Comprehensive Review of Pediatric Dentistry

Comprehensive Review of Pediatric Dentistry Provided by: American Academy of Pediatric Dentistry

Release Date December 1, 2008

1-800-284-8433 • www.cmeinfo.com 639

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

American Academy of Pediatric Dentistry Comprehensive Review of Pediatric Dentistry

Growth & Development / Orthodontics Andrew L. Sonis, D.M.D. Trauma Constance M. Killian, D.M.D. Dental Materials Steven M. Adair, D.D.S., M.S. Pulp Therapy Steven M. Adair, D.D.S., M.S. Oral Pathology / Oral Medicine / Syndromes Andrew L. Sonis, D.M.D. Oral Pathology / Oral Medicine / Syndromes (cont'd) Andrew L. Sonis, D.M.D. Prevention Steven M. Adair, D.D.S., M.S. Special Needs Patients Constance M. Killian, D.M.D. Dental Development Steven M. Adair, D.D.S., M.S. Hospital Dentistry Constance M. Killian, D.M.D. Special Needs Patients (cont'd) Constance M. Killian, D.M.D. Behavior Management Constance M. Killian, D.M.D.

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Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Comprehensive Review of Pediatric Dentistry Provided by: American Academy of Pediatric Dentistry

DVD #1

WARNING: The copyright proprietor has licensed the picture contained on this recording for personal use only and prohibits any other use, copying, reproduction, or performance in public, in whole or in part (Title 17 USC Section 501 506). © 2008

4

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

is not responsible in any way for the accuracy, medical and dental or legal content of this recording. You should be aware that substantive developments in the medical and dental fields covered by this recording may have occurred since the date of original release. Date of Original Release: December 1, 2008

This educational activity is a DVD format. The activity provides a comprehensive review of pediatric dentistry and is organized to assist American Academy of Pediatric Dentistry (AAPD) members in their preparation for the American Board of Pediatric Dentistry (ABPD) examinations. It is estimated that it should take the average learner 22 hours, including completion of the post-test and evaluation form, to complete this activity.

5

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

The American Academy of Pediatric Dentistry is recognized (May 2007 – June 2010) by the ADA Continuing Education Recognition Program (ADA CERP) to provide continuing education opportunities for dentists. Continuing education credit awarded for this activity may not apply toward license renewal in all states or meet

the requirements of other governing bodies. It is the responsibility of each practitioner or resident to verify the requirements of his or her state or governmental licensing board.

6

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

DESIGNATION The American Academy of Pediatric Dentistry designates this educational activity for a maximum of 22 hours of continuing education credits.

OBJECTIVES After viewing this program, the participant should have a better understanding of the following:

1. The major clinical and knowledge base areas of pediatric dentistry. 2. Select clinical cases. 3. The American Board of Pediatric Dentistry testing process.

7

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RAA,4%'#A'%&,'.3U&%'A#"4,'#)'%&,'@+7 !

Light, continuous forces " Osteoclasts

formed " Removing lamina dura " Tooth movement begins " This process is called “FRONTAL RESORPTION”

Frontal resorption occurs on the osseous margin adjacent to the PDL

83

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73U&%'A#"4,'.,(*3)U'%#'A"#)%(.' ",5#"/%3#)

Tooth movement (mm)

! Phase 1 – Mechanical compression and tension of the periodontium ! Phase 2 --- Mechanically induced cellular and genetic responses; no tooth movement ! Phase 3 --- Accelerated tooth movement due to frontal bone resorption

Phase 3 Phase 2 Phase 1

FYN

NGYQG

Days

RAA,4%5'#A'&,(-<'A#"4,'#)'%&,' @+7 !Heavy, continuous forces "Blood supply to PDL occluded "Aseptic necrosis "PDL becomes “hyalinized” – “HYALINIZATION” "This process is called “UNDERMINING RESORPTION”.

84

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Undermining resorption results loss of vitality of localized areas of PDL resulting in removal of alveolar bone in area of pressure

>,(-<'A#"4,'.,(*3)U'%#'D)*,"03)3)U'",5#"/%3#)

Tooth movement (mm)

! Phase 1 – Mechanical compression and tension of the periodontium ! Phase 2 --- Continuing mechanical compression; little cellular and genetic responses; no tooth movement ! Phase 3 --- Cells recruited from the undermining side of lamina dura, not within the PDL, to induce undermining bone resorption

Phase 1

85

Phase 2

Phase 3

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

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86

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Direction of Force Application !

!

Center of Rotation --- The point around which rotation occurs when an object is being moved. Center of Resistance --- A point on the tooth around which the tooth shall move. For most teeth, COR is 2/5 way between the apex and the crest of the alveolar bone.

Center of resistance

in space

in oral cavity

87

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Center of Rotation

CR

Force on the crown

CR

^

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Force

^

A force (F) is a load applied to an object that tends to move the object.

^

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89

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+3",4%3#)'()*'+,U",, #A'%&,' A#"4, ?#*3.<'0#-,0,)% 100gm needed to produce bodily movement, which is double the force needed to produce a tipping movement

Orthodontic Forces and Tooth Movement !

Optimal force levels "

“High enough to stimulate cellular activity without completely occluding blood vessels in the PDL” (Proffit et al. 2000).

90

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Degree of Force Summary

! ! !

!

In the range of 10 to 200 grams. Varies with the type of tooth movement. Light, continuous forces are currently considered to be most effective in inducing tooth movement. Heavy forces cause damage and may fail to move the teeth.

Distribution Nb'U Nb'U Nb'U Nb'U

^'L'FGG'U

91

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Distribution Nb'U Nb'U bG'U

^'L'FGG'U

Duration Force

Intermittent

Time

92

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Duration Force

Continuous and decreasing

Time

Duration Force

Continuous and Constant

Time

93

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

+D"(%3#) • Key to producing tooth movement: •application of sustained force •force must be present for a considerable percentage of time to stimulate cell differentiation .

+D"(%3#) $Relationship of duration to tooth movement $t duration- t tooth movement

94

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

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198

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Constance M. Killian, D.M.D.

3

199

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Prevention of Trauma Who is at high risk for trauma?

Prevention of Trauma Trauma is a part of Anticipatory Guidance

200

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Prevention of Trauma Custom mouthguards

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Injury Assessment

General Considerations 1. “Primum non nocere”

Do no harm 2. Never treat a stranger

202

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Injury Assessment

General Considerations Be prepared… • • • • • •

Be calm & reassuring Address behavior Communicate Know the Guidelines Have supplies ready Standardized trauma form

Diagnostic Evaluation • Medical condition of patient • • • • • • •

General health Cardiac conditions Bleeding disorders Allergies Medications Chronic conditions Name of physician

203

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Diagnostic Evaluation

History of Current Injury • • • • • •

Identify adult bringing the child What When Where How Any treatment done elsewhere for this injury

Diagnostic Evaluation

Emergency Assessment • Dental trauma is a subset of head

trauma • Assess awareness/orientation • Assure a patent airway • Observe for rhinorrhea or otorrhea

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Diagnostic Evaluation

Emergency Assessment • Bruising behind ear -

“Battle’s sign” • Abnormal vital signs

Diagnostic Evaluation

Emergency Assessment Rapid Neurologic Exam: Cranial Nerves III – Oculomotor • Penlight • PERRLA • Abnormalities

205

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Diagnostic Evaluation

Emergency Assessment Rapid Neurologic Exam: Cranial Nerves III, IV, VI: Oculomotor, Trochlear, and Abducens • •

Track movements Extraocular movements intact

Diagnostic Evaluation

Emergency Assessment Rapid Neurologic Exam: Cranial Nerves VII: Facial Ask patient to close eyes, smile, frown • No asymmetry of movement •

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Diagnostic Evaluation

Emergency Assessment • Glasgow Coma Scale – see

Appendix • • • •

Eyes Best Motor Response Best Verbal Response Maximum score 15, minimum 3

Glasgow Coma Scale Finding A. Eyes

Rating

Open spontaneously Open to verbal command Open to pain No response B. Best Motor Response Obeys verbal command Realizes pain Withdraws from pain Flexion to pain (decorticate) Extension to pain (decerebrate) No response C. Best Verbal Response Oriented and converses Confused Inappropriate words Incomprehensible sounds No response Minimal score = 3 Maximum score = 15

4 3 2 1

207

6 5 4 3 2 1 5 4 3 2 1

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Diagnostic Evaluation

Intra Cranial Injury Symptoms from clinical history • Post-traumatic seizure • Severe headache • Loss of consciousness • Vomiting • Nausea • Clinical evidence of skull fracture

Diagnostic Evaluation What else should make you think ICI? • Persistent drowsiness • Amnesia • Focal neurological signs – “seeing stars”

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Diagnostic Evaluation What overrides the dental injury? • Cervical spine injury – rare in children • Intracranial injury • Neurological injury • Bleeding that cannot be controlled

If no evidence of head trauma, proceed with dental treatment

Diagnostic Evaluation After dental treatment, follow through…. Give post-op instructions for observation • • • •

Patient is persistently sleepy Vomiting Severe headache Abnormal behavior

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Evaluation and Treatment of Orofacial Trauma

Facial Bones Extraoral: Hard Tissue - Facial bones Classification of fractures Simple Compound Comminuted Favorable Unfavorable

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Evaluation and Treatment of Orofacial Trauma

Craniofacial Trauma Causes Falls – 64% Traffic – 22% Sports – 9% Violence – 5%

Distribution Skull vault – 54% Upper/middle facial third – 37%

Concommitant injuries – 33%

Evaluation and Treatment of Orofacial Trauma

Facial Bones Forces of facial fractures High impact – requires more than 50G Low impact – requires less than 50G What facial bones are most likely to fracture?

