries and/or surgery in the oral and maxillofacial region markedly increases the potential for risks and complications in the pediatric population. Traumatic injuries involving the maxillofacial region can affect growth, development, and function adversely. For example, injuries to the mandibular condyle may not only
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result in restricted growth, but also limit mandibular function as a result of ankylosis. Surgery for acquired, congenital, or developmental malformations may, in itself, affect growth adversely. This commonly is seen in the cleft patient, for example, where palatal scarring following primary palatal repair may result in maxillary constriction.2 Developing dentition Surgery involving the maxilla and mandible of young patients is complicated by the presence of developing tooth follicles. Alteration or deviation from standard treatment modalities may be necessary to avoid injuring the follicles.9 To minimize the negative effects of surgery on the developing dentition, careful planning using radiographs, tomography10, cone beam computed tomography11, and/or 3-D imaging techniques is necessary to provide valuable information to assess the presence, absence, location, and/or quality of individual crown and root development.9 Pathology Primary and reconstructive management of tumors in children is affected by anatomical and physiological differences from those of adult patients. Tumors generally grow faster in pediatric patients and are less predictable in behavior. The same physiological factors that affect tumor growth, however, can play a favorable role in healing following primary reconstructive surgery. Pediatric patients are more resilient and heal more rapidly than their adult counterparts.2 Perioperative care Metabolic management of children following surgery frequently is more complex than that of adults. Special consideration should be given to caloric intake, fluid and electrolyte management, and blood replacement. Comprehensive management of the pediatric patient following extensive oral and maxillofacial surgery usually is best accomplished in a facility that has the expertise and experience in the management of young patients (ie, a children’s hospital).2,3
Recommendations Odontogenic infections In children, odontogenic infections may involve more than 1 tooth and usually are due to carious lesions, periodontal problems, or a history of trauma.12,13 Untreated odontogenic infections can lead to pain, abscess, and cellulitis. As a consequence of this, children are prone to dehydration—especially if they are not eating well due to pain and malaise. Prompt treatment of the source of infection is important in order to control pain and prevent the spread of infection. With infections of the upper portion of the face, patients usually complain of facial pain, fever, and inability to eat or drink. Care must be taken to rule out sinusitis, as symptoms may mimic an odontogenic infection. Occasionally in upper face infections, it may be difficult to find the true cause. Infections of the lower face usually involve pain, swelling, and
trismus.12 They frequently are associated with teeth, skin, local lymph nodes, and salivary glands.12 Swelling of the lower face more commonly has been associated with dental infection.14 Most odontogenic infections can be managed with pulp therapy, extraction, or incision and drainage.2 Infections of odontogenic origin with systemic manifestations (eg, elevated temperature of 102º to 104ºF, facial cellulitis, difficulty in breathing or swallowing, fatigue, nausea) require antibiotic therapy. Severe but rare complications of odontogenic infections include cavernous sinus thrombosis and Ludwig’s angina.2,12 These conditions can be life threatening and may require immediate hospitalization with intravenous antibiotics, incision and drainage, and referral/consultation with an oral and maxillofacial surgeon.2,12 Extraction of erupted teeth Maxillary and mandibular anterior teeth Most primary and permanent maxillary and mandibular central incisors, lateral incisors, and canines have conical single roots. In most cases, extraction of anterior teeth is accomplished with a rotational movement, due to their single root anatomies.2 However, there have been reported cases of accessory roots observed in primary canines.15-17 Radiographic examination is helpful to identify differences in root anatomy prior to extraction.15-17 Care should be taken to avoid placing any force on adjacent teeth that could become luxated or dislodged easily due to their root anatomy. Maxillary and mandibular molars Primary molars have roots that are smaller in diameter and more divergent than permanent molars. Root fracture in primary molars is not uncommon due to these characteristics as well as the potential weakening of the roots caused by the eruption of their permanent successors.2 To avoid inadvertent extraction or dislocation of or trauma to the permanent successor, careful evaluation of the relationship of the primary roots to the developing succedaneous tooth should be completed. Primary molars with roots encircling the successor’s crown may need to be sectioned to protect the permanent tooth’s location.2 Molar extractions are accomplished by using slow continuous palatal/lingual and buccal force allowing for the expansion of the alveolar bone to accommodate the divergent roots and reduce the risk of root fracture.2 When extracting mandibular molars, care should be taken to support the mandible to protect the temporomandibular joints from injury.2 Fractured primary tooth roots The dilemma to consider when treating a fractured primary tooth root is that removing the root tip may cause damage to the succedaneous tooth, while leaving the root tip may increase the chance for postoperative infection and delay eruption of the permanent successor.2 Radiographs can assist in the decision process. The literature suggests that if the fractured root tip can be removed easily, it should be removed.2 If the
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root tip is very small, located deep in the socket, situated in close proximity to the permanent successor, or unable to be retrieved after several attempts, it is best left to be resorbed.2 Unerupted and impacted teeth Impacted canines Permanent maxillary canines are second to third molars in frequency of impaction.18 Early detection of an ectopically erupting canine through visual inspection, palpation, and radiographic examination is important to minimize such an occurrence.19 Panoramic and periapical films are useful in locating potentially ectopic canines.20 Routine evaluation of patients in mid-mixed dentition should involve identifying signs such as lack of canine bulges and asymmetry in pattern of exfoliation. Eruption of canines and abnormal angulation or ectopic eruption of developing permanent cuspids can be detected with a radiograph.19 When the cusp tip of the permanent canine is just mesial to or overlaying the distal half of the long axis of the root of the permanent lateral incisor, canine palatal impaction usually occurs.20 Extraction of the primary canines is the treatment of choice when malformation or ankylosis is present, when the risk of resorption of the adjacent tooth is evident, or when trying to correct palatally impacted canines, provided there are normal space conditions and no incisor resorption.18,21-23 One study showed that 78% of ectopically-erupting permanent canines normalized within 12 months after removal of the primary canines; 64% normalized when the starting canine position overlapped the lateral incisor by more than half of the root and 91% normalized when the starting canine position overlapped the lateral incisor by less than half of the root.18 If no improvement in canine position occurs in a year, surgical and/ or orthodontic treatment were suggested.18,23 Although a Cochrane review21 yielded a lack of randomized controlled clinical studies to support extraction of primary canines to facilitate eruption of ectopic permanent maxillary canines, the literature suggests that this can be considered to minimize complications resulting from impacted canines. Consultation between the practitioner and an orthodontist may be useful in the final treatment decision. Third molars Panoramic or periapical radiographic examination is indicated in late adolescence to assess the presence, position, and development of third molars.4 AAOMS recommends that a decision to remove or retain third molars should be made before the middle of the third decade.1 Little controversy surrounds their removal when pathology (eg, cysts or tumors, caries, infection, pericoronitis, periodontal disease, detrimental changes of adjacent teeth or bone) is associated and/or the tooth is malpositioned or nonfunctional (ie, an unopposed tooth).24-26 A systematic review of research literature from 1984 to 1999 concluded there is no reliable evidence to support the prophylactic removal of disease-free impacted third molars.24 Although prophylactic removal of all impacted or unerupted
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disease-free third molars is not indicated, consideration should be given to removal by the third decade when there is a high probability of disease or pathology and/or the risks associated with early removal are less than the risks of later removal.24-26 Removing the third molars prior to complete root formation may be surgically prudent.1 AAOMS performed an age-related third molar study among board-certified oral and maxillofacial surgeons in 2001 and concluded that third molar removal in adults is safe with minimal complications and negative effects on the patient’s quality of life.25 The report showed that mandibular third molars exhibited more pathology or abnormalities. All intraoperative complications (eg, nerve injury, unexpected hemorrhage, unplanned transfusion or parenteral drugs, compromised airway, fracture, other injuries to adjacent teeth/structures) occurred at a frequency less than 1%.25 Excluding alveolar osteitis, postoperative complications (eg, paresthesia, infection, trismus, hemorrhage) were similarly low.25,26 Factors that increase the risk for complications (eg, coexisting systemic conditions, location of peripheral nerves, history of temporomandibular joint disease, presence of cysts or tumors)25,26 and position and inclination of the molar in question27 should be assessed. The age of the patient is only a secondary consideration.27 Referral to an oral and maxillofacial surgeon for consultation and subsequent treatment may be indicated. When a decision is made to retain impacted third molars, they should be monitored for change in position and/ or development of pathology, which may necessitate later removal. Supernumerary teeth Supernumerary teeth and hyperdontia are terms to describe an excess in tooth number. Supernumerary teeth are thought to be related to disturbances in the initiation and proliferation stages of dental development.15,28 Although some supernumerary teeth may be syndrome associated (eg, cleidocranial dysplasia) or of familial inheritance pattern, most supernumerary teeth occur as isolated events.15 Supernumerary teeth can occur in either the primary or permanent dentition.15,29-31 In 33% of the cases, a supernume-rary tooth in the primary dentition is followed by the supernumerary tooth complement in the permanent dentition.32,33 Reports in incidence of supernumerary teeth can be as high as 3%, with the permanent dentition being affected 5 times more frequently than the primary dentition and males being affected twice as frequently as females.15,29,30 Supernumerary teeth will occur 10 times more often in the maxillary arch versus the mandibular arch.15 Approximately 90% of all single tooth supernumerary teeth are found in the maxillary arch, with a strong predilection to the anterior region.15,31 The maxillary anterior midline is the most common site, in which case the supernumerary tooth is known as a mesiodens; the second most common site is the maxillary molar area, with the tooth known as a paramolar.15,29,31 A mesiodens can be suspected if there is an asymmetric eruption pattern of the maxillary incisors, delayed eruption of the
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maxillary incisors with or without any over-retained primary incisors, or ectopic eruption of a maxillary incisor.29,33 The diagnosis of a mesiodens can be confirmed with radiographs, including occlusal, periapical, or panoramic films,34 or computed tomography10,11. Three-dimensional information needed to determine the location of the mesiodens or impacted tooth can be obtained by taking 2 periapical radiographs using either 2 projections taken at right angles to one another or the tube shift technique (buccal object rule or Clark’s rule)34 or by cone beam computed tomography11. Complications of supernumerary teeth can include delayed and/or lack of eruption of the permanent tooth, crowding, resorption of adjacent teeth, dentigerous cyst formation, pericoronal space ossification, and crown resorption.35,36 Early diagnosis and appropriately timed treatment are important in the prevention and avoidance of these complications. Because only 25% of all mesiodens erupt spontaneously, surgical management often is necessary.33,37 A mesiodens that is conical in shape and is not inverted has a better chance for eruption than a mesiodens that is tubercular in shape and is inverted.36 The treatment objective for a nonerupting permanent mesiodens is to minimize eruption problems for the permanent incisors.36 Surgical management will vary depending on the size, shape, and number of supernumeraries and the patient’s dental development.36 The treatment objective for a nonerupting primary mesiodens differs in that the removal of these teeth usually is not recommended, as the surgical intervention may disrupt or damage the underlying developing permanent teeth.35 Erupted primary tooth mesiodens typically are left to shed normally upon the eruption of the permanent dentition.35 Extraction of an unerupted primary or permanent mesiodens is recommended during the mixed dentition to allow the normal eruptive force of the permanent incisor to bring itself into the oral cavity.36 Waiting until the adjacent incisors have at least two-thirds root development will present less risk to the developing teeth but still allow spontaneous eruption of the incisors.1 In 75% of the cases, extraction of the mesiodens during the mixed dentition results in spontaneous eruption and alignment of the adjacent teeth.35,38 If the adjacent teeth do not erupt within 6 to 12 months, surgical exposure and orthodontic treatment may be necessary to aid their eruption.37,39 The diagnosing dentist may consider a multidisciplinary approach when treating difficult or complex cases. Pediatric oral pathology Lesions of the newborn Oral pathologies occurring in newborn children include Epstein’s pearls, dental lamina cysts, Bohn’s nodules, and congenital epulis. Epstein’s pearls are common, found in about 75% to 80% of newborns.40-43 They occur in the median palatal raphe area40-44 as a result of trapped epithelial remnants along the line of fusion of the palatal halves.42,44 Dental lamina cysts, found on the crests of the dental ridges, most commonly are seen bilaterally in the region of the first primary molars.42
They result from remnants of the dental lamina. Bohn’s nodules are remnants of salivary gland epithelium and usually are found on the buccal and lingual aspects of the ridge, away from the midline.40,41,43 Epstein’s pearls, Bohn’s nodules, and dental lamina cysts typically present as asymptomatic 1 mm to 3 mm nodules or papules. They are smooth, whitish in appearance, and filled with keratin.41,42 No treatment is required, as these cysts usually disappear during the first 3 months of life.41,44 Congenital epulis of the newborn, also known as granular cell tumor or Neumann’s tumor, is a rare benign tumor seen only in newborns. This lesion is typically a protuberant mass arising from the gingival mucosa. It is most often found on the anterior maxillary ridge.45,46 Patients typically present with feeding and/or respiratory problems.46 Congenital epulis has a marked predilection for females at 8:1 to 10:1.45-47 Treatment normally consists of surgical excision.45,47 The newborn usually heals well, and no future complications or treatment should be expected. Eruption cyst (eruption hematoma) The eruption cyst is a soft tissue cyst that results from a separation of the dental follicle from the crown of an erupting tooth.41,48 Fluid accumulation occurs within this created follicular space.40,43,48,49 Eruption cysts most commonly are found in the mandibular molar region.48 Color of these lesions can range from normal to blue-black or brown, depending on the amount of blood in the cystic fluid.40,43,48,49 The blood is secondary to trauma. If trauma is intense, these blood-filled lesions sometimes are referred to as eruption hematomas.40,43,48,49 Because the tooth erupts through the lesion, no treatment is necessary.40,43,48,49 If the cyst does not rupture spontaneously or the lesion becomes infected, the roof of the cyst may be opened surgically.40,43,48 Mucocele The mucocele is a common lesion in children and adolescents resulting from the rupture of a minor salivary gland excretory duct, with subsequent leakage of mucin into the surrounding connective tissues that later may be surrounded in a fibrous capsule.41,43,50-52 Most mucoceles are well-circumscribed bluish translucent fluctuant swellings (although deeper and longstanding lesions may range from normal in color to having a whitish keratinized surface) that are firm to palpation.43,50,52 Local mechanical trauma to the minor salivary gland is often the cause of rupture.43,50-52 Mucoceles most frequently are observed on the lower lip, usually lateral to the midline.50 Mucoceles also can be found on the buccal mucosa, ventral surface of the tongue, retromolar region, and floor of the mouth (ranula).50-52 Superficial mucoceles and some other mucoceles are shortlived lesions that burst spontaneously, leaving shallow ulcers that heal within a few days.43,50-52 Many lesions, however, require treatment to minimize the risk of recurrence.43,50-52
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Structural anomalies Maxillary frenum A prominent maxillary frenum in children, although a common finding, is often a concern, especially when associated with a diastema. A comparison of attached frena with and without diastemas found no correlation between the height of the frenum attachment and diastema presence and width.53 Treatment is suggested when the attachment exerts a traumatic force on the gingiva causing the papilla to blanch when the upper lip is pulled or if or it causes a diastema to remain after eruption of the permanent canines.54,55 Interference with oral hygiene measures, esthetics, and psychological reasons are contributing factors that relate to treatment of the maxillary frenum.54,56 Treatment options can include orthodontics, restorative dentistry, surgery, or a combination of these.54 When a diastema is present, the objectives for treatment involve managing both the diastems or permanent teeth and its cause while maintaining stable results in the future.54 It is recommended that treatment be delayed until the permanent incisors and cuspids have erupted and the diastema has had an opportunity to close naturally.55 If orthodontic treatment is indicated, the frenectomy [complete excision (ie, removal of the whole frenulum)]57 should be performed only after the diastema is closed as much as possible to achieve stable results.54 When indicated, a maxillary frenectomy is a fairly simple procedure and can be performed in the office setting. Mandibular labial frenum A high frenum sometimes can present on the labial aspect of the mandibular ridge. This is most often seen in the central incisor area and frequently occurs in individuals where the vestibule is shallow.58 The mandibular anterior frenum, as it is known, occasionally inserts into the free or marginal gingival tissue.58 Movements of the lower lip cause the frenum to pull on the fibers inserting into the free marginal tissue, which, in turn, can lead to food and plaque accumulation.58 Early treatment can be considered to prevent subsequent inflammation, recession, pocket formation, and possible loss of the alveolar bone and/or tooth.58 However, if factors causing gingival/periodontal inflammation are controlled, the degree of recession and need for treatment decreases.57 Mandibular lingual frenum/ankyloglossia Ankyloglossia is a developmental anomaly of the tongue characterized by a short, thick lingual frenum resulting in limitation of tongue movement (partial ankyloglossia) or by the tongue appearing to be fused to the floor of the mouth (total ankyloglossia).44,58 The reported prevalence is 0.1-10.7% of the population.57 The exact cause of ankyloglossia remains unknown57. Ankyloglossia has been associated with problems with breastfeeding among neonates,57-61 tongue mobility and speech,54,57,62 malocclusion,57,63,64 and gingival recession.57 During breastfeeding, a short frenum can cause ineffective latch, inadequate milk transfer and intake, and persistent mater-
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nal nipple pain, all of which can affect feeding adversely.57-61 When indicated, frenuloplasty (various methods to release the tongue tie and correct the anatomic situation57) or frenectomy (simple cutting of the frenulum57) may be a successful approach to facilitate breastfeeding; however, there is a need for evidence-based research to determine indications for treatment.57-60 This indicates that there is a need to standardize a classification system and justify parameters for surgical correction of ankyloglossia among neonates.57-63 Limitations in tongue mobility and speech pathology have been associated with ankyloglossia.54,57,62 There has been varied opinion among health care professionals regarding the correlation between ankyloglossia and speech disorders.57,62 Frenuloplasty or frenectomy in conjunction with speech therapy can be a treatment option to improve tongue mobility and speech.62 Further evidence is needed to determine the benefit of surgical correction of ankyloglossia in resolving speech pathology.57 There is limited evidence to show an association between ankyloglossia and Class III malocclusion.57,64 Speculations have been made that the abnormal tongue position may affect skeletal development.57,63,64 Although there are no clear recommendations in the literature, a complete orthodontic evaluation, diagnosis, and treatment plan are necessary prior to any surgical intervention.57 Reports also have been made regarding the association between frenal attachment and gingival recession; further clinical evidence, however, is warranted to show a clear relationship between these 2 factors.57 Elimination of plaqueinduced gingival inflammation can minimize gingival recession without any surgical intervention.57 The significance and management of ankyloglossia are very controversial due to the lack of evidence-based studies to support frenotomy, frenectomy, and frenuloplasty among children and adults affected by ankyloglossia.57,62 Studies have shown a difference in treatment recommendations among speech pathologists, pediatricians, otolaryngologists, lactation specialists, surgeons, and dental specialists.57-63,65 Most professionals, however, will agree that there are certain indications for these procedures.63 A short lingual frenum can inhibit tongue movement and create deglutition problems.65 If there is no improvement in breastfeeding for a child with ankyloglossia after non-surgical intervention, frenectomy may be indicated.57 Although there is limited evidence in the literature to promote the timing, indication, and type of surgical intervention, frenectomy for functional limitations due to severe ankyloglossia should be considered on an individual basis.57 If evaluation shows that function may be improved by surgery, treatment should be considered.65 Frenectomy techniques Frenectomy involves surgical incision, establishing hemostasis, and suturing of the wound.66 Dressing placement or the use of antibiotics is not necessary.66 Recommendations include maintaining a soft diet, regular oral hygiene, and analgesics as needed.66 Although there is minimal evidence-based research
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available, the use of laser technology and electrosurgery for frenectomies have demonstrated a shorter operative working time, the ability to control bleeding quickly, reduced pain and discomfort, fewer postoperative complications (eg, pain, swelling, infection), and no need for suture removal, as well as increasing patient acceptance.66-69 These procedures require skilled technique and patient management.66,69 Natal and neonatal teeth Natal and neonatal teeth can present a challenge when deciding on appropriate treatment. Natal teeth have been defined asthose teeth present at birth, and neonatal teeth are those that erupt during the first 30 days of life.70,71 The occurrence of natal and neonatal teeth is rare; the incidence varies from 1:1,000 to 1:30,000.70,71 The teeth most often affected are the mandibular primary incisors.72 In most cases, anterior natal and neonatal teeth are part of the normal complement of the dentition.70,71 Natal or neonatal molars have been identified in the posterior region and may be associated with systemic conditions or syndromes (eg, Pfieffer syndrome, histiocytosis X).72-74 Although many theories exist as to why the teeth erupt prematurely, currently no studies confirm a causal relationship with any of the proposed theories. The superficial position of the tooth germ associated with a hereditary factor seems to be the most accepted possibility.71 If the tooth is not excessively mobile or causing feeding problems, it should be preserved and maintained in a healthy condition if at all possible.71,75 Close monitoring is indicated to ensure that the tooth remains stable. Riga-Fede disease is a condition caused by the natal or neonatal tooth rubbing the ventral surface of the tongue during feeding leading to ulceration.69,70 Failure to diagnose and properly treat this lesion can result in dehydration and inadequate nutrient intake for the infant.75 Treatment should be conservative and focus on creating round, smooth incisal edges.71-76 If conservative treatment does not correct the condition, extraction is the treatment of choice.71,76 An important consideration when deciding to extract a natal or neonatal tooth is the potential for hemorrhage. Extraction is contraindicated in newborns due to risk of hemorrhage.77 Unless the child is at least 10 days old, consultation with the pediatrician regarding adequate hemostasis may be indicated prior to extraction of the tooth.
References 1. American Association of Oral and Maxillofacial Surgeons. Parameters of Care: Clinical Practice Guidelines for Oral and Maxillofacial Surgery (AAOMS ParCare 07 Ver 4.0). J Oral Maxillofac Surg 2007:Suppl. 2. Wilson S, Montgomery RD. Local anesthesia and oral surgery in children. In: Pinkham JR, Casamassimo PS, Fields HW Jr, McTigue DJ, Nowak AJ, eds. Pediatric Dentistry: Infancy through Adolescence. 4th ed. St. Louis, Mo: Elsevier Saunders; 2005:454, 461.
3. Kaban L, Troulis M. Preoperative Assessment of the Pediatric Patient. In: Pediatric Oral and Maxillofacial Surgery. Philadelphia, Pa: Saunders; 2004:3-19. 4. American Academy of Pediatric Dentistry. Guideline on prescribing dental radiographs for infants, children, adolescents, and persons with special health care needs. Pediatr Dent 2009;31(special issue):250-2. 5. Kaban L, Troulis M. Behavior management and conscious sedation of pediatric patients in the oral surgery office. In: Pediatric Oral and Maxillofacial Surgery. Philadelphia, Pa: Saunders; 2004:75-85. 6. Kaban L, Troulis M. Deep sedation for pediatric patients. In: Pediatric Oral and Maxillofacial Surgery. Philadelphia, Pa: Saunders; 2004:86-99. 7. McDonald RE, Avery DR, Dean JA. Examination of the mouth and other relevant structures. In: Dean JA, Avery DR, McDonald RE, eds. McDonald and Avery’s Dentistry for the Child and Adolescent. 9th ed. Maryland Heights, Mo: Mosby Elsevier; 2011:3. 8. American Academy of Pediatric Dentistry. Guideline on informed consent. Pediatr Dent 2009;31(special issue): 247-9. 9. Murray DJ, Chong DK, Sandor GK, Forrest CR. Dentigerous cyst after distraction osteogenesis of the mandible. J Craniofac Surg 2007;18(16):1349-52. 10. White S, Pharoah M, Frederiksen NL. Advanced Imaging. In: White S, Pharoah M, eds. Oral Radiology: Principles and Interpretation. 6th ed. St Louis, Mo: Mosby Elsevier; 2009:207-24. 11. Scarfe WC, Farman AG. Cone Beam Computed Tomography. In: White S, Pharoah M, eds. Oral Radiology: Principles and Interpretation. 6th ed. St Louis, Mo: Mosby Elsevier; 2009:225-43. 12. Kaban L, Troulis M. Infections of the maxillofacial region. In: Pediatric Oral and Maxillofacial Surgery. Philadelphia, Pa: Saunders; 2004:171-86. 13. Seow W. Diagnosis and management of unusual dental abscesses in children. Aust Dent J 2003;43(3):156-68. 14. Dodson T, Perrott D, Kaban L. Pediatric maxillofacial infections: A retrospective study of 113 patients. J Oral Maxillofac Surg 1989;47(4):327-30. 15. Regezi J, Sciubba J, Jordan R. Abnormalities of teeth. In: Oral Pathology: Clinical-Pathologic Correlations, 5th ed. St Louis, MO: Saunders Elsevier; 2008:361-76. 16. Mochizuki K, Ohtawa Y, Kubo S, Machida Y, Yakushiji M. Bifurcation, birooted primary canines: A case report. Int J Pediatr Dent 2001;11(5):380-5. 17. Ott N, Ball R. Birooted primary canines: A report of three cases. Pediatr Dent 1996;18(4):328-30. 18. Ericson S, Kurol J. Early treatment of palatally erupting maxillary canines by extraction of the primary canines. Eur J Orthod 1988;10(4):283-95. 19. Richardson G, Russel K. A review of impacted permanent maxillary cuspids – Diagnosis and prevention. J Can Dent Assoc 2000;66(9):497-501.
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20. Lindauer SJ, Rubenstein LK, Hang WM, Andersen WC, Isaason RJ. Canine impaction identified early with panoramic radiographs. J Am Dent Assoc 1992;123(3):91-2, 95-7. Erratum in J Am Dent Assoc 1992;123(5):16. 21. Parkin N, Benson P, Shah A, et al. Extraction of primary (baby) teeth for unerupted palatally displaced permanent canine teeth in children. Cochrane Database Syst Rev 2009;15(2):CD004621. 22. Fernandez E, Bravo LA, Canteras M. Eruption of the permanent upper canines: A radiologic study. Am J Orthod Dentofacial Orthop 1998;113(4):414-20. 23. Baccetti T, Leonardi M, Armi P. A randomized clinical study of two interceptive approaches to palatally displaced canines. Eur J Orthod 2008;30(4):381-5. 24. Song F, O’Meara S, Wilson P, Goldner S, Kleijnen J. The effectiveness and cost-effectiveness of prophylactic removal of wisdom teeth. Health Technol Assess 2000;4(1): 1-55. 25. Haug R, Perrott D, Gonzalez M, Talwar R. The American Association of Oral and Maxillofacial Surgeons agerelated third molar study. J Oral Maxillofac Surg 2005; 63(8):1106-14. 26. Pogrel M, Dodson T, Swift J, et al. White paper on third molar data. American Association of Oral and Maxillofacial Surgeons. March 2007. Available at: “http://www. aaoms.org/docs/third_molar_white_paper.pdf\”. Accessed June 24, 2010. 27. Almendros-Marques N, Alaejos-Algarra E, QuinterosBorgarello M, Berini-Aytes L, Gay-Escoda C. Factors influencing the prophylactic removal of asymptomatic impacted lower third molars. Int J Oral Maxillofac Surg 2008;37(1):29-35. 28. Profitt WR. The etiology of orthodontic problems. In: Profitt WR, Fields HW Jr, Sarver DM, eds. Contemporary Orthodontics. 4th ed. St. Louis, Mo: Mosby Elsevier; 2007:138. 29. Primosch R. Anterior supernumerary teeth—Assessment and surgical intervention in children. Pediatr Dent 1981; 3(2):204-15. 30. Dummett CO Jr . Anomalies of the developing dentition. In: Pinkham JR, Casamassimo PS, Fields HW Jr, McTigue DJ, Nowak AJ, eds. Pediatric Dentistry: Infancy through Adolescence. 4th ed. St. Louis, Mo: Elsevier Saunders; 2005:61-2. 31. Neville BW, Damm DD, Allen CM, Bouquot JE. Abnormalities of the teeth. In: Oral and Maxillofacial Pathology. 3rd ed. St Louis, Mo: Saunders Elsevier; 2009:80. 32. Taylor GS. Characteristics of supernumerary teeth in the primary and permanent dentition. Trans Br Soc Study Orthod 1970-71;57:123-8. 33. American Academy of Pediatric Dentistry. Guideline on the management of the developing dentition and occlusion in pediatric dentistry. Pediatr Dent 2009;31(special issue):196-208.
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34. White S, Pharoah M. Projection geometry. In: Oral Radiology: Principles and Interpretation. 6th ed. St. Louis, Mo: Mosby Elsevier; 2009:46-52. 35. Neville BW, Damm DD, White DK. Pathology of the teeth. In: Color Atlas of Clinical Oral Pathology. 2nd ed. Baltimore, Md: Williams & Wilkins; 2003:58-60. 36. Christensen JR, Fields HW Jr. Treatment planning and management of orthodontic problems. In: Pinkham JR, Casamassimo PS, Fields HW Jr, McTigue DJ, Nowak AJ, eds. Pediatric Dentistry: Infancy through Adolescence. 4th ed. St. Louis, Mo: Elsevier Saunders; 2005:624-6. 37. Russell K, Folwarczna M. Mesiodens: Diagnosis and management of a common supernumerary tooth. J Can Dent Assoc 2003;69(6):362-6. 38. Howard R. The unerupted incisor. A study of the postoperative eruptive history of incisors delayed in their eruption by supernumerary teeth. Dent Pract Dent Rec 1967;17(9):332-41. 39. Giancotti A, Grazzini F, De Dominicis F, Romanini G, Arcuri C. Multidisciplinary evaluation and clinical management of mesiodens. J Clin Pediatr Dent 2002;26(3): 233-7. 40. Slayton R, Hughes-Brickhouse T, Adair S. Dental development, morphology, eruption and related pathologies. In: Nowak AJ, Casamassimo PS, eds. The Handbook: Pediatric Dentistry. 3rd ed. Chicago, Ill: American Academy of Pediatric Dentistry; 2007:9-28. 41. Flaitz CM. Differential diagnosis of oral lesions and developmental anomalies. In: Pinkham JR, Casamassimo PS, Fields HW Jr, McTigue DJ, Nowak AJ, eds. Pediatric Dentistry: Infancy through Adolescence. 4th ed. St. Louis, Mo: Elsevier Saunders; 2005:18. 42. Hays P. Hamartomas, eruption cysts, natal tooth, and Epstein pearls in a newborn. J Dent Child 2000;67(5): 365-8. 43. Aldred MJ, Cameron AC. Pediatric oral medicine and pathology. In: Cameron AC, Widmer RP. eds. Handbook of Pediatric Dentistry. 3rd ed. Philadelphia, Pa: Mosby Elsevier; 2008:192-216. 44. Neville BW, Damm DD, Allen CM, Bouquot JE. Developmental defects of the oral and maxillofacial region. In: Oral and Maxillofacial Pathology. 3rd ed. St. Louis, Mo: Saunders Elsevier; 2009:25-7. 45. Lapid O, Shaco-Levey R, Krieger Y, Kachko L, Sagi A. Congenital epulis. Pediatrics 2001;107(2):E22. 46. Marakoglu I, Gursoy U, Marakoglu K. Congenital epulis: Report of a case. J Dent Child 2002;69(2):191-2. 47. Neville BW, Damm DD, Allen CM, Bouquot JE. Soft tissue tumors. In: Oral and Maxillofacial Pathology. 3rd ed. St. Louis, Mo: Saunders Elsevier; 2009; 537-8. 48. Neville BW, Damm DD, Allen CM, Bouquot JE. Odontogenic cysts and tumors. In: Oral and Maxillofacial Pathology. 3rd ed. St Louis, Mo: Saunders Elsevier; 2009: 682.
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49. Regezi J, Sciubba J, Jordan R. Cysts of the oral region. In: Oral Pathology: Clinical-Pathologic Correlations. 5th ed. St. Louis, Mo: Saunders Elsevier; 2008:241-4. 50. Baurmash HD. Mucoceles and ranulas. J Oral Maxillofac Surg 2003;61(3):369–78. 51. Regezi J, Sciubba J, Jordan R. Salivary gland diseases. In: Oral Pathology: Clinical-Pathologic Correlations. 5th ed. St Louis, Mo: Saunders Elsevier; 2008:179-82. 52. Sonis A, Keels MA. Oral pathology/oral medicine/ syndromes. In: Nowak AJ, Casamassimo PS, eds. The Handbook: Pediatric Dentistry. 3 rd ed. Chicago, Ill: American Academy of Pediatric Dentistry; 2007:29-53. 53. Ceremello P. The superior labial frenum and midline diastema and their relation to growth and development of the oral structures. Am J Orthod Dentofacial Orthop 1993;39(2):120-39. 54. Gkantidis N, Kolokitha OE, Topouzelis N. Management of maxillary midline diastema with emphasis on etiology. J Clin Ped Dent 2008;32(4):265-72. 55. Griffen AL. Periodontal problems in children and adolescents. In: Pinkham JR, Casamassimo PS, Fields HW Jr, McTigue DJ, Nowak AJ, eds. Pediatric Dentistry: Infancy through Adolescence. 4th ed. St. Louis, Mo: Elsevier Saunders; 2005:417. 56. McDonald RE, Avery DR, Hartsfield JK. Acquired and developmental disturbances of the teeth. In: Dean JA, Avery DR, McDonald RE, eds. McDonald and Avery’s Dentistry for the Child and Adolescent. 9th ed. Maryland Heights, Mo: Mosby Elsevier; 2011:119-20. 57. Suter VG, Bornstein MM. Ankyloglossia: Facts and myths in diagnosis and treatment. J Periodontol 2009;80 (8):1204-19. 58. McDonald RE, Avery DR, Weddell JA. Gingivitis and periodontal disease. In: Dean JA, Avery DR, McDonald RE, eds. McDonald and Avery’s Dentistry for the Child and Adolescent. 9th ed. Maryland Heights, Mo: Mosby Elsevier; 2011:389-91. 59. Segal L, Stephenson R, Dawes M, Feldman P. Prevalence, diagnosis, and treatment of ankyloglossia. Can Fam Physician 2007;53(6):1027-33. 60. Ballard J, Auer C, Khoury J. Ankyloglossia: Assessment, incidence, and effect of frenuloplasty on the breastfeeding dyad. Pediatrics 2002;110(5):e63. 61. Geddes D, Langton D, Gollow I, Jacobs L, Hartmann P, Simmer K. Frenulotomy for breastfeeding infants with ankyloglossia: Effect on milk removal and sucking mechanism as imaged by ultrasound. Pediatrics 2008;122 (1):e188-e194.
62. Kupietzky A, Botzer E. Ankyloglossia in the infant and young child: Clinical suggestions for diagnosis and management. Pediatr Dent 2005;27(1):40-6. 63. Lalakea L, Messner A. Frenotomy and frenuloplasty: If, when and how. Oper Tech Otolaryngol Head Neck Surg 2002;13(1):93-7. 64. Neville BW, Damm DD, White DK. Developmental disturbances of the oral and maxillofacial region. Color Atlas of Clinical Oral Pathology. 2nd ed. Baltimore, Md: Williams & Wilkins; 2003:10-1. 65. Lalakea M, Messner A. Ankyloglossia: Does it matter? Pediatr Clin North Am 2003;50(2):381-97. 66. Kaban L, Troulis M. Intraoral soft tissue abnormalities. In: Pediatric Oral and Maxillofacial Surgery. Philadelphia, Pa: Saunders; 2004:147-53. 67. Shetty K. Trajtenberg C. Patel C. Streckfus C. Maxillary frenectomy using a carbon dioxide laser in a pediatric patient: A case report. Gen Dent 2008;56(1):60-3. 68. Kara C. Evaluation of patient perceptions of frenectomy: A comparison of Nd:YAG laser and conventional techniques. Photomed Laser Surg 2008;26(2):147-52. 69. Gontijo I, Navarro R, Haypek P, Ciamponi A, Haddad A. The applications of diode and Er:YAG lasers in labial frenectomy in infant patients. J Dent Child 2005;72(1):10-5. 70. Cunha RF, Boer FA, Torriani DD, Frossard WT. Natal and neonatal teeth: Review of the literature. Pediatr Dent 2001;23(2):158-62. 71. Leung A, Robson W. Natal teeth: A review. J Natl Med Assoc 2006;98(2):226-8. 72. Galassi MS, Santos-Pinto L, Ramalho T. Natal maxillary primary molars: Case report. J Clin Pediatr Dent 2004; 29(1):41-44. 73. Alvarez MP, Crespi PV, Shanske AL. Natal molars in Pfeiffer syndrome type 3: A case report. J Clin Pediatr Dent 1993;18(1):21-4. 74. Stein S, Paller A, Haut P, Mancini A. Langerhans cell histiocytosis presenting in the neonatal period: A retrospective case series. Arch Pediatr Adolesc Med 2001;155(7): 778-83. 75. Slayton RL. Treatment alternatives for sublingual traumatic ulceration (Riga-Fede disease). Pediatr Dent 2000;22 (5):413-4. 76. Goho C. Neonatal sublingual traumatic ulceration (RigaFede disease): Report of cases. J Dent Child 1996;63 (5):362-4. 77. Rushmah M. Natal and neonatal teeth: A clinical and histological study. J Clin Pediatr Dent 1991;15(4):251-3.
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Guideline on Use of Antibiotic Therapy for Pediatric Dental Patients Originating Council Council on Clinical Affairs
Review Council Council on Clinical Affairs
Adopted 2001
Revised 2005, 2009
Purpose The American Academy of Pediatric Dentistry recognizes the increasing prevalence of antibiotic-resistant micro-organisms. This guideline is intended to provide guidance in the proper and judicious use of antibiotic therapy in the treatment of oral conditions.1
Methods This revision was based upon a new systematic literature search of the MEDLINE/Pubmed electronic database using the following parameters: Terms: antibiotic therapy, antibacterial agents in children, antimicrobial agents in children, dental trauma, oral wound management, orofacial infections, periodontal disease, viral disease, and oral contraception; Field: All fields; Limits: within the last 10 years, humans, English, clinical trials, birth through age 18. Papers for review were chosen from this search and from hand searching. When data did not appear sufficient or were inconclusive, recommendations were based upon expert and/or consensus opinion by experienced researchers and clinicians.
Background The widespread use of antibiotics has permitted common bacteria to develop resistance to drugs that once controlled them.2-4 At present, there are no antibiotics to which resistance has not appeared.2,5 To diminish the rate at which resistance is increasing, health care providers must be prudent in the use of antibiotics. 1
Recommendations Conservative use of antibiotics is indicated to minimize the risk of developing resistance to current antibiotic regimens.2-11 The following general principles should be adhered to when prescribing antibiotics for the pediatric population.