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Evaluation and Treatment of Orofacial Trauma

Facial Bones Midface fractures • Rare in children • Skull fractures more common • Causes • Treatment – nonsurgical best

Evaluation and Treatment of Orofacial Trauma

Facial Bones Nasal Fracture: most common midface fracture in children Signs • • • • •

Ecchymosis Laceration Swelling Epistaxis Bony irregularities

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Evaluation and Treatment of Orofacial Trauma

Facial Bones Signs of Zygomatic Fracture • • • • • •

Periorbital swelling Ecchymosis and hematoma Conjunctival hemorrhage Palpable step deformity Paresthesia Limited upward gaze

Frontal view

Submentovertex view

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Evaluation and Treatment of Orofacial Trauma

Facial Bones • LeFort Fractures • • • •

Least common midface fracture in children Many fractures are combinations LeFort I treatment – no fixation Caution in fixation for LeFort II and III

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Evaluation and Treatment of Orofacial Trauma

Facial Bones Diagnostic Aids • Computerized Tomography (CT) • Radiographs • AP and Lateral skull • Waters • Submental vertex

Management - OMS

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Evaluation and Treatment of Orofacial Trauma

Mandible Mandibular Fracture is the most common facial skeletal injury in hospitalized pediatric trauma patients • Boys affected twice as often as girls • Younger patients: condylar/subcondylar

fractures • Adolescents: fracture of angle of mandible • Causes: bicycles, steps, swings

Evaluation and Treatment of Orofacial Trauma

Management of Mandibular Fracture Management – OMS • Timing: can defer 24-36 hrs • Stabilize mandible if deferring treatment

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Evaluation and Treatment of Orofacial Trauma

Mandibular Fracture Diagnosis: Subcondylar/Condylar fracture • Blunt injury to chin • Bite is “off” or deviated • Unilateral vs. Bilateral • Palpate external auditory meatus

Evaluation and Treatment of Orofacial Trauma

Clinical Exam for Possible Subcondylar Fracture

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Evaluation and Treatment of Orofacial Trauma

Management of Mandibular Fracture Condylar fractures carry the greatest risk of growth disturbance

• Goals of treatment

• Preserve function • Maintain ramus height

•

Treatment is usually nonsurgical

•

Complications

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Evaluation and Treatment of Orofacial Trauma

Management of Mandibular Fracture Intracapsular fracture of condyle •

•

Ankylosis risk in children less than 3 yrs. Treatment: mandibular exercises and jaw stretching

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Evaluation and Treatment of Orofacial Trauma

Management of Mandibular Fracture Fracture of body of mandible Signs/Symptoms • • • •

Ecchymosis of floor of mouth Hematoma in buccal vestibule Mobility along fracture site on palpation Possible paresthesia

Evaluation and Treatment of Orofacial Trauma

Fracture of Body of Mandible • Radiographs • Management: OMS • No benefits to prolonged post-operative

antibiotics

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Evaluation and Treatment of Orofacial Trauma

Fracture of Body of Mandible

Evaluation and Treatment of Orofacial Trauma

Types of Soft Tissue Injuries

Laceration

Contusions & Abrasion

Burn Puncture

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Evaluation and Treatment of Orofacial Trauma

Soft Tissue Injuries Soft Tissue Lacerations Identify foreign bodies • ¼ usual exposure for intraoral

xray • ½ usual exposure for extraoral xray

Evaluation and Treatment of Orofacial Trauma

Soft Tissue Injuries Goals of wound management Avoid infection Functional and esthetic scar Repair or Refer Location of injury Patient’s ability to heal

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Evaluation and Treatment of Orofacial Trauma

Soft Tissue Injuries • Timing of closure • Wound preparation • Primary wound closure

Evaluation and Treatment of Orofacial Trauma

Soft Tissue Injuries Suture technique • Trim nonvital tissue • Use reverse cutting needle • Suture inside to outside • Insert through more mobile tissue first • Use interrupted sutures • Synthetic sutures: avoid silk or cotton

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Evaluation and Treatment of Orofacial Trauma

Suturing of Soft Tissue Injuries

Evaluation and Treatment of Orofacial Trauma

Soft Tissue Lacerations Tongue Laceration • May not require sutures • Use heavy thread • Deep bites with needle • Assure good

approximation • Bury knots

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Evaluation and Treatment of Orofacial Trauma

Extraora/Intraoral Soft Tissue

Electrical Burns

Evaluation and Treatment of Orofacial Trauma

Electrical Burn: long-term scarring

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Evaluation and Treatment of Orofacial Trauma

Electrical Burn: Commisural Splint

Evaluation!and!Treatment!of!Orofacial Trauma

Extraora/Intraoral Soft!Tissue

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Evaluation and Treatment of Orofacial Trauma

Intraoral Soft Tissue • Inspect buccal vestibule • Inspect floor of mouth • Evaluate palate for any puncture wounds

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Evaluation and Treatment of Orofacial Trauma

Intraoral Hard Tissue • Note maxillary displacement • Note any changes in occlusion • Note any alveolar displacement • Note any tooth mobility • Note any dental crazing • Dental trauma – see classifications

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Intraoral Trauma

Evaluation and Classification of Dental Injuries WHO Classification of Dental Trauma • Includes primary and permanent dentition • Based on type of tissue injury • 1. Injury to hard dental structures and pulp • 2. Injury to hard dental structures, pulp, and alveolar process • 3. Injury to periodontal tissues

Primary Dentition Trauma

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Primary Dentition Trauma

General Considerations • May be first contact with dentist • Precooperative child • Long-term concerns for permanent

dentition

Primary Dentition Trauma

Epidemiology •

Maxillary primary incisors

•

2-4 years of age

•

Luxation

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Primary Dentition Trauma

Causes • Falls • Automobile accidents • Child abuse • Secondary factors

Primary Dentition Trauma

Emergencies When can treatment be deferred?

What injuries should be seen ASAP?

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Primary Dentition Trauma

Clinical Examination • Address behavior • Assessment of clinical signs in young

children: objective vs. subjective signs

Primary Dentition Trauma

Clinical Examination

Remember to look past the obvious……

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Primary Dentition Trauma

Clinical Examination And get the big picture….

Primary Dentition Trauma

Radiographic Examination • Avoid further injury • Parental assistance • Possible immobilization • Usually record size 2 film • Extraoral lateral radiographs not helpful in

intrusion

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Primary Dentition Trauma

Treatment Refer to tables in appendices: p. 32-33 •

www.iadt-dentaltrauma.org Guidelines for the management of traumatic dental injuries Flores, Guidelines III. 2007

Primary Dentition: Tooth and/or Alveolar Fractures Injury

Diagnostic Findings Clinical

Treatment / Follow-up

Radiographic

Enamel fracture or

Take one x-ray

Smooth sharp edges with sandpaper disk

Uncomplicated Crown fracture

Enamel + dentin fracture

Evaluate pulp chamber, stage of root development, root resorption

Smooth smaller fractures, place bandage restoration with glass ionomer or composite Clinical exam at 1 week Clinical and x-ray exam at 3-4 weeks

Complicated Crown fracture

Enamel + dentin fracture with pulp exposure

Take one x-ray Evaluate pulp chamber, stage of root development, root resorption

Pulpotomy, pulpectomy (if possible) or extraction Clinical exam at 1 week Clinical and x-ray exam at 3-4 weeks, 6 months, 1 year

Crown-root fracture

Coronal fragment mobile Minimal to moderate displacement

Take one x-ray - may be able to see gingival extent of fracture

Cautious extraction so as not to disturb developing permanent tooth while trying to retrieve root fragments; if necessary, leave root fragment to resorb

Coronal fragment usually mobile and may be displaced or absent

Take one x-ray – determine location of fracture (coronal, middle, or apical third)

If displaced - extract coronal fragment only. Leave apical fragment to resorb Clinical, x-ray exam annually until successor erupts

Root fracture Coronal fragment may be firm

Alveolar fracture

Patient instructions

Tooth-bearing segment is mobile and may be displaced. Step in arch form may be noted

Take one x-ray

Take one x-ray - determine if teeth are in line of alveolar fracture

If crown firm - monitor only Clinical exam at 1 week Clinical, x-ray exam at 2-3 wks, 6-8 wks, 1 year, then annually until successor erupts Reposition segment Splint to adjacent teeth 3 - 4 weeks Sutures if needed Clinical exam at 1 week Clinical, x-ray exam, splint removal at 3-4 weeks Clinical, x-ray exam at 6-8 weeks, 1 year Xray exam annually until exfoliation

Soft diet for 10 - 14 days Gentle toothbrushing after each meal, Clorhexidine swabbed on gingival twice daily, if splinted Follow-up as indicated based on type of injury