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Oral wound management Factors related to host risk (eg, age, systemic illness, malnutrition) and type of wound (eg, laceration, puncture) must be evaluated when determining the risk for infection and subsequent need for antibiotics. Wounds can be classified as clean, potentially contaminated, or contaminated/dirty. Facial lacerations may require topical antibiotic agents.12 Intraoral lacerations that appear to have been contaminated by extrinsic bacteria, open fractures, and joint injury have an increased risk of infection and should be covered with antibiotics.12 If it is determined that antibiotics would be beneficial to the healing process, the timing of the administration of antibiotics is critical to supplement the natural host resistance in bacterial killing. The drug should be administered as soon as possible for the best result. The most effective route of drug administration (intravenous vs intramuscular vs oral) must be considered. The clinical effectiveness of the drug must be monitored. If the infection is not responsive to the initial drug selection, a culture and susceptibility testing of isolates from the infective site may be indicated. The minimal duration of drug therapy should be limited to 5 days beyond the point of substantial improvement or resolution of signs and symptoms; this is usually a 5- to 7-day course of treatment dependent upon the specific drug selected.13-18 The importance of completing a full course of antibiotic must be emphasized. If the patient discontinues the antibiotic prematurely, the surviving bacteria can restart an infection that may be resistant to the original antibiotic. Special conditions Pulpitis/apical periodontitis/draining sinus tract/localized intraoral swelling Bacteria can gain access to the pulpal tissue through caries, exposed pulp or dentinal tubules, cracks into the dentin, and defective restorations. If a child presents with acute symptoms of pulpitis, treatment (ie, pulpotomy, pulpectomy, or extraction) should be rendered. Antibiotic therapy usually is not indicated
American academy of pediatric Dentistry
if the dental infection is contained within the pulpal tissue or the immediately surrounding tissue. In this case, the child will have no systemic signs of an infection (ie, no fever and no facial swelling).14,16-18
shown to cause significant decrease in the plasma concentrations of ethinyl estradiol, causing ovulation in some individuals taking oral contraceptives.36 Caution is advised with the concomitant use of antibiotics and oral contraceptives.36
Acute facial swelling of dental origin A child presenting with a facial swelling secondary to a dental infection should receive immediate dental attention. Depending on clinical findings, treatment may consist of treating or extracting the tooth/teeth in question with antibiotic coverage or prescribing antibiotics for several days to contain the spread of infection and then treating the involved tooth/teeth. The clinician should consider the ability to obtain adequate anesthesia, the severity of the infection, and the medical status of the child. Intravenous antibiotic therapy and/or referral for medical management may be indicated.16,17
References
Dental trauma Local application of an antibiotic to the root surface of an avulsed tooth with an open apex and less than 60 minutes extraoral dry time has been recommended, if available, to inhibit external resorption and aid in pulpal revascularization. 20-26 Systemic antibiotics have been recommended as adjunctive therapy for avulsed permanent incisors with an open or closed apex.20, 22-25,27 Tetracycline is the drug of choice, but consideration must be exercised in the systemic use of tetracycline due to the risk of discoloration in the developing permanent dentition.20 Penicillin V can be given as an alternative.24,25,27 The use of topical antibiotics to induce pulpal revascularization in immature non-vital traumatized teeth has been suggested.28-31 However, further randomized clinical trials are needed. Pediatric periodontal diseases In pediatric periodontal diseases (eg, neutropenias, PapillonLeFevre syndrome, leukocyte adhesion deficiency), the immune system is unable to control the growth of periodontal pathogens and, in some cases, treatment may involve antibiotic therapy. Culture and susceptibility testing of isolates from the involved sites are helpful in guiding the drug selection.32 Viral diseases Conditions such as acute primary herpetic gingivostomatitis should not be treated with antibiotic therapy unless there is strong evidence to indicate that a secondary bacterial infection exists.33 Oral contraceptive use Whenever an antibiotic is prescribed to a female patient taking oral contraceptives to prevent pregnancy, the patient must be advised to use additional techniques of birth control during antibiotic therapy and for at least 1 week beyond the last dose, as the antibiotic may render the oral contraceptive ineffective.34,35 Rifampicin has been documented to decrease the effectiveness of oral contraceptives.36 Other antibiotics, particularly tetracycline and penicillin derivatives, have been
1. Wilson W, Taubert KA, Gevitz P, et al. Prevention of infective endocarditis: Guidelines from the American Heart Association. J American Dent Assoc 2008;139(1):3S-24S. 2. Levy SB. Multidrug resistance: A sign of the times. N Engl J Med 1998;338(19):1376-8. 3. Neu HC. The crisis in antibiotic resistance. Science 1992; 257(5073):1064-73. 4. Tenover FC, Hughes JM. The challenges of emerging infectious diseases. JAMA 1996;275(4):300-4. 5. American Academy of Pediatrics, CDC, American Society for Microbiology. Your child and antibiotics: Unnecessary antibiotics can be harmful. Atlanta, Ga: CDC; 1997. 6. CDC, Food and Drug Administration, National Institutes of Health. Action plan to combat antimicrobial resistance 1999. Available at: “http://www.cdc.gov/drugresistance/ actionplan/index.htm”. Accessed November 5, 2008. 7. Dowell SF, Marcy SM, Phillips WR, Gerber MA, Schwartz B. Principles of judicious use of antimicrobial agents for pediatric upper respiratory tract infectious. Pediatrics 1998;101:163-5. 8. Finkelstein JA, Metlay JP, Davis RL, Rifas-Shiman SL, Dowell SF, Platt R. Antimicrobial use in defined populations of infants and young children. Arch Pediatr Adolesc Med 2000;154(4):395-400. 9. O’Brien KL, Dowell SF, Schwartz B, Marcy M, Phillips WR, Gerber MA. Acute sinusitis: Principles of judicious use of antimicrobial agents. Pediatrics 1998;101:174-7. 10. Schwartz B, Bell DM, Hughes JM. Preventing the emergence of antimicrobial resistance: A call to action by clinicians, public health officials, and patients. JAMA 1997;278(11):944-5. 11. Williams RJ, Heymann DL. Containment of antibiotic resistance. Science 1998;279(5354):1153-4. 12. Nakamura Y, Daya M. Use of appropriate antimicrobials in wound management. Emerg Med Clin North Am 2007;25(1)159-76. 13. Wickersham RM, Novak KK, Schweain SL, et al. Systemic anti-infectives. In: Drug Facts and Comparisons. St. Louis, Mo: Facts and Comparisons; 2004:1217-336. 14. Johnson BS. Oral infection: Principles and practice of antibiotic therapy. Infect Dis Clin North Am 1999;13 (4):851-70. 15. Kuriyama T, Karasawa T, Nakagawa K, Saiki Y, Yamamoto E, Nakamura S. Bacteriological features and antimicrobial susceptibility in isolates from orofacial odontogenic infections. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2000;90(5):600-8.
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16. Peterson LJ. Antibiotics for oral and maxillofacial infections. In: Newman MG, Kornman KS, eds. Antibiotic/ Antimicrobial Use in Dental Practice. St. Louis, Mo: Mosby; 1990:159-71. 17. Maestre Vera Jr. Treatment options in odontogenic infection. Med Oral Patol Oral Cir Bucal 2004;9(suppl S): 19-31. 18. Keenan JV, Farman AG, Fedorowicz Z, Newton JT. A Cochrane system review finds no evidence to support the use of antibiotics for pain relief in irreversible pulpitis. J Endod 2006;32(2):87-92. 19. Prieto-Prieto J, Calvo A. Microbiological basis of oral infections and sensitivity to antibiotics. Med Oral Patol Oral Cir Bucal 2004;9(suppl S):11-8. 20. Andreasen JO, Andreasen FM. Avulsions. In: Textbook and Color Atlas of Traumatic Injuries to the Teeth, 4th ed. Copenhagen, Denmark: Blackwell Munksgaard; 2007: 461, 478-88. 21. Cvek M, Cleaton-Jones P, Austin J, Kling M, Lownie J, Fatti O. Effect of topical application of doxycycline on pulp revascularization and periodontal healing in reimplanted monkey incisors. Endod Dent Traumatol 1990;6 (4):170-6. 22. Lee JY, Vann WF, Sigurdson AS. Management of avulsed permanent incisors: A decision analysis based on changing concepts. Pediatr Dent 2001;23(4):357-60. 23. Trope M. Treatment of the avulsed tooth. Pediatr Dent 2000;22(2):145-7. 24. Flores MT, Andersson L, Andreasen JO, et al. Guidelines for the management of traumatic dental injuries II. Avulsion of permanent teeth. Dental Traumatol 2007;23 (3)130-6. 25. McIntyre JD, Lee JY, Tropte M, Vann WF Jr. Management of avulsed permanent incisors: A comprehensive update. Pediatr Dent 2007;29(1):56-63.
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26. Yanpiset K, Trope M. Pulp revascularization of replanted immature dog teeth after different treatment methods. Endod Dent Traumatol 2000;16(5):211-7. 27. Sae-Lim V, Wand CY, Trope M. Effect of systemic tetracycline and amoxicillin on inflammatory root resorption of replanted dogs’ teeth. Endod Dent Traumatol 1998;14 (5):216-20. 28. Iwaya S, Ikawa M, Kubota M. Revascularization of an immature permanent tooth with apical periodontitis and sinus tract. Dent Traumatol 2001;17(4):185-7. 29. Thibodeau B, Trope M. Pulp revascularization of a necrotic infected immature permanent tooth: Case report and review of the literature. Pediatr Dent 2007;29(1):47-50. 30. Thibodeau B, Teixeira F, Yamauchi M, Caplan DJ, Trope M. Pulp revascularization of immature dog teeth with apecial periodontitis. J Endod 2007;36(6):680-9. 31. Banchs F, Trope M. Revascularization of immature permanent teeth with apical periodontitis: New treatment protocol? J Endod 2004;30(4):196-200. 32. Delaney JE, Keels MA. Pediatric oral pathology: Soft tissue and periodontal conditions. Pediatr Clin North Am 2000;47(5):1125-47. 33. American Academy of Pediatrics. Herpes simplex. In: Red Book: 2003 Report of the Committee on Infectious Diseases. 26th ed. Elk Grove Village, Ill: American Academy of Pediatrics; 2003:344-53. 34. DeRossi SS, Hersh EV. Antibiotics and oral contraceptives. Pediatr Clin North Am 2002;46(4):653-64. 35. Burroughs KE, Chambliss ML. Antibiotics and oral contraceptive failure. Arch Fam Med 2000;9(1):81-2. 36. Dickinson BD, Altman RD, Nielsen NH, Sterling ML. Drug interactions between oral contraceptives and antibiotics. Obstet Gynecol 2001;98(5Pt1):853-60.
american academy of pediatric dentistry
Guideline on Antibiotic Prophylaxis for Dental Patients at Risk for Infection Originating Committee
Clinical Affairs Committee Review Council Council on Clinical Affairs
Adopted 1990
Revised 1991, 1997, 1999, 2002, 2005, 2007, 2008
Purpose The American Academy of Pediatric Dentistry (AAPD) recognizes that numerous medical conditions predispose patients to bacteremia-induced infections. Because it is not possible to predict when a susceptible patient will develop an infection, prophylactic antibiotics are recommended when these patients undergo procedures most likely to produce bacteremia. This guideline is intended to help practitioners make appropriate decisions regarding antibiotic prophylaxis for dental patients at risk.
Methods This guideline is based on a review of current dental and medical literature pertaining to postprocedural bacteremia-induced infections. A MEDLINE search was performed using the keywords “infective endocarditis” (IE), “bacteremia”, “antibiotic prophylaxis”, and “dental infection”.
Background Bacteremia is anticipated following invasive dental procedures.1,2 Only a limited number of bacterial species commonly are implicated in resultant postoperative infections. An effective antibiotic regimen should be directed against the most likely infecting organism, with antibiotics administered shortly before the procedure. When procedures involve infected tissues, additional doses may be necessary. Antibiotic usage may result in the development of resistant organisms. Utilization of antibiotic prophylaxis for patients at risk does not provide absolute prevention of infection. Postprocedural symptoms of acute infection (eg, fever, malaise, weakness, lethargy) may indicate antibiotic failure and need for further medical evaluation. Appropriateness of antibiotic prophylaxis should be decided on an individual basis. Some medical conditions that may predispose patients to postprocedural infections are discussed below. This is not intended to be an exhaustive list; rather, the categorization should help practitioners identify children who
may be at increased risk. If a patient reports a syndrome or medical condition with which the practitioner is not familiar, it is appropriate to contact the child’s physician to determine susceptibility to bacteremia-induced infections. In 2007, the American Heart Association (AHA) released its newly revised guidelines for the prevention of IE and reducing the risk for producing resistant strains of bacteria.3 The 2007 revision was based on relevant literature and studies, in consultation with national and international experts. The AAPD, acknowledging the AHA’s expertise and efforts to produce evidenced-based recommendations, continues to endorse the AHA guideline for antibiotic prophylaxis, now entitled “Prevention of Infective Endocarditis”. The primary reasons for the revision include: • “IE is much more likely to result from frequent exposure to random bacteremias associated with daily activities than from bacteremia caused by a dental, GI tract, or GU tract procedure.”3 (Daily activities would include tooth brushing, flossing, chewing, use of toothpicks, use of water irrigation devices, and other activities.) • “Prophylaxis may prevent an exceedingly small number of cases of IE, if any, in individuals who undergo a dental, GI tract, or GU tract procedure. • The risk of antibiotic-associated adverse events exceeds the benefit, if any, from prophylactic antibiotic therapy. • Maintenance of optimal oral health and hygiene may reduce the incidence of bacteremia from daily activities and is more important than prophylactic antibiotics for a dental procedure to reduce the risk of IE.”3 The recent AHA revision was intended to clarify when antibiotic prophylaxis is/is not recommended and to provide more uniform global recommendations. Major changes from the 1997 version4 include: (1) “The Committee concluded that only an extremely small number of cases of infective endocarditis might be prevented by antibiotic prophylaxis for dental procedures even if such prophylactic therapy were 100% effective.
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(2) Infective endocarditis prophylaxis for dental procedures is reasonable only for patients with underlying cardiac conditions associated with the highest risk of adverse outcome from infective endocarditis. (3) For patients with these underlying cardiac conditions, prophylaxis is reasonable for all dental procedures that involve manipulation of gingival tissue or the periapical region of teeth or perforation of the oral mucosa. (4) Prophylaxis is not recommended based solely on an increased lifetime risk of acquisition of infective endocarditis.”3
Recommendations The conservative use of antibiotics is indicated to minimize the risk of developing resistance to current antibiotic regimens.1-13 Given the increasing number of organisms that have developed resistance to current antibiotic regimens, it is best to be prudent in the use of antibiotics for the prevention of IE and other conditions. Patients with cardiac conditions Dental practitioners should consider prophylactic measures to minimize the risk of IE in patients with underlying cardiac conditions. These patients and/or parents need to be educated and motivated to maintain personal oral hygiene through daily plaque removal, including flossing. Greater emphasis should be placed on improved access to dental care and oral health in patients with underlying cardiac conditions at high risk for IE and less focus on a dental procedure and antibiotic coverage. Professional prevention strategies should be based upon the individual’s assessed risk for caries and periodontal disease. Specific recommendations from the 2007 AHA guideline on prevention of IE are included in the following tables. The AHA recommends antibiotic prophylaxis only for those whose underlying cardiac conditions are associated with the highest risk of adverse outcome3 (see Table 1). Such conditions include prosthetic heart valves, previous history of IE, unrepaired cyanotic congenital heart disease (CHD), completely repaired congenital heart defect with prosthetic material or device during the first 6 months after the procedure, repaired CHD with residual defects at the site or adjacent to the site of a prosthetic patch or device, and cardiac transplantation recipients who develop valvulopathy.3 In addition to those diagnoses listed in the AHA guidelines, patients with a history of intravenous drug abuse may be at risk for developing bacterial endocarditis due to associated cardiac anomalies.5 Consultation with the patient’s physician may be necessary to determine susceptibility to bacteremia-induced infections. Antibiotics are recommended for all dental procedures that involve manipulation of gingival tissue or the periapical region of teeth or perforation of the oral mucosa3 (see Table 2). Specific antibiotic regimens can be found in Table 3. Practitioners and patients/parents can review the entire AHA guidelines “http:// circ.ahajournals.org/cgi/reprint/CIRCULATIONAHA.106. 183095” for additional background information as well as discussion of special circumstances (eg, patients already receiving antibiotic therapy, patients on anticoagulant therapy).
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Patients with compromised immunity Patients with a compromised immune system may not be able to tolerate a transient bacteremia following invasive dental procedures. This category includes, but is not limited to, patients with the following conditions: 1. human immunodeficiency virus (HIV); 2. severe combined immunodeficiency (SCIDS); 3. neutropenia; 4. immunosuppression; 5. sickle cell anemia; 6. status post splenectomy; 7. chronic steroid usage; 8. lupus erythematosus; 9. diabetes; 10. status post organ transplantation.
Consultation with the child’s physician is recommended for management of patients with a compromised immune system. Discussion of antibiotic prophylaxis for patients undergoing chemotherapy, irradiation, and hematopoietic cell transplantation appears in a separate AAPD guideline.14 Patients with shunts, indwelling vascular catheters, or medical devices The AHA recommends that antibiotic prophylaxis for nonvalvular devices, including indwelling vascular catheters (central lines), is indicated only at the time of placement of these devices in order to prevent surgical site infection.15 The AHA found no convincing evidence that microorganisms associated with dental procedures cause infection of nonvalvular devices at any time after implantation.15 The infections occurring after device implantation most often are caused by staphylococci, Gram-negative bacteria, or other microorganisms associated with surgical implantation or other active infections. The AHA further states that immunosuppression is not an independent risk factor for nonvalvular device infections; immunocompromised hosts who have those devices should receive antibiotic prophylaxis as advocated for immunocompetent hosts.15 Consultation with the child’s physician is recommended for management of patients with nonvalvular devices. Ventriculoatrial (VA) or ventriculovenus (VV) shunts for hydrocephalus are at risk of bacteremia-induced infections due to their vascular access. In contrast, ventriculoperitoneal (VP) shunts do not involve any vascular structures and, consequently, do not require antibiotic prophylaxis.15,16 Consultation with the child’s physician is recommended for management of patients with vascular shunts. The AAPD endorses the recommendations of the American Dental Association and the American Academy of Orthopaedic Surgeons for management of patients with prosthetic joints.17 Antibiotic prophylaxis is not indicated for dental patients with pins, plates, and screws, nor is it indicated routinely for most dental patients with total joint replacements. Antibiotics may be considered when high-risk dental procedures (Table 2) are performed for patients within 2 years following implant surgery or for patients who have had previous joint infections.
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Table 1. Cardiac Conditions Associated With the Highest Risk of Adverse OuTcome From Endocarditis for Which Prophylaxis With Dental Procedures is reasonable Prosthetic cardiac valve or prosthetic material used for cardiac valve repair Previous IE Congenital heart disease (CHD)* Unrepaired cyanotic CHD, including palliative shunts and conduits Completely repaired congenital heart defect with prosthetic material or device, whether placed by surgery or by catheter intervention, during the first 6 months after the procedure † Repaired CHD with residual defects at the site or adjacent to the site of a prosthetic patch or prosthetic device (which inhibit endothelialization) Cardiac transplantation recipients who develop cardiac valvulopathy * Except for the conditions listed above, antibiotic prophylaxis is no longer recommended for any other form of CHD. † Prophylaxis is reasonable because endothelialization of prosthetic material occurs within 6 months after the procedure.
Circulation. 2007; 116:1745. Reprinted with permission ©2007, American Heart Association, Inc.3
Table 2. DENTAL PROCEDURES FOR WHICH ENDOCARDITIS PROPHYLAXIS IS REASONABLE FOR PATIENTS IN TABLE 1 All dental procedures that involve manipulation of gingival tissue or the periapical region of teeth or perforation of the oral mucosa* * The following procedures and events do not need prophylaxis: routine anesthetic injections through non-infected tissue, taking dental radiographs, placement of removable prosthodontic or orthodontic appliances, adjustment of orthodontic appliances, placement of orthodontic brackets, shedding of deciduous teeth, and bleeding from trauma to the lips or oral mucosa. Circulation. 2007; 116:1746. Reprinted with permission ©2007, American Heart Association, Inc.3
Table 3. Regimens for a Dental Procedure Regimen: Single Dose 30 to 60 min Before Procedure
Situation Oral Unable to take oral medication
Allergic to penicillins or ampicillin-oral
Allergic to penicillin or ampicillin and unable to take oral medication
Agent
Adults
Children
Amoxicillin
2g
50 mg/kg
Ampicillin OR Cefazolin or ceftriaxone
2 g IM or IV
50 mg/kg IM or IV
1 g IM or IV
50 mg/kg IM or IV
Cephalexin *† OR Clindamycin OR Azithromycin or clarithromycin
2g
50 mg/kg
600 mg
20 mg/kg
500 mg
15 mg/kg
1g IM or IV
50 mg/kg IM or IV
600 mg IM or IV
20 mg/kg IM or IV
Cefazolin or ceftriaxone† OR Clindamycin
IM indicates intramuscular; IV, intravenous. * Or other first-or second-generation oral cephalosporin in equivalent adult or pediatric dosage. † Cephalosporins should not be used in an individual with a history of anaphylaxis, angioedema, or urticaria with penicillins or ampicillin.
Circulation. 2007; 116:1747. Reprinted with permission ©2007, American Heart Association, Inc.3
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Consultation with the child’s physician may be necessary for management of patients with other implanted devices (eg, Harrington rods, external fixation devices).
References 1. Lockhart PB, Brennan MT, Kent ML, Norton JH, Weinrib DA. Impact of amoxicillin prophylaxis on the incidence, nature, and duration of bacteremia in children after intubation and dental procedures. Circulation. 2004;109(23): 2978-84. 2. Roberts GJ, Jaffrey EC, Spract DA, Petrie A, Greville C, Wilson M. Duration, prevalence and intensity of bacteremia after dental extractions in children. Heart 2006;92 (9):1274-7. 3. Wilson W, Taubert KA, Gevitz M, et al. Prevention of infective endocarditis: Guidelines from the American Heart Association. Circulation e-published April 19, 2007. Available at: “http://circ.ahajournals.org/cgi/reprint/CIRCULA TIONAHA.106.183095”. Accessed March 30, 2008. Correction Circulation. 2007;116:e376-e377. Available at: “http://circ.ahajournals.org/cgi/content/full/116/15/1736”. Accessed May 23, 2008. 4. Dajani AS, Taubert KA, Wilson W, et al. Prevention of bacterial endocarditis: Recommendations by the American Heart Association. JAMA 1997;227(22):1794-801. 5. Dajani AS, Taubert KA. Infective endocarditis. In: Allen HD, Gutgessel HP, Clark EB, Driscoll DJ, eds. Moss and Adams’ Heart Disease in Infants, Children, and Adolescents. New York, NY: Lippincott Williams & Wilkins; 2001:1297-308. 6. Schwartz B, Bell DM, Hughes JM. Preventing the emergence of antimicrobial resistance: A call to action by clinicians, public health officials, and patients. JAMA 1997; 278(11):901-4. 7. Tenover FC, Hughes JM. The challenges of emerging infectious diseases; Development and spread of multipleresistant bacterial pathogens. JAMA 1996;75(4):300-4.
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8. American Society of Microbiology. Antibiotic resistanceCurrent status and future directions. 1994. Available at: “http://www.asm.org/Policy/Index.asp?bid=5961”. Accessed December 5, 2007. 9. CDC, US Food and Drug Administration, National Institutes of Health. Action plan to combat antimicrobial resistance 1999. Available at: “http://www.cdc.gov/ drugresistance/actionplan/index.htm”. Accessed June 17, 2007. 10. Levy SB, Marshall B. Antibacterial resistance worldwide: Causes, challenges, and responses. Nat Med 2004;10 (12 suppl):S122-9, Review. 11. Finkelstein JA, Metlay JP, Davis RL. Antimicrobial use in defined populations of infants and young children. Arch Pediatric Adolescent Med 2000;154(4);395-400. 12. O’Brien KL, Dowell SF, Schwartz B, Marcy SM, Phillip WR, Gerber MA. Acute sinusitis: Principles of judicious use of antimicrobial agents. Pediatrics 1998;101(1 suppl): 174-7. 13. Williams RJ, Heymann DL. Containment of antibiotic resistance. Science 1998;279(5354):1153-4. 14. American Academy of Pediatric Dentistry. Guideline on dental management of pediatric patients receiving chemotherapy, hematopoietic cell transplantation, and/or radiation. Pediatr Dent 2008;30(suppl):219-25. 15. Baddour LM, Bettman MA, Bolger AF, Bolger A, Ferrieri P. Nonvalvular cardiovascular device-related infections. Circ 2003;108(16):2015-31. 16. Lockhart PB, Loven B, Brennan MT, Baddour LM, Levinson M. The evidence base for the efficiency of antibiotic prophylaxis in dental practice. J Am Dent Assoc 2007; 138(4):458-74. 17. American Dental Association, American Academy of Orthopedic Surgeons. Advisory Statement: Antibiotic prophylaxis for dental patients with total joint replacements. J Am Dent Assoc 2003;134(7):895-9.
american academy of pediatric dentistry
Guideline on Dental Management of Pediatric Patients Receiving Chemotherapy, Hematopoietic Cell Transplantation, and/or Radiation Originating Committee
Clinical Affairs Committee Review Council Council on Clinical Affairs
Adopted 1986
Revised 1991, 1997, 1999, 2001, 2004, 2008
Reaffirmed 1994
Purpose The American Academy of Pediatric Dentistry recognizes that the pediatric dental professional plays an important role in the diagnosis, prevention, stabilization, and treatment of oral and dental problems that can compromise the child’s quality of life before, during, and after cancer treatment. Dental intervention with certain modifications must be done promptly and efficiently, with attention to the patient’s medical history, treatment protocol, and health status. Chemotherapy and/or radiotherapy for the treatment of cancer or in preparation for hematopoietic cell transplantation (HCT) may cause many acute and long-term side effects in the oral cavity. Furthermore, because of the immunosuppression the patients experience, any existing or potential sources of oral/ dental infections and or soft tissue trauma can compromise the medical treatment, leading to morbidity, mortality, and higher hospitalization costs. It is imperative that the pediatric dentist be familiar with the oral manifestations of the patient’s underlying condition and the treatment differences for patients undergoing chemotherapy only and those who will receive an HCT.
Methods This guideline is based on a review of the current dental and medical literature related to dental management of pediatric patients receiving chemotherapy, hematopoietic cell transplantation, and/or radiation. A MEDLINE search was conducted using the terms “pediatric cancer”, “pediatric oncology”, “hematopoietic cell transplantation”, “bone marrow transplantation”, “mucositis”, “stomatitis”, “chemotherapy”, “radiation therapy”, “acute effects”, “long-term effects”, “dental care”, “pediatric dentistry”, and “clinical practice guidelines”. Expert opinions
and best current practices were relied upon when sufficient scientific data were not available.
Background The most frequently documented source of sepsis in the immunosuppressed cancer patient is the mouth; therefore, early and definitive dental intervention, including comprehensive oral hygiene measures, reduces the risk for oral and associated systemic complications.1-13 All patients with cancer should have an oral examination before initiation of the oncology therapy, and treatment of preexisting or concomitant oral disease is essential to minimize complications in this population.6 The key to success in maintaining a healthy oral cavity during cancer therapy is patient compliance. The child and the parents should be educated regarding the possible acute side effects and the long-term sequelae of cancer therapies in the oral cavity.1-6,8,14-16 Younger patients present more oral problems than adults.2 Because there are many oncology and HCT protocols, every patient should be managed on an individual basis and appropriate consultations with physicians and other dental specialists should be sought before dental care is instituted.5
Recommendations Dental and oral care before the initiation of cancer therapy Objectives
The objectives of a dental/oral examination before cancer therapy starts are two-fold16: 1. to identify and stabilize or eliminate existing and potential sources of infection and local irritants in the oral cavity—without needlessly delaying the cancer treatment or inducing complications; and
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2. to educate the patient and parents about the importance of optimal oral care in order to minimize oral problems/ discomfort before, during, and after treatment and about the possible acute and long-term effects of the therapy in the oral cavity and the craniofacial complex. Initial evaluation Medical history review: should include, but not be limited to, type of disease/condition, treatment protocol, medications (including bisphosphonates), allergies, surgeries, secondary medical diagnoses, and immunosuppression status. For HCT patients, include type of transplant, matching status, donor, conditioning protocol, and graft versus host disease (GVHD) prophylaxis. The American Heart Assocation (AHA) recommends that antibiotic prophylaxis for nonvalvular devices, including indwelling vascular catheters (eg, central lines) is indicated only at the time of placement of these devices in order to prevent surgical site infections.17 The AHA found no convincing evidence that microorganisms associated with dental procedures cause infection of nonvalvular devices at any time after implantation.17 The infections occurring after device implantation most often are caused by staphyloccal Gram-negative bacteria or other microorganisms associated with surgical implantation or other active infections. The AHA further states that immunosuppression is not an independent risk factor for nonvalvular device infections; immunocompromised hosts who have those devices should receive antibiotic prophylaxis as advocated for immunocompetent hosts.17 Consultation with the child’s physician is recommended for management of patients with nonvalvular devices. Dental history review: includes information such as habits, trauma, symptomatic teeth, previous care, preventive practices, etc. Oral/dental assessment: should include thorough head, neck, and intraoral examinations, oral hygiene assessment and training, and radiographic evaluation based on history and clinical findings. Preventive strategies Oral hygiene: Oral hygiene includes brushing of the teeth and tongue 2 to 3 times daily with regular soft nylon brush or electric toothbrush, regardless of the hematological status.4,5,8,9,13,18 Ultrasonic brushes and dental floss should be allowed only if the patient is properly trained.1,8 Patients with poor oral hygiene and/or periodontal disease may use chlorhexidine rinses daily until the tissue health improves or mucositis develops. The high alcohol content of commercially-available chlorhexidine mouthwash may cause discomfort and dehydrate the tissues in patients with mucositis; thus, an alcohol-free solution is indicated in this situation. Diet: Dental practitioners should encourage a non-cariogenic diet and advise patients/parents about the high cariogenic potential of dietary supplements rich in carbohydrate and oral pediatric medications rich in sucrose.
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Fluoride: Preventive measures include the use of fluoridated toothpaste, fluoride supplements if indicated, neutral fluoride gels/ rinses, or applications of fluoride varnish for patients at risk for caries and/or xerostomia. A brush-on technique is convenient and may increase the likelihood of patient compliance with topical fluoride therapy.8 Trismus prevention/treatment: Patients who receive radiation therapy to the masticatory muscles may develop trismus. Thus, daily oral stretching exercises/physical therapy should start before radiation is initiated and continue throughout treatment. Therapy for trismus may include prosthetic aids to reduce the severity of fibrosis, trigger-point injections, analgesics, musclerelaxants, and other pain management strategies.3,5,10 Reduction of radiation to healthy oral tissues: In cases of radiation to the head and neck, the use of lead-lined stents, prostheses, and shields, as well as salivary gland sparing techniques (eg, 3-dimensional conformal or intensity modulated radiotherapy, concomitant cytoprotectants, surgical transfer of salivary glands), should be discussed with the radiation oncologist. Education: Patient/parent education includes the importance of optimal oral care in order to minimize oral problems/discomfort before, during, and after treatment and the possible acute and long-term effects of the therapy in the craniofacial complex. Dental care Hematological considerations: 1. Absolute neutrophil count (ANC): • >1,000/mm3: no need for antibiotic prophylaxis. 10 However, some authors5 suggest that antibiotic coverage (dosed per AHA recommendations19) may be prescribed when the ANC is between 1,000 and 2,000/mm 3. If ininfection is present or unclear, more aggressive antibiotic therapy may be indicated and should be discussed with the medical team • <1,000/mm3: defer elective dental care until the ANC rises. In dental emergency cases, discuss antibiotic coverage beyond endocarditis prophylaxis with medical team before proceeding with treatment. The patient may need hospitalization for dental management.12 2. Platelet count5,10: • >75,000/mm3: no additional support needed but the dentist should be prepared to treat prolonged bleeding by using sutures, hemostatic agents, pressure packs, gelatin foams, etc. • 40,000 to 75,000/mm3: platelet transfusions may be considered pre- and 24 hours post-operatively. Localized procedures to manage prolonged bleeding may include sutures, hemostatic agents, pressure packs, and/or gelatin foams. • <40,000/mm3: defer care. In dental emergency cases, contact the patient’s physician to discuss supportive measures (eg, platelet transfusions, bleeding control, hospital admission) before proceeding.
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3. Other coagulation tests may be in order for individual patients. Dental procedures: 1. In general terms, most oncology/hematology protocols (exclusive of HCT, which will be discussed later) are divided into phases (cycles) of chemotherapy, in addition to other therapies (eg, radiotherapy, surgery). The patient’s blood counts normally start falling 5 to 7 days after the beginning of each cycle, staying low for approximately 14-21 days, before rising again to normal levels for a few days until the next cycle begins. Ideally, all dental care should be completed before cancer therapy is initiated. When that is not feasible, temporary restorations may be placed and non-acute dental treatment may be delayed until the patient’s hematological status is stable,5,8,10,11 2. Prioritizing procedures: When all dental needs cannot be treated before cancer therapy is initiated, priorities should be infections, extractions, periodontal care (eg, scaling, prophylaxis), and sources of tissue irritation before the treatment of carious teeth, root canal therapy for permanent teeth, and replacement of faulty restorations.10 The risk for pulpal infection and pain determine which carious lesions should be treated first.8 Incipient to small carious lesions may be treated with fluorides and/or sealants until definitive care can be accomplished.5 It is important for the practitioner to be aware that the signs and symptoms of periodontal disease may be decreased in immunosuppressed patients.5 3. Pulp therapy in primary teeth: Although there have been no studies to date that address the safety of performing pulp therapy in primary teeth prior to the initiation of chemotherapy and/or radiotherapy, many clinicians choose to provide a more definitive treatment in the form of extraction because pulpal/periapical/furcal infections during immunosuppression periods can have a significant impact on cancer treatment and become life-threatening.5,8,11 Teeth that already have been treated pulpally and are clinically and radiographically sound present minimal risk. 4. Endodontic treatment in permanent teeth: Symptomatic non-vital permanent teeth should receive root canal treatment at least 1 week before initiation of cancer therapy to allow sufficient time to assess treatment success before the chemotherapy.5,10 If that is not possible, extraction is indicated. Extraction is also the treatment of choice for teeth that cannot be treated by definitive endodontic treatment in a single visit. In that case, the extraction should be followed by antibiotic therapy (penicillin or for penicillin-allergic patients, clindamycin) for about 1 week.5,10,12 Asymptomatic endodontic needs in permanent teeth may be delayed until the hematological status of the patient is stable.10,11,20 It is important that the etiology of periapical lesions associated with previously endodontically treated teeth be determined because they can be due to a number of factors including pulpal infections, inflammatory reactions, apical scars, cysts, and malignancy.8 If a periapical lesion is associated with an
endodontically treated tooth and no signs or symptoms of infection are present, there is no need for retreatment or extraction since the radiolucency likely is due to an apical scar.20 5. Orthodontic appliances and space maintainers: Poorly-fitting appliances can abrade oral mucosa and increase the risk of microbial invasion into deeper tissues.5 Appliances should be removed if the patient has poor oral hygiene and/or the treatment protocol or HCT conditioning regimen carries a risk for the development of moderate to severe mucositis. Simple appliances (eg, band and loops, fixed lower lingual arches) that are not irritating to the soft tissues may be left in place in patients who present good oral hygiene.1,8 Removable appliances and retainers that fit well may be worn as long as tolerated by the patient who maintains good oral care.5,8,21 Patients should be instructed to changes appliance soaking solutions daily and routinely clean appliance cases with an antimicrobial solution to prevent contamination and reduce the risk of appliance-associated oral infections.5 If band removal is not possible, vinyl mouth guards or orthodontic wax should be used to decrease tissue trauma.8 6. Periodontal considerations: Partially erupted molars can become a source of infection because of pericoronitis. The overlying gingival tissue should be excised if the dentist believes it is a potential risk and if the hematological status permits.8,10 Patients should have a periodontal assessment and appropriate therapy prior to receiving bisphosphonates as part of cancer treatment.22,23 If the patient has had bisphosphonates and an invasive periodontal procedure is indicated, risks must be discussed with the patient, parents, and physicians prior to the procedure. 7. Extractions: There are no clear recommendations for the use of prophylactic antibiotics for extractions. Recommendations generally have been empiric or based on anecdotal experience. Surgical procedures must be as atraumatic as possible, with no sharp bony edges remaining and satisfactory closure of the wounds. 5,8,10-12 If there is documented infection associated with the tooth, antibiotics–ideally chosen with the benefit of sensitivity testing–should be administered for about 1 week.5,8,10,12 • To minimize the risk of development of osteonecrosis or osteoradionecrosis, patients who will receive bisphosphonates or radiation to the jaws as part of the cancer treatment must have all oral surgical procedures completed before those measures are instituted.22,23 If the patient has received bisphosphonates or radiation to the jaws and an oral surgical procedure is necessary, risks must be discussed with the patient, parents, and physician prior to the procedure. • Loose primary teeth should be allowed to exfoliate naturally, and the patient should be counseled to not play with them in order to avoid bacteremia. When the patient cannot comply with this recommendation, the teeth should be removed if the hematologic parameters allow. • Nonrestorable teeth, root tips, teeth with periodontal pockets >6 mm, symptomatic impacted teeth, and teeth
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exhibiting acute infections, significant bone loss, involvement of the furcation, or mobility should be removed ideally 2 weeks (or at least 7 to 10 days) before cancer therapy is initiated to allow adequate healing.1,5,8,10,11 • Some practitioners prefer to extract all third molars that are not fully erupted, particularly prior to HCT, while others favor a more conservative approach, recommending extraction of third molars at risk for pulpal infection or those associated with significant periodontal infection, including pericoronitis.8 Dental and oral care during immunosupression periods Objectives The objectives of a dental/oral care during cancer therapy are three-fold: 1. to maintain optimal oral health during cancer therapy; 2. to manage any oral side effects that may develop as a consequence of the cancer therapy; and 3. to reinforce the patient and parents’ education regarding the importance of optimal oral care in order to minimize oral problems/discomfort during treatment. Preventive strategies Oral hygiene: Intensive oral care is of paramount importance because it reduces the risk of developing moderate/severe mucositis without causing an increase in septicemia and infections in the oral cavity.1-12 Thrombocytopenia should not be the sole determinant of oral hygiene as patients are able to brush without bleeding at widely different levels of platelet count.8,9,13 Patients should use a soft nylon brush 2 to 3 times daily and replace it on a regular (every 2-3 months) basis.8 Fluoridated toothpaste may be used but, if the patient does not tolerate it during periods of mucositis due to oral burning or stinging sensations, it may be discontinued and the patient should brush with water alone. If moderate to severe mucositis develops and the patient cannot tolerate a regular soft nylon toothbrush or an end-tufted brush, foam brushes or super soft brushes soaked in chlorhexidine may be used.9,17 Otherwise, foam or super soft brushes should be discouraged because they do not allow for effective cleaning.9,19 The use of a regular brush should be resumed as soon as the mucositis improves.8 Brushes should be air-dried between uses.8 Electric or ultrasonic brushes are acceptable if the patient is capable of using them without causing trauma and irritation.1,8 If patients are skilled at flossing without traumatizing the tissues, it is reasonable to continue flossing throughout treatment.8 Toothpicks and water irrigation devices should not be used when the patient is pancytopenic to avoid tissue trauma.8,10 Diet: Dental practitioners should encourage a non-cariogenic diet and advise patients/parents about the high cariogenic potential of dietary supplements rich in carbohydrate and oral pediatric medications rich in sucrose. Fluoride: Preventive measures include the use of fluoridated toothpaste, fluoride supplements if indicated, neutral fluoride
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gels/rinses, or applications of fluoride varnish for patients at risk for caries and/or xerostomia. A brush-on technique is convenient, familiar, and simple and may increase the likelihood of patient compliance with topical fluoride therapy.8 Lip care: Lanolin-based creams and ointments are more effective in moisturizing and protecting against damage than petrolatum-based products.8,11 Education: Patient/parent education includes reinforcing the importance of optimal oral hygiene and teaching strategies to manage soft tissue changes (eg, mucositis, oral bleeding, xerostomia) in order to minimize oral problems/discomfort during treatment and the possible acute and long-term effects of the therapy in the craniofacial complex. Dental care During immunosuppression, elective dental care must not be provided. If a dental emergency arises, the treatment plan should be discussed with the patient’s physician who will make recommendations for supportive medical therapies (eg, antibiotics, platelet transfusions, analgesia). The patient should be seen every 6 months (or in shorter intervals if there is a risk of xerostomia, caries, trismus, and/or chronic oral GVHD) for an oral health evaluation during treatment, in times of stable hematological status and always after reviewing the medical history. If a central line is still in place and an invasive dental procedure is planned, consultation with the oncologist is recommended.17 Management of oral conditions related to cancer therapies Mucositis: Mucositis care remains focused on palliation of symptoms and efforts to reduce the influence of secondary factors on mucositis.5,10,12 The Multinational Association of Supportive Care in Cancer/International Society of Oral Oncology has published guidelines (which are updated regularly) for treatment of mucositis.24 Studies on the use of chlorhexidine for mucositis have given conflicting results. Most studies have not demonstrated a prophylactic impact, although reduced colonization of candidial species has been shown.7,12,24 Patient-controlled analgesia has been helpful in relieving pain associated with mucositis, reducing the requirement for oral analgesics. There is no significant evidence of the effectiveness or tolerability of mixtures containing topical anesthetics (eg, “Philadelphia mouthwash”, “magic mouthwash”).24 The use of topical anesthetics often is recommended for pain management although there are no studies available to assess the benefit and potential for toxicity. Lidocaine use may obtund or diminish taste and the gag reflex and/or result in a burning sensation, in addition to possible cardiovsascular and central nervous system effects. Local application may be useful for painful ulcers.7 Oral mucosal infections: The signs of inflammation and infection may be greatly diminished during neutropenic periods. Thus, the clinical appearance of infections may differ significantly from the normal.1,10 Close monitoring of the oral cavity
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allows for timely diagnosis and treatment of fungal, viral, and bacterial infections. Prophylactic nystatin is not effective for the prevention and/or treatment of fungal infections.5,26 Oral cultures and/or biopsies of all suspicious lesions should be performed and prophylactic medications should be initiated until more specific therapy can be prescribed.1,5,8-12
Fluoride: Preventive measures include the use of fluoridated toothpaste, fluoride supplements if indicated, neutral fluoride gels/rinses, or applications of fluoride varnish for patients at risk for caries and/or xerostomia. A brush-on technique is convenient, familiar, and simple and may increase the likelihood of patient compliance with topical fluoride therapy.8
Oral bleeding: Oral bleeding occurs due to thrombocytopenia, disturbance of coagulation factors, and/or damaged vascular integrity. Management should consist of local approaches (eg, pressure packs, antifibrinolytic rinses, gelatin sponges) and systemic measures (eg, platelet transfusions, aminocaproic acid).5,6,8,10
Lip care: Lanolin-based creams and ointments are more effective in moisturizing and protecting against damage than petrolatum-based products.8,11
Dental sensitivity/pain: Tooth sensitivity could be related to decreased secretion of saliva during radiation therapy and the lowered salivary pH.5,8,10 Patients who are using plant alkaloid chemotherapeutic agents (eg, vincristine, vinblastine) may present with deep, constant pain affecting the mandibular molars with greater frequency, in the absence of odontogenic pathology. The pain usually is transient and generally subsides shortly after dose reduction and/or cessation of chemotherapy.5,8,10 Xerostomia: Sugar-free chewing gum or candy, sucking tablets, special dentifrices for oral dryness, saliva substitutes, frequent sipping of water, alcohol-free oral rinses, and/or oral moisturizers are recommended.8,27 Placing a humidifier by bedside at night may be useful.10 Saliva stimulating drugs are not approved for use in children. Fluoride rinses and gels are recommended highly for caries prevention in these patients. Trismus: Daily oral stretching exercises/physical therapy must continue during radiation treatment. Management of trismus may include prosthetic aids to reduce the severity of fibrosis, trigger-point injections, analgesics, muscle relaxants, and other pain management strategies.3,5,10 Dental and oral care after the cancer therapy is completed (exclusive of HCT) Objectives The objectives of a dental/oral examination after cancer therapy ends are two-fold: 1. to maintain optimal oral health; and 2. to reinforce to the patient/parents the importance of optimal oral and dental care for life. Preventive strategies Oral hygiene: Patients must brush their teeth 2 to 3 times daily with a soft nylon toothbrush. Brushes should be airdried between uses.8 Patients should floss daily. Diet: Dental practitioners should encourage a non-cariogenic diet and advise patients/parents about the high cariogenic potential of dietary supplements rich in carbohydrate and oral pediatric medications rich in sucrose.