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Primary Dentition: Luxated or Avulsed Teeth Injury

Diagnostic Findings Clinical

Radiographic

Treatment / Follow-up

Concussion

Percussion sensitive No mobility or sulcular bleeding

Take one x-ray No abnormalities expected

Observation Clinical exam at 1 week Clinical and x-ray exam at 6-8 weeks

Subluxation

Tooth mobile but not displaced Sulcular bleeding

Take one x-ray No abnormalities expected Increased PDL space may be noted

If no occlusal interference - observation Clinical and x-ray exam at 6-8 weeks

Lateral luxation

Tooth displaced laterally, usually in a palatal/lingual direction

Take one x-ray May see increased periodontal space at apex of tooth

Treatment depends on degree of displacement/occlusal interference: Observation, extraction Clinical exam at 2-3 wks Clinical, xray exam at 6-8 wks, 1 year

Intrusion

Tooth may not be visible. Check orientation of crown Check for apex through labial bone

Take one or two x-ray{s} If displaced toward labial bone, tooth appears shorter and more opaque If displaced toward permanent successor, tooth appears longer

Observation for re-eruption Clinical exam at 1 week, Clinical, xray exam at 3-4 wks Clinical exam at 6-8 wks Clinical, xray exam at 6 months, 1 year, then annually until successor erupts Extraction x-ray annually until successor erupts

Avulsion

Tooth out of socket

Take one x-ray - confirm avulsion

Do not replant. Suture if needed Clinical exam at 1 week Clinical, x-ray exam at 6 months, 1 year, then annually until successor erupts

Patient instructions

Soft diet for 10 - 14 days Gentle toothbrushing after each meal, Clorhexidine BID if splinted Follow-up as indicated based on type of injury

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Primary Dentition Trauma

Complications in Primary Teeth • Color changes – 53% • Pulp necrosis – 25% • Pulp canal obliteration – 36% • Gingival retraction – 6% • Disturbances in physiologic resorption -4% • Premature tooth loss – 46% • Ankylosis

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Primary Dentition Trauma

Primary Tooth Complications Discolored primary incisors • • • •

>50% dark coronal discoloration fades Yellowish teeth develop less pathology >50% of dark teeth remain asymptomatic Root canal treatment not indicated

When to extract? • • • •

Swelling Sinus tract Increased mobility Sensitivity to percussion

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Primary!Dentition!Trauma

Primary!Tooth!Complications:! Pulp!Canal!Obliteration

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Primary!Dentition!Trauma

Intrusion!Injury

Primary Dentition Trauma

Intrusion Injury Considerations • 80% of intruded teeth pushed labially • Majority re-erupt and survive >36mos • Common findings • Role of systemic antibiotics

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Primary!Dentition!Trauma

Intrusion!Injury!Sequence

Baseline

Baseline

4 weeks

12 weeks

Primary Dentition Trauma

Luxated or Avulsed Teeth: Avulsion

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Age 1

Age 3.5

Primary Dentition Trauma

Complications in Permanent Successors What primary tooth trauma poses the greatest risk to permanent successor ? •Intrusion and avulsion of primary teeth •Age less than 3 years at time of trauma

245

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Primary!Dentition!Trauma

Complications!in!Permanent!Successors

What are the possible consequences to permanent successors?

Primary!Dentition!Trauma

Complications!in!Permanent!Successors:! Discoloration/Hypoplasia

246

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3.3 yrs

4.5 yrs

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7 yrs 8.5 yrs

8 yrs of age

9 yrs

8.5 yrs

10 yrs

248

12 yrs

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249

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Primary Dentition Trauma

Parental Discussion Topics The parents want to know what will happen as a result of the trauma. How do you respond?

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Permanent Dentition Trauma

Permanent Tooth Trauma

General Considerations • • • • • •

Age of patient Medical status Cooperation Type of trauma Dental development Parental desires/concerns

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Permanent Tooth Trauma

Treatment Timing Should be seen immediately • Avulsion • Alveolar fracture • Extrusive or lateral luxation

Can be deferred several hours • • • • •

Intrusion Concussion Subluxation Root fracture Crown fracture with pulp exposure

Treatment may be deferred • Crown fracture without pulp exposure

Permanent Tooth Trauma

Treatment Refer to tables in appendicies: p. 3438 •

www.iadt-dentaltrauma.org Guidelines for the management of traumatic dental injuries Flores, Guidelines I. 2007 Flores, Guidelines II. 2007

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Permanent Dentition: Tooth and/or Alveolar Fractures Injury Uncomplicated Crown fracture

Diagnostic Findings Clinical Enamel fracture Enamel + dentin fracture

Treatment / Followup

Radiographic Take x-rays from 3 angulations Radiograph of lip or cheek lacerations Evaluate pulp chamber, stage of root development Baseline pulp test

Smooth with sandpaper disk or bond with composite resin as needed Rebond fractured segment if intact. Bandage restoration with glass ionomer or composite Clinical,xray exam at 6-8 weeks, 1 year

Complicated Crown fracture

Enamel + dentin fracture with pulp exposure

Take x-rays from 3 angulations Radiograph of lip or cheek lacerations Evaluate pulp chamber, stage of root development

Partial pulpotomy with Ca(OH)2 Restore with composite Pulpectomy for some mature teeth depending on time pulp exposed and pulp condition Clinical exam, xray at 6-8 weeks, 1 year

Crown-root fracture

Enamel, dentin and root fracture Pulp may or may not be exposed Coronal fragment mobile Minimal to moderate displacement

Take x-rays from more than one angle to detect fracture Pulp test usually positive

Reposition / splint coronal fragment as needed Longterm: Subgingival fracture site may require crown lengthening and/or orthodontic extrusion Clinical exam, xray, splint removal at 3-4 wks Clinical exam, xray at 6-8 wks, 6 mos, 1 year

Root fracture

Coronal segment may be mobile/displaced Transient crown discoloration

Take xray from more than one angle Consider occlusal xray for fractures in cervical 1/3 Pulp test is usually negative initially – monitor over time at clinical exams

Reposition coronal segment, splint 4 weeks with flexible splint; If fracture is in cervical 1/3 splint longer, up to 4 months Clinical exam, xray, splint removal at 4 wks Clinical exam, xray 6-8 wks, 4 mos, 6 mos, 1 year, then annually for 5 years

Alveolar fracture

Tooth containing segment mobile and may be displaced. Step in arch form noted

Take x-ray; panograph is helpful in determining fracture lines Pulp test may or may not be positive

Reposition segment and splint 4 weeks. Sutures if needed Clinical exam, xray, splint removal at 3-4 wks Clinical exam, xray at 6-8 wks, 6 mos, 1 year

Patient instructions

Soft diet for 10 - 14 days Gentle toothbrushing after each meal, Clorhexidine BID if splinted Follow-up as indicated based on type of injury

Permanent Tooth Trauma

Crown Fracture Crown fracture with/without pulp exposure

• Injury to enamel, dentin, pulp • Factors affecting pulpal healing • Management

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Permanent Tooth Trauma

Crown Fracture: Uncomplicated Enamel & Dentin Fracture Crown fracture with/without pulp exposure – what are the likely outcomes?

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Permanent Tooth Trauma

Crown Fracture: Complicated Enamel & Dentin Fracture

Crown fracture with pulp exposure

• Within hours and small exposure • Longer interval and larger exposures

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Permanent Tooth Trauma

Intra-Alveolar Root Fractures • Injury to pulp, PDL, cementum, dentin • Coronal displacement – considered as luxation • Healing depends on bacterial contamination of

pulp • Importance of radiographs at multiple angles • Treatment delay possible

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Permanent Tooth Trauma

Intra-Alveolar Root Fractures To Splint or not to Splint… • • •

Non-displaced teeth with no mobility Fracture in middle third – mobile fragment Fracture in cervical third

Antibiotics?

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Permanent Tooth Trauma

Intra-Alveolar Root Fractures Types of healing • Hard tissue: dentin & cementum form • Connective tissue: cells from pdl form • Non-healing: necrosis in coronal

segment

Permanent Tooth Trauma

Intra-Alveolar Root Fractures Monitor pulpal vitality in coronal segment • Open apex: necrosis rare • Pulp necrosis in coronal segment: treat

as immature permanent tooth • Apical root segment: no treatment

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Permanent Tooth Trauma

Intra-Alveolar Root Fractures • Calcium hydroxide as pulp canal

medicament • Apexification • Disinfection of root canals • Weakens dentin walls

Permanent Tooth Trauma

Intra-Alveolar Root Fractures • Mineral Trioxide Aggregate (MTA)

as pulp canal medicament • Alkaline, like Ca(OH)2 • Grainy texture • Hydrophilic • No thinning of dentinal walls

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Permanent Tooth Trauma

Benefits of MTA • Biocompatible • Stimulates interleukin regulation • Calcium from MTA diffuses through dentin to

resorptive lesions • May help stop inflammatory root resorption • Does not thin dentinal walls • Better fracture resistance over time than Ca(OH)2

Permanent Tooth Trauma

Fracture resistance: MTA vs. Ca(OH)2

Hatibovic-Kofman et al, 2008

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Permanent Tooth Trauma

Luxation Injuries: Concussion Concussion • Sensitive to percussion • No mobility • No sulcular bleeding

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Permanent Tooth Trauma

Luxation Injuries: Subluxation • Subluxation • Sensitive to percussion • Mobile • No displacement

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Permanent!Tooth!Trauma

Luxation Injuries:!Subluxation

Permanent!Tooth!Trauma

Luxation Injuries:!Subluxation

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Permanent!Tooth!Trauma

Luxation Injuries:!Subluxation As time goes by …

Injury

6 mos

3.5 yrs

270

1yr 9 mos

4.5 yrs

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Permanent Tooth Trauma

Luxation Injuries: Lateral Luxation • Lateral luxation - displacement in a

direction other than axial • Pulp supply is ruptured • PDL becomes compressed • Sequelae

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Age 8 yrs.