Education: The importance of optimal oral and dental care for life must be reinforced. It is also important to emphasize the need for regular follow-ups with a dental professional, especially for patients who are at risk for or have developed GVHD and/or xerostomia and those less than 6 years of age during treatment due to potential dental developmental problems caused by cancer therapies. Dental care Periodic evaluation: The patient should be seen at least every 6 months (or in shorter intervals if issues such as chronic oral GVHD, xerostomia, or trismus are present). Patients who have experienced moderate or severe mucositis and/or chronic oral GVHD should be followed closely for malignant transformation of their oral mucosa (eg, oral squamous cell carcinoma).6,25 Orthodontic treatment: Orthodontic care may start or resume after completion of all therapy and after at least a 2 year disease-free survival when the risk of relapse is decreased and the patient is no longer using immunosuppressive drugs.21 A thorough assessment of any dental developmental disturbances caused by the cancer therapy must be performed before initiating orthodontic treatment. The following strategies should be considered when providing orthodontic care for patients with dental sequelae: (1) use appliances that minimize the risk of root resorption, (2) use lighter forces, (3) terminate treatment earlier than normal, (4) choose the simplest method for the treatment needs, and (5) do not treat the lower jaw.28 However, specific guidelines for orthodontic management, including optimal force and pace, remain undefined. Patients who have used or will be given bisphosphonates in the future present a challenge for orthodontic care. Although bisphosphonate inhibition of tooth movement has been reported in animals, it has not been quantified for any dose or duration of therapy in humans.29 Consultation with the patient’s parents and physician regarding the risks and benefits of orthodontic care in this situation is recommended. Oral surgery: Consultation with an oral surgeon and/or periodontist and the patient’s physician is recommended for non-elective oral surgical and invasive periodontal procedures in patients who have used or are using bisphosphonates or those who received radiation therapy to the jaws in order to devise
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strategies to decrease the risk of osteonecrosis and osteoradionecrosis, respectively. Elective invasive procedures should be avoided in these patients.28 Xerostomia: Sugar-free chewing gum or candy, special dentifrices for oral dryness, saliva substitutes, frequent sipping of water, alcohol-free oral rinses, and/or oral moisturizers are recommended.8,27 Placing a humidifier by bedside at night may be useful10. Saliva stimulating drugs are not approved for use in children. Fluoride rinses and gels are recommended highly for caries prevention in these patients. Trismus: Daily oral stretching exercises/physical therapy should continue after radiation therapy is finished in order to prevent or ameliorate trismus. Management of trismus may include prosthetic aids to reduce the severity of fibrosis, trigger-point injections, analgesics, muscle-relaxants, and other pain management strategies.3,5,10 Hematopoietic cell transplantation Specific oral complications can be correlated with phases of HCT.8,14,15 Phase I: Pre-transplantation The oral complications are related to the current systemic and oral health, oral manifestations of the underlying condition, and oral complications of recent medical therapy. Most of the principles of dental and oral care before the transplant are similar to those discussed for pediatric cancer.16 The 2 major differences are: 1) in HCT, the patient receives all the chemotherapy and/or total body irradiation in just a few days before the transplant, and 2) there will be prolonged immunosuppression following the transplant. Elective dentistry will need to be postponed until immunological recovery has occurred, which may take as long as 9 to 12 months after HCT, or longer if chronic GVHD or other complications are present.5,8 Therefore, all dental treatment must be completed before the patient becomes immunosuppressed. Phase II: Conditioning/neutropenic phase In this phase, which encompasses the day the patient is admitted to the hospital to begin the transplant conditioning to 30 days post-HCT, the oral complications are related to the conditioning regimen and supportive medical therapies.8 Mucositis, xerostomia, oral pain, oral bleeding, opportunistic infections, and taste dysfunction may be seen. The patient should be followed closely to monitor and manage the oral changes and to reinforce the importance of optimal oral care. Dental procedures usually are not allowed in this phase due to the patient’s severe immunosuppression. Phase III: Initial engraftment to hematopoietic reconstitution The intensity and severity of complications begin to decrease normally 3 to 4 weeks after transplantation. Oral fungal infections and herpes simplex virus infection are most notable. Oral GVHD can become a concern for allogeneic graft recipients. A dental /oral examination should be performed and invasive
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dental procedures, including dental cleanings and soft tissue curettage, should be done only if authorized by the HCT team because of the patient’s continued immunosuppression.8 Patients should be encouraged to optimize oral hygiene and avoid a cariogenic diet. Attention to xerostomia and oral GVHD manifestations is crucial. HCT patients are particularly sensitive to intraoral thermal stimuli between 2 and 4 months post-transplant.8 The mechanism is not well understood, but the symptoms usually resolve spontaneously within a few months. Topical application of neutral fluoride or desensitizing toothpastes helps reduce the symptoms.8 Phase IV: Immune reconstitution/ late posttransplantation After day 100 post-HCT, the oral complications predominantly are related to the chronic toxicity associated with the conditioning regimen, including salivary dysfunction, craniofacial growth abnormalities (especially in patients less than 6 years of age at the time of treatment), late viral infections, oral chronic GVHD, and oral squamous cell carcinoma.8 Periodic dental examinations with radiographs can be performed, but invasive dental treatment should be avoided in patients with profound impairment of immune function.8 Consultation with the pa-tient’s physician and parents regarding the risks and benefits of orthodontic care is recommended.
References 1. Barker GJ. Current practices in the oral management of the patient undergoing chemotherapy or bone marrow transplantation. Support Care Cancer 1999;7(1):17-20. 2. Sonis S, Kunz A. Impact of improved dental services on the frequency of oral complications of cancer therapy for patients with non-head-and-neck malignancies. Oral Surg Oral Med Oral Pathol 1988;65(1):19-22. 3. Scully C, Epstein JB. Oral health care for the cancer patient. Eur J Cancer B Oral Oncol 1996;32B(5):281-92. 4. Toth BB, Martin JW, Fleming TJ. Oral and dental care associated with cancer therapy. Cancer Bull 1991;43: 397-402. 5. Schubert MM, Epstein JB, Peterson DE. Oral complications of cancer therapy. In: Yagiela JA, Dowd FJ, Neidle EA, eds. Pharmacology and Therapeutics for Dentistry. 5th ed. St. Louis Mo: Mosby-Year Book Inc; 2004:797-813. 6. National Institutes of Health, National Cancer Institute. Consensus Development Conference on Oral Complications of Cancer Therapies: Diagnosis, Prevention, and Treatment. National Cancer Institute Monograph No. 9. Bethesda, Md: National Institutes of Health; 1990. 7. Epstein JB, Schubert MM. Oral mucositis in myelosuppressive cancer therapy. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1999;88(3):273-6. 8. Schubert MM, Peterson DE, Lloid ME. Oral complications. In: Blume KG, Forman SJ, Appelbaum RF, eds. Thomas’ Hematopoietic Cell Transplantation, 3 rd ed. Malden, Mass: Blackwell Science, Inc; 2004:911-28.
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9. Bavier AR. Nursing management of acute oral complications of cancer. Consensus Development Conference on Oral Complications of Cancer Therapies: Diagnosis, Prevention, and Treatment. National Cancer Institute Monograph No. 9. Bethesda, Md: National Institutes of Health; 1990:23-128. 10. Little JW, Falace DA, Miller CS, Rhodus NL. Dental Management of the Medically Compromised Patient, 7th ed. St. Louis, Mo: Mosby; 2008:433-61. 11. Semba SE, Mealy BL, Hallmon WW. Dentistry and the cancer patient: Part 2: Oral health management of the chemotherapy patient. Compend 1994;15(11):1378, 1380-7; quiz 1388. 12. Sonis S, Fazio RC, Fang L. Principles and Practice of Oral Medicine. 2nd ed. Philadelphia, Pa: WB Saunders Co; 1995:426-54. 13. Borowski B, Benhamou E, Pico JL, Laplanche A, Margainaud JP, Hayat M. Prevention of oral mucositis in patients treated with high-dose chemotherapy and bone marrow transplantation: A randomised controlled trial comparing two protocols of dental care. Eur J Cancer B Oral Oncol 1994;30B(2):93-7. 14. da Fonseca MA. Pediatric bone marrow transplantation: Oral complications and recommendations for care. Pediatr Dent 1998;20(7):386-94. 15. da Fonseca MA. Long-term oral and craniofacial complications following pediatric bone marrow transplantation. Pediatr Dent 2000;22(1):57-62. 16. da Fonseca MA. Dental care of the pediatric cancer patient. Pediatr Dent 2004;26(1):53-7. 17. Baddour LM, Bettman MA, Bolger AF, et al. Nonvalvular cardiovascular device-related infections. Circ 2003; 108(16):2015-31. 18. Ransier A, Epstein JB, Lunn R, Spinelli J. A combined analysis of a toothbrush, foam brush, and a chlorhexidinesoaked foam brush in maintaining oral hygiene. Canc Nurs 1995;18(5):393-6. 19. Wilson W, Taubert KA, Gevitz M, et al. Prevention of infective endocarditis: Guidelines from the American Heart Association. Circulation e-published April 19, 2007. Available at: “http://circ.ahajournals.org/cgi/reprint/CIRCU LATIONAHA.106.183095”. Accessed March 30, 2008. Correction Circulation 2007;116e376-e377. Available at: “http://circ.ahajournals.org/cgi/content/full/116/15/1736”. Accessed May 23, 2008.
20. Peters E, Monopoli M, Woo SB, Sonis S. Assessment of the need for treatment of postendodontic asymptomatic periapical radiolucencies in bone marrow transplant recipients. Oral Surg Oral Med Oral Pathol 1993;76(1): 45-8. 21. Sheller B, Williams B. Orthodontic management of patients with hematologic malignancies. Am J Orthod Dentofacial Orthop 1996;109(6):575-80. 22. Migliorati CA, Casiglia J, Epstein J, Jacobsen PL, Siegel MA, Woo SB. Managing the care of patients with bisphosphonate-associated osteonecrosis. An American Academy of Oral Medicine position paper. J Am Dent Assoc 2005;136(12):1658-68. Erratum in: 2006;137 (1):26. 23. Ruggiero SL, Fantasia J, Carlson E. Bisphosphonaterelated osteonecrosis of the jaw: Background and guidelines for diagnosis, staging and management. Oral Surg Oral Med Oral Pathol Oral Radiol Endodont 2006; 102(3):433-41. 24. Keefe DM, Schubert MM, Elting LS, et al. Updated clinical practice guidelines for the prevention and treatment of mucositis. Cancer 2007;109(5):820-831. Available at: “http://www.mascc.org/content/125.html”. Accessed June 9, 2008. 25. Euvrard S, Kanitakis J, Claudy A. Skin cancers after organ transplantation. N Engl J Med 2003;348(17):1681-91. 26. Gøtzche PC, Johansen HK. Nystatin prophylaxis and treatment in severely immunocompromised patients. Cochrane Database Syst Rev 2002;(2):CD002033. Update in Cochrane Database Syst Rev 2002;(4):CD002033. 27. Nieuw Amerongen AV, Veerman ECI. Current therapies for xerostomia and salivary gland hypofunction associated with cancer therapies. Support Care Cancer 2003;11 (4):226-31. 28. Dahllöf G, Jönsson A, Ulmner M, Huggare J. Orthodontic treatment in long-term survivors after bone marrow transplantation. Am J Orthod Dentofacial Orthop 2001; 120(5):459-65. 29. Zahrowski JJ. Bisphosphonate treatment: An orthodontic concern for a proactive approach. Am J Orthod Dentofacial Orthop 2007;131(3):311-20.
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Guideline on Record-keeping Originating Council Council on Clinical Affairs
Review Council Council on Clinical Affairs
Adopted 2004
Revised 2007
Purpose
This guideline was developed through reviews of current literature, recommendations of the American Dental Association, and current record-keeping by pediatric dental residency programs, dental schools, and pediatric dental practitioners, as well as consultation with experts in risk management. A MEDLINE search was conducted using the keywords “record-keeping”, “dental chart”, “dental record”, “risk management”, “electronic patient record”, and “electronic oral health record”.
data interchange with other professional and third parties. The software must contain all the essential elements of a traditional paper record. The elements of record-keeping addressed in this guideline are general charting considerations; initial patient record; components of a patient record; patient medical and dental histories; comprehensive and limited clinical examinations; treatment planning and informed consent; progress notes; correspondence, consultations, and ancillary documents; and confidential notes. Additionally, appendices to this guideline illustrate items for consideration in the development of patient medical and dental histories and examination forms. These lists, developed by experts in pediatric dentistry and offered to facilitate excellence in practice, should be modified as needed by individual practitioners. These samples do not establish or evidence a standard of care. In issuing this information, the AAPD is not engaged in rendering legal or other professional advice. If such services are required, competent legal or other professional counsel should be sought.
Background
Recommendations
The patient record provides all privileged parties with the history and details of patient assessment and communications between dentist and patient, as well as specific treatment recommendations, alternatives, risks, and care provided. The patient record is an important legal document in third party relationships. Poor or inadequate documentation of patient care consistently is reported as a major contributing factor in unfavorable legal judgments against dentists.1,2 Therefore, the AAPD recognizes that a guideline on record-keeping may provide dentists the inform-ation needed to compile an accurate and complete patient chart that can be interpreted by a knowledgeable third party. An electronic patient record is becoming more commonplace.3,4 Advantages include quality assurance by allowing comparative analysis of groups of patients or providers, medical and dental history profiles for demographic data, support for decision making based on signs and symptoms, administrative management for patient education and recall, and electronic
General charting considerations The dental record must be authentic, accurate, legible, and objective. Each patient should have an individual dental record. Chart entries should contain the initials or name of the individual making the note. Abbreviations should be standardized for the practice. Risk management experts recommend a problem-oriented record.5 After data collection, a list is compiled that includes medical considerations, psychological/ behavior constraints, and the oral health needs to be addressed. Problems are listed in order of importance in a standardized fashion making it less likely that an area might be overlooked. The plan identifies a general course of treatment for each problem. This plan can result in the need for additional information, consultation with other practitioners, patient education, and preventive strategies.
The American Academy of Pediatric Dentistry (AAPD) recognizes the patient record is an essential component of the delivery of competent and quality oral health care. It serves as an information source for the care provider and patient, as well as any authorized third party. This guideline will assist the practitioner in assimilating and maintaining a comprehensive, uniform, and organized record addressing patient care. However, it is not intended to create a standard of care.
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Initial patient record The parent’s/patient’s initial contact with the dental practice, usually via telephone, allows both parties an opportunity to address the patient’s primary oral health needs and to confirm the appropriateness of scheduling an appointment with that particular practitioner. During this conversation, the receptionist may record basic patient information such as: • Patient’s name, nickname, and date of birth • Name, address, and telephone number of parent • Name of referring party • Significant medical history • Chief complaint Such information constitutes the initial dental record. At the first visit to the dental office, additional information would be obtained and a permanent dental record developed. Components of a patient record The dental record must include each of the following specific components: 1. Medical history 2. Dental history 3. Clinical assessment 4. Diagnosis 5. Treatment recommendations 6. Progress notes When applicable, the following should be incorporated into the patient’s record as well: 1. Radiographic assessment 2. Caries risk assessment 3. Informed consent documentation 4. Sedation/general anesthesia records 5. Trauma records 6. Orthodontic records 7. Consultations/referrals 8. Laboratory orders 9. Test results 10. Additional ancillary records Medical history1,2,6-8 An accurate, comprehensive, and up-to-date medical history is necessary for correct diagnosis and effective treatment planning. Familiarity with the patient’s medical history is essential to decreasing the risk of aggravating a medical condition while rendering dental care. The practitioner, or staff under the supervision of the practitioner, must obtain a medical history from the parent (if the patient is under the age of 18) before commencing patient care. When the parent cannot provide adequate details regarding a patient’s medical history, or if the dentist providing care is unfamiliar with the patient’s medical diagnosis, consultation with the medical health care provider may be indicated. Documentation of the patient’s medical history includes the following elements of information, with elaboration of positive findings: • Medical conditions and/or illnesses • Name and, if available, telephone number of primary and specialty medical care providers
• Hospitalizations/surgeries • Anesthetic experiences • Current medications • Allergies/reactions to medications • Other allergies/sensitivities • Immunization status • Review of systems • Family history • Social history Appendix I provides suggestions for specific information that may be included in the written medical questionnaire or during discussions with the patient/parent. The history form should provide the parent additional space for information regarding positive historical findings, as well any medical conditions not listed. There should be areas on the form indicating the date of completion, the signature of the person providing the history (along with his/her relationship to the patient), and the signature of the staff member reviewing the history with the parent/guardian. Records of patients with significant medical conditions should be marked “Medical Alert” in a conspicuous yet confidential manner. Medical history for adolescents9 The adolescent can present particular psychosocial characteristics that impact the health status of the oral cavity, care seeking, and compliance. Integrating positive youth development8 into the practice, the practitioner should obtain additional information confidentially from teenagers. Topics to be discussed may include nutritional and dietary considerations, eating disorders, alcohol and substance abuse, tobacco usage, over-the-counter medications and supplements, body art (eg, intra- and extraoral piercings, tattoos), and pregnancy. Medical updates At each patient visit, the history should be consulted and updated. Recent medical attention for illness or injury, newly diag-nosed medical conditions, and changes in medications should be documented. A written update should be obtained at each recall visit. Dental history2,6,10,11 A thorough dental history is essential to guide the practitioner’s clinical assessment, make an accurate diagnosis, and develop a comprehensive preventive and therapeutic program for each patient. The dental history should address the following: • Chief complaint • Previous dental experience • Date of last dental visit/radiographs • Oral hygiene practices • Fluoride use/exposure history • Dietary habits (including bottle/no-spill training cup use in young children) • Oral habits • Previous orofacial trauma • Temporomandibular joint (TMJ) history clinical guidelines
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• Family history of caries • Social development Appendix II provides suggestions for specific information that may be included in the written dental questionnaire or during discussions with the patient/parent. Comprehensive clinical examination2,7,12 The clinical examination is tailored to the patient’s chief complaint (eg, initial visit to establish a dental home, acute traumatic injury, second opinion). A visual examination should precede other diagnostic procedures. Components of a comprehensive oral examination include: • General health/growth assessment • Pain assessment • Extraoral soft tissue examination • TMJ assessment • Intraoral soft tissue examination • Oral hygiene and periodontal health assessment • Assessment of the developing occlusion • Intraoral hard tissue examination • Radiographic assessment, if indicated13 • Caries risk assessment14 • Assessed behavior of child Appendix III provides suggestions for specific information that may be included in the oral examination. The dentist may employ additional diagnostic tools to complete the oral health assessment. Such diagnostic aids may include electric or thermal pulp testing, photographs, laboratory tests, and study casts. If the child is old enough to talk, the speech may be evaluated and provide additional diagnostic information. Examinations of a limited nature If a patient is seen for limited care, a consultation, an emergency, or a second opinion, a medical and dental history should be obtained, along with a hard and soft tissue examination as deemed necessary by the practitioner. The parent should be informed of the limited nature of the treatment and counseled to seek routine comprehensive care. The AAPD’s Guideline on Management of Acute Dental Trauma15 provides greater details on diagnostic procedures and documentation for this clinical circumstance. Treatment recommendations and informed consent Once the clinician has obtained the medical and dental histories and evaluated the facts obtained during the diagnostic procedures, the diagnoses should be derived and a sequential prioritized treatment plan developed. The treatment plan would include specific information regarding the nature of the procedures/materials to be used, number of appointments/time frame needed to accomplish this care, behavior guidance techniques, and fee for proposed procedures. The dentist is obligated to educate the parent on the need for and benefits of the recommended care, as well as risks, alternatives, and expectations if no intervention is provided. When deemed appropriate, the
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patient should be included in these discussions. The dentist should not attempt to decide what the parent will accept or can afford. After the treatment plan is presented, the parent should have the opportunity to ask questions regarding the proposed care and have concerns satisfied prior to giving informed consent. Documentation should include that the parent appeared to understand and accepted the proposed procedures. Any special restrictions of the parent should be documented. Progress notes An entry must be made in the patient’s record that accurately and objectively summarizes each visit. The following information should be included: • Date of visit • Reason for visit/chief complaint • Adult accompanying child • Verification of compliance with preoperative instructions • Changes in the medical history, if any • Radiographic exposures and interpretation • Reference to supplemental documents • Treatment rendered, including anesthetic agents16 and/or nitrous oxide/oxygen17 • Patient behavior • Post-operative instructions and prescriptions • Anticipated follow-up visit A standardized format may provide the practitioner a way to record the essential aspects of care on a consistent basis. One example of documentation is the SOAP note.18 SOAP is an acronym for “subjective” (S) or the patient’s response and feeling to treatment, “objective” (O) or the observations of the clinician, “assessment” (A) or diagnosis of the problem, and “procedures accomplished and plans” (P) for subsequent problem resolving activities. The signature or initials of the office staff member documenting the visit should be entered. When sedation or general anesthesia is employed, additional documentation on a time-based record is required, as discussed in the AAPD’s Guideline for Monitoring and Management of Pediatric Patients During and After Sedation for Diagnostic and Therapeutic Procedures.19 Progress notes also should include telephone conversations regarding the patient’s care, appointment history (ie, cancellations, failures, tardiness), non-compliance with treatment recommendations, and educational materials utilized (both video and written), along with identification of the staff member making the entry in the dental record. Orthodontic treatment The AAPD’s Guideline on Management of the Developing Dentition and Occlusion in Pediatric Dentistry20 and the American Board of Pediatric Dentistry site visit requirements8 provide general recommendations on the documentation of orthodontic care. Signs and/or symptoms of TMJ disorders should be recorded when they occur before, during, or after orthodontic treatment.21 During orthodontic treatment, progress
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notes should include deficiencies in oral hygiene, loose bands and brackets, patient complaints, caries, root resorption, and cancellations and failures. Correspondence, consultations, and ancillary documents The primary care dentist often consults with other health care providers in the course of delivery of comprehensive oral health care, especially for patients with special health care needs or complex oral conditions. Communications with medical care providers or dental specialists should be incorporated into the dental record. Written referrals to other care providers should include the specific nature of the referral, as well as pertinent patient history and clinical findings. A progress note should be made on correspondence sent or received regarding a referral, indicating documentation filed elsewhere in the patient’s chart. Copies of test results, prescriptions, laboratory work orders, and other ancillary documents should be maintained as part of the dental record. Confidential notes The practitioner may elect to keep on a separate form subjective notes addressing impressions and opinions of the doctor and/or staff concerning parent/patient interactions that may or did result in negative consequences.
Appendices* *The information included in the following samples, developed by the AAPD, is provided as a tool for pediatric dentists and other dentists treating children. It was developed by experts in pediatric dentistry and is offered to facilitate excellence in practice. However, these samples do not establish or evidence a standard of care. In issuing this information, the AAPD is not engaged in rendering legal or other professional advice. If such services are required, competent legal or other professional counsel should be sought.
Appendix I—Medical history* Name and nickname Date of birth Gender Race/ethnicity Height, weight by report Name, address, and telephone number of all physicians Date of last physical examination Immunization status Summary of health problems Any health conditions that necessitate antibiotics prior to dental treatment Allergies/sensitivities/reactions Anesthetics, local and general Sedative agents Drugs or medications
Environmental (including latex, food, dyes, metal, acrylic) Medications (including over-the-counter analgesics, vitamins, and herbal supplements) Dose Frequency Reactions Hospitalizations—reason, date, and outcome Surgeries—reason, date, and outcome Significant injuries—description, date, and outcome General Complications during pregnancy and/or birth Prematurity Congenital anomalies Cleft lip/palate Inherited disorders Nutritional deficiencies Problems of growth or stature Head, ears, eyes, nose, throat Lesions in/around mouth Chronic adenoid/tonsil infections Chronic ear infections Ear problems Hearing impairments Eye problems Visual impairments Sinusitis Speech impairments Apnea/snoring Mouth breathing Cardiovascular Congenital heart defect/disease Heart murmur High blood pressure Rheumatic fever Rheumatic heart disease Respiratory Asthma—medications, triggers, last attack, hospitalizations Tuberculosis Cystic fibrosis Frequent colds/coughs Respiratory syncytial virus Reactive airway disease/breathing problems Smoking Gastrointestinal Eating disorder Ulcer Excessive gagging
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Gastroesophageal/acid reflux disease Hepatitis Jaundice Liver disease Intestinal problems Prolonged diarrhea Unintentional weight loss Lactose intolerance Dietary restrictions Genitourinary Bladder infections Kidney infections Pregnancy Systemic birth control Sexually transmitted diseases Musculoskeletal Arthritis Scoliosis Bone/joint problems TMJ problems—popping, clicking, locking, difficulties opening or chewing Integumetary Fever blisters Eczema Rash/hives Dermatologic conditions Neurologic Fainting Dizziness Autism Developmental disorders Learning problems/delays Mental disability Brain injury Cerebral palsy Convulsions/seizures Epilepsy Headaches/migraines Hydrocephaly Shunts—ventriculoperitoneal, ventriculoatrial, ventriculovenous Psychiatric Abuse
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Alcohol and chemical dependency Emotional disturbance Hyperactivity/attention deficit hyperactivity disorder Psychiatric problems/treatment Endocrine Diabetes Growth delays Hormonal problems Precocious puberty Thyroid problems Hematologic/lymphatic/immunologic Anemia Blood disorder Transfusion Excessive bleeding Bruising easily Hemophilia Sickle cell disease/trait Cancer, tumor, other malignancy Immune disorder Chemotherapy Radiation therapy Hematopoietic cell (bone marrow) transplant Infectious disease Measles Mumps Rubella Scarlet fever Varicella (chicken pox) Mononucleosis Cytomegalovirus (CMV) Pertussis (whooping cough) Human immunodeficiency virus/acquired immune deficiency syndrome (HIV/AIDS) Family history Genetic disorders Problems with general anesthesia Serious medical conditions or illnesses Social concerns Passive smoke exposure Religious or philosophical objections to treatment
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Appendix II—Dental History* Previous dentist, address, telephone number Family dentist Date of last visit Date of last dental radiographs, number and type taken, if known Prenatal/natal history Family history of caries, including parents and siblings History of smoking in the home Medications or disorders that would impair salivary flow Injuries to teeth and jaws, including TMJ trauma When Treatment required Dental pain and infections Habits (past and present) such as finger, thumb, pacifier, tongue or lip sucking, bruxism, clenching Snoring Diet and dietary habits Breast feeding—frequency Bottle feeding/no-spill training (sippy) cup use Frequency Formula, milk water, juice Weaned/when Sodas, fruit juice, sports drinks, beverages— amount, frequency Snacks—type, frequency Meals—balanced Oral hygiene Frequency of brushing, flossing Assisted/supervised Fluoride exposure Primary source of drinking water—home, daycare, other Water—tap, bottled, well, reverse osmosis Systemic supplementation—tablets, drops Topical—toothpaste, rinses, prescription Previous orthodontic treatment Behavior of child during past dental treatment Behavior anticipated for future treatment
Appendix III—Clinical Examination* General health/growth assessment Growth appropriate for age Height/weight/frame size/body mass index (BMI) Vital signs Blood pressure Pulse Extraoral examination Facial features Nasal breathing Lip posture Symmetry Pathologies Skin health Temporomandibular joint/disorder (TMJ/TMD)12 Signs of clenching/bruxism Headaches from TMD Pain Joint sounds Limitations or disturbance of movement or function Intra-oral soft tissue examination Tongue Roof of mouth Frenulae Floor of mouth Tonsils/pharynx Lips Pathologies noted Oral hygiene and periodontal assessment22,23 Oral hygiene, including an index or score Gingival health, including an index or score Probing of pocket depth, when indicated Marginal discrepancies Calculus Bone level discrepancies that are pathologic Recession/inadequate attached gingiva Mobility Bleeding/suppuration Furcation involvement Assessment of the developing occlusion Facial profile Canine relationships Molar relationships Overjet Overbite
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Midline Crossbite Alignment Crowding Centric relation/centric occlusion discrepancy Influence of oral habits Appliances present Intraoral hard tissue examination Teeth present Supernumerary/missing teeth Dental development status Over-retained primary teeth Ankylosed teeth Ectopic eruption Anomalies/pathologies noted Tooth size, shape discrepancies Tooth discoloration Enamel hypoplasia Congenital defects Existing restorations Defective restorations Caries Pulpal pathology24 Traumatic injuries Third molars Radiographic examination25 Developmental anomalies Eruptive patterns/tooth positions/root resorption Crestal alveolar bone level Pulpal/furcation/periapical pathology Caries – presence, proximity to pulp space, demineralization/remineralization Existing pulpal therapy/restorations Traumatic injury Calculus deposits Occult disease Explanation of inability to obtain diagnostic image when indicated Caries-risk assessment14
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References 1. Lawney M. For the record: Understanding patient recordkeeping. N Y State Dent J 1998;64(5):34-43. 2. Bressman JK. Risk management for the ‘90s. J Am Dent Assoc 1993;124(3):63-7. 3. Heid DW, Chasteen J, Forrey AW. The electronic oral health record. J Contemp Dent Pract 2002;3(1);43-5. 4. Atkinson JC, Zeller GG, Shah C. Electronic patient records for dental school clinics: More than paperless systems. J Dent Educ 2002;66(5):634-42. 5. Valenza JA. Medical risk report: Improving patient management and record keeping through a problem-oriented approach. J Greater Houston Dent Soc 1994;65(9):46-8. 6. Nelson GV. Guidelines to the prevention of problems in record keeping. Part I. Pediatr Dent 1989;11(2):174-7. 7. Nelson GV. Records, charting, and problem areas in documentation: Part II. Pediatr Dent 1989;11(3):240-2. 8. American Board of Pediatric Dentistry. Site Visit Handbook, 2006-2007. Available at: “http://www.abpd.org/ pamphlets/sitevisit_handbook.pdf ”. Accessed March 18, 2007. 9. American Academy of Pediatric Dentistry. Guideline on adolescent oral health care. Pediatr Dent 2006;28(suppl): 77-84. 10. American Academy of Pediatric Dentistry. Guideline on infant oral health care. Pediatr Dent 2006;28(suppl): 73-6. 11. American Academy of Pediatric Dentistry. Guideline on periodicity of examination, preventive dental services, anticipatory guidance, and oral treatment for children. Pediatr Dent 2007:29(suppl):102-8. 12. American Academy of Pediatric Dentistry. Guideline on acquired temporomandibular disorders in infants, children, and adolescents. Pediatr Dent 2006;28(suppl): 170-2. 13. American Academy of Pediatric Dentistry. Guideline on prescribing dental radiographs for infants, children, adolescents, and persons with special health care needs. Pediatr Dent 2006;28(suppl):200-1. 14. American Academy of Pediatric Dentistry. Policy on use of caries-risk assessment tool (CAT) for infants, children, and adolescents. Pediatr Dent 2006;28(suppl):24-8. 15. American Academy of Pediatric Dentistry. Guideline on management of acute dental trauma. Pediatr Dent 2007; 29(suppl):168-76. 16. American Academy of Pediatric Dentistry. Guideline on appropriate use of local anesthesia for pediatric dental patients. Pediatr Dent 2006;28(suppl):106-11. 17. American Academy of Pediatric Dentistry. Guideline on appropriate use of nitrous oxide for pediatric dental patients. Pediatr Dent 2006;28(suppl):112-4. 18. Chasteen JE, Cameron CA, Phillips SL. An audit system for assessing dental record keeping. J Dent Educ 1996; 60(12):978-86.
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19. American Academy of Pediatric Dentistry. Guidelines on monitoring and management of pediatric patients during and after sedation for diagnostic and therapeutic procedures. Pediatr Dent 2006;28(suppl):115-32. 20. American Academy of Pediatric Dentistry. Guideline on management of the developing dentition and occlusion in pediatric dentistry. Pediatr Dent 2006;28(suppl):157-69. 21. Machen DE. Legal aspects of orthodontic practice: Risk management concepts. Am J Orthod Dentofac Orthop 1989;96(2):173-5. 22. Greenwell H. American Academy of Periodontology Committee on Research, Science, and Therapy. Periodontal therapy. J Periodontol 2001;72(11):1624-8.
23. Califano JV. American Academy of Periodontology Research, Science, and Therapy Committee. Periodontal diseases of children and adolescents. J Periodontol 2003; 74(11):1696-704. 24. American Academy of Pediatric Dentistry. Guideline on pulp therapy for primary and young permanent teeth Pediatr Dent 2006;28(suppl):144-8. 25. Stigers JI, Burke R. Radiology. In: Nowak AJ, Casamassimo PS, eds. The Handbook of Pediatric Dentistry, 3rd ed. American Academy of Pediatric Dentistry Chicago, Ill; 2007:61-7.
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Guideline on Informed Consent Originating Council Council on Clinical Affairs
Review Council Council on Clinical Affairs
Adopted 2005
Revised 2009
Purpose The American Academy of Pediatric Dentistry recognizes that informed consent is essential in the delivery of health care. The informed consent process allows the patient or the custodial parent or, in the case of minors, legal guardian to participate in and retain autonomy over the health care received. Informed consent also may decrease the practitioner’s liability from claims associated with miscommunication. This guideline reflects that informed consent is governed by the statutes and case laws of individual states and that oral care providers should review applicable state law and regulations.