Age 20 years

Permanent Tooth Trauma

Luxation Injuries: Intrusive Luxation Factors in Intrusive Luxation • Age of patient: <12-fewer complications • Concurrent gingival laceration: more

necrosis • Root development: immature = necrosis • Multiple intrusions – more bone loss

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Permanent Tooth Trauma

Luxation Injuries: Intrusive Luxation Permanent Intrusion Injuries • Rare injury • More common in boys • Maxillary central and lateral incisors • Multiple intrusions occur often • Intrusions >7mm –more complications • Intrusions 1-3mm – less root resorption

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Permanent Tooth Trauma

Avulsion Factors affecting Prognosis • • • •

•

Extraoral time Loss of PDL vitality Storage media Handling of tooth before replantation Patient immune response

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Permanent Tooth Trauma

Avulsion Effect of storage media on PDL cell apoptosis • Apoptosis: programmed cell death (differs from necrosis) • In vitro study comparing milk, HBSS, Gatorade, and

contact lens solution as storage media • At 24 & 72 hours, Gatorade and contact lens solution displayed greatest % apoptotic cells • Cells treated in the solutions on ice showed less apoptosis than those at room temperature Chamorro, Regan et al, 2008

•

Permanent Tooth Trauma

Avulsion Contraindications to replantation • • • • •

Severe cardiac disease Seizure disorder Severe mental disability Compromised healing Poor alveolar support

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Permanent Tooth Trauma

Avulsion Tooth cannot be found •

Verify avulsion

•

Assess labial plate of bone

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After bone grafting

Permanent Tooth Trauma

Avulsion Replantation Basics Extraoral period <60 min • On-site replantation is best • Meet patient/parent at office • Place tooth in reconstituting media (HBSS) • Take clinical photo, radiograph as indicated • Review procedure and likely outcomes

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Permanent Tooth Trauma

Avulsion Replantation Basics • Obtain informed consent • Provide local anesthesia • Curette socket, remove clot • Replace tooth • Place flexible splint

Permanent Tooth Trauma

Avulsion Replantation Basics • Systemic antibiotics • •

> 12 years: Doxycycline < 12 years: Penicillin V

• Post-op instructions

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Permanent Tooth Trauma

Avulsion How does root development affect pulp therapy in avulsed teeth? • Closed apex • Open apex

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1 year

2 years

3 years

6 months

4 years

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5 years

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3 years

Permanent Tooth Trauma

Avulsion Delayed Replantation Extraoral period >60 minutes • Emphasize poor prognosis • Remove necrotic tissue from root • Root canal treatment • Tooth in 2% sodium fluoride - 20 minutes • Replant tooth and stabilize

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Permanent Tooth Trauma

Avulsion Healing mechanism in avulsion • 4 days: pulp revascularization begins • 1 week: gingival attachment re-established • 2 weeks: PDL at original state

Permanent Tooth Trauma

Avulsion How can PDL and Pulp Problems affect outcome for avulsed teeth? Replacement vs. Inflammatory Resorption

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Permanent Tooth Trauma

Avulsion Closed Apex Outcomes • Favorable • Unfavorable

Permanent Tooth Trauma

Avulsion Open Apex Outcomes • Favorable • Unfavorable

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Permanent Tooth Trauma

Avulsion Inflammatory Resorption • Begins as early as 2-3 weeks • Radiolucencies: bone and/or cementum • Endodontic treatment necessary • Enamel matrix protein derivative

Permanent Tooth Trauma

Avulsion Replacement Resorption • Begins within 2 weeks • Tooth gradually replaced by bone • Transient or permanent • Enamel protein matrix derivative

(Emdogain) not beneficial

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8 yrs post avulsion (age 15)

Permanent Tooth Trauma

Avulsion • Decoronation: conservative therapy • Indications • Technique • Timing • 7-10 years: within 2 yrs. • 10-12 years: decide each case individually • >12 years: as soon as detected • Further procedures: ridge augmentation

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Permanent Tooth Trauma

Avulsion Plan for future restoration • Interdisciplinary approach • Alveolar development near completion • Extraction of tooth – plan for bone graft • Orthodontic closure of space

Splinting for luxations, avulsions and root fractures: a review • Reviewed 12 clinical studies and 9 animal studies • Assessed splinting’s biological processes that affect healing • Prognosis is determined by type of injury rather than factors associated with splinting • Problems with some studies – did not simulate injury • Current protocols by IADT & AAE: Best Practice Kahler & Heithersay, 2008

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Child Abuse

Child Abuse

Reporting Requirements • Failure to report suspected child abuse is a misdemeanor • Know state guidelines • Organizations for support: • Childhelp National Child Abuse Hotline • Prevent Abuse and Neglect through Dental

Awareness

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Child Abuse

Statistics National Pediatric Trauma Registry (NPTR): • Physical abuse: 11% of all blunt trauma ages 0• • • •

4 Premature birth: high risk factor Intracranial injury more common with abuse Injuries to thorax and abdomen more common Increased hospital stays for abused children

Child Abuse

Orofacial Injuries Injuries to head, face, mouth and neck are present in over 50% of physically abused children

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Child Abuse

Child Characteristics Which children are at higher risk? • Low birth weight • Physical disability • Mental disability • Hyperactivity or aggressivity • One of many (4 or more) siblings • Age 2-4 years

Child Abuse

Neighborhood Characteristics Where is child abuse more likely? In neighborhoods with: • • • • • • • •

Increased number of one-parent families Increased unemployment Many children younger than 6 years Many families at poverty level Families living at current address <1 year Many vacant houses Many families isolated from kin Low number of single family dwellings

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Child Abuse

Characteristics of Abuser • • • • • • • • •

Young maternal age Single marital status Low level of education Low level of employment Poverty level income Low self esteem Substance abuse Mother not living with her mother at age 14 Presence of surrogate in home

Child Abuse

Other Characteristics Perpetrator, location and mechanism of injury • 27% mother • 26% father • 13% mother’s partner • 53% in home • 23% punched or slapped around head, neck, or face • 17% struck by object

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Child Abuse

Forms of Child Abuse • Physical abuse • • • •

•

Non-accidental injuries Parent punishing child Parental frustration and lack of self-control Physical presentation not consistent with history Bruises, welts, fractures, burns, lacerations

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Child Abuse

Forms of Child Abuse Sexual abuse • •

Trauma to mouth Various infections

Child Abuse

Forms of Child Abuse Neglect Emotional or verbal

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Child Abuse

Physical Indicators Injury and explanation don’t match • • • •

Handprint on face is not from a fall Accounts that change over time Conflicting accounts Unwitnessed injury

Child Abuse

Physical Indicators What injuries are seen in abused children? • • •

<1 year 2-5 yrs 6-12 years

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Child Abuse

Behavioral Indicators • Child • Adult

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Child Abuse

In the Medical Setting Munchausen syndrome by proxy • Parent

fabricates pediatric illness • Child subjected to unnecessary tests/procedures

Child Abuse

Role of the Dentist Role of dentist who suspects child abuse • • • •

Dental and general physical exam History from child and parent Ask questions If suspicious of abuse, contact protective agency

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Trauma: A Case Presentation This 14-year-old boy fell and struck his mouth on the edge of a fence. How do you proceed?

Discuss the components of your examination of this patient. • Medical history review, identifying the adult

with the patient • History of the injury • •

What, When, Where, How Any care sought elsewhere?

• Physical assessment for head trauma • • •

Orientation Rapid neurological exam Physical examination of head/neck

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The medical history is noncontributory, and your physical assessment is within normal limits. The parents say the accident happened about 3 hours ago and he broke off part of his front tooth. It hurts when he breaths in. What other information do you need to complete your diagnosis? • Continue with dental/soft tissue examination – extraoral, intraoral • It looks like he also has a lip laceration – that may need suturing after I treat his dental injury • I would examine his mouth intraorally to examine the traumatized area, and then I would probably record some radiographs.

The following images represent the condition of the patient at your office:

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You mentioned that you would record radiographs; what radiographs would you record? Based on my clinical findings – assuming no problems with any other teeth, I would record a few periapical radiographs of the injured tooth, taken from different angles.

The following radiographs were recorded:

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What is your diagnosis? This is a complicated enamel and dentin fracture of tooth #10, involving the mesial, distal, labial, lingual, and incisal surfaces. There is also a lip laceration, just coming up to the vermillion border on the left maxillary lip.