Methods This revision included a systematic literature search of the MEDLINE/Pubmed electronic database using the following parameters: Terms: “informed consent”, “pediatric consent”, “pediatric informed consent”, and “consent”; Fields: all fields; Limits: within the last 10 years, humans, English, review of legal cases. One hundred seven articles matched these criteria. Papers for review were chosen from this list and from references within selected articles. When data did not appear sufficient or were inconclusive, recommendations were based upon expert and/or consensus opinion by experienced researchers and legal practitioners.
Background Informed consent is the process of providing the patient or, in the case of a minor or incompetent adult, the custodial parent or legal guardian with relevant information regarding diagnosis and treatment needs so that an educated decision regarding treatment can be made by the patient or custodial parent/legal guardian. The American Dental Association’s Principles of Ethics states “the dentist should inform the patient of the proposed treatment, and any reasonable alternatives, in a manner that allows the patient to become involved in treatment decisions.”1 State laws and court decisions determine the criteria for informed consent.2 In 1914, a New York state court ruled that “every human being of adult years and sound mind has a right to determine what shall be done with his own body….”3 Al-
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though most cases have involved other health professionals, oral health care providers should follow the rulings established by these cases. Ruling from the Supreme Court of North Dakota found that laws pertaining to a physician’s duty to obtain informed consent also pertained to dentists.4 As court rulings and laws differ in each state, it is difficult to develop an inclusive guideline. The law generally has several criteria for selecting information to provide to a patient/parent/guardian as part of an informed consent. Some states follow a patient-oriented standard—that information which a reasonably prudent patient in same or similar circumstances would wish to know.5,6 Other states follow a practitioner-oriented standard—that information which a health care provider, practicing within the standard of care, would reasonably provide to a patient in the same circumstances.5,7 A hybrid approach, combining the patient-oriented and practitioner-oriented standards, is followed by some states.5-7 Whichever standard a state applies, the treating practitioner must disclose information that he/she considers material to the patient’s decision-making process and provide a warning of death or serious bodily injury where that is a known risk of the procedure.2,5,8 The informed consent process generally excludes adverse consequences associated with a simple procedure if the risk of occurrence is considered remote and when such circumstances commonly are understood by the profession to be so. It generally is understood that the person granting consent is the patient of the age of majority. Patients under the age of majority or adults with diminished mental capacity should have treatment consent obtained from a parent or legal guardian.2,5 The adult accompanying the pediatric patient may not be a legal guardian allowed by law to consent to medical procedures. Examples of this include a grandparent, stepparent, noncustodial parent in instances of divorce, babysitter, or friend of the family. A child in foster care or a ward of the state may be accompanied by a caretaker who may or may not be allowed to consent to medical procedures, according to individual state law. It is advisable that the oral health care provider obtain a copy of court orders appointing a guardian to verify who is authorized to consent for medical treatment for the patient.2 One option
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to consider is obtaining a parent/guardian’s authorization via a consent by proxy or power of attorney agreement for any other individual to make dental treatment decisions for a child.9 In situations where individuals other than the parent/guardian regularly bring the child to the dental office, this can help eliminate doubt as to whether such individual has the legal authority to provide informed consent. Practitioners, however, should consult their own attorney in deciding whether to utilize such a form in their own practice. Written consent is required by some states before treatment of a patient.2,5 Even if not mandated by state law, written consent is advisable as it may decrease the liability from miscommunication. A patient’s or parent/guardian’s signing a consent form should not preclude a thorough discussion. Studies have shown that even when seemingly adequate information has been presented to patients, their ability to fully understand the information may be limited.10-11 Supplements such as informational booklets or videos may be helpful to the patient or custodial parent or legal guardian in understanding a proposed procedure. The oral discussion between provider and patient, not the completion of a form, is the important issue of informed consent. The consent form should document the oral discussion of the proposed therapy, including risks, benefits, and possible alternative therapy. When a form is utilized, it is best to use simple words and phrases, avoiding technical terms, so that it may be easily understood. A modified or customized consent form is preferred over a standard form and should be in a format that is readily understandable to a lay person.12 Overly broad statements such as “any and all treatment deemed necessary…” or “all treatment which the doctor in his/her best medical judgment deems necessary, including but not limited to…” should be avoided. Courts have determined it to be so broad and unspecific that it does not satisfy the duty of informed consent. Informed consent discussion, when possible, should occur on a day separate from the treatment and the practitioner should avoid downplaying the risks involved with the proposed therapy. Items appearing on a consent form should include: 1. name and date of birth of pediatric patient; 2. name, relationship to patient, and legal basis for adult to consent on behalf of minor; 3. description of specific treatment in simple terms; 4. alternatives to treatment; 5. potential adverse sequelae specific to the procedure; 6. an area for the patient or parent/guardian to indicate all questions have been answered; 7. signature lines for the dentist, parent or legal guardian, and a witness. Consent forms should be procedure specific, with multiple forms likely to be used. For example, risks associated with restorative procedure will differ from those associated with an extraction. Separate forms, or separate areas outlining each procedure on the same form, would be necessary to accurately advise the patient regarding each procedure. Consent for sedation or behavior guidance techniques such as protective
stabilization (ie, immobilization) should be obtained separately from consent for other procedures. Consent may need to be updated or changed accordingly as changes in treatment plans occur. For example, a primary tooth originally planned for pulp therapy is determined to be nonrestorable at the time of treatment. Consent will need to be updated to reflect the change in treatment.
Recommendations Informed consent is the process of providing the patient or, in the case of a minor or incompetent adult, the custodial parent or legal guardian with relevant information regarding diagnosis and treatment needs so that an educated decision regarding treatment can be made by the patient or custodial parent or legal guardian. Statutes and case law of individual states govern informed consent. Some states allow oral discussions, which should be documented in the medical record, while others may require written consent. Oral health practitioners should review applicable state laws to determine their level of compliance. Consent forms should be procedure specific, utilize simple terms, and avoid overly broad statements. When a practitioner utilizes an “informed consent” form, the following should be included: 1. name and date of birth of pediatric patient; 2. name and relationship to the pediatric patient/legal basis on which the person is consenting on behalf of the patient; 3. description of the procedure in simple terms; 4. disclosure of known adverse risk(s) of the proposed treatment specific to that procedure; 5. professionally-recognized or evidence-based alterna tive treatment(s) to recommended therapy and risk(s); 6. place for custodial parent or legal guardian to indicate that all questions have been asked and adequately answered; 7. places for signatures of the custodial parent or legal guardian, dentist, and an office staff member as a witness.
References 1. American Dental Association. Principles of Ethics and Code of Professional Conduct. Available at: “http://www. ada.org/prof/prac/law/code/index.asp”. Accessed April 12, 2008. 2. Sfikis P. A duty to disclose: Issues to consider in securing informed consent. J Am Dent Assoc 2003;134(10): 1329-33. 3. Schloendorffer v Society of New York Hospital, 105 NE92 (1914). 4. Koapke v Herfendal, 660 NW 2d 206 (ND 2003). 5. LeBlang TR, Rosoff AJ, White C. Informed consent to medical and surgical treatment. In: Legal Medicine. 6th ed. Philadelphia, Pa: Mosby; 2004. 6. Canterbury v Spence, 464 F2d 786 (DC Cir 1972).
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7. Nathanson v Kline, 350 P2d 1093 (Kan 1960). 8. Harris DM. Contemporary Issues in Healthcare Law and Ethics. 3rd ed. Chicago, Ill: Health Administration Press; 2007:198-203. 9. American Academy of Pediatrics Committee on Medical Liability. Consent by proxy for nonurgent pediatric care. Pediatrics 2003;112(5):1186-95. 10. Tahir MA, Mason C, Hind V. Informed consent: Optimism versus reality. Br Dent J 2002;192(4):221-4.
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11. Adewumi A, Hector MP, King JM. Children and informed consent: A study of children’s perceptions and involvement in consent to dental treatment. Br Dent J 2001;191(5):256-9. 12. Tait AR, Voepel-Lewis T, Malviya S, Philipson SJ. Improving the readability and processability of a pediatric informed consent document. Arch Pediatr Adolesc Med 2005;159(4):347-52.
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Guideline on Prescribing Dental Radiographs for Infants, Children, Adolescents, and Persons with Special Health Care Needs Originating Committee Ad Hoc Committee on Pedodontic Radiology
Review Council Council on Clinical Affairs
Adopted 1981
Revised 1992, 1995, 2001, 2005, 2009
Reaffirmed 1997
Purpose The American Academy of Pediatric Dentistry (AAPD) intends this guideline to help practitioners make clinical decisions concerning appropriate selection of dental radiographs as part of an oral evaluation of infants, children, adolescents, and persons with special health care needs. The guideline can be used to optimize patient care, minimize radiation burden, and allocate health care resources responsibly.
Methods The American Dental Association (ADA) initiated a review of The Selection of Patients for X-ray Examinations: Dental Radiographic Examinations1 in 2002. The AAPD, along with other dental specialty organizations, participated in the review and revision of these guidelines. The Food and Drug Administration (FDA) accepted them in November 2004.2 This review included a new systematic literature search of the MEDLINE/ Pubmed electronic database using the following parameters: Terms: “dental radiology”, “dental radiographs”, “dental radiography”, “cone beam computed tomography” AND “guidelines”, “recommendations”; Fields: all fields; Limits: within the last 10 years, humans, and English. In 2006, the ADA Council on Scientific Affairs published an update to their recommendations for dental radiographs.3 The AAPD continues to endorse the ADA/FDA’s recommendations.
Background Radiographs are valuable aids in the oral health care of infants, children, adolescents, and persons with special health care needs. They are used to diagnose oral diseases and to monitor dentofacial development and the progress of therapy. The recommendations in the ADA/FDA guidelines were developed
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to serve as an adjunct to the dentist’s professional judgment. The timing of the initial radiographic examination should not be based upon the patient’s age, but upon each child’s individual circumstances. Because each patient is unique, the need for dental radiographs can be determined only after reviewing the patient’s medical and dental histories, completing a clinical examination, and assessing the patient’s vulnerability to environmental factors that affect oral health. Radiographs should be taken only when there is an expectation that the diagnostic yield will affect patient care. The AAPD recognizes that there may be clinical circumstances for which a radiograph is indicated, but a diagnostic image cannot be obtained. For example, the patient may be unable to cooperate or the dentist may have privileges in a health care facility lacking intraoral radiographic capabilities. If radiographs of diagnostic quality are unobtainable, the dentist should confer with the parent to determine appropriate management techniques (eg, preventive/restorative interventions, advanced behavior guidance modalities, deferral, referral), giving consideration to the relative risks and benefits of the various treatment options for the patient. Because the effects of radiation exposure accumulate over time, every effort must be made to minimize the patient’s exposure. Good radiological practices (eg, use of lead apron, thyroid collars, and high-speed film; beam collimation) are important. The dentist must weigh the benefits of obtaining radiographs against the patient’s risk of exposure. New imaging technologies [ie, cone beam computed tomography (CBCT)] have added 3-dimensional capabilities that have many applications in dentistry. Evidence-based guidelines and policies currently are under development by organizations such as the American Academy of Oral and
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Guidelines for Prescribing Dental Radiographs Patient Age and Dental Developmental Stage Child with Primary Dentition (prior to eruption of first permanent tooth)
Child with Transitional Dentition (after eruption of first permanent tooth)
Adolescent with Permanent Dentition (prior to eruption of third molars)
New patient* being evaluated for dental diseases and dental development
Individualized radiographic exam consisting of selected periapical/occlusal views and/or posterior bitewings if proximal surfaces cannot be visualized or probed. Patients without evidence of disease and with open proximal contacts may not require a radiographic exam at this time.
Individualized radiographic exam consisting of posterior bitewings with panoramic exam or posterior bitewings and selected periapical images.
Individualized radiographic exam consisting of posterior bitewings with panoramic exam or posterior bitewings and selected periapical images. A full mouth intraoral radiographic exam is preferred when the patient has clinical evidence of generalized dental disease or a history of extensive dental treatment.
Recall patient* with clinical caries or at increased risk for caries**
Posterior bitewing exam at 6-12 month intervals if proximal surfaces cannot be examined visually or with a probe
Posterior bitewing exam at 6-18 month intervals
Not applicable
Recall patient* with no clinical caries and not at increased risk for caries**
Posterior bitewing exam at 12-24 month intervals if proximal surfaces cannot be examined visually or with a probe
Posterior bitewing exam at 24-36 month intervals
Not applicable
Recall patient* with periodontal disease
Clinical judgment as to the need for and type of radiographic images for the evaluation of periodontal disease. Imaging may consist of, but is not limited to, selected bitewing and/or periapical images of areas where periodontal disease (other than nonspecific gingivitis) can be identified clinically.
Patient for monitoring of growth and development
Clinical judgment as to need for and type of radiographic images for evaluation and/or monitoring of dentofacial growth and development
Patient with other circumstances including, but not limited to, proposed or existing implants, pathology, restorative/endodontic needs, treated periodontal disease and caries remineralization
Clinical judgment as to need for and type of radiographic images for evaluation and/or monitoring in these circumstances.
Type of Encounter
* Clinical situations for which radiographs may be indicated include but are not limited to: A. 1. 2. 3. 4. 5. 6.
Positive Historical Findings Previous periodontal or endodontic treatment History of pain or trauma Familial history of dental anomalies Postoperative evaluation of healing Remineralization monitoring Presence of implants or evaluation for implant placement
B. 1. 2. 3. 4. 5. 6. 7. 8.
Positive Clinical Signs/Symptoms Clinical evidence of periodontal disease Large or deep restorations Deep carious lesions Malposed or clinically impacted teeth Swelling Evidence of dental/facial trauma Mobility of teeth Sinus tract (“fistula”)
Posterior bitewing exam at 18-36 month intervals
Clinical judgment as to need for and type of radiographic images for evaluation and/or monitoring of dentofacial growth and development. Panoramic or periapical exam to assess developing third molars
9. Clinically suspected sinus pathology 10. Growth abnormalities 11. Oral involvement in known or suspected systemic disease 12. Positive neurologic findings in the head and neck 13. Evidence of foreign objects 14. Pain and/or dysfunction of the temporomandibular joint 15. Facial asymmetry 16. Abutment teeth for fixed or removable partial prosthesis 17. Unexplained bleeding 18. Unexplained sensitivity of teeth 19. Unusual eruption, spacing or migration of teeth 20. Unusual tooth morphology, calcification or color 21. Unexplained absence of teeth 22. Clinical erosion
Adult, Dentate or Partially Edentulous
Adult, Edentulous
Individualized radiographic exam, based on clinical signs and symptoms.
Not applicable
Usually not indicated
** Factors increasing risk for caries may include but are not limited to: 1. High level of caries experience or demineralization 2. History of recurrent caries 3. High titers of cariogenic bacteria 4. Existing restoration(s) of poor quality 5. Poor oral hygiene 6. Inadequate fluoride exposure 7. Prolonged nursing (bottle or breast) 8. Frequent high sucrose content in diet 9. Poor family dental health 10. Developmental or acquired enamel defects 11. Developmental or acquired disability 12. Xerostomia 13. Genetic abnormality of teeth 14. Many multisurface restorations 15. Chemo/radiation therapy 16. Eating disorders 17. Drug/alcohol abuse 18. Irregular dental care
* From: American Dental Association, US Food & Drug Administration. The Selection of Patients For Dental Radiograph Examinations. Available on “www.ada.org”. endorsements
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Maxillofacial Radiology (AAOMR).4 The usefulness and future of CBCT have been reviewed with an introduction to issues related to criteria, ramifications, and medico-legal considerations.5 Certain principles clearly are emerging and point to the need for standards of provisions of care. Because this technology has potential to produce vast amounts of data and imaging information beyond initial intentions, it is important to interpret all information obtained, including that which may be beyond the immediate diagnostic needs of the practitioner.
Recommendations The recommendations of the ADA/FDA guidelines are contained within the accompanying table. “The recommendations in this chart are subject to clinical judgment and may not apply to every patient. They are to be used by dentists only after reviewing the patient’s health history and completing a clinical examination. Because every precaution should be taken to minimize radiation exposure, protective thyroid collars and aprons should be used whenever possible. This practice is strongly recommended for children, women of childbearing age, and pregnant women.”2 Although standards are not officially developed for the use of CBCT, this advance in orofacial dental imaging is an excellent adjunct for improvements in dental care. The executive opinion statement of the AAOMR provides initial guidance for the use of this technology.4 Their recommendations relate to the need for practices of qualified individuals to use this technology with selection criteria which include clear indications
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that minimize radiation exposure while maximizing diagnostic information obtained. When using CBCT, the resulting imaging is required to be supplemented with a written report placed in the patient’s records that includes full interpretation of the findings.
References 1. Joseph LP. The Selection of Patients for X-ray Examinations: Dental Radiographic Examinations. Rockville, Md: The Dental Radiographic Patient Selection Criteria Panel, US Dept of Health and Humans Services, Center for Devices and Radiological Health; 1987. HHS Publication No. FDA 88-8273. 2. American Dental Association, US Dept of Health and Humans Services. The selection of patients for dental radiographic examinations—2004. Available at: “http:// www.ada.org/prof/resources/topics/radiography.asp”. Accessed November 21, 2008. 3. American Dental Association Council on Scientific Affairs. The use of dental radiographs: Update and recommendations. J Am Dent Assoc 2006;137(9):1304-12. 4. Carter L, Farman AG, Geist J, et al. American Academy of Oral and Maxillofacial Radiology executive opinion statement on performing and interpreting diagnostic cone beam computed tomography. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2008;106(4):561-2. 5. Farman AG, Scarfe WC, Haskell BS. Cone beam computed tomography. Seminars in Orthodontics 2009;15 (1):1-77.
american academy of pediatric dentistry
Policy on Management of Patients With Cleft Lip/ Palate and Other Craniofacial Anomalies Originating Committee Clinical Affairs Committee
Review Council Council on Clinical Affairs
Adopted 1999
Revised 2003, 2008
Reaffirmed 2007
The American Academy of Pediatric Dentistry (AAPD), in its efforts to promote optimal health for children with cleft lip/ palate and other craniofacial anomalies, endorses the current statements of the American Cleft Palate-Craniofacial Association (ACPA).1,2 A child born with cleft lip/palate or other craniofacial anomalies has multiple and complex problems, including early feeding and nutritional concerns, middle ear disease, hearing deficiencies, deviations in speech and resonance, dentofacial and orthodontic abnormalities, and psychosocial adjustment problems. A report on children with special needs3 issued in 1987 by the US Surgeon General stressed that the care of these children should be comprehensive, coordinated, culturally sensitive, specific to the needs of the individual, and readily accessible. Recognizing that children with clefts and other craniofacial anomalies have special needs, the Maternal and Child Health Bureau in 1991 provided funding to ACPA to develop parameters of care for these patients. As part of these parameters1, several fundamental principles were identified as critical to optimal cleft/craniofacial care. These principles are: 1. Management of patients with craniofacial anomalies is best provided by an interdisciplinary team of spe cialists. 2. Optimal care for patients with craniofacial anomalies is provided by teams that see sufficient numbers of these patients each year to maintain clinical expertise in diagnosis and treatment. 3. Although referral for team evaluation and manage ment is appropriate for patients of any age, the optimal time for the first evaluation is within the first few weeks of life and, whenever possible, within the first few days.
4. From the time of first contact with the child and family, every effort must be made to assist the family in adjusting to the birth of a child with a craniofacial anomaly and the consequent demands and stress placed upon that family. 5. Parents/caregivers must be given information about recommended treatment procedures, options, risk fac tors, benefits, and costs to assist them in: (1) making informed decisions on the child’s behalf; and (2) pre paring the child and themselves for all recommended procedures. The team should actively solicit family participation and collaboration in treatment planning and, when the child is mature enough to do so, he or she should also participate in treatment decisions. 6. Treatment plans should be developed and imple mented on the basis of team recommendations. 7. Care should be coordinated by the team, but should be provided at the local level whenever possible; how ever, complex diagnostic or surgical procedures should be restricted to major centers with appropriate treat ment facilities and experienced care providers. 8. It is the responsibility of each team to be sensitive to linguistic, cultural, ethnic, psychosocial, economic, and physical factors that affect the dynamic relationship between the team, patient, and family. 9. It is the responsibility of the team to monitor both short-term and long-term outcomes. Thus, longitudi nal follow up of patients, including appropriate docu mentation and record-keeping, is essential. 10. Evaluation of treatment outcomes must take into ac count the satisfaction and psychosocial well-being of the patient, as well as effects on growth, function, and appearance.
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As members of the interdisciplinary team of physicians, dentists, speech pathologists, and other allied health professionals, pediatric dentists should provide dental services in close cooperation with their orthodontic, oral and maxillofacial surgery, and prosthodontic colleagues. All dental specialists should ensure that: 1. Dental radiographs, cephalometric radiographs, and other imaging modalities as indicated should be uti lized to evaluate and monitor dental and facial growth and development. 2. Diagnostic records, including properly occluded dental study models, should be collected at appropriate in tervals for patients at risk for developing malocclusion or maxillary-mandibular discrepancies. 3. As the primary dentition erupts, the team evaluation should include a dental examination and, if such ser vices are not already being provided, referral to appro priate providers for caries control, preventive measures, and space management. 4. Before the primary dentition has completed eruption, the skeletal and dental components should be evalu ated to determine if a malocclusion is present or developing. 5. Depending upon the specific goals to be accomplished and also upon the age at which the patient is initially evaluated, orthodontic management of the malocclu sion may be performed in the primary, mixed, or permanent dentition. In some cases, orthodontic treat ment may be necessary in all 3 stages. 6. While continuous active orthodontic treatment from early mixed dentition to permanent dentition should be avoided, each stage of orthodontic therapy may be followed by retention and regular observation. Orthodontic retention for the permanent dentition may extend into adulthood.
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7. For some patients with craniofacial anomalies, func tional orthodontic appliances may be indicated. 8. For patients with craniofacial anomalies, orthodontic treatment may be needed in conjunction with surgi cal correction of the facial deformity. 9. Congenitally missing teeth may be replaced with a removable appliance, fixed restorative bridgework, or osseointegrated implants. 10. Patients should be closely monitored for dental and periodontal disease. 11. Prosthetic obturation of palatal fistulae may be neces sary in some patients. 12. A prosthetic speech device may be used to treat velo pharyngeal inadequacy in some patients.
References 1. American Cleft Palate-Craniofacial Association. Parameters for evaluation and treatment of patients with cleft lip/palate or other craniofacial anomalies. Chapel Hill, NC: The Maternal and Child Health Bureau, Title V, Social Security Act, Health Resources and Services Administration, US Public Health Service, DHHS; November 2007. Grant #MCJ-425074. Available at: “http://www. acpa-cpf.org/teamcare/parameters07rev.pdf ”. Accessed April 1, 2008. 2. American Cleft Palate-Craniofacial Association, Team Standards Committee. The cleft and craniofacial team. Chapel Hill, NC: American Cleft Palate-Craniofacial Association; 1996. 3. US Dept of Health and Human Services. A report of the Surgeon General: Children with special health care needs. Rockville, Md: Office of Maternal and Child Health, US Dept of Health and Human Services; 1987.
american academy of pediatric dentistry
Periodontal Diseases of Children and Adolescents Originating Group American Academy of Periodontology – Research, Science and Therapy Committee
Endorsed/Reaffirmed by the American Academy of Pediatric Dentistry 1992, 1995, 2004
Epidemiologic studies indicate that gingivitis of varying severity is nearly universal in children and adolescents.1-19 These studies also indicate that the prevalence of destructive forms of periodontal disease is lower in young individuals than in adults. Epidemiologic surveys in young individuals have been performed in many parts of the world and among individuals with a widely varied background. For the most part, these surveys indicated that loss of periodontal attachment and supporting bone is relatively uncommon in the young but that the incidence increases in adolescents aged 12 to 17 when compared to children aged 5 to 11.15-22 In general, in the United States, epidemiologic studies indicate that the prevalence of severe attachment loss on multiple teeth among children and young adults is approximately 0.2% to 0.5%.23 Despite this low prevalence, children and adolescents should receive periodic periodontal evaluation as a component of routine dental visits. On October 30-November 2, 1999, the American Academy of Periodontology assembled an International Workshop for a Classification of Periodontal Diseases and Conditions, which resulted in a new classification.24 Periodontal diseases discussed here will reflect the new classification system. Clinically distinct periodontal infections that can affect young individuals include: 1) dental plaque-induced gingival diseases; 2) chronic periodontitis; 3) aggressive periodontitis; 4) periodontitis as a manifestation of systemic diseases; and 5) necrotizing periodontal diseases.
Dental plaque-induced gingival diseases Gingivitis Associated with Dental Plaque Only and Gingival Diseases Modified by Systemic Factors Associated with the Endocrine System Gingivitis characterized by the presence of gingival inflammation without detectable loss of bone or clinical attachment is common in children.1-19,25 Although the microbiology of this disease has not been completely characterized, increased subgingival levels of Actinomyces sp., Capnocytophaga sp., Leptotrichia sp., and Selenomonas sp. have been found in experimental gingivitis in
children when compared to gingivitis in adults. These species may therefore be important in its etiology and pathogenesis.26,27 Normal and abnormal fluctuation in hormone levels, including changes in gonadotrophic hormone levels during the onset of puberty, can modify the gingival inflammatory response to dental plaque.28,29 Similarly, alterations in insulin levels in patients with diabetes can affect gingival health.28,29 In both situations, there is an increased inflammatory response to plaque.28,29 However, the gingival condition usually responds to thorough removal of bacterial deposits and improved daily oral hygiene.28,29
Periodontitis Aggressive Periodontitis, Chronic Periodontitis, and Periodontitis as a Manifestation of Systemic Diseases Children and adolescents can have any of the several forms of periodontitis as described in the proceedings of the 1999 International Workshop for a Classification of Periodontal Diseases and Conditions (aggressive periodontitis, chronic periodontitis, and periodontitis as a manifestation of systemic diseases). However, chronic periodontitis is more common in adults, while aggressive periodontitis may be more common in children and adolescents.24 The primary features of aggressive periodontitis include a history of rapid attachment and bone loss with familial aggregation. Secondary features include phagocyte abnormalities and a hyperresponsive macrophage phenotype.24 Aggressive periodontitis can be localized or generalized. Localized aggressive periodontitis (LAgP) patients have interproximal attachment loss on at least two permanent first molars and incisors, with attachment loss on no more than two teeth other than first molars and incisors. Generalized aggressive periodontitis (GAgP) patients exhibit generalized interproximal attachment loss including at least three teeth that are not first molars and incisors. In young individuals, the onset of these diseases is often circumpubertal. Some investigators have found that the localized form appears to be self-limiting,30 while others suggest that it is not.20 Some patients initially diagnosed as having
Copyright© 2004 by the American Academy of Periodontology; all rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, or otherwise without written permission of the publisher. Periodontal diseases of children and adolescents. J Periodontol 2003;74:1696-704. Available through the American Academy of Periodontology, Department of Scientific, Clinical and Educational Affairs, 737 North Michigan Avenue, #800, Chicago, IL 60611-2690, Phone: 312-787-5518, Fax: 312-787-3670. Approved by the American Academy of Periodontology Board of Trustees, April 1991.
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LAgP were found to have GAgP or to be periodontally healthy at a 6-year follow-up exam.31,32 LAgP occurs in children and adolescents without clinical evidence of systemic disease and is characterized by the severe loss of alveolar bone around permanent teeth.31 Frequently, the disease is localized to the permanent first molars and incisors. However, some retrospective data obtained from LAgP patients suggest that bone loss around the primary teeth can be an early finding in the disease.33 Linkage studies of the Brandywine population (a segregated group of people in Maryland that represents a relatively closed gene pool) have found a gene conferring increased risk for LAgP on chromosome 4.34 Subsequent linkage studies of African American and Caucasian families did not confirm linkage to this locus, suggesting that there may be genetic and/or etiologic heterogeneity for aggressive periodontitis.35-37 Reported estimates of the prevalence of LAgP in geographically diverse adolescent populations range from 0.1% to 15%.23,3335,37-42 Most reports suggest a low prevalence (0.2%), which is markedly greater in African American populations (2.5%). Many reports suggest that patients with LAgP generally form very little supragingival dental plaque or calculus.31,43 In contrast, other investigators find plaque and calculus at levels similar to other periodontal diseases.44,45 Bacteria of probable etiologic importance include highly virulent strains of Actinobacillus actinomycetemcomitans in combination with Bacteroides-like species.46-49 In some populations, Eubacterium sp. have been associated with the presence of LAgP.50,51 To date, however, no single species is found in all cases of LAgP.52 A variety of functional defects have been reported in neutrophils from patients with LAgP.53-55 These include anomalies of chemotaxis,56-58 phagocytosis,59,60 bactericidal activity,61 superoxide production,62-66 FcgIIIB (CD16) expression,67 leukotriene B4 generation,68,69 and Ca2+–channel and second messenger activation.70-75 The defect in chemotaxis is thought to be an intrinsic defect by some investigators56-58 and an induced defect by others.76 The influence of these functional defects on the susceptibility of individuals to LAgP is unknown, but it is possible that they play a role in the clinical course of disease in some patients. Indeed, in some cases exhibiting phagocyte abnormalities, neutrophil defects may still be present after treatment.77 Molecular markers of LAgP can include an abnormally low number of chemoattractant receptors78-81 and an abnormally low amount of another cell surface glycoprotein designated GP110.82,83 Adherence receptors on neutrophils and monocytes, such as LFA-1 and Mac-1, are normal in LAgP patients.82,83 GAgP, often considered to be a disease of adolescents and young adults, can begin at any age and often affects the entire dentition.84,85 Individuals with GAgP exhibit marked periodontal inflammation and have heavy accumulations of plaque and calculus.84 In the United States, the reported prevalence of GAgP in adolescents (14 to 17 years of age) is 0.13%.23 Subgingival sites from affected teeth harbor high percentages of non-motile, facultatively anaerobic, Gram-negative rods including Porphyromonas gingivalis.86,87 In one report, the levels of P. gingivalis and Treponema denticola were significantly higher in
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GAgP and LAgP patients compared to matched controls, with GAgP patients having the highest levels.88 Neutrophils from patients with GAgP frequently exhibit suppressed chemotaxis as observed in LAgP77,87 with a concomitant reduction in GP-110. This suggests a relationship between the two variants of aggressive periodontitis.82,83 Alterations in immunologic factors such as immunoglobulins are known to be present in aggressive periodontitis. Immunoglobulins appear to be influenced by both genetic and environmental factors and have important protective diseaselimiting effects in aggressive periodontitis patients.89-93 Human IgG antibody molecules (immunoglobulin G) are categorized into four subclasses designated as IgG1-4. Most of the antibody reactive with A. actinomycetemcomitans is specific for high molecular weight lipopolysaccharide and is of the IgG2 subclass. This antibody response appears to be protective, as early-onset periodontitis patients having high concentrations of antibody reactive with A. actinomycetemcomitans lipopolysaccharide have significantly less attachment loss (a measure of disease severity) than patients who lack this antibody.89,90 Overall levels of IgG2 in serum are under genetic control.91 These levels have also been shown to be affected by periodontal diagnosis (LAgP patients have very high levels), race (African Americans have higher levels than Caucasians), and smoking (smokers have lower levels of IgG2, with notable exceptions in some patient groups).91,92,94,95 These factors also influence specific antibody responses to A. actinomycetemcomitans.91-93,95 Thus, the protective antibody response afforded by IgG2, as well as the clinical manifestations of aggressive periodontitis, is modified by patients’ genetic background as well as environmental factors such as smoking and bacterial infection.89,91-93,95,96 Successful treatment of aggressive periodontitis depends on early diagnosis, directing therapy against the infecting microorganisms and providing an environment for healing that is free of infection.97 While there is some disagreement among individual studies regarding treatment of LAgP, most authors recommend a combination of surgical or non-surgical root debridement in conjunction with antimicrobial (antibiotic) therapy.47,98 These findings are supported by other work in which meticulous and repeated mechanical therapy with antibiotics proved to be sufficient to arrest most cases of LAgP.99 However, surgical treat ment may be effective in eliminating A. actinomycetemcomitans without the use of antibiotics.100 In a study of 25 deep periodontal lesions (probing depths 5 to 11 mm) in young LAgP patients, scaling and root planing alone were ineffective for the elimination of A. actinomycetemcomitans, while surgical therapy was effective.100 It is not known, however, if A. actinomycetemcomitans is the only organism involved in disease pathogenesis. The majority of reports suggest that the use of antibiotics is usually beneficial in the treatment of LAgP. Two reports described using antibiotics exclusively.97,101 In both reports, LAgP patients attained significant clinical attachment gain when assessed after 12 months with tetracycline therapy alone. Most reports in the past 10 years, however, have recommended combination therapy using antibiotics and surgical or
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non-surgical root debridement as the optimal treatment for LAgP.98,102-116 The most successful antibiotics reported are the tetracyclines, sometimes prescribed sequentially with metronidazole.103,117,118 Metronidazole in combination with amoxicillin has also been utilized, especially where tetracyline-resistant A. actinomycetemcomitans are present.111 A single randomized control study in which oral penicillin was used reported that therapy was successful with or without the antibiotic.119 While the use of antibiotics in conjunction with surgical or non-surgical root debridement appears to be quite effective for the treatment of LAgP, GAgP does not always respond well to conventional mechanical therapy or to antibiotics commonly used to treat periodontitis.30,118,120 Alternative antibiotics may be required, based upon the character of the pathogenic flora. In GAgP patients who have failed to respond to standard periodontal therapy, laboratory tests of plaque samples may identify periodontal pathogens that are resistant to antibiotics typically used to treat periodontitis.103 It has been suggested that follow-up tests after additional antibiotic or other therapy is provided may be helpful in confirming elimination of targeted pathogenic organisms.103 Chronic periodontitis is most prevalent in adults, but can occur in children and adolescents. It can be localized (less than 30% of the dentition affected) or generalized (greater than 30% of the dentition affected) and is characterized by a slow to moderate rate of progression that may include periods of rapid destruction. Furthermore, the severity of disease can be mild (1 to 2 mm clinical attachment loss), moderate (3 to 4 mm clinical attachment loss), or severe (≥5 mm clinical attachment loss). Children and young adults with this form of disease were previously studied along with patients having LAgP and GAgP. Therefore, published data are lacking for this group. In patients with one of several systemic diseases that predispose to highly destructive disease of the primary teeth, the diagnosis is periodontitis as a manifestation of systemic disease. As with adults, periodontitis associated with systemic diseases occurs in children and adolescents. Such diseases include PapillonLefévre syndrome,121-125 cyclic neutropenia,126-130 agranulocytosis,131,132 Down syndrome,133-135 hypophosphatasia,136 and leukocyte adherence deficiency.137,138 It is probable that defects in neutrophil and immune cell function associated with these diseases play an important role in increased susceptibility to periodontitis and other infections. In Down’s syndrome, for example, the amount of periodontal destruction has been shown to be positively correlated with the severity of the neutrophil chemotaxis defect.135 In some cases, specific genes have been associated with these diseases. Examples include the cathepsin C gene and Papillon-Lefévre syndrome139-141 and the tissue nonspecific alkaline phosphatase gene and hypophosphatasia.136 The consensus report of the 1999 Workshop specifically excluded diabetes-associated periodontitis as a specific form of periodontitis associated with systemic disease. Participants concluded that diabetes is a significant modifier of all forms of periodontitis. In a survey of 263 type 1 diabetics, 11 to 18 years of age, 10% were found to have overt periodontitis often
localized to first molars and incisors, although periodontitis was also found in a generalized pattern.142 Affected subgingival sites harbored A. actinomycetemcomitans and Capnocytophaga sp.143 Periodontitis as a manifestation of systemic disease in children is a rare disease that often begins between the time of eruption of the primary teeth up to the age of 4 or 5.144,145 The disease occurs in localized and generalized forms. In the localized form, affected sites exhibit rapid bone loss and minimal gingival inflammation.144 In the generalized form, there is rapid bone loss around nearly all teeth and marked gingival inflammation. Neutrophils from some children with a clinical diagnosis of periodontitis as a manifestation of systemic disease have abnormalities in a cell surface glycoprotein (LFA-1, leukocyte functional antigen–1, also known as CD11, and Mac-1). The neutrophils in these patients having LAD (leukocyte adhesion deficiency) are likely to have a decreased ability to move from the circulation to sites of inflammation and infection.137 Affected sites harbor elevated percentages of putative periodontal pathogens such as A. actinomycetemcomitans, Prevotella intermedia, Eikenella corrodens, and Capnocytophaga sputigena.146,147 Treatment of periodontitis as a manifestation of systemic disease in children is similar to the treatment of localized and generalized aggressive periodontitis in the permanent dentition and has been reported to include surgical or non-surgical mechanical debridement and antimicrobial therapy.124,127-130,132, 134,142,144 Localized lesions have been treated successfully with this approach,144,145 but the degree of predictable success in managing generalized periodontitis is low when systemic diseases are contributing factors.144,145 In many cases, the affected teeth had to be extracted.138,144,145
Necrotizing periodontal diseases Necrotizing periodontal diseases (NPD) occur with varying but low frequency (less than 1%) in North American and European children. It is seen with greater frequency (2% to 5%) in certain populations of children and adolescents from developing areas of Africa, Asia, and South America.148-150 The two most significant findings used in the diagnosis of NPD are the presence of interproximal necrosis and ulceration and the rapid onset of gingival pain. Patients with NPD can often be febrile. Necrotizing ulcerative gingivitis/periodontitis sites harbor high levels of spirochetes and P. intermedia,151 and invasion of the tissues by spirochetes has been shown to occur.152 Factors that predispose children to NPD include viral infections (including HIV), malnutrition, emotional stress, lack of sleep, and a variety of systemic diseases.148150,153 Treatment involves mechanical debridement, oral hygiene instruction, and careful follow-up.154-156 Debridement with ultrasonics has been shown to be particularly effective and results in a rapid decrease in symptoms.157 If the patient is febrile, antibiotics may be an important adjunct to therapy. Metronidazole and penicillin have been suggested as drugs of choice.151,158
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Summary Children and adolescents are subject to several periodontal diseases. Although there is a much lower prevalence of destructive periodontal diseases in children than in adults, children can develop severe forms of periodontitis.23 In some cases, this destructive disease is a manifestation of a known underlying systemic disease. In other young patients, the underlying cause for increased susceptibility and early onset of disease is unknown. These diseases are often familial, suggesting a genetic predisposition for aggressive disease. Current modalities for managing periodontal diseases of children and adolescents may include antibiotic therapy in combination with non-surgical and/or surgical therapy. Since early diagnosis ensures the greatest chance for successful treatment,97 it is important that children receive a periodontal examination as part of their routine dental visits.
Acknowlegments The primary author for this paper is Dr. Joseph V. Califano. Members of the 2002-2003 Research, Science and Therapy Committee include: Drs. Terry D. Rees, Chair; Christopher Cutler; Petros Damoulis; Joseph Fiorellini; William Giannobile; Henry Greenwell; Angelo Mariotti; Steven Offenbacher; Leslie Salkin; Brian Nicoll, Board Liaison; Robert J. Genco, Consultant.