Describe in detail your management of this patient.

• I would anesthetize the tooth with local anesthesia • Since it had been 3 hours since the trauma, I would likely do a Cvek pulpotomy – maybe a pulp cap, if the injury were still fresh. • Then, I would restore the tooth with composite resin, or reattach the segment if the parents had it.

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Describe the Cvek Pulpotomy procedure. • The coronal pulp is removed (1-2 mm), making sure that the tissue is fresh and vital • Cover the pulp stump with calcium hydroxide, then restore the tooth. • The goal is for the pulp further down in the canal to retain its vitality.

What are your post-operative instructions to the patient and his parents? When do you want to see the patient again, and what will you do at that appointment? • I would tell them to seek medical care regarding the lip laceration, and I would tell them to watch for any signs of head trauma (vomiting, sleepiness, etc.). If these occur, they should head to the ED • I would tell them to give him acetaminophen or ibuprofen for any pain, and to try to keep his diet soft for the next several days. Additionally, I would encourage him to be thorough with his oral hygiene. • I would want to see him in about 4 weeks; at that time, I would check the pulp vitality of #10, and assess for any color change, mobility, etc. I would also record a follow-up radiograph.

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The parents ask you about the long-term consequences of the injury. What do you tell them? • I would tell them that there is always a possiblity that the tooth could undergo necrosis (the nerve dying), and that it may require endodontic therapy. • I would also tell them that it would at some time likely need a full coronal restoration. • We won’t know about the long-term survival of the tooth for a while, but we’ll monitor it for about 5 years.

If the injury had occurred 2 days ago, would your treatment recommendations be the same? If it occurred two days ago, there would be more bacteria entering the pulp, and if I were to attempt a Cvek pulpotomy, I’d have to go further into the chamber, and possibly into the canal to get to vital tissue. Most likely, though, the tooth would need endodontic therapy, if I wasn’t able to get to a bleeding pulp in the chamber or canal

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If the patient were 8 years old, with incomplete root formation, would your immediate treatment be the same? Yes, my immediate treatment would be the same (assuming that we’re now talking about the accident happening 3 hours ago); the goal of treatment is continued vascularity of the pulp so that the apex of the tooth can continue to develop normally. I would hope that in an 8-year-old, the pulp would be able to retain its vascularity and provide the healthy tissue needed for the apex to develop. Still, I would need to make the parents aware of the challenges we face with this type of injury.

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Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.



308

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

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Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Steven M. Adair, DDS, MS Medical College of Georgia

•

75% of direct restorations placed in last 50 years

•

Most widely used restorative material for permanent teeth in past

•

Ratio of amalgams to composites has fallen below 50:50

310

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Study

Number

Results

Braff

150 Cl. II

11.3% success over 33.5 months

Holland et al

1139

3y survival: Ds 38%; Es 48%

Qvist et al

1715

50% failed by 2y

Levering and Messer

1177 Cl. II

76% success

Roberts and Sheriff

706 Cl. II

5y survival 67%

Study Holland

Patient Age at Placement 3 years

11 months

Holland

7-8 years

44 months

Levering/Messer

<4 years

5 years (51%)

Levering/Messer

>4 years

5 years (70%)

Roberts/Sherriff

4-5 years

>7.5 years

Welbury et al.

5-11 years

41.4 months

311

MST

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Wide range of failure rates reported (058%)

•

Failure rates in context of controlled clinical environment: 0-22%

•

Concluded that amalgam remains appropriate choice for restoration of primary teeth

Kilpatrick!&!Neumann!2007

•

Children 6-10 randomized to receive • amalgams only (N=267), or • compomers in primary teeth, and • composites in permanent teeth (N=267)

•

Follow-up scheduled q6mo for 5 y

Soncini et!al!2007

312

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Primary teeth: overall: 6% compomers, 4% amalgams ! NS

2ry caries: 3% compomers, 0.5% amalgams ! statistically significant

Permanent teeth: overall: 15% composites, 11% amalgams ! NS

repairs: 3% composites, 0.4% amalgams ! statistically significant (7X difference)

•

472 children ages 8-12

•

Randomly assigned to receive posterior restorations with • amalgam (N=856) • composite s (N=892)

•

Followed for up to to 7 years Bernardo!et!al!2007

313

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Overall failure rate: 10% Survival rates amalgam: 95% composite: 86%

Annual failure rates amalgam: 0.16-3% composite: 1-9%

Primary failure reason: 2ry caries 3.5X higher for composites

•

ADA Council on Scientific Affairs (1998): “no justification for discontinuing the use of dental amalgam”

•

Supported by USPHS (“no solid evidence of any harm”) and NIH (“no scientific evidence… (of) significant side effects (from dental restoratives)”

•

Amalgam disposal issue

314

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Dalen et al J Dent 2003 • No correlation was detected between

memory variables and exposure to amalgam

•

Hujoel et a Am J Epidemiol 2005 • No evidence that mercury-containing dental

fillings placed during pregnancy increased low-birth-weight risk

•

Bellinger et al 2007 • no evidence that exposure from dental

amalgam is associated with any adverse neuropsychological effects over 5 years •

Lauterbach et al 2008 • exposure to Hg from amalgams does not

advesely affect neurological status of chilren

315

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Roberts et al 2008 • no measurable change in level of resistance to

Hg or antibiotic resistance in children with / without amalgam restorations •

DeRouen et al 2006 • no statistically significant differences in

neurobehavioral assessments or nerve conduction velocity over 7 years in children with amalgam vs. composite restorations

•

2006: review called for more studies on amalgam safety • did not ban amalgam

•

2008: set deadline (7/28/09) to complete reclassification process for amalgam

•

Beazoglou et al 2007 • economic impact of amalgam ban estimated to

be $8.2 billion first year (2005) and >$98 billion in US 2015-2020 • reductions in access to care

316

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Restoration longevity is no longer the primary factor

•

Restoration esthetics is more important

•

Parents may be concerned about mercury “issue”

•

Parents are generally not aware of the estrogenicity “issue” with resin composites

Introduced in 1950 Chrome-steel (18-8) and nickel-chrome alloys (older; not in use)

Chrome-steel properties

heating does not increase strength work hardens high chromium reduces corrosion soldering w/ flux reduces corrosion resistance

317

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Age of patient at SSC placement Years of Service

<4 years

>4 years

1

92%

97%

5

76%

80%

10

64%

61% Messer!and!Levering!1988

•

Data collected from 10 studies

•

Failure rates of SSCs: 1.9 to 30.3%

•

Failure rates of amalgams: 11.6 to 88.7%

•

1.5 - 9 failed amalgams for every failed SSC

•

Odds ratio 0.23 (95% CI 0.19, 0.28) Randall!et!al!JADA!2000

318

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

No studies met inclusion criteria • no randomized prospective studies

Evidence to support SSCs over other types of fillings for primary molars (but low quality) • Strong need for prospective RCTs • Lower levels of evidence consistently favor SSCs • Should not be misinterpreted as lack of evidence for SSC efficacy •

Materials Continuum

Glass ionomer cements – evolved from search for replacement for silicate cement

Resin modified glass ionomers – “glass ionomer hybrids”

Polyacid modified resin composites “compomers”

319

Resin composites

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Historical development • acrylic and other resins, early composites

•

Composition filler particles; various; hydrophilic resin matrix; dimethacrylate resin; hydrophobic silane coupling agent pigments, stabilizers, polymerization inhibitor, photoinitiator, radiopaquing agents

• • • •

•

Filler - range of materials, sizes

Category

Particle size (microns)

w/w% Filler

Filler Type

Characteristics

Traditional

8-12

>80

quartz

rough

Small particle

1-5

60-78

quartz/glass

better stress resistance

Microfilled

0.04-0.4

50-60

silica/ppc

esthetic

Hybrid

0.4, 1-5 blend

50-75

silica/glass

esthetic

Nanofilled

5-25 nm 75-80 75-100 nm clusters

320

nanosilica, highly esthetic zrconium/silica

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Particle size 0.005 – 0.01 "m though 40 nm particles present in microfills

Comparisons: hydrogen atom: 0.1 – 0.2 nm small bacterium: 1000 nm (1 "m)

Reduced interstitial spacing of filler particles Increased filler loading Better properties (?) Longer retention of surface polish

•

“Finishability” • nanofilled > microfilled > hybrid > small particle >

traditional •

Tensile strength • small particle = hybrid = nanofilled > traditional >

microfilled •

Compressive strength • small particle > hybrid = nanofilled > microfilled =

traditional

321

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

•

Reduce polymerization shrinkage

•

Decrease coefficient of thermal expansion

•

Increase hardness

Composite resin polymerization shrinkage: 2 – 3.5% • leads to gap formation/microleakage, and cusp

deflection

•

Necessitates incremental filling technique

Layering technique

Gap formation

From Ruiz & Mitra 2006

322

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Bonding agent strength must be >17 MPa to overcome shrinkage stress (1MPa=150 psi) • Less shrinkage if cured in contact with a set RMGI liner (“stress breaker”) • Composite shrinks toward strongest area of bond •

•

Not truly condensable

•

SureFil, ALERT, Filtek P60

•

Fillers • fibrous, porous, or irregularly-shaped

particles • different sizes of particles •

Wear rates similar to amalgam (?)