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11. Blankenstein R, Murray JJ, Lind OP. Prevalence of chronic periodontitis in 13-15-year-old children. A radiographic study. J Clin Periodontol 1978;5:285-92. 12. Latcham NL, Powell RN, Jago JD, Seymour GJ, Aitken JF. A radiographic study of chronic periodontitis in 15-year-old Queensland children. J Clin Periodontol 1983;10:37-45. 13. Gjermo P, Bellini HT, Santos VP, Martens JG, Ferracyoli JR. Prevalence of bone loss in a group of Brazilian teenagers assessed in bitewing radiographs. J Clin Periodontol 1984;11:104-13. 14. Hansen BF, Gjermo P, Bergwitz-Larsen KR. Periodontal bone loss in 15-year-old Norwegians. J Clin Periodontol 1984;11:125-31. 15. Wolfe MD, Carlos JP. Periodontal disease in adolescents: Epidemiologic findings in Navajo Indians. Community Dent Oral Epidemiol 1987;15:33-40. 16. Wei SJY, Yang S, Barmes DE. Needs and implementation of preventive dentistry in China. Community Dent Oral Epidemiol 1986;14:19-23. 17. Durward CS, Wright FA. The dental health of IndoChinese and Australian-born adolescents. Austr Dent J 1989;34(3):233-9. 18. Miyazaki H, Hanada N, Andoh MI, et al. Periodontal disease prevalence in different age groups in Japan as assessed according to the CPITN. Community Dent Oral Epidemiol 1989;17:71-4. 19. Pilot T, Barmes DE, Leclercq MH, McCombie BJ, Sardo IJ. Periodontal conditions in adolescents, 15-19 years of age: An overview of CPITN data in the WHO Global Oral Data Bank. Community Dent Oral Epidemiol 1987;15: 336-8. 20. Brown LJ, Albandar JM, Brunelle JA, Löe H. Early onset periodontitis: Progression of attachment loss during 6 years. J Periodontol 1996;67:968-75. 21. Oliver RC, Brown LJ, Löe H. Periodontal diseases in the United States population. J Periodontol 1998;69:269-78. 22. Perry DA, Newman MG. Occurrence of periodontitis in an urban adolescent population. J Periodontol 1990;61:185-8. 23. Löe H, Brown LJ. Early onset periodontitis in the United States of America. J Periodontol 1991;62:608-16. 24. Armitage G. Development of a classification system for periodontal diseases and conditions. Ann Periodontol 1999;4:1-6. 25. Arnlaugsson S, Magnusson TE. Prevalence of gingivitis in 6-year-olds in Reykjavik, Iceland. Acta Odontol Scand 1996;54:247-50. 26. Moore W, Holdeman L, Smibert R, et al. Bacteriology of experimental gingivitis in children. Infect Immun 1984; 46:1-6. 27. Slots J, Moenbo D, Langebaek J, Frandsen A. Microbiota of gingivitis in man. Scand J Dent 1978;86:174-81. 28. Nakagawa S, Fujii H, Machida Y, Okuda K. A longitudinal study from prepuberty to puberty of gingivitis. Correlation between the occurrence of Prevotella intermedia and sex hormones. J Clin Periodontol 1994;21:658-65.
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29. De Pommereau V, Dargent-Par C, Robert JJ, Brion M. Periodontal status in insulin-dependent diabetic adolescents. J Clin Periodontol 1992;19:628-32. 30. Gunsolley JC, Califano JV, Koertge TE, Burmeister JA, Cooper LC, Schenkein HA. Longitudinal assessment of early onset periodontitis. J Periodontol 1995;66:321-8. 31. Baer PN. The case for periodontosis as a clinical entity. J Periodontol 1971;42:516-20. 32. Albandar JM, Brown LJ, Genco RJ, Löe H. Clinical classification of periodontitis in adolescents and young adults. J Periodontol 1997;68:545-55. 33. Sjödin B, Matsson L, Unell L, Egelberg J. Marginal bone loss in the primary dentition of patients with juvenile periodontitis. J Clin Periodontol 1993;20:32-6. 34. Boughman JA, Halloran SL, Roulston D, et al. An autosomal dominant form of juvenile periodontitis: Its localization to chromosome 4 and linkage to dentinogenesis imperfecta and Gc. J Craniofac Genet Dev Biol 1986;6: 341-50. 35. Marazita ML, Burmeister JA, Gunsolley JC, Koertge TE, Lake K, Schenkein HA. Evidence for autosomal dominant inheritance and race-specific heterogeneity in early onset periodontitis. J Periodontol 1994;65:623-30. 36. Hart TC, Kornman KS. Genetic factors in the pathogenesis of periodontitis. Periodontol 2000 1997;14:202-15. 37. Hart TC, Marazita ML, McCanna KM, Schenkein HA, Diehl SR. Reevaluation of the chromosome 4q candidate region for early onset periodontitis. Hum Genet 1993;91:416-22. 38. Saxén L. Juvenile periodontitis. J Clin Periodontol 1980; 7:1-19. 39. Saxén L. Prevalence of juvenile periodontitis in Finland. J Clin Periodontol 1980;7:177-86. 40. Kronauer E, Borsa G, Lang NP. Prevalence of incipient juvenile periodontitis at age 16 years in Switzerland. J Clin Periodontol 1986;13:103-8. 41. Harley AF, Floyd PD. Prevalence of juvenile periodontitis in schoolchildren in Lagos, Nigeria. Community Dent Oral Epidemiol 1988;16:299-301. 42. Neely AL. Prevalence of juvenile periodontitis in a circumpubertal population. J Clin Periodontol 1992;19:367-72. 43. Butler J. A familial pattern of juvenile periodontitis (periodontosis) J Periodontol 1969;40:115-8. 44. Albandar JM, Brown LJ, Brunelle JA, Löe H. Gingival state and dental calculus in early-onset periodontitis. J Periodontol 1996;67:953-9. 45. Burmeister JA, Best AM, Palcanis KG, Caine FA, Ranney RR. Localized juvenile periodontitis and generalized severe periodontitis: Clinical findings. J Clin Periodontol 1984;11:18192. 46. Haraszthy V, Hariharan G, Tinoco E, et al. Evidence for the role of highly leukotoxic Actinobacillus actinomycetemcomitans in the pathogenesis of localized and other forms of early-onset periodontitis J Periodontol 2000;71:912-22. 47. Kornman KS, Robertson PB. Clinical and microbiological evaluation of therapy for juvenile periodontitis. J Periodontol 1985;56:443-6.
48. Genco RJ, Zambon JJ, Christersson LA. The origin of periodontal infections. Adv Dent Res 1988;2:245-59. 49. Zambon JJ. Actinobacillus actinomycetemcomitans in human periodontal disease. J Clin Periodontol 1985;12:1-20. 50. Moore WEC, Holdeman LV, Cato EP, et al. Comparative bacteriology of juvenile periodontitis. Infect Immun 1985;48:507-19. 51. Han N, Xiao X, Zhang L, et al. Bacteriological study of juvenile periodontitis in China. J Periodont Res 1991;26: 409-14. 52. Moore W, Moore L. The bacteria of periodontal diseases. Periodontol 2000 1994;5:66-77. 53. Daniel MA, Van Dyke TE. Alterations in phagocyte function and periodontal infection. J Periodontol 1996; 67:1070-5. 54. Dennison DK, Van Dyke TE. The acute inflammatory response and the role of phagocytic cells in periodontal health and disease. Periodontol 2000 1997;14:54-78. 55. Van Dyke TE, Lester MA, Shapira L. The role of host response in periodontal disease progression: Implications for future treatment strategies. J Periodontol 1993;64: 792-806. 56. Genco RJ, Van Dyke TE, Levine MJ, Nelson RD, Wilson ME. Molecular factors influencing neutrophil defects in periodontal disease. J Dent Res 1986;65:1379-91. 57. Van Dyke TE, Levine MJ, Genco RJ. Neutrophil function and oral disease. J Oral Pathol 1985;14:95-120. 58. Van Dyke TE, Hoop GA. Neutrophil function and oral disease. Crit Rev Oral Biol Med 1990;1:117-33. 59. Van Dyke TE, Zinney W, Winkel K, Taufig A, Offenbacher S, Arnold RR. Neutrophil function in localized juvenile periodontitis: Phagocytosis, superoxide production and specific granule release. J Periodontol 1986;57:703-8. 60. Cogen RB, Roseman JM, Al-Joburi W, et al. Host factors in juvenile periodontitis J Dent Res 1986;65:394-9. 61. Kalmar JR, Arnold RR, Van Dyke TE. Direct interaction of Actinobacillus actinomycetemcomitans with normal and defective (LJP) neutrophils. J Periodont Res 1987; 22:179-81. 62. Å sman B, Bergström K, Wijkaner P, Lockowandt B. Influence of plasma components on luminol-enhanced chemiluminescence from peripheral granulocytes in juvenile periodontitis. J Clin Periodontol 1986;13:850-5. 63. Åsman B, Bergström K, Wijkander P, Lockowandt B. Peripheral PMN cell activity in relation to treatment of juvenile periodontitis. Scand J Dent Res 1988;96:418-20. 64. Zafiropoulos GG, Flores-de-Jacoby L, Czerch W, Kolb G, Markitzu A, Havemann K. Neutrophil function in patients with localized juvenile periodontitis and rapidly progressive periodontitis. J Biol Buccale 1988;16:151-6. 65. Zafiropoulos GG, Flores-de-Jacoby L, Plate VM, Eckle I, Kolb G. Polymorphonuclear neutrophil chemiluminescence in periodontal disease. J Clin Periodontol 1991;18:634-9. 66. Shapira L, Borinski R, Sela MN, Soskolne A. Superoxide formation and chemiluminescence of peripheral polymorphonuclear leukocytes in rapidly progressive periodontitis patients. J Clin Periodontol 1991;18:44-8. endorsements
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67. Nemoto E, Nakamura M, Shoji S, Horiuchi H. Circulating promyelocytes and low levels of CD16 expression on polymorphonuclear leukocytes accompany early onset periodontitis. Infect Immun 1997;65:3906-12. 68. Offenbacher S, Scott SS, Odle BM, Wilson-Burrows C, Van Dyke TE. Depressed leukotriene B4 chemotactic response of neutrophils from localized juvenile periodontitis patients. J Periodontol 1987;58:602-6. 69. Van Dyke TE, Offenbacher S, Kalmar J, Arnold RR. Neutrophil defects and host parasite interactions in the pathogenesis of localized juvenile periodontitis. Adv Dent Res 1988; 2:354-8. 70. Agarwal S, Reynolds MA, Duckett LD, Suzuki JB. Altered free cytosolic calcium changes and neutrophil chemotaxis in patients with juvenile periodontitis. Adv Dent Res 1989;24:149-54. 71. Daniel MA, McDonald G, Offenbacher S, Van Dyke TE. Defective chemotaxis and calcium response in localized juvenile periodontitis neutrophils. J Periodontol 1993;64: 617-21. 72. Hurttia HM, Pelto LM, Leino L. Evidence of an association between functional abnormalities and defective diacylglycerol kinase activity in peripheral blood neutrophils from patients with localized juvenile periodontitis. J Periodont Res 1997;32:401-7. 73. Kurihara H, Murayama Y, Warbington ML, Champagne C, Van Dyke TE. Depressed protein kinase C (PKC) activity of neutrophils in localized juvenile periodontitis. Infect Immun 1993;61:3137-42. 74. Leino L, Hurttia H, Peltonen E. Diacylglycerol in peri-pheral blood neutrophils from patients with localized juvenile periodontitis. J Periodont Res 1994;29:334-8. 75. Tyagi SR, Uhlinger DJ, Lambeth JD, Champagne C, Van Dyke TE. Altered diacylglycerol level and metabolism in localized juvenile periodontitis neutrophils. Infect Immun 1992;60:2481-7. 76. Agarwal S, Suzuki J. Altered neutrophil function in localized juvenile periodontitis: Intrinsic cellular defect or effect of immune mediators? J Periodont Res 1991; 26:276-8. 77. Van Dyke TE, Levine MJ, Genco RJ. Periodontal diseases and neutrophil abnormalities. In: Genco RJ, Mergenhagen SE, eds. Host-Parasite Interactions in Periodontal Diseases. Washington, DC: American Society for Microbiology; 1982:235-45. 78. Van Dyke T. The role of neutrophils in host defense to periodontal infections. In: Hamada S, Holt S, McGhee J, eds. Periodontal Disease: Pathogens and Host Immune Res-ponses. Tokyo: Quintessence Publishing Co; 1991:251-61. 79. Van Dyke T, Levine M, Tabak L, Genco R. Reduced chemotactic peptide binding in juvenile periodontitis: A model for neutrophil function. Biochem Biophys Res Commun 1981;100:1278-84. 80. Van Dyke T, Levine M, Tabak L, Genco R. Juvenile periodontitis as a model for neutrophil function: Reduced binding of complement chemotactic fragment, C5a. J Dent Res 1983;62:870-2. 282
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81. Van Dyke T, Schweinebraten M, Cianciola U, Offenbacher S, Genco R. Neutrophil chemotaxis in families with localized juvenile periodontitis. J Periodont Res 1985;20:503-14. 82. Van Dyke TE, Wilson-Burrows C, Offenbacher S, Hensen P. Association of an abnormality of neutrophil chemotaxis in human periodontal disease with a cell surface protein. Infect Immun 1987;55:2262-7. 83. Van Dyke TE, Warbington M, Gardner M, Offenbacher S. Neutrophil surface protein markers as indicators of defective chemotaxis in LJP. J Periodontol 1990;61:180-4. 84. Page RC, Altman LC, Ebersole JL, et al. Rapidly progressive periodontitis: A distinct clinical condition. J Periodontol 1983;54:197-209. 85. Spektor MD, Vandesteen GE, Page RC. Clinical studies of one family manifesting rapidly progressive, juvenile and prepubertal periodontitis. J Periodontol 1985;56:93-101. 86. Slots J. Importance of black-pigmented Bacteroides in human periodontal disease. In: Genco RJ, Mergenhagen SE, eds. Host-Parasite Interactions in Periodontal Diseases. Washington, DC: American Society for Microbiology; 1982:27-45. 87. Wilson ME, Zambon JJ, Suzuki JB, Genco RJ. Generalized juvenile periodontitis, defective neutrophil chemotaxis and Bacteroides gingivalis in a 13-year-old female. J Periodontol 1985;56:457-63. 88. Albandar JM, Brown LJ, Le H. Putative periodontal pathogens in subgingival plaque of young adults with and without early-onset periodontitis. J Periodontol 1997;68: 973-81. 89. Califano JV, Gunsolley JC, Nakashima K, Schenkein HA, Wilson ME, Tew JG. Influence of anti-Actinobacillus actinomycetemcomitans Y4 (serotype b) lipopolysaccharide on severity of generalized early-onset periodontitis. Infect Immun 1996;64:3908-10. 90. Califano JV, Pace BE, Gunsolley JC, Schenkein HA, Lally ET, Tew JG. Antibody reactive with Actinobacillus actinomycetemcomitans leukotoxin in early-onset periodontitis patients. Oral Microbiol Immunol 1997;12:20-6. 91. Marazita ML, Lu H, Cooper ME, et al. Genetic segregation analyses of serum IgG2 levels. Am J Hum Genet 1996; 58:1042-9. 92. Quinn SM, Zhang JB, Gunsolley JC, Schenkein JG, Schenkein HA, Tew JG. Influence of smoking and race on immunoglobulin G subclass concentrations in early-onset periodontitis patients. Infect Immun 1996;64:2500-5. 93. Tangada SD, Califano JV, Nakashima K, et al. The effect of smoking on serum IgG2 reactive with Actinobacillus actinomycetemcomitans in early-onset periodontitis patients. J Periodontol 1997;68:842-50. 94. Lu H, Wang M, Gunsolley JC, Schenkein HA, Tew JG. Serum immunoglobulin G subclass concentrations in periodontally healthy and diseased individuals. Infect Immun 1994;62:1677-82. 95. Quinn SM, Zhang JB, Gunsolley JC, Schenkein HA, Tew JG. The influence of smoking and race on adult periodontitis and serum IgG2 levels. J Periodontol 1998;69:171-7.
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96. Schenkein HA, Gunsolley JC, Koertge TE, Schenkein JG, Tew JG. Smoking and its effects on early-onset periodontitis. J Am Dent Assoc 1995;126:1107-13. 97. Novak MJ, Stamatelakys C, Adair SM. Resolution of early lesions of juvenile periodontitis with tetracycline therapy alone: Long-term observations of 4 cases. J Periodontol 1991;62:628-33. Erratum 1992;63:148. 98. Mandell RL, Socranksy SS. Microbiological and clinical effects of surgery plus doxycycline on juvenile periodontitis. J Periodontol 1988;59:373-9. 99. Gjermo P. Chemotherapy in juvenile periodontitis. J Clin Periodontol 1986;13:982-6. 100. Christersson LA, Slots J, Rosling BG, Genco RJ. Microbiological and clinical effects of surgical treatment of localized juvenile periodontitis. J Clin Periodontol 1985; 12:465-76. 101. Christersson LA, Zambon JJ. Suppression of Actinobacillus actinomycetemcomitans in localized juvenile periodontitis with systemic tetracycline. J Clin Periodontol 1993; 20:395-401. 1 02. Seymour RA, Heasman PA. Pharmacological control of periodontal disease. II. Antimicrobial agents. J Dent 1995;23:5-14. 103. van Winkelhoff AJ, Rams TE, Slots J. Systemic antibiotic therapy in periodontics. Periodontol 2000 1996;10:45-78. 104. Palmer RM, Watts TL, Wilson RF. A double-blind trial of tetracycline in the management of early onset periodontitis. J Clin Periodontol 1996;23:670-4. 105. Saxén L, Asikainen S. Metronidazole in the treatment of localized juvenile periodontitis. J Clin Periodontol 1993; 20:166-71. 106. Mandell RL, Tripodi LS, Savitt E, Goodson JM, Socransky SS. The effect of treatment on Actinobacillus actinomycetemcomitans in localized juvenile periodontitis. J Periodontol 1986;57:94-9. 107. Zambon JJ, Christersson LA, Genco RJ. Diagnosis and treatment of localized juvenile periodontitis. J Am Dent Assoc 1986;113:295-9. 108. Sterrett JD. Atypical localized juvenile periodontitis. A case report and review of current treatment considerations. J Periodontol 1986;57:486-91. 109. Levine RA. Localized juvenile periodontitis: Historical background and therapy. Compendium Continuing Educ Dent 1986;7:552-6. 110. Krill DB, Fry HR. Treatment of localized juvenile periodontitis (periodontosis). A review. J Periodontol 1987;58:1-8. 111. van Winkelhoff AJ, Rodenburg JP, Goene RJ, Abbas F, Winkel EG, de Graaff J. Metronidazole plus amoxycillin in the treatment of Actinobacillus actinomycetemcomitansassociated periodontitis. J Clin Periodontol 1989;16:128-31. 112. Saxon L, Asikainen SKA, Kaneroo A, Kari K, Jousimies- Somer H. The long-term efficacy of systemic doxycycline medication in the treatment of localized juvenile periodontitis. Arch Oral Biol 1990;35(suppl):227S-9S.
113. Muller HP, Lange DE, Muller RF. A 2-year study of adjunctive minocycline-HCl in Actinobacillus actinomycetemcomitans- associated periodontitis. J Periodontol 1993; 64:509-19. 114. Donly KJ, Ashkenazi M. Juvenile periodontitis: A review of pathogenesis, diagnosis, and treatment. J Clin Pediatr Dent 1992;16:73-8. 115. Gordon JM, Walker CB. Current status of systemic antibiotic usage in destructive periodontal disease. J Periodontol 1993;64:760-71. 116. Wisner-Lynch A, Giannobile WV. Current concepts in juvenile periodontitis. Curr Opin Periodontol 1993;28-42. 117. Aitken S, Birek P, Kulkarni G, Lee W, McCulloch C. Serial doxycyline and metronidazole in prevention of recurrent periodontitis in high risk patients. J Periodontol 1992; 63:87-92. 118. van Winkelhoff AJ, de Graaff J. Microbiology in the management of destructive periodontal disease. J Clin Periodontol 1991;18:406-10. 119. Kunihira DM, Caine FA, Palcanis KG, Best AM, Ranney RR. A clinical trial of phenoxymethyl penicillin for adjunctive treatment of juvenile periodontitis. J Periodontol 1985;56:352-8. 120. Asikainen S, Jousimies-Somer H, Kanervo A, Saxén L. The immediate efficacy of adjunctive doxycycline treatment of localized juvenile periodontitis. Arch Oral Biol 1990;35(suppl):231S-4S. 121. Hart TC, Stabholz A, Meyle J, et al. Genetic studies of syndromes with severe periodontitis and palmoplantar hyperkeratosis. J Periodont Res 1997;32:81-9. 122. Gorlin RJ, Sedano H, Anderson V. The syndrome palmarplantar hyperkeratosis and premature periodontal destruction of teeth. A clinical and genetic analysis of the Papillon-Lefévre syndrome J Pediatr 1964;65:895-908. 123. Schroeder HE, Segar RA, Keller HU, Rateitschak-Plüss EM. Behavior of neutrophilic granulocytes in a case of Papillon-Lefévre syndrome. J Clin Periodontol 1983;10: 618-35. 1 24. Rateitschak-Plüss EM, Schroeder HE. History of periodontitis in a child with Papillon-Lefévre syndrome. A case report. J Periodontol 1984;55:35-46. 1 25. Tinanoff N, Tanzer JM, Kornman KS, Maderazo EG. Treatment of the periodontal component of Papillon- Lefévre syndrome. J Clin Periodontol 1986;13:6-10. 126. Andrews RG, Benjamin S, Shore N, Canter S. Chronic benign neutropenia of childhood with associated oral manifestations. Oral Surg Oral Med Oral Pathol 1965;20: 719-25. 127. Deasy MJ, Vogel RI, Macedo-Sobrinho B, Gertzman G, Simon B. Familial benign chronic neutropenia associated with periodontal disease. A case report. J Periodontol 1980;51:206-10. 128. Baehini PC, Payot T, Tsai CC, Cimasoni G. Periodontal status associated with chronic neutropenia. J Clin Peri-odontol 1983;10:222-30.
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129. Prichard JF, Ferguson DM, Windmiller J, Hurt WC. Prepubertal periodontitis affecting the deciduous and permanent dentition in a patient with cyclic neutropenia. J Periodontol 1984;55:114-22. 130. Kirstilä V, Sewón L, Laine J. Periodontal disease in three siblings with familial neutropenia. J Periodontol 1993; 64:566-70. 131. Davey KW, Konchak PA. Agranulocytosis. Oral Surg Oral Med Oral Pathol 1969;28:166-71. 132. Awbrey JJ, Hibbard ED. Cogenital agranulocytosis. Oral Surg Oral Med Oral Pathol 1973;35:526-30. 133. Cohen MM, Winer RA, Schwartz S, Shklar G. Oral aspects of mongolism. I. Periodontal disease in mongolism. Oral Surg Oral Med Oral Pathol 1961;14:92-107. 134. Orner G. Periodontal disease among children with Down syndrome and their siblings. J Dent Res 1976;55:778-82. 135. Izumi Y, Sugiyama S, Shinozuki O, Yamazaki T, Ohyama T, Ishikawa I. Defective neutrophil chemotaxis in Down syndrome patients and its relationship to periodontal destruction. J Periodontol 1989;60:238-42. 136. Watanabe H, Goseki-Sone M, Iimura T, Oida S, Orimo H, Ishikawa I. Molecular diagnosis of hypophosphatasia with severe periodontitis. J Periodontol 1999;70:688-91. 137. Page RC, Beatty P, Waldrop TC. Molecular basis for the functional abnormality in neutrophils from patients with generalized prepubertal periodontitis. J Periodont Res 1987;22:182-3. 138. Waldrop TC, Anderson DC, Hallmon WW, Schmalstieg FC, Jacobs RL. Periodontal manifestations of the heritable Mac-1, LFA-1 syndrome —Clinical, histopathologic and molecular characteristics. J Periodontol 1987;58:400-16. 139. Hart TC, Hart PS, Bowden DW, et al. Mutations of the cathepsin C gene are responsible for Papillon-Lefévre syndrome. J Med Genet 1999;36:881-7. 140. Hart TC, Hart PS, Michalec MD, et al. Localization of a gene for prepubertal periodontitis to chromosome 11q14 and identification of a cathepsin C gene mutation. J Med Genet 2000;37:95-101. 141. Hart TC, Shapira L. Papillon-Lefévre syndrome. Periodontol 2000, 1994;6:88-100. 142. Cianciola LJ, Park BH, Bruck E, Mosovich L, Genco RJ. Prevalence of periodontal disease in insulin-dependent diabetes mellitus (juvenile diabetes). J Am Dent Assoc 1982;104:653-60. 143. Mashimo PA, Yamamoto Y, Slots J, Park BH, Genco RJ. The periodontal microflora of juvenile diabetics. Culture, immunofluorescence, and serum antibody studies. J Periodontol 1983;54:420-30. 144. Page RC, Bowen T, Altman L, et al. Prepubertal periodontitis. I. Definition of a clinical entity. J Periodontol 1983;54:257-71. 145. Watanabe K. Prepubertal periodontitis: A review of diagnostic criteria, pathogenesis, and differential diagnosis. J Periodont Res 1990;25:31-48.
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146. Sweeney EA, Alcoforado GAP, Nyman S, Slots J. Prevalence and microbiology of localized prepubertal periodontitis. Oral Microbiol Immunol 1987;2:65-70. 147. Delaney DE, Kornman KS. Microbiology of subgingival plaque from children with localized prepubertal periodontitis. Oral Microbiol Immunol 1987;2:71-6. 148. Taiwo JO. Severity of necrotizing ulcerative gingivitis in Nigerian children. Periodontal Clin Investig 1995;17:24-7. 149. Smith BW, Dennison DK, Newland JR. Acquired HIV deficiency syndrome: Implications for the practicing dentist. Va Dent J 1987;63:38-42. 150. Contreras A, Falkler WA Jr., Enwonwu CO, et al. Human Herpes viridae in acute necrotizing ulcerative gingivitis in children in Nigeria. Oral Microbiol Immunol 1997; 12:259-65. 151. Loesche WJ, Syed SA, Laughon BE, Stoll J. The bacteriology of acute necrotizing ulcerative gingivitis. J Periodontol 1982;53:223-30. 152. Listgarten M. Electron microscopic observations on the bacterial flora of acute necrotizing ulcerative gingivitis. J Periodontol 1965;36:328-39. 153. Horning G, Cohen M. Necrotizing ulcerative gingivitis, periodontitis, stomatitis: Clinical staging and predisposing factors. J Periodontol 1995;66:990-8. 154. Enwonwu CO. Epidemiological and biochemical studies of necrotizing ulcerative gingivitis and noma (cancrum oris) in Nigerian children. Arch Oral Biol 1972;17: 1357-71. 155. Jimenez LM, Baer PN. Necrotizing ulcerative gingivitis in children: A 9-year clinical study. J Periodontol 1975; 46:715-20. 156. Pindborg JJ, Bhat M, Devanath KR, Narayana HR, Ramachandra S. Occurrence of acute necrotizing gingivitis in South Indian children. J Periodontol 1966;37:14-9. 157. Fitch H, Bethant H, Alling C, Munns C. Acute necrotizing ulcerative gingivitis. J Periodontol 1963;34:422-6. 158. Johnson B, Engel D. Acute necrotizing ulcerative gingivitis. A review of diagnosis, etiology and treatment. J Periodontol 1986;57:141-50.
Individual copies of this paper may be obtained on the Academy’s website at: “http://www.perio.org”. Members of the American Academy of Periodontology have permission of the Academy, as copyright holder, to reproduce up to 150 copies of this document for not-for-profit, educational purposes only. For information on reproduction of the document for any other use or distribution, please contact Rita Shafer at the Academy Central Office; voice: (312) 573- 3221; fax: (312) 573-3225; or e-mail:
[email protected].
american academy of pediatric dentistry
Guideline for Periodontal Therapy Originating Group American Academy of Periodontology
Endorsed/Reaffirmed by the American Academy of Pediatric Dentistry 1992, 1993, 2000, 2001, 2003
Research has provided evidence that chronic inflammatory periodontal diseases are treatable.1-8 Studies have also been directed at providing information to permit better understanding of mechanisms of disease progression and pathogenesis in order to make treatment of periodontal diseases more effective and predictable.9-11 As a result of advances in knowledge and therapy, the great majority of patients retain their dentition over their lifetime with proper treatment, reasonable plaque control, and continuing maintenance care.12-21 However, there are some situations when traditional therapy is not effective in arresting the disease. In these instances, the progression of the disease may be slowed, but eventually the teeth may be lost.14-21 Adherence to the following guidelines will not guarantee a successful outcome and will not obviate all complications or postcare problems in periodontal therapy. Additionally, these guidelines should not be deemed inclusive of all methods of care, or exclusive of treatment reasonably directed at obtaining the same results. It should also be noted that these guidelines describe summaries of patient evaluation and treatment procedures that have been presented in considerably more detail within textbooks of periodontology as well as in the medical and dental literature. Ultimately judgments regarding the appropriateness of any specific procedure must be made by the practitioner in light of all the circumstances presented by the individual patient.
Scope of periodontics Periodontics is the specialty of dentistry that encompasses prevention, diagnosis, and treatment of diseases of the supporting and surrounding tissues of teeth and dental implants. The specialty includes maintenance of the health, function, and esthetics of all supporting structures and tissues (gingiva, periodontal ligament, cementum, alveolar bone, and sites for tooth replacements). Tissue regeneration, management of periodontal-endodontic lesions, and providing dental implants as tooth replacements are, when indicated, integral components of comprehensive periodontal therapy. Tooth extraction and implant site development may accompany either periodontal or implant therapy. Patient management during therapy may include the administration of intravenous conscious sedation.
The goals of periodontal therapy are to preserve the natural dentition, periodontium and peri-implant tissues; to maintain and improve periodontal and peri-implant health, comfort, esthetics, and function. Currently accepted clinical signs of a healthy periodontium include the absence of inflammatory signs of disease such as redness, swelling, suppuration, and bleeding on probing; maintenance of a functional periodontal attachment level; minimal or no recession in the absence of inter-proximal bone loss; and functional dental implants.
Periodontal examination All patients should receive a comprehensive periodontal examination. Such an examination includes discussion with the patient regarding the chief complaint, medical and dental history review, clinical examination, and radiographic analysis. Microbiologic, genetic, biochemical, or other diagnostic tests may also be useful, on an individual basis, for assessing the periodontal status of selected patients or sites. Some or all of the following procedures may be included in a comprehensive periodontal examination: 1. Extra- and intraoral examination to detect non periodontal oral diseases or conditions. 2. General periodontal examination to evaluate the to pography of the gingiva and related structures; to as sess probing depth, recession, and attachment level; to evaluate the health of the subgingival area with measures such as bleeding on probing and suppura tion; to assess clinical furcation status; and to detect endodontic-periodontal lesions. 3. Assessment of the presence, degree and/or distribu tion of plaque, calculus and gingival inflammation. 4. Dental examination, including caries assessment, proxi mal contact relationships, the status of dental resto rations and prosthetic appliances, and other tooth- or implant-related problems. 5. Determination of the degree of mobility of teeth and dental implants. 6. Occlusal examination. 7. Interpretation of a satisfactory number of updated, diagnostic quality periapical and bite-wing radio graphs or other diagnostic imaging needed for im plant therapy.
Copyright© 1993, 2000, 2001 by the American Academy of Periodontology. Copyrighted and reproduced with permission from the American Academy of Periodontolgy. Periodontal therapy. J Periodontol 2001;72:1624-8.
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8. Evaluation of potential periodontal systemic inter relationships. 9. Assessment of suitability to receive dental implants.
Establishing a diagnosis and prognosis The purpose of the comprehensive periodontal examination is to determine the periodontal diagnosis and prognosis and/or suitability for dental implants. This process includes an evaluation of periodontal and peri-implant tissues to determine the suitability of the patient for treatments including nonsurgical, surgical, regenerative and reconstructive therapy, or dental implant placement. This information should be recorded in the patient’s chart and communicated to the patient and the referring dentist when appropriate.
Periodontal diseases and conditions Diseases of the periodontium may be categorized as gingival diseases, periodontitis, necrotizing periodontal diseases, abscesses of the periodontium, and developmental or acquired deformities and conditions.22 Gingivitis is gingival inflammation without attachment loss or with non-progressing attachment loss. Other gingival diseases may be modified by systemic factors, medications or malnutrition. Periodontitis is gingival inflammation with progressing attachment loss. Different forms include, but are not limited to, chronic periodontitis, aggressive periodontitis, periodontitis as a manifestation of systemic disease, necrotizing ulcerative periodontitis, and periodontitis associated with endodontic lesions. Periodontitis may be further characterized by degree of attachment loss as slight, moderate, or severe; by extent as localized or generalized; and by post-treatment status as recurrent or refractory. Facial recession involving loss of periodontal attachment and gingival tissue affects children and adults. The prevalence increases with age and adults over 50 have the greatest degree of involvement. This mucogingival condition is often treatable.23 Edentulous ridge defects result from loss of osseous tissue and can compromise esthetics or complicate future implant placement. Other diseases and anomalies not explicitly described herein may also involve the periodontium.
Development of a treatment plan The clinical findings together with a diagnosis and prognosis should be used to develop a logical plan of treatment in order to eliminate or alleviate the signs and symptoms of periodontal diseases and thereby arrest or slow further disease progression. The treatment plan should be used to establish the methods and sequence of delivering appropriate periodontal treatment. When indicated, the plan should include: 1. Medical consultation or referral for treatment when appropriate. 2. Periodontal procedures to be performed. 3. Consideration of adjunctive restorative, prosthetic, orthodontic and/or endodontic consultation or treatment. 4. Provision for reevaluation during and after periodontal or dental implant therapy.
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Consideration of chemotherapeutic agents for adjunctive treatment. Consideration of diagnostic testing that may include microbiological, genetic or biochemical assessment or monitoring during the course of periodontal therapy. Periodontal maintenance program.
Informed consent and patient records Where reasonably foreseeable risks, potential complications, or the possibility of failure are associated with treatment, informed consent should be obtained prior to the commencement of therapy. The information given to the patient in these circumstances should include the following: 1. The diagnosis, etiology, proposed therapy, possible alternative treatment(s), and the prognosis with and without the proposed therapy or possible alternatives. 2. Recommendations for referral to other health care providers as necessary. 3. The reasonably foreseeable inherent risks and potential complications associated with the proposed therapy, including failure with the ultimate loss of teeth or dental implants. 4. The need for periodontal maintenance treatment after active therapy due to the potential for disease recurrence. A record of the patient’s consent to the proposed therapy should be maintained. Moreover, complete records of diagnosis, treatment, results, and recommended follow-up are essential, starting with the initial examination and continuing for as long as the patient is under care. Where reasonably foreseeable risks, potential complications, or the possibility of failure are associated with treatment, it is advisable to obtain the informed consent in writing prior to commencement of therapy.
Treatment procedures A broad range of therapies exist in periodontics. No single treatment approach can provide the only means of treating any one or all periodontal diseases. One treatment modality may be appropriate for one section of the mouth while another approach may be suitable at other sites. When indicated, treatment should include: 1. Patient education, training in personal oral hygiene, and counseling on control of risk factors (eg, smoking, medical status, stress) with referral when appropriate. 2. Removal of supragingival and accessible subgingival bacterial plaque and calculus is accomplished by periodontal scaling. Comprehensive periodontal root planing is used to treat root surface irregularities or alterations caused by periodontal pathoses. In some instances, these procedures may be incorporated into the surgical treatment. 3. Finishing procedures, which include post-treatment evaluation with review and reinforcement of personal daily oral hygiene when appropriate.
american academy of pediatric dentistry
The following courses of treatment may be indicated in addition to the above outlined procedures: 1. Chemotherapeutic agents. These agents may be used to reduce, eliminate, or change the quality of micro bial pathogens; or alter the host response through local or systemic delivery of appropriate agent(s). 2. Resective procedures. These procedures are designed to reduce or eliminate periodontal pockets and create an acceptable gingival form that will facilitate effective oral hygiene and periodontal maintenance treatment. Soft tissue procedures include gingivectomy, gingivo plasty, and various mucogingival flap procedures. Os seous procedures include ostectomy and osteoplasty. Dental tissue procedures include root resection, tooth hemisection, and odontoplasty. Combined osseous and dental tissue procedures may be required for management of endodontic-periodontal lesions. 3. Periodontal regenerative procedures include: soft tissue grafts, bone replacement grafts, root biomodification, guided tissue regeneration, and combinations of these procedures for osseous, furcation, and recession de fects. Periodontal reconstructive procedures include: guided bone regeneration, ridge augmentation, ridge preservation, implant site development, and sinus grafting. 4. Periodontal plastic surgery for gingival augmentation, for correction of recession or soft tissue defects, or for other enhancement of oral esthetics. 5. Occlusal therapy, which may include: minor tooth movement, occlusal adjustment, splinting, or provision of devices to reduce occlusal trauma. 6. Preprosthetic periodontal procedures include: exploratory flap surgery, resective procedures, regenerative or reconstructive procedures, or crown lengthening sur gery, performed to facilitate restorative or prosthetic treatment plans. 7. Selective extraction of teeth, roots, or implants when indicated, in order to facilitate periodontal therapy, implant therapy, implant site development, or im plant, restorative and/or prosthetic treatment plans. 8. Replacement of teeth by dental implants. 9. Procedures to facilitate orthodontic treatment includ ing, but not limited to, tooth exposure, frenulectomy, fiberotomy, gingival augmentation, and implant placement. 10. Management of periodontal systemic interrelation ships when appropriate.
Periodontal maintenance therapy Upon completion of active periodontal treatment, follow-up periodontal maintenance visits should include: 1. Update of medical and dental histories. 2. Evaluation of current extra- and intraoral, periodontal and peri-implant soft tissues as well as dental hard tissues and referral when indicated (eg, for treatment of carious lesions, pulpal pathosis, or other conditions).
3. Assessment of the oral hygiene status with reinstruc tion when indicated. 4. Mechanical toothcleaning to disrupt/remove dental plaque and biofilms, stain, and calculus. Local delivery or systemic chemotherapeutic agents may be used as adjunctive treatment for recurrent or refractory disease. 5. Elimination or mitigation of new or persistent risk and etiologic factors with appropriate treatment. 6. Identification and treatment of new, recurrent, or re fractory areas of periodontal pathoses. 7. Establishment of an appropriate, individualized inter val for periodontal maintenance treatment. The patient should be kept informed of: 1. Areas of persistent, recurrent, refractory, or new perio dontal disease. 2. Changes in the periodontal prognosis. 3. Advisability of further periodontal treatment or re treatment of indicated sites. 4. Status of dental implants. 5. Other oral health problems noted that may include caries, defective restorations, and non-periodontal mucosal diseases or conditions.