•

Must place incrementally (polymerization shrinkage)

323

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

•

• • •

Lower filler volumes (45-70 w/w%), same particle size as hybrids, decreased viscosity/stiffness Increased polymerization shrinkage, decreased wear resistance, decreased strength, bond strength 8-10 MPa Most contain fluoride Designed as sealants, but used as restorative agents Radiopacity important if used beneath resin composites

Materials Continuum

Glass ionomer cements – evolved from search for replacement for silicate cement

Resin modified glass ionomers – “glass ionomer hybrids”

Polyacid modified resin composites “compomers”

324

Resin composites

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Type I: luting cements

•

Type II: restorative materials • II.1 esthetic • II.2 reinforced

•

Type III: lining materials and fissure sealants

Sealant Luting cement Crown cementation Orthodontic band cementation Orthodontic bracket adhesive

Cavity liner Dentinal adhesive Sandwich technique or dentin “replacement” Tooth restoration, including ITR (ART)

325

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Chelation bond to dentin and enamel

•

Leaches fluoride (how long? “burst” effect? rechargeable? antimicrobial effects?)

•

Biologically compatible with connective tissue

•

Thermal expansion similar to enamel and dentin

•

Low setting shrinkage

•

Bond strength 0.5-4.0 MPa to dentin

Technique sensitive - moisture imbibition and dessication Bond strength less than composite/dentin Brittle Porosity Surface finish not as smooth as composite Surface wear greater than composite

326

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Clean surface required for good chelation

•

10% polyacrylic acid, water rinse

•

Removes smear layer, tubules plugged

•

Must cover GIC with varnish or unfilled resin immediately after placement

•

Initial finishing delayed ~3-5 minutes

•

Finish using standard techs (hand instruments?)

327

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Cover again with varnish or sealant

•

No pressure for 1 hour

•

Cracks caused by dehydration can be closed by rehydration

•

Effect was greater for RMGIs than conventional GICs Sidhu et al 2004

•

Proper dentin conditioning

•

Proper manipulation of material

•

Protection during setting or whenever dessication might occur

328

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Materials Continuum

Glass ionomer cements – evolved from search for replacement for silicate cement

Polyacid modified resin composites “compomers”

Resin modified glass ionomers – “glass ionomer hybrids”

•

Resin modified with hydrophilic monomers that contain no water

•

Specialized fillers, dehydrated polyalkenoic acid

•

LC plus auxiliary acid-base reaction with uptake of water (insufficient in dark)

•

Require use of primers and adhesives; acid etching recommended

329

Resin composites

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Low fluoride release with water uptake (20% of GIC); limited reservoir effect Weaker, more likely to wear than RCs and RMGIs Excellent handling characteristics Water uptake degrades some physical characteristics, buffers acidic environment, affects color stabiliby

Advantages no mixing easy to place and polish; excellent handling good esthetics less susceptible to dehydration radiopaque stronger than GICs higher bond strengths than RMGIs clinical success rates similar to amalgam, GI, RMGI, resin composites

330

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Disadvantages • bonding agent required • more leakage than RMGIs • expand from water sorption over time • wear more readily than resin composites • fluoride release into tooth structure inhibited by

resin bonding agent • limited fluoride uptake (recharge) • no major advantages over resin composites

Materials Continuum

Glass ionomer cements – evolved from search for replacement for silicate cement

Resin modified glass ionomers – “glass ionomer hybrids”

Polyacid modified resin composites “compomers”

331

Resin composites

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

80% GIC + 20% LC composite resin

•

Powder similar to conventional GIC

•

Liquid is HEMA, water, and a polyacid; significant acid-base reaction

Fuji II LC

Setting reactions:

acid-base reaction (self-cure) photoinitiated (light cure) chemically-activated polymerization (resin cure)

Fluoride release similar to/less than GICs: initially high, decreases rapidly; can be “recharged” F in filler particles, radiopaquing agent, resin matrix

332

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Strength and solubility intermediate to GIC and composites Less prone to hydration problems than GIC F release equal to GIC; can be recharged Ease of use intermediate to GIC and composites; requires mixing

•

• • •

Vitrebond Plus

•

Esthetics intermediate to GIC and composites

•

Bond to tooth structure > GIC

•

Less microleakage than GIC

•

Coefficient of thermal expansion lower than GIC

333

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

In comparison to flowable composites RMGIs have: lower adhesion to dentin fluoride release coefficient of thermal expansion closer that that of natural tooth lower (better) modulus of elasticity – can act as stress-absorbing buffer for polymerization contraction forces

•

RMGI + composite resin performs better than flowable + composite resin

RMGI absorbs contraction stress, counterbalances cusp deformation

334

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

15-60 sec etch with 37% phosphoric acid

•

Resin tag formation - 1075 "m

•

Hydrophobic bis-GMA or urethane dimethacrylate resins

•

Bond strengths >20 MPa

•

Type I – rod cores

•

Type II – peripheries of rods

•

Type III – delineation of rods not evident

335

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Dentin histology is major factor in bonding success

Factors smear layer dentinal tubule density, size, length dentin sclerosis (caries-affected)

1 - 5" thick; dentin chips, debris Partly porous, but reduces fluid flow from tubules Weak attachment to dentin - ~6 MPa Biological “band-aid” Permeability increased by primers

336

Courtesy of Dr. Jorge Perdigao

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Tubule diameter increases with depth toward pulp Superficial dentin fewer tubules per surface area less area for lateral diffusion of bonding agent

Bond strength decreases with progressive depth from DEJ water in dentinal fluid competes with collagen for hydrophilic monomers fluid dilutes concentration of monomer less intertubular dentin available for creation of hybrid layer

337

Courtesy of Dr. Jorge Perdigao

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Sclerotic dentin denser in mineral content

•

Reduces penetration of bonding agent

•

Additional/extended etching on cariesaffected dentin increases tensile bond strength (Arrais et al 2004)

•

Removes or modifies smear layer, increases permeability

•

Demineralizes underlying dentin

•

Chemistry • • • • •

EDTA phosphoric acid maleic acid phosphoric/nitric acid/Al oxalate others

338

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Current systems use hydrophilic wetting agents

•

Provides micro-mechanical retention to modified dentin

•

Wets/penetrates collagen meshwork, creates “hybrid layer,” increases wetability of dentin

Unfilled resin Bonds with composite restorative material Bonds with primer in hybrid layer Courtesy of Dr. Jorge Perdigao

339

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Two-bottle etch and rinse system (total etch/complex)

One-bottle etch and rinse system (total etch/simplified)

Two-bottle self-etch system (self-etch/complex)

One-step self-etch system (self-etch/simplified) De Munck et al 2005

•

Etch-rinse-prime-bond (two bottle) system: • gold standard for bonding agents

•

Any simplification in the procedure results in loss of bonding effectiveness

•

Only two-step self-etch primer + adhesive approaches the gold standard

340

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Self-etch systems modify but do not remove the smear layer

•

May result in less postoperative sensitivity

•

Not as good as total etch systems for enamel bonding

•

“Total etch technique”

•

Dentin is left slightly wet - “glistening”

•

Enamel and dentin bond strengths 21-30 MPa for permanent, 10-18 primary

341

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Smear layer removed more easily than in permanent teeth 25-30% thicker hybrid layer Greater reactivity of primary dentin to conditioner; deeper demineralized zone; precludes complete penetration of primer and adhesive? Recommended less time for conditioning primary teeth (7 vs. 15 sec) Nor et al 1996, Torres et al 2007

•

Microtensile bond strength of adhesive systems similar with permanent and primary dentin (Soares et al 2005)

Shorter etch times may not be necessary with self-etch products

342

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Osseointegrated (endosseous) implants • titanium or titanium alloy • surface treatments to enhance

osseointegration

• acid etching • grit blasting / acid etching

• surface treatment with hydroxyapatite

leads to biointegration

• direct biochemical bond of bone to implant surface independent of mechanical interlocking

•

Implants behave as ankylosed teeth

•

Can interfere with position of adjacent tooth germs, eruption of adjacent teeth

•

May become dislocated or lost as result of jaw growth

343

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Cannot participate in drift and displacement mechanisms of growth in maxilla

Fixed!implants!that cross!the!midline!will restrict!maxillary!growth

•

In mandible, however, increases in width are generally related to posterior growth at rami Transverse!growth!in anterior!region!ends!in early!childhood

344

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Most risky areas for implant placement in growing child are: • anterior and posterior maxilla • posterior mandible

•

Best site: • anterior mandible (but not for single tooth

replacement)

•

Mandibular rotation and resorption of anterior alveolar ridge may lead to displacement / loss of implants

345

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Prior to placing implants, use a conventional prosthesis to: gain information on function and esthetics allow for as much growth as possible

Problem with prosthetic approach: retention Examples of implants in children with ectodermal dysplasia: see Kramer et al 2007, Guckes et al 1997

346

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

6-year-old white male with ectodermal dysplasia

Rockman RA, Hall KB, Fiebiger M. JADA 2007

Rexillium alloy copings cemented to maxillary and mandibular primaryteeth; copings used to hold “keeper” magnets

347

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Cast metal frameworks

Magnets were attached with cold cure resin Some dental anatomy placed in maxillary posterior acrylic Mandibular acrylic left as monoplane

348

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

349

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

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Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Pulp Therapy in Primary and Young Permanent Teeth Steven M. Adair, DDS, MS Medical College of Georgia

Histologic Components of Primary Pulp •

Lymph vessels

•

Blood vessels

•

Nerve tissue

•

Collagenous fibers

•

Fibroblasts

•

Defense cells •

•

Lymphocytes

•

Odontoblasts

•

Odonto-/osteoclasts

•

macrophages, neutrophils

351

Histologically similar to young permanent pulp – cell rich, vascular

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Comparative Morphology •

Increased number of accessory canals

•

Curved roots

•

Ribbon-like radicular pulp

•

Relatively longer roots in molars

•

Coronal pulp position

•

Apical resorption

•

Position/proximity of premolars

•

Larger pulp relative to crown size

•

Mesial pulp horns closer to DEJ than distal

Clinical Assessment of Pulp Status •

Problem: making histologic assessment from clinical signs and symptoms In general, the correlation between the clinical findings and the histologic condition is weak.

352

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Assessment of Pain Types of Pain

Pulp Status

Spontaneous Nocturnal

Irreversible: Non-vital treatment

Constant Thermal Reversible: Vital treatment

Chemical Intermittent

Further Clinical Assessment •

Extent of lesion •

•

location, color

Mobility •

•

R/O root resorption

•

Soft tissue swelling

•

Lymphadenopathy

Sensitivity to percussion •

•

Pulp exposure •

•

hemorrhagic v necrotic

Pulp testing • • •

353

reliable in primary teeth

electrical thermal percussion

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Reliability of Pulp Testing Teeth:

Primary

Young permanent

Mature permanent

Electrical

---

+

+

Thermal

+

+

++

Percussion

++

+

+

No single diagnostic test is reliable

Radiographic Criteria for Healthy Pulp •

Adequate periodontal support

•

No decalcified lesions or root fractures

•

No internal/external resorption or radiolucency

•

Integrity of lamina dura

•

See manual for more

354

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Radiographic vs. Histologic Assessment Moss et al 1965: accessory canals in furcation area no vital pulp tissue with interradicular bone loss increased porosity of pulpal floor when infected

Wrbas et al 1997: 77.5% of mandibular primary molars had accessory canals in floor of chamber

Vital Pulp Therapy •

Protective base/liner

•

Indirect pulp treatment (IPT)

•

Direct pulp capping (DPC)

•

Pulpotomy • •

•

pharmacotherapeutic non-pharmacotherapeutic

Partial pulpotomy (permanent teeth)

355

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Protective Base/Liner Indications (AAPD):

•

• • • • •

normal pulp dentin tubules exposed by cavity prep all caries removed minimize injury to pulp minimize post-op sensitivity

Objectives

•

• • • •

preserve pulpal vitality promote pulpal healing promote tertiary dentin formation minimize microleakage/sensitivity

Indirect Pulp Treatment •

Indications • • • • •

•

deep carious lesion no/reversible pulpitis incomplete caries removal no pulp exposure pulp vital

Objectives •

complete seal, preserve vitality, no post-tx signs or symptoms, no harm to succedaneous teeth, continued root development in permanent teeth

356

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

IPT Technique •

Apply medicament/material over carious or sound dentin [Ca(OH)2 most commonly used]

•

Vitality should be preserved

•

If planning to re-enter, wait 6-8 weeks for tertiary dentin; remove remaining caries, restore; eliminate microleakage

IPT Technique •

Need to re-enter controversial

•

Radiolucency beneath IPT decreased in size or did not increase under Dycal/ZOE in majority of cases (Maltz et al 2007)

•

Success rate up to ~90%

•

Stepwise excavation leads to fewer pulp exposures in young permanent teeth

357

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

IPT in Primary Teeth •

Recent data: •

•

•

•

IPT (GIC) had higher success rate than FMC pulpotomies Farooq et al 2000; Vij et al 2004 total etch technique more successful in primary molars than IPT (Ca[OH]2) Falster et al 2002 IPT (Ca[OH]2) success rate in primary molars was 95% in retrospective study Al-Zayer et al 2003 Carious dentin undergoes mineral gain when sealed in IPT Oliveira et al 2006

Indirect Pulp Treatment •

Vij et al 2004 0-1 year

1-2 years

2-3 years

>3 years

FMC success

95%

84%

76%

70%

IPT success

98%

96%

94%

94%

Treatment of deep dentinal lesions with caries control procedures prior to FMC or IPT improved the success of both.

358

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Direct Pulp Cap •

Indications •

•

•

Small mechanical or traumatic exposure in primary teeth with normal pulp Small carious or mechanical exposure in permanent teeth with normal pulp

Contraindicated for carious exposure in primary teeth

Direct Pulp Cap: Objectives (AAPD) •

Preserve vitality

•

No post-treatment signs or symptoms

•

Pulp healing

•

Tertiary dentin

•

No pathologic changes

•

No harm to successors

•

Continued apexogenesis for permanent teeth

359

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Pulp Capping Agents •

Ca(OH)2 still widely used and taught

•

ZOE - chronic inflammation

•

•

Mineral trioxide aggregate (MTA; permanent teeth) Total etch technique

Direct Pulp Cap - Bleeding • •

•

•

Success inversely related to bleeding at site Debris at exposure site: clean out with saline or anesthetic to prevent inflammation caused by dentinal chips; keep pulp moist Clot will prevent contact of material with the pulp; clot may release products that attract bacteria Success rate up to 80-90%; 50% if pulp inflamed

360

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Biocompatibility of Materials with Dental Pulp •

Pulpal response to contact with a variety of materials is severe inflammation when bacterial microleakage occurs

•

Biocompatibility with dental materials allows pulpal healing in absence of microleakage

•

Dentin bridge formation possible even in contact with sterile food in germ-free environment

•

Biocompatibility is a function of microleakage

Partial Pulpotomy - Criteria •

No/recent pain of short duration

•

No swelling, mobility, rxn to percussion

•

No internal/external resorption, changes in PDL, radiographic abnormalities

•

Pulp exposure 1-2 mm, bleeding stops <1-2 min

•

Inflammation, infection superficial only

•

Only superficial pulp removed Mass et al 1995

361

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Partial Pulpotomy Technique •

Enlarge exposure

•

Partial extirpation

•

Place capping material

•

Place leak-proof seal •

ZOE covered with GIC or CH if resin composite is to be used

Partial Pulpotomy – Objectives (AAPD) •

Remaining pulp stays vital

•

No adverse clinical signs/symptoms

•

Continued apexogenesis in immature teeth

362

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Partial Pulpotomy •

Advantages • • • • • • • • •

removes inflamed, infected portion of pulp preserves cell-rich coronal pulp facilitates washing away carious debris allows better contact with more material increases healing potential physiologic apposition of cervical dentin no need for RCT natural color/translucency preserved maintenance of vitalometer response

Pulpotomy for Primary Teeth •

Indications •

• • •

•

deep lesion adjacent to pulp that is normal or reversibly inflamed, or pulp exposed by trauma coronal tissue can be amputated remaining radicular tissue vital (clinically and radiographically)

Objectives • • • •

preserve vitality of radicular pulp no adverse signs or symptoms no radiographic changes no harm to succedaneous teeth

363

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Technique •

Prepare tooth for restoration (typically SSC)

•

Excavate carious dentin, unroof pulp chamber

•

Amputate coronal pulp

•

Hemostasis (diagnostic value)

•

Treat remaining pulp (medicament/energy)

•

Seal and restore

Pulpotomy: Clinical Indications •

Mechanical/carious exposure, trauma

•

Inflammation limited to coronal pulp

•

Absence of spontaneous pain (?)

•

•

Absence of swelling or alveolar abscess formation Restorable tooth

364

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Pulpotomy Contraindications •

•

•

•

History of unprovoked pain (?)

•

Presence of fistula or swelling

•

Evidence of necrotic pulp

•

Uncontrolled pulpal hemorrhage

•

Periapical or bifurcation radiolucency Pathologic resorption Dystrophic calcification More than 1/3 root resorption

Pulp Treatment Medicaments 1883 At a meeting of the American Dental Association in St. Louis in 1883, Dr. F.A. Hunter claimed a 98% success rate using a pulp capping agent made from one pint of sorghum molasses and one pound of the droppings from the English sparrow.

365

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Categories of Medicaments •

Fixatives •

•

•

Ca(OH)2

Palliative sealers •

•

FMC, glutaraldehyde

Mineralizing and/or bacteriostatic agents •

•

•

erythromycin, others

Tissue healing agents

•

•

mineral trioxide aggregate

epi, ferric sulfate, aluminum chloride

Antibiotics/Antimicrobials

•

ZOE

Obturators •

Coagulants

•

collagen, BMP

Glucocorticoids

•

•

corticosteroids

Medicament Combinations •

Vitapex •

•

Maisto’s paste •

•

iodoform, Ca(OH)2 iodoform, parachlorophenol, camphor/menthol

Ledermix • •

dimethylchlorotetracycline triamcinolone

366

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Formocresol Pulpotomy Success Rates Range of success rates in literature: 62-100% depending on study and criteria used Clinical>Radiographic>Histological

Formocresol pulpotomies may be empirical clinical successes, but histologically they are failures to one degree or another.