Factors modifying results The results of periodontal treatment may be adversely affected by circumstances beyond the control of the dentist.10 Examples of such circumstances include systemic diseases; inadequate plaque control by the patient; unknown or undeterminable etiologic factors which current therapy has not controlled; pulpalperiodontal problems; inability or failure of the patient to follow the suggested treatment or maintenance program; adverse health factors such as smoking, stress, and occlusal dysfunction; and uncorrectable anatomic, structural, or iatrogenic factors.10,19,24-28 The goals of periodontal therapy occasionally may be compromised when: 1) a patient refuses to have the recommended treatment, or to have hopeless teeth or implants removed; or 2) a practitioner elects to temporarily retain a hopeless tooth or replacement because it is serving as an abutment for a fixed or removable partial denture or is maintaining vertical dimension.29 Individuals who are unable or unwilling to undergo procedures required to achieve a healthy periodontium and the goal(s) of periodontal therapy or who are medically compromised are examples of patients that may be best treated with a limited therapeutic program.30 The prognosis of cases treated with a limited therapeutic program may be less favorable.
Evaluation of therapy Upon completion of planned periodontal therapy, the record should document that: 1. The patient has been counseled on why and how to perform an effective daily personal oral hygiene program. 2. Accepted therapeutic procedures have been performed to arrest the progression of the periodontal disease(s).
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Periodontal root planing has left subgingival root surfaces without clinically detectable calculus deposits or rough areas. Gingival crevices are generally without bleeding on probing or suppuration. A recommendation has been made for the correction of any tooth form, tooth position, restoration, or prosthesis considered to be contributing to the periodontal disease process. An appropriate periodontal maintenance program, specific to individual circumstances, has been recommended to the patient for long-term control of the disease, as well as for the maintenance of dental implants, if present.
References 1. Hill RW, Ramfjord SP, Morrison EC, et al. Four types of periodontal treatment compared over two years. J Periodontol 1981;52:655-62. 2. Nyman S, Lindhe J. A longitudinal study of combined periodontal and prosthodontic treatment of patients with advanced periodontal disease. J Periodontol 1979; 50:163-9. 3. Pihlstrom BL, McHugh RB, Oliphant TH, Ortiz-Campos C. Comparison of surgical and nonsurgical treatment of periodontal disease. A review of current studies and additional results after 6 1/2 years. J Clin Periodontol 1983; 10:524-41. 4. Isidor F, Karring T. Long-term effect of surgical and nonsurgical periodontal treatment. A 5-year clinical study. J Periodont Res 1986;21:462-72. 5. Becker W, Becker BE, Ochsenbein C, et al. A longitudinal study comparing scaling, osseous surgery, and modified Widman procedures. Results after one year. J Periodontol 1988;59:351-65. 6. Olsen CT, Ammons WF, van Belle G. A longitudinal study comparing apically repositioned flaps with and without osseous surgery. Int J Periodontics Restorative Dent 1985; 5:10-33. 7. Kaldahl WB, Kalkwarf KL, Patil KD, Molvar MP, Dyer JK. Long-term evaluation of periodontal therapy: I. Response to 4 therapeutic modalities. J Periodontol 1996;67: 93-102. 8. Kaldahl WB, Kalkwarf KL, Patil KD, Molvar MP, Dyer JK. Long-term evaluation of periodontal therapy: II. Incidence of sites breaking down. J Periodontol 1996; 67:103-8. 9. Goodson J, Tanner A, Haffajee A, Sornberger G, Socransky S. Patterns of progression and regression of advanced destructive periodontal disease. J Clin Periodontol 1982; 9:472-81. 10. Genco RJ. Current view of risk factors for periodontal diseases. J Periodontol 1996;67(Suppl.):1041-9. 11. Page RC, Offenbacher S, Schroeder HE, Seymour GJ, Kornman KS. Advances in the pathogenesis of periodontitis: Summary of developments, clinical implications, and future directions. Periodontol 2000 1997;14:216-48. 288
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12. Löe H, Anerud A, Boysen H, Smith M. The natural history of periodontal disease in man. Tooth mortality rates before 40 years of age. J Periodont Res 1978;13:563-72. 13. Löe H, Anerud A, Boysen H, Smith M. The natural history of periodontal disease in man. The rate of periodontal destruction before 40 years of age. J Periodontol 1978;49:607-20. 14. Hirschfeld I, Wasserman B. A long-term survey of tooth loss in 600 treated periodontal patients. J Periodontol 1978;49:225-37. 15. McFall W. Tooth loss in 100 treated patients with periodontal disease. A long-term study. J Periodontol 1982;53:539-49. 16. Meador H, Lane J, Suddick R. The long-term effectiveness of periodontal therapy in a clinical practice. J Periodontol 1985;56:253-8. 17. Goldman M, Ross I, Goteiner D. Effect of periodontal therapy on patients maintained for 15 years or longer. J Periodontol 1986;57:347-53. 18. Oliver R. Tooth loss with and without periodontal therapy. J West Soc Periodontol 1969;17:8-9. 19. Wilson T, Glover M, Malik A, Schoen J, Dorsett D. Tooth loss in maintenance patients in a private periodontal practice. J Periodontol 1987;58:231-5. 20. Nabers C, Stalker W, Esparza D, Naylor B, Canales S. Tooth loss in 1535 treated periodontal patients. J Periodontol 1988;59:297-300. 21. Chace R, Low S. Survival characteristics of periodontally involved teeth: A 40-year study. J Periodontol 1993; 64:701-5. 22. Armitage GC. Development of a classification system for periodontal diseases and conditions. Ann Periodontol 1999;4:1-6. 23. Albandar JM, Kingman A. Gingival recession, gingival bleeding and dental calculus in adults 30 years of age and older in the United States, 1988-1994. J Periodontol 1999; 70:30-43. 24. Mealey B. Diabetes and periodontal diseases (position paper). J Periodontol 2000;71:664-78. 25. Axelsson P, Lindhe J. The significance of maintenance care in the treatment of periodontal disease. J Clin Periodontol 1981;8:281-94. 26. Lindhe J, Westfelt E, Nyman S, Socransky S, Haffajee A. Long-term effect of surgical/non-surgical treatment of periodontal disease. J Clin Periodontol 1984;11:448-58. 27. Johnson GK. Tobacco use and the periodontal patient (position paper). J Periodontol 1999;70:1419-27. 28. Pennel B, Keagle J. Predisposing factors in the etiology of chronic inflammatory periodontal disease. J Periodontol 1977;48:517-32. 29. Machtei E, Zubrey Y, Yehuda B, Soskolne A. Proximal bone loss adjacent to periodontally hopeless teeth with and without extraction. J Periodontol 1989;60:512-5. 30. Rose LF, Steinberg BJ, Atlas SL. Periodontal management of the medically compromised patient. Periodontol 2000 1995;9:165-75.
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Acknowledgments The primary author for the revision of this position paper is Dr. Henry Greenwell. It replaces the paper titled Guidelines for Periodontal Therapy which had been revised by Dr. Robert E. Cohen and approved by the Board of Trustees in December 1997. Members of the 2000-2001 Research, Science and Therapy Committee include: Drs. David Cochran, Chair; Timothy Blieden; Otis J. Bouwsma; Robert E. Cohen; Petros Damoulis; Connie H. Drisko; Joseph P. Fiorellini; Gary Greenstein; Vincent J. Iacono; Martha J. Somerman; Terry D. Rees; Angelo Mariotti, Consultant; Robert J. Genco, Consultant; and Brian L. Mealey, Board Liaison.
Individual copies of this position paper may be obtained by accessing the Academy’s Web site at: “http://www.perio.org”. Members of the American Academy of Periodontology have permission of the Academy, as copyright holder, to reproduce up to 150 copies of this document for not-for-profit, educational purposes only. For information on reproduction of the document for any other use or distribution, please contact Rita Shafer at the Academy Central Office; voice: 312/573-3221; fax: 312/573-3225; or e-mail: rita@ perio.org.
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Treatment of Plaque-induced Gingivitis, Chronic Periodontitis, and Other Clinical Conditions Originating Group American Academy of Periodontology - Research, Science, and Therapy Committee
Endorsed by the American Academy of Pediatric Dentistry 2004
Gingivitis and periodontitis are the 2 major forms of inflammatory diseases affecting the periodontium. Their primary etiology is bacterial plaque, which can initiate destruction of the gingival tissues and periodontal attachment apparatus.1,2 Gingivitis is inflammation of the gingiva that does not result in clinical attachment loss. Periodontitis is inflammation of the gingiva and the adjacent attachment apparatus and is characterized by loss of connective tissue attachment and alveolar bone. Each of these diseases may be subclassified based upon etiology, clinical presentation, or associated complicating factors.3 Gingivitis is a reversible disease. Therapy is aimed primarily at reduction of etiologic factors to reduce or eliminate inflammation, thereby allowing gingival tissues to heal. Appropriate supportive periodontal maintenance that includes personal and professional care is important in preventing re-initiation of inflammation. Therapeutic approaches for periodontitis fall into 2 major categories: 1) anti-infective treatment, which is designed to halt the progression of periodontal attachment loss by removing etiologic factors; and 2) regenerative therapy, which includes anti-infective treatment and is intended to restore structures destroyed by disease. Essential to both treatment approaches is the inclusion of periodontal maintenance procedures.4 Inflammation of the periodontium may result from many causes (eg, bacteria, trauma). However, most forms of gingivitis and periodontitis result from the accumulation of toothadherent microorganisms.5-7 Prominent risk factors for development of chronic periodontitis include the presence of specific subgingival bacteria,8-10 tobacco use,9-13 diabetes,9,10,14 age,9,10 and male gender.9,10 Furthermore, there is evidence that other factors can contribute to periodontal disease pathogenesis: environmental, genetic, and systemic (eg, diabetes).14,15 This paper primarily reviews the treatment of plaqueinduced gingivitis and chronic periodontitis, but there might be some situations where the described therapies will not resolve disease or arrest disease progression. Furthermore, the
treatments discussed should not be deemed inclusive of all possible therapies, or exclusive of methods of care reasonably directed at obtaining good results. The ultimate decision regarding the appropriateness of any specific procedure must be made by the practitioner in light of the circumstances presented by an individual patient.
Plaque-induced Gingivitis Therapy for individuals with chronic gingivitis is initially directed at reduction of oral bacteria and associated calcified and noncalcified deposits. Patients with chronic gingivitis, but without significant calculus, alterations in gingival morphology, or systemic diseases that affect oral health, may respond to a therapeutic regimen consisting of improved personal plaque control alone.16 The periodontal literature documents the shortand long-term effects following self-treatment of gingivitis by personal plaque control.16-20 However, while it may be possible under controlled conditions to remove most plaque with a variety of mechanical oral hygiene aids, many patients lack the motivation or skill to attain and maintain a plaque-free state for significant periods of time.21-23 Clinical trials also indicate that self-administered plaque control programs alone, without periodic professional reinforcement, are inconsistent in providing long-term inhibition of gingivitis.19,24,25 Many patients with gingivitis have calculus or other associated local factors (eg, defective dental restorations) that interfere with personal oral hygiene and the ability to remove bacterial plaque. An acceptable therapeutic result for these individuals is usually obtained when personal plaque control measures are performed in conjunction with professional removal of plaque, calculus, and other local contributing factors.26,27 Removal of dental calculus is accomplished by scaling and root planing procedures using hand, sonic, or ultrasonic instruments. The therapeutic objective of scaling and root planing is to remove plaque and calculus to reduce subgingival bacteria below a threshold level capable of initiating clinical inflammation.
Copyright© 2004 by the American Academy of Periodontology; all rights reserved. Copyrighted and reproduced with permission from the American Academy of Periodontology. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, or otherwise without written permission of the publisher. Treatment of Plaque-induced Gingivitis, Chronic Periodontitis, and Other Clinical Conditions. J Periodontol 2001;72:1790-1800. Available through the American Academy of Periodontology, Department of Scientific, Clinical and Educational Affairs, 737 North Michigan Avenue, #800, Chicago, IL 60611-2690, Phone: (312) 787-5518, Fax: (312) 787-3670.
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The success of instrumentation is determined by evaluating the periodontal tissues following treatment and during the maintenance phase of therapy. The use of topical antibacterial agents to help reduce bacterial plaque may be beneficial for the prevention and treatment of gingivitis in some patients.28-30 A number of these agents in oral rinses and dentifrices have been tested in clinical trials.28 However, to be accepted by the American Dental Association (ADA) Council on Dental Therapeutics as an effective agent for the treatment of gingivitis, a product must reduce plaque and demonstrate effective reduction of gingival inflammation over a period of at least 6 months. The agent must also be safe and not induce adverse side effects. Three medicaments have been given the ADA Seal of Acceptance for the control of gingivitis. The active ingredients of one product are thymol, menthol, eucalyptol, and methyl salicylate.29 Active ingredients in the other two are chlorhexidine digluconate and triclosan.29 If properly used, the addition of a topical anti-plaque agent to a gingivitis treatment regimen for patients with deficient plaque control will likely result in reduction of gingivitis.30 However, experimental evidence indicates that penetration of topically applied agents into the gingival crevice is minimal.31 Therefore, these agents are useful for the control of supragingival, but not subgingival plaque. Among individuals who do not perform excellent oral hygiene, supragingival irrigation with and without medicaments is capable of reducing gingival inflammation beyond that normally achieved by toothbrushing alone. This effect is likely due to the flushing out of subgingival bacteria.32 If gingivitis remains following the removal of plaque and other contributing local factors, thorough evaluation should be undertaken of systemic factors (eg, diabetes, pregnancy, etc.). If such conditions are present, gingival health may be attained once the systemic problem is resolved and plaque control is maintained. Acute Periodontal Diseases Necrotizing ulcerative gingivitis (NUG) is associated with specific bacterial accumulations occurring in individuals with lowered host resistance.1 NUG usually responds rapidly to the reduction of oral bacteria by a combination of personal plaque control and professional debridement. If lymphadenopathy or fever accompanies oral symptoms, administration of systemic antibiotics may be indicated. The use of chemotherapeutic rinses by the patient may be beneficial during the initial treatment stages. After the acute inflammation of the NUG lesion is resolved, additional intervention may be indicated to prevent disease recurrence or to correct resultant soft tissue deformities. Necrotizing ulcerative periodontitis (NUP) manifests as rapid necrosis and destruction of the gingiva and periodontal attachment apparatus. It may initiate gingival bleeding and pain, and it usually represents an extension of necrotizing ulcerative gingivitis in individuals with lowered host resistance. NUP has been reported among both HIV-positive and negative individuals, but its true prevalence is unknown.33-38 Management of
NUP involves debridement which may be combined with irrigation with antiseptics (eg, povidone iodine), antimicrobial mouth rinses (eg, chlorhexidine), and administration of systemic antibiotics.39 There is also evidence that HIV-immune deficiency may be associated with severe loss of periodontal attachment that does not necessarily present clinically as an ulcerative lesion.40 Although not an acute disease, linear gingival erythema (LGE) occurs in some HIV-infected individuals and does not appear to respond to conventional scaling, root planing, and plaque control.39 Antibiotic therapy should be used in HIV-positive patients with caution due to the possibility of inducing opportunistic infections.39,40 The oral manifestations of a primary herpes simplex virus type I infection often include gingivitis. By the time gingivitis is present, patients are usually febrile, in pain, and have lymphadenopathy. Diagnosis is generally made from the clinical appearance of the oral soft tissues. Although not performed routinely, a viral culture may provide definitive identification of the infective agent. In otherwise healthy patients, treatment for herpetic gingivitis consists of palliative therapy. The infection is self-limiting and usually resolves in 7 to 10 days. Systemic antiviral therapy with acyclovir is appropriate for immunocompromised patients with herpetic gingivitis.41 Gingival Enlargement Chronic gingival inflammation may result in gingival enlargement. This overgrowth of gingiva may be exaggerated in patients with genetic or drug-related systemic factors (eg, anticonvulsants, cyclosporine and calcium channel blocking drugs).42-46 Among individuals taking phenytoin, gingival overgrowth may be minimized with appropriate personal oral hygiene and professional maintenance.47,48 However, root debridement in patients with gingival overgrowth often does not return the periodontium to normal contour. The residual overgrowth may not only complicate the patient’s ability to adequately clean the dentition, but it may also present esthetic and functional problems.49 For patients with gingival overgrowth, the modification of tissue topography by surgical recontouring may be undertaken to create a maintainable oral environment.47,50 Postoperative management following tissue resection is important. The benefits of surgical reduction may be lost due to rapid proliferation of the tissues during the post-therapy phase.51 Recurrence is common in many patients with drug-induced gingival overgrowth.51 For these patients, consultation with the patient’s physician is advisable to determine if it is possible to use an alternative drug therapy that does not induce gingival overgrowth. If not, then repeated surgical and/or non-surgical intervention may be required.
Chronic Periodontitis Appropriate therapy for patients with periodontitis varies considerably with the extent and pattern of attachment loss, local anatomical variations, type of periodontal disease, and therapeutic objectives. Periodontitis destroys the attachment
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apparatus of teeth resulting in periodontal pocket formation and alteration of normal osseous anatomy. The primary objectives of therapy for patients with chronic periodontitis are to halt disease progression and to resolve inflammation. Therapy at a diseased site is aimed at reducing etiologic factors below the threshold capable of producing breakdown, thereby allowing repair of the affected region. Regeneration of lost periodontal structures can be enhanced by specific procedures. However, many variables responsible for complete regeneration of the periodontium are unknown and research is ongoing in this area. Scaling and Root Planing The beneficial effects of scaling and root planing combined with personal plaque control in the treatment of chronic periodontitis have been validated.52-65 These include reduction of clinical inflammation, microbial shifts to a less pathogenic subgingival flora, decreased probing depth, gain of clinical attachment, and less disease progression.52-65 Scaling and root planing procedures are technically demanding and time-consuming. Studies show that clinical conditions generally improve following root planing; nonetheless, some sites still do not respond to this therapy.62,63,66,67 The addition of gingival curettage to root planing in the treatment of generalized chronic periodontitis with shallow suprabony pockets does not significantly reduce probing depth or gain clinical attachment beyond that attained by scaling and root planing alone.68,69 The following factors may limit the success of treatment by root planing: root anatomy (eg, concavities, furrows etc.), furcations,66 and deep probing depths.70-72 Several weeks following the completion of root planing and efforts to improve personal plaque control, re-evaluation should be conducted to determine the treatment response. Several factors must be considered at sites that continue to exhibit signs of disease. If the patient’s daily personal plaque control is not adequate to maintain gingival health, then additional instruction and motivation in personal plaque control and/or the use of topical chemotherapeutics (eg, mouthrinses, local drug delivery devices) may be indicated. Anatomical factors that can limit the effectiveness of root instrumentation or limit the patient’s ability to perform personal plaque control (eg, deep probing depths, root concavities, furcations) may require additional therapy including surgery. Host response may also have an effect on treatment outcome and patients with systemic conditions (eg, diabetes, pregnancy, stress, AIDS, immunodeficiencies, and blood dyscrasias) may not respond well to therapy that is directed solely at controlling local factors. In such patients, it is important that attempts be made to control the contributing systemic factors. Pharmacological Therapy Pharmacotherapeutics may have an adjunctive role in the management of periodontitis in certain patients.73 These adjunctive therapies are categorized by their route of administration to diseased sites: systemic or local drug delivery.
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Systemic Drug Administration Numerous investigations73 have assessed the use of systemic antibiotics to halt or slow the progression of periodontitis or to improve periodontal status. The adjunctive use of systemically delivered antibiotics may be indicated in the following situations: patients with multiple sites unresponsive to mechanical debridement, acute infections, medically compromised patients, presence of tissue-invasive organisms and ongoing disease progression.74-77 The administration of antibiotics for the treatment of chronic periodontitis should follow accepted pharmacological principles including, when appropriate, identification of pathogenic organisms and antibiotic sensitivity testing. Considerable research efforts have focused on systemic application of host modulating agents such as non-steroidal anti-inflammatory drugs (NSAIDS)78-80 and subantimicrobial dose doxycycline.81-84 Investigators have reported some benefit when these medications are incorporated into treatment protocols.78,81-84 Recently [year 2000], the United States Food and Drug Administration (FDA) approved the use of a systemically delivered collagenase inhibitor consisting of a 20-mg capsule of doxycycline hyclate as an adjunct to scaling and root planing for the treatment of periodontitis. Benefits included a statistically significant reduction in probing depths, a gain in clinical attachment levels and a reduction in the incidence of disease progression.82-84 Overall, the data suggest that use of subantimicrobial dose doxycycline as an adjunct to scaling and root planing provides defined but limited improvement in periodontal status. It is important to consider the potential benefits and side effects of systemic pharmacological therapy. Benefits may include the ability to treat patients unresponsive to conventional therapy or an individual with multiple sites experiencing recurrent periodonitits. In contrast, potential risks associated with systemically administered antibiotics include development of resistant bacterial strains,85 emergence of opportunistic infections, and possible allergic sensitization of patients.73 With regard to the prolonged administration of NSAIDS, harmful effects may include gastrointestinal upset and hemorrhage, renal and hepatic impairment, central nervous system disturbances, inhibition of platelet aggregation, prolonged bleeding time, bone marrow damage, and hypersensitivity reactions.73 At present, the incidence of negative side effects reported after root planing with or without administration of subantimicrobial dose doxycycline has been similar. In general, since patients with chronic periodontitis respond to conventional therapy, it is unnecessary to routinely administer systemic medications such as antibiotics, NSAIDS, or subantimicrobial dosing with doxycycline. Local Delivery Controlled delivery of chemotherapeutic agents within periodontal pockets can alter the pathogenic flora and improve clinical signs of periodontitis.86-94 Local drug delivery systems provide several benefits; the drug can be delivered to the site of disease activity at a bactericidal concentration and it can facilitate prolonged drug delivery. The FDA has approved the
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use of an ethylene vinyl acetate fiber that contains tetracycline,86-91 a gelatin chip that contains chlorhexidine93 and a minocycline polymer formulation92 as adjuncts to scaling and root planing. The FDA has also approved doxycycline hyclate in a bioabsorbable polymer gel as a stand-alone therapy for the reduction of probing depths, bleeding upon probing, and gain of clinical attachment.94 Local delivery systems have potential limitations and benefits. If used as a monotherapy, problems associated with local delivery can include allergic reaction, possible inability to disrupt biofilms, and failure to remove calculus.95 The benefits include the ease of application, selectively targeting a limited number of diseased sites that were unresponsive to conventional therapy, and possibly enhanced treatment results at specific locations. Local delivery modalities have shown beneficial clinical improvements with regard to probing depth reduction and gain in clinical attachment.91-94 Furthermore, there are limited data to suggest that local delivery of antibiotics may also be beneficial in preventing recurrent attachment loss in the absence of maintenance therapy.90 Utilization of antibiotics at an individual site will depend on the discretion of the treating therapist after consultation with the patient. The greatest potential of local delivery devices may be to enhance therapy at sites that do not respond to conventional treatment. Ultimately, the results of local drug delivery must be evaluated with regard to the magnitude of improvement that can be attained relative to disease severity. A more complete review of local drug delivery can be found in the American Academy of Periodontology position paper The Role of Controlled Drug Delivery for Periodontitis.87 Surgical Therapy Surgical access to facilitate mechanical instrumentation of the roots has been utilized to treat chronic periodontitis for decades. A surgical approach to the treatment of periodontitis is utilized in an attempt to: 1) provide better access for removal of etiologic factors; 2) reduce deep probing depths; and 3) regenerate or reconstruct lost periodontal tissues.96-98 Clinical trials indicate that both surgical and nonsurgical approaches can be effective in achieving stability of clinical attachment levels.60-65,99-103 Flap reflection is capable, however, of increasing the efficacy of root debridement, especially at sites with deep probing depths or furcations.60-65,70,72,99-104 Nevertheless, complete calculus removal, even with surgical access, may not always be achieved.70,72,104 The addition of osseous resection during surgical procedures appears to produce greater reduction of probing depth due to gingival recession,62,64,65 particularly in furcations.66 Regardless of the type of therapy, furcated teeth are problematic since they are still more likely to lose clinical attachment than nonfurcated teeth.66,67,105 While these overall findings are helpful, the practitioner should base specific decisions for therapy on findings for each individual patient.
Regenerative Surgical Therapy The optimal goal of therapy for individuals who have lost a significant amount of periodontal attachment is regeneration of lost tissues. While root debridement in combination with plaque control has demonstrated efficacy in resolving inflammation and arresting periodontitis,26,27,60-65 healing typically results in the formation of a long junctional epithelium106-108 with remodeling of the alveolus.109 Similarly, surgical debridement alone does not induce significant amounts of new connective tissue attachment.110,111 However, some bone fill may occur in selected sites.107,112 Clinical trials suggest that obtaining new periodontal attachment or regenerating lost tissues is enhanced by the use of adjunctive surgical technique devices and materials. Chemical agents that modify the root surface, while promoting new attachment, have shown variable results when used in humans.113-118 Bone grafting119-125 and guided tissue regeneration (GTR) techniques, with or without bone replacement grafts,126-133 may be successful when used at selected sites with advanced attachment loss. The use of biologically engineered tissue inductive proteins (eg, growth factors, extracellular matrix proteins, and bone morphogenic proteins) to stimulate periodontal or osseous regeneration has also shown promise.134-142 Literature reviews on periodontal regeneration143,144 and mucogingival therapy145 provide additional information regarding these therapies. Regenerative therapy and other treatment modalities can be affected by several risk factors (eg, diabetes and tobacco use) which can diminish periodontal treatment outcomes.146 In this regard, cigarette smoking is associated with a high risk for progressive periodontitis9-13,147 and treatment for periodontitis may be less effective in smokers than non-smokers.148-150 These factors are reviewed in more depth in the Academy’s position paper Tobacco Use and the Periodontal Patient.151 To maximize effective prevention and treatment of periodontitis, patients should be encouraged to stop smoking and to stop using smokeless tobacco.
Occlusal Management Several studies indicated that excessive occlusal forces do not initiate plaque-induced periodontal disease or connective tissue attachment loss (periodontitis).152-155 However, other investigations suggest that tooth mobility may be associated with adverse effects on the periodontium and affect the response to therapy with respect to gaining clinical attachment.156,157 With regards to treatment, occlusal therapy may aid in reducing tooth mobility and gaining some bone lost due to traumatic occlusal forces.158 Occlusal equilibration also may be used to ameliorate a variety of clinical problems related to occlusal instability and restorative needs.159 Clinicians should use their judgment as to whether or not to perform an occlusal adjustment as a component of periodontal therapy based upon an evaluation of clinical factors related to patient comfort, health and function.160
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Periodontal Maintenance Procedures Periodic monitoring of periodontal status and appropriate maintenance procedures should be part of the long-term treatment plan for managing chronic periodontitis.28 Although experimental studies have demonstrated very successful treatment outcomes when patients are professionally maintained at 2-week intervals,161 such a program is impractical for most chronic periodontitis patients. Therefore, to maximize successful therapeutic outcomes, patients must maintain effective daily plaque control. It also appears that in-office periodontal maintenance at 3 to 4 month intervals can be effective in maintaining most patients.4 A more comprehensive review on this subject can be found in the American Academy of Periodontology’s position paper entitled Supportive Periodontal Therapy (SPT).162
Summary The inflammatory components of plaque induced gingivitis and chronic periodontitis can be managed effectively for the majority of patients with a plaque control program and nonsurgical and/or surgical root debridement coupled with continued periodontal maintenance procedures. Some patients may need additional therapeutic procedures. All of the therapeutic modalities reviewed in this position paper may be utilized by the clinician at various times over the long-term management of the patient’s periodontal condition.
References 1. American Academy of Periodontology. The pathogenesis of periodontal diseases (position paper). J Periodontol 1999;70:457-70. 2. American Academy of Periodontology. Diagnosis of Periodontal Diseases (position paper). Chicago, Ill: The American Academy of Periodontology; April 1995. 3. Armitage GC. Development of a classification system for periodontal diseases and conditions. Ann Periodontol 1999;4:1-6. 4. Ramfjord SP. Maintenance care and supportive periodontal therapy. Quintessence Int 1993;24:465-71. 5. Page RC. Gingivitis. J Clin Periodontol 1986;13:345-59. 6. Ranney RR, Debski BF, Tew JG. Pathogenesis of gingivitis and periodontal disease in children and young adults. Pediatr Dent 1981;3:89-100. 7. Socransky SS, Haffajee AD. Microbial mechanisms in the pathogenesis of destructive periodontal diseases: A critical assessment. J Periodont Res 1991;26:195-212. 8. Wolff L, Dahlen G, Aeppli D. Bacteria as risk markers for periodontitis. J Periodontol 1994;65:498-510. 9. Grossi SG, Zambon JJ, Ho AW, et al. Assessment of risk for periodontal disease. I. Risk indicators for attachment loss. J Periodontol 1994;65:260-7. 10. Grossi SG, Genco RJ, Machtei EE, et al. Assessment of risk for periodontal disease. II. Risk indicators for alveolar bone loss. J Periodontol 1995;66:23-9.
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11. Ismail A, Morrison E, Burt B, Caffesse R, Kavanaugh Natural history of periodontal disease in adults: Findings from the Tecumseh Periodontal Disease Study, 1959-1987. J Dent Res 1990;69:430-5. 12. Haber J, Wattles J, Crowley M, Mandell R, Joshipurak K, Kent RL. Evidence for cigarette smoking as a major risk factor for periodontitis. J Periodontol 1993;64:16-23. 13. Bergstrom J, Preber H. Tobacco use as a risk factor. J Periodontol 1994;65:545-50. 14. Oliver RC, Tervonen T. Diabetes: A risk factor for periodontitis in adults? J Periodontol 1994;65:530-8. 15. Michalowicz BS. Genetic and heritable risk factors in periodontal disease. J Periodontol 1994;65:479-88. 16. Löe H, Theilade E, Jensen SB. Experimental gingivitis in man. J Periodontol 1965;36:177-87. 17. Theilade E, Wright WH, Jensen SB, Löe H. Experimental gingivitis in man. II. A longitudinal clinical and bacteriological investigation. J Periodont Res 1966;1:1-13. 18. Lindhe J, Axelsson P. The effect of a preventive programme on dental plaque, gingivitis, and caries in school children. Results after one and two years. J Clin Periodontol 1974; 1:126-38. 19. Suomi JD, Greene JC, Vermillion JR, Doyle J, Chang JJ, Leatherwood EC. The effect of controlled oral hygiene procedures on the progression of periodontal disease in adults: Results after third and final year. J Periodontol 1971;42:152-60. 20. Axelsson P, Lindhe J. Effect of controlled oral hygiene procedures on caries and periodontal disease in adults. Results after 6 years. J Clin Periodontol 1981;8:239-48. 21. De la Rosa M, Guerra JZ, Johnston DA, Radike AW. Plaque growth and removal with daily toothbrushing. J Periodontol 1979;50:661-4. 22. MacGregor IDM, Rugg-Gunn AJ, Gordon PH. Plaque levels in relation to the number of toothbrushing strokes in uninstructed English schoolchildren. J Periodont Res 1986;21:577-82. 23. Lang NP, Cumming BR, Löe H. Toothbrushing frequency as it relates to plaque development and gingival health. J Periodontol 1973;44:396-405. 24. Listgarten MA, Schifter CC, Laster L. 3-year longitudinal study of the periodontal status of an adult population with gingivitis. J Clin Periodontol 1985;12:225-38. 25. Agerbaek N, Melsen B, Lind OP, Glavind L, Kristiansen B. Effect of regular small group instruction per se on oral health status of Danish schoolchildren. Community Dent Oral Epidemiol 1979;7:17-20. 26. Tagge DL, O’Leary TJ, El-Kafrawy AH. The clinical and histological response of periodontal pockets to root planing and oral hygiene. J Periodontol 1975;46:527-33. 27. Lövdal A, Arno A, Schei O, Waerhaug J. Combined effect of subgingival scaling and controlled oral hygiene on the incidence of gingivitis. Acta Odontol Scand 1961;19: 537-55.
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28. Hancock EB. Prevention. Ann Periodontol 1996;1:223-49. 29. Mandel ID. Antimicrobial mouthrinses: Overview and update. J Am Dent Assoc 1994;125(suppl 2):2S-10S. 30. Brecx M, Brownstone E, MacDonald L, Gelskey S, Cheang M. Efficacy of Listerine, Meridol, and chlorhexidine as supplements to regular tooth-cleaning measures. J Clin Periodontol 1992;19:202-7. 31. Pitcher GR, Newman HN, Strahan JD. Access to subgingival plaque by disclosing agents using mouthrinsing and direct irrigation. J Clin Periodontol 1980;7:300-8. 32. American Academy of Periodontology. The role of supraand subgingival irrigation in the treatment of periodontal diseases (position paper). Chicago, Ill: The American Academy of Periodontology; April 1995. 33. Mealey BL. Periodontal implications: Medically compromised patients. Ann Periodontol 1996;1:293-303. 34. Drinkard CR, Decher L, Little JW, et al. Periodontal status of individuals in early stages of human immunodeficiency virus infection. Community Dent Oral Epidemiol 1991; 19:281-5. 35. Friedman RB, Gunsolley J, Gentry A, Dinius A, Kaplowitz L, Settle J. Periodontal status of HIV seropositive and AIDS patients. J Periodontol 1991;62:623-7. 36. Riley C, London JP, Burmeister JA. Periodontal health in 200 HIV-positive patients. J Oral Pathol Med 1992;21: 124-7. 37. Masouredis CM, Katz MH, Greenspan D, et al. Prevalence of HIV-associated periodontitis and gingivitis in HIVinfected patients attending an AIDS clinic. J Acquir Immune Defic Syndr 1992;5:479-83. 38. Glick M, Muzyka BC, Salkin LM, Lurie D. Necrotizing ulcerative periodontitis: A marker for immune deterioration and a predictor for the diagnosis of AIDS. J Periodontol 1994;65:393-7. 39. American Academy of Periodontology. Periodontal considerations in the HIV-positive patient (position paper). Chicago, Ill: The American Academy of Periodontology; April 1994. 40. Tomar SL, Swango PA, Kleinman DV, Burt BA. Loss of periodontal attachment in HIV-seropositive military personnel. J Periodontol 1995;66:421-8. 41. Redding SW, Montgomery MT. Acyclovir prophylaxis for oral herpes simplex infection in patients with bone marrow transplants. Oral Surg Oral Med Oral Pathol 1989;67:680-3. 42. Hassell TM, Hefti AF. Drug induced gingival overgrowth: Old problem, new problem. Crit Rev Oral Biol Med 1991;2:103-37. 43. Butler RT, Kalkwarf KL, Kaldahl WB. Drug-induced gingival hyperplasia: Phenytoin, cyclosporine, and nifedipine. J Am Dent Assoc 1987;114:56-60. 44. Miller CS, Damm DD. Incidence of verapamil-induced gingival hyperplasia in a dental population. J Periodontol 1992;63:453-6. 45. Nery EB, Edson RG, Lee KK, Pruthi VK, Watson J. Prevalence of nifedipine-induced gingival hyperplasia. J Periodontol 1995;66:572-8.
46. Mealey BL. Periodontal implications: Medically compromised patients. Ann Periodontol 1996;1:303-8. 47. Pihlstrom B. Prevention and treatment of dilantin associated gingival enlargement. Compendium Continuing Educ Dent 1990;11(suppl 14):S506-S510. 48. Hall WB. Dilantin hyperplasia: A preventable lesion? Compendium Continuing Educ Dent 1990;11(suppl 14): S502-5. 49. Jones JE, Weddell JA, McKown CG. Incidence and indications for surgical management of phenytoin-induced gingival overgrowth in a cerebral palsy population. J Oral Maxillofac Surg 1998;46:385-90. 50. Hall EE. Prevention and treatment considerations in patients with drug-induced gingival enlargement. Curr Opin Periodontol 1997;4:59-63. 51. Ilgenli T, Atilla G, Baylas H. Effectiveness of periodontal therapy in patients with drug-induced gingival overgrowth. Long-term results. J Periodontol 1999;70:967-72. 52. Morrison EC, Ramfjord SP, Hill RW. Short-term effects of initial, nonsurgical periodontal treatment (hygienic phase). J Clin Periodontol 1980;7:199-211. 53. Garrett JS. Effects of nonsurgical periodontal therapy on periodontitis in humans. A review. J Clin Periodontol 1983; 10:515-23. 54. Badersten A, Nilveus R, Egelberg J. Effect of nonsurgical periodontal therapy. I. Moderately advanced periodontitis. J Clin Periodontol 1981;8:57-72. 55. Badersten A, Nilveus R, Egelberg J. Effect of nonsurgical periodontal therapy. II. Severely advanced periodontitis. J Clin Periodontol 1984;11:63-76. 56. Badersten A, Nilveus R, Egelberg J. Effect of nonsurgical periodontal therapy. III. Single versus repeated instrumentation. J Clin Periodontol 1984;11:114-24. 57. Hughes TP, Caffesse RG. Gingival changes following scaling, root planing and oral hygiene - A biometric evaluation. J Periodontol 1978;49:245-52. 58. Magnusson I, Lindhe J, Yoneyama T, Liljenberg B. Recolonization of subgingival microbiota following scaling in deep pockets. J Clin Periodontol 1984;11:193-207. 59. Mosques T, Listgarten MA, Phillips RW. Effect of scaling and root planing on the composition of the human subgingival microbial flora. J Periodont Res 1980;15:144-51. 60. Pihlstrom BL, McHugh RB, Oliphant TH, Ortiz-Campos C. Comparison of surgical and nonsurgical treatment of periodontal disease. A review of current studies and additional results after 6-1/2 years. J Clin Periodontol 1983; 10:524-44. 61. Hill RW, Ramfjord SP, Morrison EC, et al. Four types of periodontal treatment compared over two years. J Periodontol 1981;52:655-62. 62. Kaldahl WB, Kalkwarf KL, Patil KD, Dyer JK, Bates RE Jr. Evaluation of four modalities of periodontal therapy. Mean probing depth, probing attachment level, and recession changes. J Periodontol 1988;59:783-93.
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63. Becker W, Becker BE, Ochsenbein C, et al. A longitudinal study comparing scaling, osseous surgery, and modified Widman procedures. Results after one year. J Periodontol 1988;59:351-65. 64. Ramfjord SP, Caffesse RG, Morrison EC, et al. 4 modalities of periodontal treatment compared over 5 years. J Clin Periodontol 1987;14:445-52. 65. Kaldahl WB, Kalkwarf KL, Kashinath D, Patil D, Molvar MP, Dyer JK. Long-term evaluation of periodontal therapy: I. Response to 4 therapeutic modalities. J Periodontol 1996;67:93-102. 66. Kalkwarf KL, Kaldahl WB, Patil KD. Evaluation of furcation region response to periodontal therapy. J Periodontol 1988;59:794-804. 67. Kaldahl WB, Kalkwarf KL, Kashinath D, Patil D, Molvar MP, Dyer JK. Long-term evaluation of periodontal therapy: II. Incidence of sites breaking down. J Periodontol 1996;67:103-8. 68. Ainslie P, Caffesse R. A biometric evaluation of gingival curettage (II). Quintessence Int 1981;6:609-14. 69. Echeverra JJ, Caffesse RG. Effects of gingival curettage when performed 1 month after root instrumentation. A biometric evaluation. J Clin Periodontol 1983;10:277-86. 70. Caffesse RG, Sweeney PL, Smith BA. Scaling and root planing with and without periodontal flap surgery. J Clin Periodontol 1986;13:205-10. 71. Rabbani GM, Ash MM, Caffesse RG. The effectiveness of subgingival scaling and root planing in calculus removal. J Periodontol 1981;52:119-23. 72. Fleischer HC, Mellonig JT, Brayer WK, Gray JL, Barnett JD. Scaling and root planing efficacy in multirooted teeth. J Periodontol 1989;60:402-9. 73. Drisko CH. Non-surgical pocket therapy: Pharmacotherapeutics. Ann Periodontol 1996;1:491-566. 74. Magnusson I, Low SB, McArthur WP, et al. Treatment of subjects with refractory periodontal disease. J Clin Periodontol 1994;21:628-37. 75. van Winkelhoff AJ, Tijhof CJ, de Graaff J. Microbiological and clinical results of metronidazole plus amoxicillin therapy in Actinobacillus actinomycetem omitans-associated periodontitis. J Periodontol 1992;63:52-7. 76. Magnusson I, Clark WB, Low SB, Maruniak J, Marks RG, Walker CB. Effect of non-surgical periodontal therapy combined with adjunctive antibiotics in subjects with “refractory” periodontal disease. I. Clinical results. J Clin Periodontol 1989;16:647-53. 77. Kornman KS, Robertson PB. Clinical and microbiological evaluation of therapy for juvenile periodontitis. J Periodontol 1985;56:443-6. 78. Williams R, Jeffcoat M, Howell T, et al. Altering the progression of human alveolar bone loss with the nonsteroidal anti-inflammatory drug flurbiprofen. J Periodontol 1989;60:485-90.
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79. Williams RC, Jeffcoat MK, Howell TH, et al. Ibuprofen: An inhibitor of alveolar bone resorption in beagles. J Periodont Res 1988;23:225-9. 80. Howell TH, Jeffcoat MK, Goldhaber P, et al. Inhibition of alveolar bone loss in beagles with the NSAID naproxen. J Periodont Res 1991;26:498-501. 81. Crout RJ, Lee HM, Schroeder H, et al. The “cyclic” regimen of low-dose doxycycline for adult periodontitis: A preliminary study. J Periodontol 1996;67:506-14. 82. Golub LM, McNamara TF, Ryan ME, et al. Adjunctive treatment with subantimicrobial doses of doxycycline: Effects on gingival fluid collagenase activity and attachment loss in adult periodontitis. J Clin Periodontol 2001;28:146-56. 83. Caton J. Evaluation of Periostat for patient management. Compend Continuing Educ Dent 1999;20:451-62. 84. Caton J, Ciancio SG, Bleiden TM, et al. Treatment with subantimicrobial dose doxycycline improves the efficacy of scaling and root planing in patients with adult periodontitis. J Periodontol 2000;71:521-32. 85. Walker CB. The acquisition of antibiotic resistance in the periodontal microflora. Periodontol 2000 1996;10:79-88. 86. Goodson JM, Cugini MA, Kent RL, et al. Multicenter evaluation of tetracycline fiber therapy: II. Clinical response. J Periodont Res 1991;26:371-9. 87. American Academy of Periodontology. The role of controlled drug delivery for periodontitis (position paper). J Periodontol 2000;71:125-40. 88. Goodson JM, Tanner A, McArdle S, Dix K, Watanabe SM. Multicenter evaluation of tetracycline fiber therapy: III. Microbiological response. J Periodont Res 1991;26:440-51. 89. Drisko CH, Cobb CM, Killoy WJ, et al. Evaluation of periodontal treatments using controlled release tetracycline fibers: Clinical response. J Periodontol 1995;66:692-9. 90. Michalowicz BS, Pihlstrom BL, Drisko CH, et al. Evaluation of periodontal treatments using controlledrelease tetracycline fibers: Maintenance response. J Periodontol 1995; 66:708-15. 91. Newman MG, Kornman KS, Doherty FM. A 6-month multi-center evaluation of adjunctive tetracycline fiber therapy used in conjunction with scaling and root planing in maintenance patients: Clinical results. J Periodontol 1994;65:685-91. 92. Williams RC, Paquette DW, Offenbacher S, et al. Treatment of periodontitis by local administration of minocycline microspheres: A controlled clinical trial. J Periodontol 2001;72(11):1535-44. 93. Jeffcoat MK, Bray KS, Ciancio SG, et al. use of a subgingival controlled-release chlorhexidine chip reduces probing depth and improves attachment level compared with scaling and root planing alone. J Periodontol 1998;69:989-97. 94. Garrett S, Johnson L, Drisko CH, et al. Two multicenter studies evaluating locally delivered doxycycline hyclate, placebo control, oral hygiene, and scaling and root planing in the treatment of periodontitis. J Periodontol 1999;70; 490-503.
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95. Darveau PR, Tanner A, Page RC. The microbial challenge in periodontics. Periodontol 2000 1997;14:12-32. 96. Consensus Report: Surgical pocket therapy. Ann Periodontol 1996;1:618-20. 97. Consensus Report: Periodontal regeneration around natural teeth. Ann Periodontol 1996;1:667-70. 98. Consensus Report: Mucogingival therapy. Ann Periodontol 1996;1:702-6. 99. Antczak-Bouckoms A, Joshipura K, Burdick E, Tolloch JFC. Meta-analysis of surgical versus non-surgical methods of treatment for periodontal disease. J Clin Periodontol 1993;20:259-68. 100. Ramfjord SP, Knowles JW, Nissle RR, Schick RA, Burgett FG. Longitudinal study of periodontal therapy. J Periodontol 1973;44:66-77. 101. Pihlstrom BL, Oliphant TH, McHugh RB. Molar and nonmolar teeth compared over 6 1/2 years following two methods of periodontal therapy. J Periodontol 1984;55: 499-504. 102. Lindhe J, Westfelt E, Nyman S, Socransky S, Heijl L, Bratthall G. Healing following surgical/nonsurgical treatment of periodontal disease. A clinical study. J Clin Periodontol 1982;9:115-28. 103. Berkey CS, Antczak-Bouckoms A, Hoaglin DC, Mosteller F, Pihlstrom BL. Multiple-outcomes metaanalysis of treatments for periodontal disease. J Dent Res 1995;74:1030-9. 104. Buchanan SA, Robertson PB. Calculus removal by scaling/ root planing with and without surgical access. J Periodontol 1987;58:159-63. 105. Wang HL, Burgett FG, Shyr Y, Ramfjord S. The influence of molar furcation involvement and mobility on future clinical periodontal attachment loss. J Periodontol 1994;65:25-9. 106. Caton JG, Zander HA. The attachment between tooth and gingival tissues after periodic root planing and soft tissue curettage. J Periodontol 1979;50:462-6. 107. Caton J, Nyman S. Histometric evaluation of periodontal surgery. I. The modified Widman flap procedure. J Clin Periodontol 1980;7:212-23. 108. Caton J, Nyman S, Zander H. Histometric evaluation of periodontal surgery. II. Connective tissue attachment levels after four regenerative procedures. J Clin Periodontol 1980; 7:224-31. 109. Isidor F, Attström R, Karring T. Regeneration of alveolar bone following surgical and non-surgical periodontal treatment. J Clin Periodontol 1985;12:687-96. 110. Listgarten MA, Rosenberg MM. Histological study of repair following new attachment procedures in human periodontal lesions. J Periodontol 1979;50:333-44. 111. Stahl SS, Froum SJ, Kushner L. Periodontal healing following open flap debridement procedures. II. Histologic observations. J Periodontol 1982;53:15-21. 112. Froum SJ, Coran M, Thaller B, Kushner L, Scopp IW, Stahl SS. Periodontal healing following open debridement procedures. I. Clinical assessment of soft tissue and osseous repair. J Periodontol 1982;53:8-14.
113. Cole RT, Crigger M, Bogle G, Egelberg J, Selvig KA. Connective tissue regeneration to periodontally diseased teeth. A histological study. J Periodont Res 1980;15:1-9. 114. Albair WB, Cobb CM, Killoy WJ. Connective tissue attachment to periodontally diseased roots after citric acid demineralization. J Periodontol 1982;53:515-26. 115. Froum SJ, Kushner L, Stahl SS. Healing responses of human intraosseous lesions following the use of debridement, grafting and citric acid root treatment. I. Clinical and histologic observations six months postsurgery. J Periodontol 1983;54:67-76. 116. Stahl SS, Froum SJ, Kushner L. Healing responses of human intraosseous lesions following the use of debridement, graftingand citric acid root treatment. II. Clinical and histologic observations: One year postsurgery. J Periodontol 1983;54:325-38. 117. Peltzman B, Bowers GM, Reddi AH, Bergquist JJ. Treatment of furcations involvements with Fibronectin and intraoral autogenous bone grafts: Preliminary observations. Int J Periodontics Restorative Dent 1988;8(5):51-63. 118. Wikesjö UME, Baker PJ, Christersson LA, et al. A biochemical approach to periodontal regeneration: Tetracycline treatment conditions dentin surfaces. J Periodont Res 1986;21:322-9. 119. Dragoo MR, Sullivan HC. A clinical and histologic evaluation of autogenous iliac bone grafts in humans: Part I. Wound healing 2 to 8 months. J Periodontol 1973;44: 599-613. 120. Dragoo MR, Sullivan HC. A clinical and histologic evaluation of autogenous iliac bone grafts in humans: Part II. External root resorption. J Periodontol 1973;44:614-25. 121. Mellonig JT. Decalcified freeze-dried bone allograft as an implant material in human periodontal defects. Int J Periodontics Restorative Dent 1984;4(6):40-55. 122. Bowers GM, Chadroff B, Carnevale R, et al. Histologic evaluation of new human attachment apparatus formation in humans, Part I. J Periodontol 1989;60:664-74. 123. Bowers GM, Chadroff B, Carnevale R, et al. Histologic evaluation of new human attachment apparatus formation in humans, Part II. J Periodontol 1989;60:675-82. 124. Bowers GM, Chadroff B, Carnevale R, et al. Histologic evaluation of new human attachment apparatus formation in humans, Part III. J Periodontol 1989;60:683-93. 125. Rummelhart JM, Mellonig JT, Gray JL, Towle HJ. A comparison of freeze-dried bone allograft and demineralized freeze-dried bone allograft in human periodontal osseous defects. J Periodontol 1989;60:655-63. 126. Gottlow J, Nyman S, Karring T, Lindhe J. New attachment formation as the result of controlled tissue regeneration. J Clin Periodontol 1984;11:494-503. 127. Magnusson I, Nyman S, Karring T, Egelberg J. Connective tissue attachment formation following exclusion of gingival connective tissue and epithelium during healing. J Periodont Res 1985;20:201-8.
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128. Becker W, Becker BE, Berg L, Prichard J, Caffesse R, Rosenberg E. New attachment after treatment with root isolation procedures: Report for treated class III and class II furcations and vertical osseous defects. Int J Periodontics Restorative Dent 1988;8(3):9-23. 129. McClain PH, Schallhorn RG. Long-term assessment of combined osseous composite grafting, root conditioning, and guided tissue regeneration. Int J Periodontics Restorative Dent 1993;13:9-27. 130. Machtei EE, Grossi SG, Dunford R, Zambon JJ, Genco RJ. Long-term stability of Class II furcation defects treated with barrier membranes. J Periodontol 1996;67:523-7. 131. Garrett S, Polson AM, Stoller NH, et al. Comparison of a bioresorbable GTR barrier to a non-absorbable barrier in treating human class II furcation defects. A multi-center parallel design randomized single-blind trial. J Periodontol 1997;68:667-75. 132. Rosen PS, Reynolds MA. Polymer-assisted regenerative therapy: case reports of 22 consecutively treated periodontal defects with a novel combined surgical approach. J Periodontol 1999;70;554-61. 133. Cortellini P, Pini Prato G, Tonetti MS. Periodontal regeneration of human intrabony defects with bioresorbable membranes. A controlled clinical trial. J Periodontol 1996; 67:217-23. 134. Bowers G, Felton F, Middleton C, et al. Histologic comparison of regeneration in human intrabony defects when osteogenin is combined with demineralized freeze-dried bone allograft and with purified bovine collagen. J Periodontol 1991;62:690-702. 135. Caffesse, RG, Quinones CR. Polypeptide growth factors and attachment proteins in periodontal wound healing and regeneration. Periodontol 2000 1993;1:69-79. 136. Seyedin SM. Osteoinduction: A report on the discovery and research of unique protein growth factors mediating bone development. Oral Surg Oral Med Oral Pathol 1989;68:527-30. 137. Lynch SE, Williams RC, Polson AM, Howell TH, Reddy MS, Zappa UE. A combination of platelet-derived and insulin-like growth factors enhances periodontal regeneration. J Clin Periodontol 1989;16:545-8. 138. Wozney JM. The potential role of bone morphogenetic proteins in periodontal reconstruction. J Periodontol 1995;66:506-10. 139. Mellonig JT. Enamel matrix derivative for periodontal reconstructive surgery: Technique and clinical and histologic case report. Int J Perodontics Restorative Dent 1999;19:9-19. 140. Yukna RA, Callan DP, Krauser JT, et al. Multi-center clinical evaluation of combination anorganic bovinederived hydroxyapatite matrix (ABM)/cell binding peptide (P-15) as a bone replacement graft material in human periodontal osseous defects. 6-month results. J Periodontol 1998; 69:655-63.
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141. Sculean A, Donos N, Blaes A, et al. Comparison of enamel matrix proteins and bioabsorbable membranes in the treatment of intrabony periodontal defects. A split-mouth study. J Periodontol 1999;70:255-62. 142. Pontoriero R, Wennstrom J, Lindhe J. The use of barrier membranes and enamel matrix proteins in the treatment of angular bone defects. A prospective controlled clinical trial. J Clin Periodontol 1999;26:833-40. 143. American Academy of Periodontology. Periodontal regeneration (position paper). Chicago, Ill: The American Academy of Periodontology; May 1993. 144. Garrett S. Periodontal regeneration around natural teeth. Ann Periodontol 1996;1:621-66. 145. American Academy of Periodontology. Reconstructive periodontal surgery (position paper) Chicago, Ill: The American Academy of Periodontology; May 1992. 146. Grossi SG, Skrepcinski FB, DeCaro T, Zambon JJ, Cummins D, Genco RJ. Response to periodontal therapy in diabetics and smokers. J Periodontol 1996;67:1094-102. 147. Zambon JJ, Grossi SG, Machtei EE, Ho AW, Dunford R, Genco RJ. Cigarette smoking increases the risk for subgingival infection with periodontal pathogens. J Periodontol 1996;67:1050-4. 148. Rosen PS, Marks MH, Reynolds MA. Influence of smoking on long-term clinical results of intrabony defects treated with regenerative therapy. J Periodontol 1996;67:1159-63. 149. Preber H, Bergström J. The effect of non-surgical treatment on periodontal pockets in smokers and nonsmokers. J Clin Periodontol 1986;13:319-23. 150. Preber H, Bergström J. Effect of cigarette smoking on periodontal healing following surgical therapy. J Clin Periodontol 1990;17:324-8. 151. American Academy of Periodontology. Tobacco use and the periodontal patient (position paper). Chicago, Ill: The American Academy of Periodontology; September 1995. 152. Comar MD, Kollar, Gargiulo AW. Local irritation and occlusal trauma as co-factors in the periodontal disease process. J Periodontol 1969;40:193-200. 153. Polson AM, Meitner SW, Zander HA. Trauma and progression of marginal periodontitis in squirrel monkeys. III. Adaptation of interproximal alveolar bone to repetitive injury. J Periodont Res 1976;11:278-89. 154. Polson AM, Meitner SW, Zander HA. Trauma and progression of marginal periodontitis in squirrel monkeys. IV. Reversibility of bone loss due to trauma alone and trauma superimposed upon periodontitis. J Periodont Res 1976;11:290-7. 155. Perrier M, Polson A. The effect of progressive and increasing tooth hypermobility on reduced but healthy periodontal supporting tissues. J Periodontol 1982;53:152-7. 156. Lindhe J, Ericsson I. The effect of elimination of jiggling forces on periodontally exposed teeth in the dog. J Periodontol 1982;53:562-7.
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157. Neiderud A-M, Ericsson I, Lindhe J. Probing pocket depth at mobile and nonmobile teeth. J Clin Periodontol 1992; 19:754-9. 158. Burgett FG, Ramfjord SP, Nissle RR et al. A randomized trial of occlusal adjustment in the treatment of periodontitis patients. J Clin Periodontol 1992;19:381-7. 159. Harrel SK, Nunn ME. The effect of occlusal discrepancies on periodontitis. II. Relationship of occlusal treatment to the progression of periodontal disease. J Periodontol 2001; 72:495-505. 160. Gehr M. Non-surgical pocket therapy: Dental occlusion. Ann Periodontol 1996;1:567-80. 161. Rosling B, Nyman S, Lindhe J, Jern B. The healing potential of the periodontal tissues following different techniques of periodontal surgery in plaque-free dentitions. J Clin Periodontol 1976;3:233-50. 162. American Academy of Periodontology. Supportive periodontal therapy (SPT) (position paper). Chicago,Ill: The American Academy of Periodontology December, 1997.
Acknowledgments This paper was revised by Dr. Paul S. Rosen. It replaces the paper entitled Treatment of Gingivitis and Periodontitis which was authored by Drs. William F. Ammons, Kenneth L. Kalkwarf, and Stephen T. Sonis in May 1993 and revised by Dr. Bruce L. Pihlstrom and William F. Ammons in September 1997. Members of the 2000-2001 Research, Science and Therapy Committee include: Drs. David Cochran, Chair; Timothy Blieden; Otis J. Bouwsma; Robert E. Cohen; Petros Damoulis; Connie H. Drisko; Joseph P. Fiorellini; Gary Greenstein; Vincent J. Iacono; Martha J. Somerman; Terry D. Rees; Angelo Mariotti, Consultant; Robert J. Genco, Consultant; and Brian L. Mealey, Board Liaison. Individual copies of this position paper may be obtained by accessing: “http://www.perio.org”. Members of the American Academy of Periodontology have permission of the Academy, as copyright holder, to reproduce up to 150 copies of this document for not-forprofit, educational purposes only. For information on reproduction of the document for any other use or distribution, please contact Rita Shafer at the Academy Central Office; voice: (312) 573-3221; fax: (312) 573-3225; or e-mail:
[email protected].
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American Academy of Pediatric Dentistry
Dental Growth and Development Primary Dentition Calcification begins at
Formation complete at
Eruption Maxillary Mandibular
Exfoliation Maxillary Mandibular
Central incisors
4th fetal mo
18-24 mo
6-10 mo
5-8 mo
7-8 y
6-7 y
Lateral incisors
4th fetal mo
18-24 mo
8-12 mo
7-10 mo
8-9 y
7-8 y
Canines
4th fetal mo
30-39 mo
16-20 mo
16-20 mo
11-12 y
9-11 y
First molars
4th fetal mo
24-30 mo
11-18 mo
11-18 mo
9-11 y
10-12 y
Second molars
4th fetal mo
36 mo
20-30 mo
20-30 mo
9-12 y
11-13 y
Permanent Dentition Calcification begins at
Crown (enamel) complete at
Roots complete at
Central incisiors
3-4 mo
4-5 y
9-10 y
7-8 y (3)
6-7 y (2)
Lateral incisors
Maxilla: 10-12 mo
4-5 y
11 y
8-9 y (5)
7-8 y (4)
Mandible: 3-4 mo
4-5 y
10 y
4-5 y
6-7 y
12-15 y
11-12 y (11)
9-11 y (6)
First premolars
18-24 mo
5-6 y
12-13 y
10-11 y (7)
10-12 y (8)
Second premolars
24-30 mo
6-7 y
12-14 y
10-12 y (9)
11-13 y (10)
Birth
30-36 mo
9-10 y
5.5-7 y (1)
5.5-7 y (1a)
Second molars
30-36 mo
7-8 y
14-16 y
12-14 y (12)
12-14 y (12a)
Third molars
Maxilla: 7-9 y
4-5 y
17-30 y (13)
17-30 y (13a)
Canines
First molars
Eruption* Maxillary Mandibular
Mandible: 8-10 y
* Figures in parentheses indicate order of eruption. Many otherwise normal infants do not conform strictly to the stated schedule. Logan WHG, Kronfeld R. Development of the human jaws and surrounding structures from birth to the age of fifteen years. J Am Dent Assoc 1933;20 (3):379-427. Copyright © 1933 American Dental Association. All rights reserved. Adapted 2003 by permission.
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Food Pyramid
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American Academy of Pediatric Dentistry
Speech and Language Milestones What should my child be able to do? Hearing and Understanding
Talking
Birth-3 Months
Birth-3 Months
• • • •
• Makes pleasure sounds (cooing, gooing). • Cries differently for different needs. • Smiles when sees you.
Startles to loud sounds. Quiets or smiles when spoken to. Seems to recognize your voice and quiets if crying. Increases or decreases sucking behavior in response to sound.
4-6 Months
4-6 Months
• • • •
• Babbling sounds more speech-like with many different sounds, including p, b, and m. • Chuckles and giggles. • Vocalizes excitement and displeasure. • Makes gurgling sounds when left alone and when playing with you.
Moves eyes in direction of sounds. Responds to changes in tone of your voice. Notices toys that make sounds. Pays attention to music.
7 Months-1 Year
7 Months-1 Year
• • • •
Enjoys games like peek-o-boo and pat-a-cake. Turns and looks in direction of sounds. Listens when spoken to. Recognizes words for common items like “cup”, “shoe”, “book”, or “juice”. • Begins to respond to requests (e.g. “Come here” or “Want more?”).
• Babbling has both long and short groups of sounds such as “tata upup bibibibi.” • Uses speech or non-crying sounds to get and keep attention. • Uses gestures to communication (waving, holding arms to be picked up) • Imitates different speech sounds. • Has one or two words (hi, dog, dada, mama) around first birthday, although sounds may not be clear.
One to Two Years
One to Two Years
• Points to a few body parts when asked. • Follows simple commands and understands simple questions (“Roll the ball”, “Kiss the baby”, “Where’s your shoe?”). • Listens to simple stories, songs, and rhymes. • Points to pictures in a book when named.
• Says more words every month. • Uses some one- or two- word questions (“Where kitty?”, “Go bye-bye?”, “What’s that?”). • Puts two words together (“more cookie”, “no juice”, “mommy book”). • Uses many different consonant sounds of the beginning of words.
Two to Three Years
Two to Three Years
• Understands differences in meaning (“go-stop”, “in-on”, “big-little”, “up-down”). • Follows two requests (“Get the book and put it on the table”). • Listens to and enjoys hearing stories for longer periods of time.
• • • • •
Three to Four Years
Three to Four Years
• Hears you when call from another room. • Hears television or radio at the same loudness level as other family members. • Answers simple, “who?”, “what?”, “where?”, and “why?” questions.
• • • •
Four to Five Years
Four to Five Years
• Pays attention to a short story and answers simple questions about them. • Hears and understands most of what is said at home and in school.
• • • • • • •
Has a word for almost everything. Uses two- or three- words to talk about and ask for things. Uses k, g, f, t, d, and n sounds. Speech is understood by familiar listeners most of the time. Often asks for or directs attention to objects by naming them.
Talks about activities at school or at friends’ homes. People outside family usually understand child’s speech. Uses a lot of sentences that have 4 or more words. Usually talks easily without repeating syllables or words.
Uses sentences that give lots of details (“The biggest peach is mine”). Tells stories that stick to topic. Communicates easily with other children and adults. Says most sounds correctly except a few like l, s, r, v, z, ch, sh, th. Says rhyming words. Names some letters and numbers. Uses the same grammar as the rest of the family.
Reprinted with permission from How does your child hear and talk? (n.d.) Available from the website of the American Speech-LanguageHearing Association: “http://www.asha.org/public/speech/development/chart.htm.” All rights reserved. resource sec tion
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Decision Trees for Management of an Avulsed Permanent Tooth Management of an Avulsed Permanent Incisor with an Open Apex (Apex ≥1 mm)*
↓
OR:
Immediately replanted at the accident site.
↓
Assess medical history and rule out any neurologic and nondental injuries. Diagnostic tests: • Rule out alveolar fracture. • 3 radiographs angulated differently to rule out root fractures. • Pulp vitality test maxillary and mandibular anteriors.
OR:
Extraoral dry storage time <20 minutes and tooth was transported in Hank’s Balanced Salt Solution (HBSS) or milk for 20 minutes to 6 hours.
↓ If tooth was kept moist (in water, saliva or other non-physiologic media) for 20 to 60 minutes.
↓
OR:
↓
OR:
20 to 60 minutes extraoral dry time/storage.
Change transport to HBSS. If HBSS is not available, place in cold milk.
Soak in doxycycline or ArestinTM solution for 5 minutes.
>60 minutes extraoral dry time/storage.
Debride with soft pumice prophylaxis, gauze, gentle scaling/root planing, or 3% citric acid for 3 minutes, and rinse well to remove periodontal ligament.
Place in 1.23% sodium fluoride (eg, acidulated phosphate fluoride) for 5 to 20 minutes.
• • • •
Replant and/or reposition. Obtain periapical radiographs to verify position. Place flexible splint for approximately 2 weeks; 4 weeks for dry time >60 minutes. Rx: Antibiotics (eg, doxycyline or penicillin V potassium for non-allergic patients) for 7 days; Chlorhexidine rinse for 1 week. • Assess tetanus vaccination: if needed, get booster within 48 hours. • Provide post-operative instructions; inform of prognosis. • Follow up in 7 to 10 days.
• Monitor every 4 weeks + pulp test + radiographs. • Ideal outcome: revascularization and/or apexogenesis occurs over the next 12 to 18 months. • Alternative outcomes: – Initiate apexification with mineral trioxide aggregate (MTA) or calcium hydroxide or root canal therapy if clinical and/or radiographic pathology presents. – Consider decoronation procedure when clinical infraposition of the tooth appears and/or clinical and radiographic findings of ankylosis manifest. • Follow-up: 1 week, 1 month, 3 months, 6 months, 12 months, and annually for 5 years.
* Adapted with permission from: McIntyre J, Lee J, Trope M, Vann WJ, Permanent tooth replantation following avulsion: Using a decision tree to achieve the best outcome. Pediatr Dent 2009;31(2):137-44. 314
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Management of an Avulsed Permanent Incisor with an Closed Apex (Apex <1 mm)*
↓
OR:
Immediately replanted at the accident site.
↓
Assess medical history and rule out any neurologic and nondental injuries. Diagnostic tests:
• Rule out alveolar fracture. • 3 radiographs angulated differently to rule out root fractures. • Pulp vitality test maxillary and mandibular anteriors.
OR:
Extraoral dry storage time was <20 minutes and tooth was transported in Hank’s Balanced Salt Solution (HBSS) or milk for 20 minutes to 6 hours.
↓ If tooth was kept moist (in water, saliva or other non-physiologic media) for 20 to 60 minutes.
OR:
↓
↓
OR:
>60 minutes extraoral dry time/storage.
20 to 60 minutes extraoral dry time/storage.
Debride with soft pumice prophylaxis, gauze , gentle scaling/root planing, or 3% citric acid for 3 minutes, and rinse well to remove periodontal ligament.
Change transport to HBSS. If HBSS is not available, place in cold milk.
• • • • • • • •
Place in 1.23% sodium fluoride (eg, acidulated phosphate fluoride) for 5 to 20 minutes.
Replant and/or reposition. Obtain periapical radiographs to verify position. Place flexible splint for approximately 2 weeks; 4 weeks for dry time >60 minutes. Rx: Antibiotics (eg, doxycyline or penicillin V potassium for non-allergic patients) for 7 days; Chlorhexidine rinse for 1 week. Assess tetanus vaccination: if needed, get booster within 48 hours. Provide post-operative instructions; inform of prognosis. Follow up in 7 to 10 days. Initiate pulpectomy/debridement on all teeth within 7 to 10 days.
If root canal therapy was initiated, complete within 1 month. OR If patient does not present until >2 weeks after trauma and/or if radiographic resorption is present:
• Pulpectomy/debridement as soon as possible. • Long-term calcium hydroxide therapy/slurry and change every 3 months. • Complete root canal therapy when periodontal ligament/lamina dura is observed/healthy. Follow-up: 1 week, 1 month, 3 months, 6 months, 12 months, and annually for 5 years.
* Adapted with permission from: McIntyre J, Lee J, Trope M, Vann WJ, Permanent tooth replantation following avulsion: Using a decision tree to achieve the best outcome. Pediatr Dent 2009;31(2):137-44.
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Preparing for Your Child’s Sedation Visit Patient: ______________________________ Sedation appointment: ___________at _______am/pm We have recommended sedation for your child’s safety and comfort during dental procedures. Sedation can help increase cooperation and reduce anxiety and/or discomfort associated with dental treatment. Various medications can be used to sedate a child; medicines will be selected based upon your child’s overall health, level of anxiety, and dental treatment recommendations. Once the medications have been administered, it may take up to an hour before your child shows signs of sedation and is ready for dental treatment. Most children become relaxed and/or drowsy and may drift into a light sleep from which they can be aroused easily. Unlike general anesthesia, sedation is not intended to make a patient unconscious or unresponsive. Some children may not experience relaxation but an opposite reaction such as agitation or crying. These also are common responses to the medicines and may prevent us from completing the dental procedures. In any case, our staff will observe your child’s response to the medications and provide assistance as needed. You, as parent/legal guardian, play a key role in your child’s dental care. Children often perceive a parent’s anxiety which makes them more fearful. They tolerate procedures best when their parents understand what to expect and prepare them for the experience. If you have any questions about the sedation process, please ask. As you become more confident, so will your child. For your child’s safety, you must follow the instructions below. Prior to your child’s sedation appointment: • Please notify our office of any change in your child’s health and/or medical condition. Fever, ear infection, nasal
or chest congestion, or recent head trauma could place your child at increased risk for complications. Should your child become ill just prior to a sedation appointment, contact our office to see if it is necessary to postpone the sedation. • Tell us about any prescribed, over-the-counter, or herbal medications your child is taking. Check with us to see if routine medications should be taken the day of the sedation. Also, report any allergies or reactions to medications that your child has experienced. • Food and liquids must be restricted in the hours prior to sedation. Fasting decreases the risk of vomiting and aspirating stomach contents into the lungs, a potentially life-threatening problem. We will not proceed with the sedation if you do not comply with the following requirements. TYPE OF FOOD/LIQUID
MINIMUM FASTING PERIOD
Clear liquids (water, juice without pulp, and other beverages you can see through when held up to light)
2 hours before sedation
Breast milk
4 hours before sedation
Formula, non-human milk, and light foods (NOT fried or fatty foods or meat)
6 hours before sedation
• Dress your child in loose-fitting, comfortable clothing. This will allow us to place monitors that evaluate your child’s response to the medications and help ensure your child’s safety. These monitors may measure effects on your child’s breathing, heart rate, and blood pressure. • Try not to bring other children to this appointment so you can focus your attention on your child undergoing the sedation. • If you will be traveling home by automobile or if you must bring any other children with you to this appointment, it is preferable to have 2 adults accompany the patient home. On the way home, one individual should be able to observe the child’s breathing without any distractions, especially if the patient falls asleep while in the car or safety seat. 316
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During the sedation appointment:
• If any sedative medications are administered before your child is taken to the treatment room, we will ask you to watch your child closely as he/she may become sleepy, dizzy, unsteady, uncoordinated, or irritable. You will need to remain next to your child to prevent injuries that may occur from stumbling/falling. Keeping your child calm but distracted from the unfamiliar surroundings often is helpful. • You, as the child’s parent/legal guardian, must remain at the office throughout the sedation appointment. You may not leave the office for any reason. • The doctor and staff will evaluate your child’s health status before he/she will be discharged home. Children recover from effects of sedatives at different rates so be prepared to remain at our office until the doctor has determined your child is stable and the after-effects are minimal. At discharge, your child should be responsive but may be drowsy, crying, or fussy. After the sedation appointment: • Once home, your child will still be drowsy and must remain under adult supervision until fully recovered from the effects of the sedation. If your child wants to sleep, position your child on his/her side with the head supported and the chin up. During this period, check your child’s breathing and airway every 3-5 minutes. If your child is snoring, reposition the head until the snoring disappears and your child breathes normally. If breathing becomes abnormal or you are unable to arouse your child, contact emergency services (call 911 or _____________) immediately. • Nausea and vomiting are occasional side effects of sedation. If vomiting occurs, immediately clear the material from your child’s mouth. Once again, be sure that breathing is normal. If breathing becomes abnormal or you are unable to arouse your child, contact emergency services (call 911 or ___________) immediately. If vomiting persists for 20 to 40 minutes, contact our office immediately. • Your child may be drowsy for some time after the sedation appointment. Restrict activities for the remainder of the day. Prohibit potentially harmful activities such as bike riding, swimming, using playground equipment, or any activity where balance is important. • In addition to the sedative medications, we often use local anesthetic to numb the mouth during dental treatment. The numbness usually lasts 2-4 hours. Watch to see that your child does not bite, scratch, or injure the cheek, lips, or tongue during this time. • Children may be irritable after treatment. If this occurs, stay with your child and provide a calm environment. If you believe the irritability is caused by discomfort, you may give your child acetaminophen (Tylenol®) or ibuprofen (Motrin®, Advil®). Follow the instructions on the bottle for dosing based upon your child’s age/weight. • Once your child is alert, you may give him/her sips of clear liquids to prevent nausea and dehydration. Small drinks taken repeatedly are preferable to large amounts. The first meal should be something light and easily digestible (eg, soup, Jell-O®, apple sauce). Do not give fatty or spicy foods (eg, French fries, tacos, salsa, milk, cheese, yogurt). • A slight fever (temperature to 100.5°F) is not uncommon after sedation. You may give your child acetaminophen (Tylenol®) or ibuprofen (Motrin®, Advil®). Follow the instructions on the bottle for dosing based upon your child’s age/weight. Because dehydration may cause a slight increase in temperature, clear fluids may help correct this condition. If a higher fever develops or the fever persists, call our office. • Please feel free to call the office for any questions or concerns that you might have. • Additional instructions: ________________________________________________________________ _______ __________________________________________________________________________________________ __________________________________________________________________________________________ ________________________________________________________________________________________ Contact Numbers:
Office: ___________________________ After Hours: __________________________
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Sedation Record
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SEDATION RECORD
TIME N2O/O2 (%)
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Post-operative Instructions for Extractions/ Oral Surgery Patient: __________________________________________________________ Your child had the following procedure performed today: ❒ Frenectomy
❒ Biopsy
❒ Gingivectomy
Date: _______________________________
❒ Extraction
❒ Exposure of unerupted tooth
❒ Gingival graft
❒ Other: _________________________________
This will require special care and attention over the next few days. Please follow the instructions checked below. Contact us with questions or
if unusual symptoms develop. ❒ Numbness: The mouth will be numb approximately 2-4 hours. Watch to see that your child does not bite, scratch, or injure the cheek, lips, or tongue during this time. ❒ Bleeding: Bleeding was controlled before we discharged your child, but some occasional oozing (pink or blood-tinged saliva) may occur. Hold gauze with firm pressure against the surgical site until oozing has stopped. You may need to change the gauze or repeat this step. If bleeding continues for more than 2 hours, contact us. ❒ Surgical Site Care: Today, do not disturb the surgical site. Do not stretch the lips or cheeks to look at the area. Do not rinse vigorously, use mouthwash, or probe the area with fingers or other objects. Beginning tomorrow, you may rinse with warm salt water (½ teaspoon salt with 1 cup water) after meals. ❒ Sutures: Sutures (stitches) were placed to help control bleeding and promote healing. These sutures ❒ will dissolve and do not need to be removed OR ❒ will be removed at your follow-up visit. If the stitches come out during the first 48 hours, call our office.
❒ Daily Activities: Today, avoid physical exercise and exertion. Return to normal activities as tolerated. Smoking is never good for one’s health and may delay healing following oral surgery. ❒ Diet: After all bleeding has stopped, the patient may drink cool non-carbonated liquids but should NOT use a straw. Encourage fluids to help avoid dehydration. Cold soft foods (eg, ice cream, gelatin, Instant Breakfast®, pudding, yogurt) are ideal the first day. By the second day, consistency of foods can progress as tolerated. Until healing is more established, avoid foods such as nuts, sunflower seeds, and popcorn that may get lodged in the surgical areas. ❒ Oral Hygiene: Keeping the mouth clean is essential. Today, teeth may be brushed and flossed gently, but avoid stimulating the surgical site. Soreness and swelling may not permit vigorous brushing of all areas, but please make every effort to clean the teeth within the bounds of comfort. ❒ Pain : Because some discomfort is expected, you may give your child acetaminophen (Tylenol®) or ibuprofen (Motrin®, Advil®) before the numbness wears off. Do NOT give aspirin to your child. Follow the instructions on the bottle for dosing based upon your child’s age/weight. If pain is not relieved by one of these medications, a prescription may be needed. Take prescription pain medication with a small amount of food to avoid nausea. ❒ Prescription: You were prescribed ❒ pain medicine ❒ antibiotics ❒ oral rinse ❒ other ______________________ Directions: _____________________________________________________________________________________________ ______________________________________________________________________________________________________ ❒ Other: _________________________________________________________________________________________________ ______________________________________________________________________________________________________ ❒ Watch for: ❒ Swelling: Slight swelling and inflammation may occur for the next 2 days. If swelling occurs, ice packs may be used for the first 24 hours (10 minutes on then 10 minutes off ) to decrease swelling and/or bruising. If swelling persists after 24 hours, warm/moist compresses (10 minutes on then 10 minutes off ) may help. If swelling occurs after 48 hours, call our office. ❒ Fever: A slight fever (temperature to 100.5°F) is not uncommon the first 48 hours after surgery. If a higher fever develops or the fever persists, call our office. ❒ Dry Socket: Premature dissolving or loss of a blood clot following removal of a permanent tooth may result in a “dry socket”. This typically occurs on the 3rd to 5th day after the extraction, with a persistent throbbing pain in the jaw. Call our office if this occurs. ❒ follow-up: Schedule your child’s next visit for ____________________________________ in _________ days/weeks/months. Contact Numbers: Office: _____________________________________ 320
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Record Transfer Date: ____________________
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Release for School Absences A Message to Parents and School Administrators Regarding School Absence for Dental Appointments Tooth decay in children can be painful, just as it is in adults. Although largely preventable with proper home care and regular dental visits, untreated tooth decay diminishes a child’s ability to eat, sleep, and function well at home or at school. The unesthetic nature of tooth decay and dental malocclusion also may compromise the child’s selfesteem and social development. Prevention, early diagnosis, and treatment of oral health conditions require professional care. The American Academy of Pediatric Dentistry recognizes the importance of regular school attendance and the effect of chronic absence on academic performance. We encourage our members to work with parents and educators to minimize school absence whenever possible. It is not always possible or appropriate to provide all the care children need during non-school hours. School policies that prevent legitimate school absence for the purpose of dental visits may have a negative impact on the health and well being of children. The American Academy of Pediatric Dentistry urges parents, school administrators, and member dentists to work together to ensure that children receive needed health care while minimizing school absences. The American Academy of Pediatric Dentistry encourages parents to return their children to school for the remainder of the day after their dental visit when possible. In the case of an appointment later in the day, a child should attend school and be excused prior to his/her dental appointment.
School Attendance Release Student: _________________________________ had an appointment in this office on ______________________ from ____________ to ____________ for necessary oral health care.
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Common Laboratory Values Common Laboratory Values
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CBC Test
Normal value
Function
Significance
Hemoglobin
12-18 g/100 mL
Measures oxygen carrying capacity of blood
Low: hemorrhage, anemia High: polycythemia
Hematocrit
35%-50%
Measures relative volume of cells and plasma in blood
Low: hemorrhage, anemia High: polycythemia, dehydration
Red blood cell
4-6 million/mm3
Measures oxygen-carrying capacity of blood
Low: hemorrhage, anemia High: polycythemia, heart disease, pulmonary disease
White blood cell Infant 4-7 y 8-18 y
8,000-15,000/mm3 6,000-15,000/mm3 4,500-13,500/mm3
Test
Normal value
Measures host defense against inflammatory agents Low: aplastic anemia, drug toxicity, specific infections High: inflammation, trauma, toxicity, leukemia Differential Count Significance
Neutrophils
54%-62%
Increase in bacterial infections, hemorrhage, diabetic acidosis
Lymphocytes
25%-30%
Viral and bacterial infection, acute and chronic lymphocytic leukemia, antigen reaction
Eosinophils
1%-3%
Increase in parasitic and allergic conditions, blood dyscrasias, pernicious anemia
Basophils
1%
Increase in types of blood dyscrasias
Monocytes
0%-9%
Hodgkin’s disease, lipid storage disease, recovery from severe infections, monocytic leukemia Absolute Neutrophil Count (ANC) Normal value Significance
Calculation
(% Polymorphonuclear Leukocytes + % Bands)×Total White Cell Count 100 Bleeding Screen Test Normal value Function
>1500
<1000 Patient at increased risk for infection; defer elective dental care
Significance
Prothrombin time
1-18 sec
Measures extrinsic clotting factors
Prolonged in liver disease, impaired Vitamin K production, surgical trauma with blood loss
Partial thromboplastin time
By laboratory control
Measures intrinsic Prolonged in hemophilia A,B, and C and clotting of blood, Von Willebrand’s disease congenital clotting disorders
Platelets
140,000-340,000/mL
Measures clotting potential
Bleeding time
1-6 min
Measures quality of platelets Prolonged in thrombocytopenia
International Normalized Ratio (INR)
Without anticoagulant therapy: 1 Measures extrinsic Anticoagulant therapy clotting function target range: 2-3
Increased in polycythemia, leukemia, severe hemorrhage; decreased in thrombocytopenia purpura Increased with anticoagulant therapy
Urinalysis Test
Normal value
Volume
day 1,000-2,000 mL/d
Function
Specific gravity
1.015-1.025
Measures the degree of tubular reabsorption and dehydration
Increase in diabetes mellitus; decrease in acute nephritis, diabetes insipidus, aldosteronism
pH
6-8
Reflects acidosis and alkalosis
Acidic: diabetes, acidosis, prolonged fever Alkaline: urinary tract infection, alkalosis
Casts
1-2 per high power field
Renal tubule degeneration occurring occuring in in cardiac failure, pregnancy, and hemoglobinuric-nephrosis
Test
Normal value
Electrolytes Function
Sodium (Na)
135-147 mEq
Reflects acid-base balance
Potassium (K)
3.5-5 mEq
Bicarbonate (HCO3)
24-30 mEq
Chloride (Cl)
100-106 mEq
Significance Increase in diabetes mellitus, chronic nephritis
Significance Increase in Cushing’s syndrome Increase in tissue breakdown
Reflects acid-base balance
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Common Pediatric Medications* Antibiotics
Analgesics
Amoxicillin
Acetaminophen
Forms: Liquid, tablet, capsule
Forms: Liquid, tablet, capsule, rectal suppository
Usual oral dosage1,2: Children > 3 months of age up to 40 kg: 20-40 mg/kg/day in divided doses every 8 hours OR 25-45 mg/kg/day in divided doses every 12 hours Children > 40 kg & adults: 250-500 mg every 8 hours OR 500-875 mg every 12 hours
Usual oral dosage4: Children < 12 years: 10-15 mg/kg/dose every 4-6 hours as needed. Do not exceed 5 doses (2.6 g) in 24 hours
Endocarditis prophylaxis3: 50mg/kg (maximum 2 g 30-60 minutes before procedure
Forms: Liquid, tablet
Amoxicillin clavulanate (Augmentin®) Forms: Liquid, tablet Usual oral dosage1 (based on amoxicillin component): Children > 3 months of age up to 40 kg: 25-45 mg/kg/day in divided doses every 12 hours (Rx suspension or chewable tablet due to clavulanic acid component) Children > 40 kg & adults: 500-875 mg every 12 hours (Rx tablet)
Cephalexin Forms: Liquid, tablet, capsule Usual oral dosage2: Children: 25-50 mg/kg/day in divided doses Adults: 250 mg every 6 hours Endocarditis prophylaxis3: 50 mg/kg (maximum 2 g) 30-60 minutes before procedure
Clindamycin HCl Forms: Liquid, tablet, capsule, injectable Usual oral dosage2: Children: 8-20 mg/kg/day in 3-4 divided doses Adults: 150-450 mg every 6 hours Usual parenteral dose4: Children > 1 mo old: 20-40 mg/kg/day in 3-4 divided doses Children > 12 & adults: 1.2-1.8 g/day in 2-4 divided doses Endocarditis prophylaxis3: 20 mg/kg (maximum 600 mg) orally, IM, or IV 30-60 minutes before procedure
Penicillin V Potassium Forms: liquid, tablet Usual oral dosage4: Children < 12: 25-50 mg/kg/day in 3-4 divided doses Children > 12 & adults: 125-500 mg q 6-8 hrs
Children > 12 years & adults: 325-650 mg every 4-6 hours as needed not to exceed 4g/day
Acetaminophen with codeine4 Elixir: No. 2: No. 3: No. 4:
120 mg acetaminophen & 12 mg codeine/5 mL with alcohol 7% 300 mg acetaminophen and 1 5 mg codeine 300 mg acetaminophen and 30 mg codeine 300 mg acetaminophen and 60 mg codeine
Usual oral dosage: Children < 12 years: 0.5-1 mg codeine/kg/dose every 4-6 hours as needed; 10-15 mg acetaminophen/ kg/dose every 4 hours as needed not to exceed 2.8 g acetaminophen/24 hours OR 3-6 years: 5 mL 3-4 times/day 7-12 years: 10 mL 3-4 times/day > 12 years: 15 mL every 4 hours Adults (based on codeine component): 30-60 mg dose every 4-6 hours as needed not to exceed 360 mg codeine or 4 g acetaminophen per 24 hours
Ibuprofen Forms: Liquid, tablet Usual oral dosage: Children4: 4-10 mg/kg/dose every 6-8 hours Children > 12 years4: 200 mg every 4-6 hours as needed (maximum 1200 mg/24 hrs) Adults2: 400 mg/dose every 4-6 hours
* Pediatric dosage should not exceed adult dosage. Sources: 1. PDR.net. Available at: “http://www.pdr.net/home/pdrHome.aspx”. Accessed May 18, 2008. 2. RxList – The internet drug index. Available at: “http://www.rxlist. com”. Accessed May 18, 2008. 3. Wilson W, Taubert KA, Gewitz M, et al. Prevention of infective endocarditis: Guidelines from the American Heart Association. Circulation. 2007;116(15):1736-1754. Correction Circulation. 2007; 116:e376-e377. Available at: “http://circ.ahajournals.org/cgi/content/ full/116/15/1736”. Accessed May 23, 2008. 4. Wynn RL, Meiller TF, Crossley HL. Drug Information Handbook for Dentistry, 13th edition. Lexi-Comp, Hudson, Ohio. 2007.
DISCLAIMER: Drug information is constantly changing and is often subject to interpretation. While care has been taken to ensure the accuracy of the information presented, the AAPD is not responsible for the continued currency of the information, errors, omissions, or the resulting consequences. Decisions about drug therapy must be based upon the independent judgment of the clinician, changing drug information, and evolving healthcare practices. 324
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Management of Medical Emergencies Management of Medical Emergencies Reference Manual 2006-2007
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For all emergencies 1. Discontinue dental treatment 2. Call for assistance/someone to bring oxygen and emergency kit 3. Position patient: ensure open and unobstructed airway 4. Monitor vital signs 5. Be prepared to support respiration, support circulation, call for additional help Condition
Signs and symptoms
Treatment
Allergic reaction (mild or delayed)
Hives; itching; edema; erythema– skin, mucosa, conjunctiva
1. Discontinue all sources of Diphenhydramine 1 mg/kg allergy-causing substances Child: 10-25 mg qid 2. Administer diphenhydramine Adult: 25-50 mg qid
Oral
Allergic reaction (sudden onset): anaphylaxis
Urticaria–itching, flushing, hives; rhinitis; wheezing/difficulty breathing; bronchospasm; laryngeal edema; weak pulse; marked fall in blood pressure; loss of consciousness
This is a true, lifethreatening emergency 1. Call for medical help 2. Administer epinephrine 3. Administer oxygen 4. Monitor vital signs
IM or SubQ
Acute asthmatic attack
Shortness of breath; wheezing; coughing; tightness in chest; cyanosis; tachycardia
1. Sit patient upright or in a 1. Try patient’s inhaler or Inhale comfortable position one from emergency kit 2. Administer oxygen 2. Epinephrine 1:1000 IM or SubQ 3. Administer bronchodilator 0.01 mg/kg every 15 min 4. If bronchodilator is ineffective, as needed administer epinephrine
Anesthetic toxicity
Light-headedness; changes in vision and/or speech; changes in mental status–confusion; agitation; tinnitis; tremor; seizure; tachypnea; bradycardia; unconsciousness; cardiac arrest
1. Assess and support airway, breathing, and circulation 2. Administer oxygen 3. Monitor vital signs 4. Transport to emergency center as indicated
Supplemental oxygen
Mask
1. Reassure patient 2. Assess and support airway, breathing, and circulation 3. Administer oxygen 4. Monitor vital signs 5. Transport to emergency center as indicated
Supplemental oxygen
Mask
Anesthetic reaction: Anxiety; tachycardia/palpitations; vasoconstrictor restlessness; headache; tachypnea; chest pain; cardiac arrest
Drug dosage
Epinephrine 1:1000 0.01 mg/kg every 5 min until recovery or until help arrives
Drug delivery
Overdose: benzodiazepine
Somnolence; confusion; diminished 1. Assess and support airway, reflexes; respiratory depression; breathing, and circulation apnea; respiratory arrest; 2. Administer oxygen cardiac arrest 3. Monitor vital signs 4. Establish IV access and reverse with flumazenil 5. Monitor recovery
Flumazenil 0.01 mg/kg IV (not to exceed a total of 1 mg) at a rate not to exceed 0.2 mg/min
Overdose: narcotic
Decreased responsiveness; 1. Assess and support airway, respiratory depression; respiratory breathing, and circulation arrest; cardiac arrest 2. Administer oxygen 3. Monitor vital signs 4. Reverse with naloxone 5. Monitor recovery
Naloxone 0.01 mg/kg (may repeat after 2-3 min)
IV, IM, or SubQ
Seizure
Warning aura–disorientation, blinking, or blank stare; uncontrolled muscle movements; muscle rigidity; unconsciousness; postictal phase–sleepiness, confusion, amnesia, slow recovery
1. Recline and position to prevent injury 2. Ensure open airway and adequate ventilation 3. Monitor vital signs 4. If status is epilepticus, give diazepam
Diazepam Child up to 5 y: 0.2-0.5 mg slowly every 2-5 min with maximum=5 mg Child 5 y and up: 1 mg every 2-5 min with maximum=10 mg
IV
Syncope (fainting)
Feeling of warmth; skin pale and moist; pulse rapid initially then gets slow and weak; dizziness; hypotension; cold extremities; unconsciouness
1. Recline, feet up 2. Loosen clothing that may be binding 3. Ammonia inhaler 4. Administer oxygen 5. Cold towel on back of neck 6. Monitor recovery
Ammonia in vials
Inhale
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Cardiopulmonary Resuscitation
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american academy of pediatric dentistry
Delineation of Privileges Standard Hospital Privilege Form Hospitals and ambulatory surgery centers require credentialing of dentists and delineation of pediatric dentistry privileges to ensure quality patient care and to protect the patient from unqualified or incompetent practitioners. The American Academy of Pediatric Dentistry suggests that the following qualifications and core privileges best characterize the training, experience, and competence of an educationally-qualified pediatric dentist.
Qualifications Granting privileges in pediatric dentistry requires a review of an individual’s qualifications that are evidenced, in part, by:
asic Education B DDS, DMD, or equivalent Training Successful completion of a pediatric dentistry residency program accredited by the American Dental Association. Experience Reflects the skills of an educationally-qualified, board candidate/board certified pediatric dentist. Scope of practice includes primary and comprehensive preventive and therapeutic oral health care for infants and children through adolescence. Treatment also may be provided to patients beyond the age of majority who demonstrate physical, developmental, mental, sensory, behavioral, cognitive, or emotional impairment conditions that require specialized care. Certification May be granted by the American Board of Pediatric Dentistry
Privileges Privileges included in the pediatric dentistry core may include, but are not limited to:
dmissions and Consultations A Inpatient and outpatient care including ward, operating room, and emergency department settings. Diagnostic Services and Oral Medicine Orofacial examination, oral and maxillofacial radiography, diagnosis and management of oral and perioral lesions and anomalies, treatment of common oral diseases, uncomplicated biopsies and adjunctive diagnostic tests (eg, exfoliative cytology, microbial cultures, mutans streptococcus testing, other laboratory testing), caries risk assessment, assessment and documentation of oral/ dental neglect/abuse. Preventive Procedures Dental prophylaxis, dietary counseling, sealant application, fluoride therapies, mouthguards/occlusal guards, anticipatory guidance, tobacco cessation counseling. Restorative Dentistry and Oral Rehabilitation Comprehensive restorative care including fixed and removable prosthetic techniques for the primary, mixed, and permanent dentitions; cleft palate, maxillofacial, and speech prostheses; dental bleaching, microabrasion, and esthetic restorations. Management of the Developing Dentition and Occlusion/Orthodontic Procedures Treatment of non-nutritive oral habits, space maintenance, space regaining, correction of dental crossbites and functional shifts, headgear, functional appliances, fixed appliance therapy, infant maxillary orthopedics, orthodontic treatment in conjunction with orthognathic surgery, temporomandibular joint procedures of orthodontic nature, occlusal adjustment. Trauma/Emergency Procedures Evaluation, diagnosis, and treatment of trauma to the primary, mixed, and permanent dentitions (eg, repositioning, replantation, and stabilization of intruded, extruded, luxated, and avulsed teeth; restoration of complicated and uncomplicated dental fractures),
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the pulpal, periodontal, and associated soft tissues, the dental alveolus, and orofacial soft tissues; treatment of infections of the maxillofacial region by surgical and medical therapy; thermal mouth burns.
Periodontal Procedures Gingival curettage, scaling, root planing, local or systemic chemotherapeutic therapy, dental splinting, frenectomy (including correction of ankyloglossia), gingivectomy, gingival grafts. Endodontic Procedures Pulp capping, pulpotomy, pulpectomy and root filling of primary and permanent teeth; apicoectomy; management of periradicular tissues. Anesthesia and Pain Control Local anesthesia of intraoral and perioral tissues; nitrous oxide/oxygen analgesia/anxiolysis; minimal, moderate, or deep sedation; pain management by systemic chemotherapeutic agents. Oral and Maxillofacial Surgery Procedures Extractions of erupted teeth, surgical exposure and/or removal of impacted or unerupted teeth, biopsy of lesions, incision and drainage, removal of minor cysts and foreign bodies.
Additional or Special Procedures • List procedures (eg, laser surgery, implants): Qualifications:
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Analysis and Policy Recommendations Concerning Mid-level Dental Providers Access to oral health care for children is an important concern that has received considerable attention since publication of the US Surgeon General’s report, Oral Health in America: A Report of the Surgeon General, in 2000.1 The Surgeon General’s report concluded that for certain large groups of disadvantaged children there is a “silent epidemic” of dental disease, and that the US public health infrastructure for oral health is insufficient to address the needs of disadvantaged groups. That report also identified dental caries (tooth decay) as the most common chronic disease of children in the United States, noting that 80 percent of tooth decay is found in 20-25 percent of children, large portions of whom live in poverty or low-income households and lack access to an ongoing source of quality dental care (ie, a dental home). Addressing the disparities between these disadvantaged children and the tens of millions of US children who enjoy access to quality oral health care and unprecedented levels of oral health is a major focus of the advoc acy efforts of the American Academy of Pediatric Dentistry (AAPD). AAPD is a recognized leader in advancing policies and programs geared tow ard achieving optimal oral health for all children. Notable activities in the area of policy include annual publication of oral health policies and clinical guidelines 2; support of Title VII authorization and funding by Congress to expand pediatric and general dentistry residency training programs; revision of the Centers for Medicare and Medicaid Services (CMS) Guide to Children’s Dental Care in Medicaid 3; adoption (in 2001) and promotion of a formal oral health policy on the “dental home” for children4; and ongoing federal and state advocacy efforts to improve the performance of public programs whose purpose is to provide access to dental services for disadvantaged children [eg, Medicaid, Children’s Health Insurance Program (CHIP)]. Prominent program-related activities include a major national initiative supported through an ongoing partnership with the Office of Head Start to provide quality dental homes for the roughly one million preschool children enrolled annually in Head Start and Early Head programs throughout the US.5 Additional activities include leadership in advancing oral health care for young children and children with special health care needs and sponsorship of various professional education programs aimed at increasing general dentists’ ability to provide quality dental care for children. Medicaid is a major federal program designed to provide access to care for children with the greatest need for diagnostic, prevention and treatment services. Medicaid Early and Periodic Screening, Diagnostic, and Treatment (EPSDT) provisions require that a broad range of dental services necessary for the diagnosis, prevention, and treatment of disease-related or developmental conditions be provided to eligible children on
an ongoing periodic basis from birth through late adolescence.3 However, numerous studies – including several by the US Congress and Department of Health and Human Services – and recurring federal legal actions have documented that State Medicaid programs generally do not devote sufficient resources to provide adequate access to dental care for Medicaid children. With few exceptions, Medicaid reimbursement rates for dental providers have remained appallingly low, below market-based levels, and often less than the overhead costs of most private practices. This leads general and pediatric dentists in many states to opt out of Medicaid, thereby restricting much-needed care for this sizeable segment of the population. AAPD recognizes that Medicaid programs generally have failed to provide adequate dental care for American children who are most in need of dental services, and that these programs must be improved to address the oral health care needs of America’s most vulnerable children. Growing concern and attention to access to care issues have prompted a variety of proposals that call for workforce strategies involving greater use and, in some cases, the development of new so-called ‘mid-level providers.’ Examples include various types of dental therapists, an advanced dental hygiene practitioner, and a community dental health coordinator. These examples are in addition to the more established expanded function dental auxiliary/assistant (EFDA) mid-level model currently employed in many states and governmentsponsored programs throughout the US. In light of these circumstances, the AAPD created a Task Force on Workforce Issues in 2008 to examine various midlevel dental provider models. This Position Statement builds on the Task Force’s findings 6 and offers AAPD’s policy recommendations regarding the use of mid-level providers in dental care for children.
Review of Existing Mid-Level Models Three of the models reviewed are very similar in design and function and are closely related in history and development: the New Zealand Dental Nurse/Therapist, the Canadian Dental Therapist, and the Alaskan Dental Health Aide Therapist. Of these 3, only the Alaskan Dental Health Aide Therapist model has been employed in the US since 2005 under circumstances described below. Expanded Function Dental Assistants have been employed in the US for over 30 years, and are currently used in more than 20 states throughout the US and in programs operated by the Armed Forces and several other federal agencies. New Zealand Dental Nurse/Therapist. The New Zealand Dental Nurse/Therapist (NZDN/T) model dates from 1921 when a group of 30 ‘dental nurses’ began a two-year training
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program sponsored by the New Zealand federal government to address high levels of dental disease in children.6-8 Students/ federal employees were educated to perform oral examinations, develop treatment plans, provide preventive services, administer local anesthesia, prepare and restore primary and young permanent teeth, and extract primary teeth. Initially, the primary target for the NZDN/T services was pre-adolescent school-age children, with care delivered under the general supervision of a Ministry of Health dentist. Today, they operate under the supervision of a principal dental officer of the district health board and provide dental services for a high percentage of New Zealand children. Therapist training is limited to 2 university-based program. The term ‘dental nurse’ was changed to ‘dental therapist’ in the mid-1990s. At the time of the program’s inception, New Zealand had only a few modest-sized towns and cities. The remainder of New Zealand’s population was clustered sparingly in very small communities throughout the country, the vast majority of which were not large enough to support a resident dental practitioner. Thus, demographics were a large factor in the inability of many New Zealanders to receive adequate oral health care. New Zealand’s approximately 660 dental therapists work as part of a team, one member of which must be a dentist. For the most part, they work in particular geographic areas and visit a number of schools equipped with dental facilities on a regular basis; however recent changes now allow therapists to work in private practices. The New Zealand dental therapists provide low-to-moderate levels of oral health care and health promotion, and refer patients to dentists (or other health care providers) for services which are beyond the therapists’ skill set.9 Use of dental therapists in New Zealand is being restructured based on recent views which revealed that the School Dental Service models are not adequately addressing oral health disparities and community needs.10 Canadian Dental Therapist. The New Zealand model was used as a template for a Canadian Dental Therapy Program which began in 1972. 6,11 Training occurs at the National School of Dental Therapy which produces 15-20 graduates per year. The Canadian Dental Therapist (CDT) was introduced to address the shortage of dentists in remote northern regions of Canada. The three northern territories of Canada – the Yukon, Northwest Territories, and Nunavut – have a total landmass of 3,683,456 square kilometers, approximately 5.6 times the size of Texas. The total population in the 3 northern territories is approximately 330,000, which comprises about 1% of the total Canadian population. These regions and the northern parts of 7 of Canada’s 13 provinces are inhabited mainly by indigenous people, such as First Nations and Inuit. Providing access to oral health care in these isolated communities is a major challenge which Canadian officials chose to address through development of the CDT program. The CDT is almost identical to the NZDN/T with respect to training and services provided. Upon completion of a two-year training program, Canada’s approximately 300 dental therapists now may work in various practice settings in most provinces and territories of
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Canada. Some of these settings include: private practice dental offices; federal, provincial, territorial and First Nations government programs; and local health boards. In all the above settings, dental therapists work in conjunction with licensed dentists under general supervision. In many settings, dental therapists work within broader systems of care comprising other oral health care professionals as well as with nurses, physicians and other community-based health care service providers. In First Nation communities, the dental therapist, while functioning as part of the overall health care team, also functions as an important resource for school staff and other social programs within the community. The use of a broadly defined scope of practice allows dental therapists to provide a wide range of basic dental services, many of which are irreversible, in the community. While dental therapists most often provide services to school-age children, dental therapists can and do provide services to any age group. Therefore anyone in the community who requires basic dental care can be treated by dental therapists under the general supervision of a licensed dentist. More extensive dental procedures are referred to community-based dentists or to providers outside the community.11 Dental therapists employed by the First Nations and Inuit Health Branch fall under the professional and general supervision of the Regional Dental Officer position. Professional supervision provides a formal relationship that is the vehicle for liability coverage by the federal government. General supervision ensures that basic dental care services are available in First Nation communities, even if no dentist resides in the community.11 Alaskan Dental Health Aide Therapist. Geographically, the state of Alaska is by far the largest US state in terms of size with a land mass equal to one-fifth the combined size of the lower 48 states. Alaska ranks 47th among states with respect to population (approximately 680,000) and has approximately 475 dentists within the state. About 85,000 Alaska Natives live in approximately 200 small villages of 300-400 people, accessible only by small aircraft, boat, snow-machine, or dog sled. This population has overwhelming, unmet oral health needs. Absent access to dental homes, the children in these areas have been unable to obtain routine access to even emergent dental care.6,12 Developed as a model similar to the NZDN/T and the CDT, the Alaskan Dental Health Aide Therapist (DHAT) Program began working in Alaskan villages in 2005.12 The program was developed as an attempt to improve access to dental care in remote outlying areas within tribal lands. Alaska’s DHATs provide oral health care in the context of the Community Health Aide (CHA) program, a program authorized by federal statute, in which tribes provide primary health care throughout Alaska. Using a primary care team approach, students learn to work with other health professionals – physicians, physician assistants, nurse practitioners, and nurses – and integrate their work into existing community-based medical prevention programs. DHATs must meet specified training requirements, undergo a protracted preceptorship, and have
AMERICAN ACADEMY OF PEDIATRIC DENTISTRY
their skills reevaluated every 2 years. Continuing education is required for continued certification. DHATs are recruited from villages that they will return to serve. As of 2008, there were approximately a dozen DHATs working in Alaska. Dentists are responsible for writing standing orders, being the point of contact for DHATs, and evaluating DHATs’ skills through direct observation. DHATs must demonstrate their ability to perform each procedure for their scope of practice before being allowed to practice under a dentist’s general supervision. Supervising dentists must be employed by a recognized tribal health organization and be familiar with the DHAT certification standards.12 A number of studies have addressed the technical quality of restorative procedures performed by dental therapists. In general, these studies have found that, within the scope of services and circumstances to which therapists are limited, the technical quality of restorations placed by therapists is comparable to that produced by dentists. However, there appears to be no evidence-based material addressing comparisons between dentists and dental therapists on the broader set of competencies, knowledge and skills (eg, diagnosis, general health assessment, treatment planning, and behavior management) required in the delivery of comprehensive dental care to children, including children with special health care needs, under a broad range of circumstances. Expanded Function Dental Auxiliaries/Assistants. Expanded Function Dental Auxili aries/Assistants (EFDAs) are allied health professionals who, under the direct supervision of a licensed dentist, can perform various reversible restorative procedures and other specified services. EFDAs generally include those who were previously trained and have experience as dental assistants, certified dental assistants, or dental hygienists. The utilization of EFDAs in the US has been permitted under numerous state dental practice acts since the 1970’s. EFDAs also are used by the Armed Forces and programs sponsored by several other federal agencies and have a long history in Europe and Canada.6,13 The scope of permissible EFDA practices varies from state to state. In the private sector, the specific functions permitted and training required for EFDAs are determined by each state legislature and corresponding dental practice act. The utilization of EFDAs and the procedures they are allowed to perform vary widely across the country. Likewise, educational programs for training EFDAs vary from state to state. American Dental Association (ADA) surveys from 1972 to 2008 show a trend towards more states allowing greater delegation of procedures.14 Numerous studies have demonstrated that EFDAs enhance dental practice productivity and efficiency without compromising technical quality of care.15-17
Summary of Existing Mid-Level Models The 4 existing models noted above represent mid-level dental providers who work as part of teams of dental professionals and deliver a limited scope of services under varying levels of dentist supervision. Studies have demonstrated that the technical quality of restorative care provided under these conditions generally is comparable to that provided directly by
dentists. However, it is essential that policymakers recognize that evaluations which demonstrate comparable levels of technical quality merely indicate that individuals know how to provide certain services, not that those providers have the knowledge and experience necessary to determine whether and when various procedures should be performed or not performed or to manage individuals’ overall oral health care. The Canadian and Alaskan therap ist models were designed primarily to provide basic dental services to disadvantaged, underserved populations in remote locations. These mid-level providers are employed primarily by various governmental or tribal agencies following a minimum of 2 years of training, which generally is highly subsidized by government payments. The New Zealand model originally was designed and staffed similar to the Alaskan and Canadian models, but subsequently has been expanded to serve a wide range of school-age children. However, studies conducted in the US and New Zealand have raised questions concerning the efficiency and cost-effect iveness of school-based programs.10,18 With the exception of the EFDA model, the performance of these models has not been thoroughly evaluated in diverse US settings, nor has the cost-effectiveness of existing models been rigorously evaluated. Moreover, evidence from several developed countries that have initiated dental therapist programs suggests that when afforded an opportunity, therapists often gravitate toward private practice settings in less-remote areas, thereby diminishing the impact of these mid-level providers in terms of the care for the underserved, the very purpose for which they were initially created.
Review of Proposed Mid-Level Models Advanced Dental Hygiene Practitioner. Efforts to institute a new type of dental services provider, labeled as the Advanced Dental Hygiene Practitioner (ADHP), have been proposed by the American Dental Hygienists’ Association (ADHA).19 As proposed, this new model would have the authority to practice without the supervision of a dentist, and would mirror many of the same services performed by dentists, including rendering diagnoses and providing irreversible procedures (eg, restorations, extractions). Eff orts to promote this mid-level provider have, as their foundation, the assumptive argument that access to dental services (or lack thereof ) in underserved populations is primarily the result of a lack of dental providers, and the speculative assertion that the introduction of the ADHP would mitigate the assumed workforce shortage or provider maldistribution.6 In its 2008 Position Statement on the ADHP, the Academy of General Dentistry (AGD) noted that, “Unlike alternative allied dental models, such as Alaska’s Dental Health Aide Therapists (DHAT) and the ADA’s proposed community dental health coordinator (CDHC), an ADHP may work without direct, indirect, or general supervision by a dentist, and without any standing orders or dentist review. That is, the ADHP may fall completely outside the scope of the dental team concept.” 20 The AGD has expressed a number of concerns with the ADHP model, citing challenges of providing the care that patients require in a timely manner
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when working without a dentist or outside the traditional dental team; economic challenges of maintaining an independent practice without a dentist, especially in remote areas and when treating a high proportion of economically disadvantaged individuals; challenges related to managing complications and compromised systemic health conditions in disadvantaged patients (who typically have more severe levels of dental disease and multiple co-morbidities) in light of the ADHP’s limited education and traini ng; difficulty in establishing referrals to and working relationships with dentists, especially for patients seen in remote areas; establishing a lower standard of education and care for the treatment of disadvantaged populations; and lack of evidence that independent dental hygiene practice is economically viable or substantially expands access to care for disadvantaged populations. The AAPD Task Force on Workforce Issues shared many of these concerns and remains highly skeptical about the viability and potential impact of the ADHP model on access to care for disadvantaged populations.6 This concern is based in part on Colorado’s experience with independent dental hygiene practice. Specifically, prior analysis suggests that unsupervised dental hygiene practice has not had a notable effect on access to care in Colorado.21 The impact of existing independent practices was limited in 2 important ways: 1) there were very few practices; and 2) they were located in areas served by dental offices with dental hygienists functioning in traditional capacities. Comparisons suggest that the economic viability of the unsupervised hygienist business model is questionable because their fees, on average, are not different from traditional dental practices, which have the advantage of providing a full range of dental services.19 This may explain why independent hygienist practices have not expanded substantially in the state where they are permitted. The prior analysis also demonstrates the assumption that unsupervised hygiene practices would locate in underserved communities has not been realized. Minnesota Dental Therapist Model(s). In 2009, the State of Minnesota adopted legislation to begin training 2 proposed types or levels of mid-level providers: dental therapists and advanced dental therapists. According to published reports, the new Minnesota mid-level models resemble existing dental therapist models described above in terms of scope of services and requirements to function as part of dental teams under the supervision of dentists.22 Dental therapists will require onsite supervision by licensed dentists and will not be able to extract permanent teeth. Advanced dental therapists will need at least 2,000 hours of practice as a dental therapist and additional education, testing, and certification beyond that of a dental therapist in order to treat patients without a dentist onsite. Advanced therapists will be allowed to assess patients, but must receive approval for treatment plans from supervising dentists before performing restorative and surgical procedures, and will be able to perform some additional procedures, such as non-surgical extraction of periodontally involved permanent teeth, when authorized by supervising dentists. Neither
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dental therapists nor advanced dental therapists will be able to prescribe medications. In Minnesota, the discipline of dental therapy will remain distinct and separate from dental hygiene. A comprehensive outcomes assessment will be conducted to study the impact and quality of care provided by dental therapists.23 Community Dental Health Coordinator. In 2006, the House of Delegates of the ADA established the Workforce Models National Coordinating and Developm ent Committee to develop workforce models focusing on the treatment needs of the entire population. Subsequently, the ADA House of Delegates directed the development of 2 new workforce positions to support the dental profession and expanded scope of practice for members of the current workforce. This directive has led to the creation of the Community Dental Health Coordinator (CDHC) and Oral Preventive Assistant (OPA) model training programs to extend oral health care to underserved communities. Only the CDHC model is addressed within the context of this paper, as the OPA model falls short of generally accepted notions of mid-level dental providers.24 The ADA’s plans call for CDHCs to be specifically trained to help organize community programs and function in remote locations and other underserved areas. CDHCs will be trained to promote oral health and provide preventive services including screenings, fluoride treatments, sealants, temporary fillings and simple teeth cleanings until patients can receive more comprehensive services from a dent ist or dental hygienist. CDHCs working in facilities without the continuous presence of a dentist could perform limited palliative services for conditions requiring urgent care prior to subsequent diagnosis and treatment by a dentist. Perhaps most notably, the CDHC will be in a position to link patients who would not or could not otherwise access care with health providers by coordinating the logistics of appointments and helping patients become eligible for dental programs.24 Promoters of this model assert that CDHCs will: be of particular value to public programs, but also could be useful in larger private practices; enable the existing workforce to expand its reach deep into underserved communities; and influence local health and community organizations to adopt initiatives to promote oral health. CDHCs will work under a dentist’s supervision – not necessarily in dental offices, but under ‘remote supervision’ as a member of a dental team. Schools, community health centers, churches, senior citizen centers and Head Start programs are all health and community settings in which a CDHC may work. Much like Alaskan DHATs, CDHCs will be recruited from the comm unities where they will work to bridge the gap between local cultures and dental health care systems, navigate community members through the delivery system and help diverse populations overcome barriers that prevent them from accessing dental health services.
Summary of Proposed Mid-Level Models The proposed mid-level models summarized above present radically different approaches to expanding care for under-served
AMERICAN ACADEMY OF PEDIATRIC DENTISTRY
populations. The ADHP model proposes to create a new independent practitioner with subs tantially less education and training than is presently required for the practice of dentistry to essentially practice dentistry in disadvantaged populations. The CDHC model, on the other hand, proposes to train a new type of mid-level provider who will work with dentists and other health care professionals as part of teams with expanded capabilities to address the full range of oral health needs of underserved communities. The Minnesota dental therapist model is being developed along the lines of other dental therapist models.
AAPD Values and Principles Concerning Oral Healthcare for All Children and the Dental Home AAPD believes that all children deserve access to quality oral health care. Addressing disparities in children’s oral health and oral health care is the major focus of AAPD’s advocacy efforts. The core values of AAPD include the following elements: • Health and health care equity. • Child and adolescent welfare and safety. • An effective, efficient and competent dental workforce. • Effective, efficient public programs. • Oral health promotion, disease prevention and medically necessary dental services. • Science, education, research and evidence-based care. AAPD believes that the dental home concept is essential for ensuring optimal oral health for all children. Establishing a dental home means that each child’s oral health care is delivered in a comprehensive, continuously accessible, coordinated and family-centered way by or under the supervision of a licensed dentist. 4 The concept of the dental home reflects AAPD’s oral health policies and clinical guidelines2, which promote optimal oral health for all children. The dental home concept, which includes the age 1 dental visit, underlies the dental profession’s efforts to assist children and their parents and caretakers in establishing the foundation for a lifetime of good oral health. Each child’s dental home should include the capacity to arrange referrals to other dentists when a child’s primary care dentist cannot provide all needed care.
Policy Recommendations Existing and proposed mid-level dental provider models that are conceptually compatible with AAPD core values, oral health policies and clinical guidelines, and definition of the dental home include: EFDAs (Expanded Function Dental Auxiliaries), Dental Therapists working under the supervision of dentists, and CDHCs (Community Dental Health Coordinators). Use of EFDAs has been thoroughly evaluated, and is a part of accepted practice in over 20 states and several federal programs. Therefore: 1. AAPD supports greater use of EFDAs based on extensive evaluations of their effectiveness and efficiency in a wide range of private and public settings as part of dental teams.
On the other hand, additional evaluation of the performance, safety and efficiency of other models that are consistent with AAPD’s core values and definition of a dental home (ie, dental therapist and CDHC models) is warranted. Therefore: 2. AAPD recommends further evaluation of Dental Therapist and Community Dental Health Coordinator (CDHC) models prior to policy decisions regarding their use. AAPD has serious reservations about the premise, potential viability, and presumed impact of the Advanced Dental Hyg iene Practitioner (ADHP) model, which are shared by other organizations that have embraced the dental home concept. Therefore: 3. AAPD joins others in rejecting the ADHP model on the basis of its incompatibility with the principle that dental care should be provided directly by or under the supervision of a dentist. Existing and proposed mid-level dental providers that do not meet the criteria for a dental home may serve as valuable members of the dental care delivery team under arrangements that have been demonstrated to expand access to care without compromising quality or safety. Therefore: 4. AAPD supports the use of mid-level dental providers who perform or assist in the delivery of specified reversible procedures and certain surgical procedures under the general supervision of a dentist, provided that such arrangements have been thoroughly evaluated and demonstrated to be safe, effective, and efficient and to not compromise quality of care in similar settings.
Conclusion AAPD believes that all children deserve access to quality dental care. Some may offer proposals based on what has been characterized as the “something is better than nothing” approach to care. However, AAPD believes that the oral health needs of all children are best met through ongoing, comprehensive dental care provided through the collaborative efforts of dental teams comprised of adequately trained oral health professionals under the direction of competent dentists – in short, in quality dental homes. AAPD looks forward to working with all who embrace this concept and seek to achieve this goal for all children.
Acknowledgments Drafts of this document were developed by James J. Crall, D.D.S., Sc.D., on behalf of the American Academy of Pediatric Dentistry. Initial preliminary analysis was provided by a Task Force on Workforce Issues whose members included: H. Pitts Hinson (Chair), William C. Berlocher, Joel H. Berg, James J. Crall, David K. Curtis, Jessica Y. Lee, John R. Liu, Keith R. Morley and Ross M. Wezmar.
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