Actions of Formocresol •

Composition (open to interpretation) •

•

19% formaldehyde, 35% cresol in vehicle of 15% glycerin and water

Fixation with progressive fibrosis • • •

acidophilic zone: fixation pale staining zone: atrophy broad zone of inflammatory cells

•

Bactericidal - biggest benefit?

•

No dentin bridging

367

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Fixation Preserves cellular detail Minimizes alteration from tissue in living state Inhibits autolytic changes and bacterial growth Coagulates protoplasm rendering it insoluble Increases affinity for particular stains

Dr. Suzi Seale

Histology Glutaraldehyde pulpotomy in monkey incisor

One week

Three weeks

368

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Effects on Succedaneous Teeth Pruhs et al (1977)

Rolling and Poulsen (1978)

It is possible that enamel defects in premolars were caused by inflammation prior to the pulpotomy

Dilution of Formocresol •

1:5 dilution •

1 part FMC, 4 parts vehicle (3 parts glycerin, 1 part distilled water)

•

Histology and clinical success comparable to full strength

•

Neither produces ideal histology

•

Long-term clinical success of 1:5 still questioned by some

369

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Glutaraldehyde •

Powerful fixing agent

•

Antibacterial

•

Large molecule

•

Minimal systemic distribution

•

Low antigenicity

•

Treatment concentration 2-5%

Ferric Sulfate •

FS forms protein complex, occludes capillaries; no antibacterial action

•

Must assume healthy radicular pulp (?)

370

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Systematic Review of Ferric Sulfate •

Loh et al. 2004; 3 RCTs, 10 CTs analyzed

•

Clinically, FS significantly more successful than formocresol: OR 1.95

•

Radiographically, no difference between medicaments: OR 0.90

•

Conclusion: Pulpotomies performed with either material are likely to have similar clinical/radiographic success.

Meta-analysis of Ferric Sulfate vs FMC •

6 prospective controlled trials

•

Both treatments similar in clinical outcomes, radiographic success, other findings

•

Overall clinical success of FS: 78—100%

•

Overall radiographic success of FS: 42-97%

371

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Mineral Trioxide Aggregate •

Gray: tricalcium silicate, tricalcium phosphate, tricalcium oxide, Fe, Al

•

Broadly similar to Portland cement

•

White: more esthetic

•

Hydrophilic particles set in presence of moisture 3-4 hours; compressive strength similar to IRM

•

Better seal than amalgam

•

Pricey (~$325/box of 5 1g packets)

MTA vs FMC Controlled Trials •

Aeinehchi et al 2007 •

•

•

significantly more teeth with root resorption in FMC group no root resorption in MTA group

Noorollahian 2004 •

no significant difference in radiographic success rates between FMC and MTA

372

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Sodium Hypochlorite •

Vargas et al 2006

•

Compared NaOCl (N=32) and FS (N=28)

•

12 months: •

NaOCl: 100% clinical, 79% radiographic success

•

FS: 85% clinical, 62% radiographic success

Non-pharmacotherapeutic Pulpotomy •

Basic principles: • •

amputate infected coronal pulp treat remaining radicular pulp by controlled energy

•

neutralize residual infectious process

•

avoid dystrophic pulpal changes

•

avoid breakdown of periradicular supporting tissues

373

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Electrosurgical Pulpotomy

Disadvantages Advantages heat leads to tissue destruction quick persistent inflammation self-limiting energy cannot be isolated to surface hemostasis root resorption good visibility pulp inflammation no systemic effect

RCT of Primary Pulpotomy Techniques •

Huth et al 2005

•

Prospective randomized controlled trial

•

200 primary molars, 107 patients

•

Treatments: • • • •

50 dilute FMC (control group) 50 Er:Yag laser 50 calcium hydroxide 50 ferric sulfate

374

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Huth et al 2005 •

Pulp hemostatis was an inclusion criterion

•

All treatment followed by ZOE, GIC

•

Final restoration: SSC or composite resin, based on amount of tooth destruction

•

Clinical and radiographic follow-up at 6, 12, 18, and 24 months •

•

2 blinded examiners (neither was an operator)

Some teeth lost to follow-up (exfoliation, patient drop-out): final sample – 175

Huth et al 2005 Total success rate %

12 months

24 months

FMC

96

85

Laser

93

78

Ca(OH)2

86

53*

Ferric sulfate

86

86

Clinical success rates were higher in all cases; *statistically significantly different

375

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Huth et al 2005 •

Only calcium hydroxide performed significantly worse than FMC (p<.001) at 24 months

•

Larger sample size, more statistical power, needed to determine whether the nonsignificant differences between FMC, laser, and ferric sulfate are, in fact, truly not different

Pulpotomy in Permanent Teeth Indications: can remove infected or affected tissue; time/money constraints prevent RTC (closed apices)

376

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Agents for Permanent Tooth Pulpotomy •

Ca(OH)2 most widely used

•

Formocresol • •

•

Glutaraldehyde •

•

limited circumstances short-term preservation of permanent molar not well tested in permanent teeth

MTA

Apexogenesis •

Encourage continued root formation

•

Promote tertiary dentin formation

•

No evidence of inflammatory resorption

•

No evidence of root and periradicular pathosis

•

Immediately obturate canal or observe?

377

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MTA vs Ca(OH)2 Pulpotomy •

El Meligy & Avery 2006

•

Immature permanent teeth 15 received MTA 15 received Ca(OH)2

• •

2 Ca(OH)2 failures at 6 & 12 months

•

pain, swelling

•

•

No MTA failures

•

MTA judged to be suitable alternative to Ca(OH)2

Non-vital Pulp Therapy •

Indications for primary teeth •

irreversible pulpitis

•

pulpal necrosis

•

•

excessive hemorrhage from radicular pulp in tooth planned for pulpotomy minimal/no root resorption

378

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Non-vital Pulp Therapy for Primary Teeth •

Pulpectomy •

•

necrotic pulp/irreversible inflammation abscessed (in very limited instances - strategic importance of tooth is major consideration)

Primary Tooth Pulpectomy Other indications: tooth of strategic/esthetic importance restorable poor chance of success with vital therapy adequate root remaining cooperative patient

Reserve for incisors, 2nd molars

379

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Primary Pulpectomy Technique Remove coronal pulp Remove radicular pulp remnants up to size 35 file Irrigate repeatedly; dry; treat with medicament?; one-visit, two-visit? Obturate with resorbable paste

Criteria for Ideal Obturant •

Antiseptic

•

Resorbable

•

Harmless to adjacent tooth germ

•

Radiopaque

•

Non-impinging on erupting permanent tooth

•

Easily inserted and removed

•

Biocompatible

380

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Zinc Oxide and Eugenol Most widely used to date Biocompatibility is questionable; effects are related to concentration of free eugenol Resorbability is questionable

Calcium Hydroxide in Pulpectomies •

Good biocompatibility

•

Longevity of material and action is questionable - too resorbable

•

Other materials • • •

•

Kri-1 paste Vitapex (iodoform, calcium hydroxide) Ciprofloxacin/metronidazole/minocycline (Takushige et al 2004) Endoflas (Moskovitz et al 2005)

381

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ZOE vs. Vitapex •

Mortazavi & Mesbahi 2004

•

29 ZOE, 26 Vitapex; randomly assigned

•

3- and 10-16 mo follow-ups

•

More short fills with ZOE; more overfills with Vitapex

•

Overall success at 10-16 months • • •

Vitapex 100% ZOE 78% statistically significant

Pulpectomy Success Rates •

Success rates in molars & incisors comparable

•

Predictors of success: • •

•

• •

minimal root resorption ZOE fill to or slightly short of apex

Enamel defects in succedaneous teeth (19%) related to pre-tx root resorption Extraction of molars required about 20% of time 20% chance of altering eruption path of succedaneous tooth

382

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FS Pulpotomy vs. Pulpectomy •

Casas et al 2004

•

Compared FS pulpotomies (n=15) and ZOE pulpectomies (n=14)

•

3-year survival probabilities: • • •

•

0.62 for FS pulpotomies 0.92 for ZOE pulpectomies statistically significant difference

Pulpectomies demonstrated significantly greater survival than FS pulpotomies after 3 years

Systematic Review of Pulp Therapies •

Nadin et al, Cochrane Database, 2004

•

82 studies identified: FMC, FS pulpotomies; electrosurg; ZOE pulpectomy

•

Conclusion: no reliable evidence to support superiority of one type of pulp treatment for primary molars

383

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Non-vital Tx: Young Permanent Teeth •

Objectives: • •

•

promote continued apical development achieve apical closure (Frank technique)

Technique: apexification • •

•

necrotic tissue removal short of apex place agent (calcium hydroxide) to achieve closure or apical stop MTA being used in place of calcium hydroxide

MTA vs Ca(OH)2 Apexification •

El Meligy & Avery 2006

•

Necrotic permanent teeth requiring root-end closure • •

15 received MTA 15 received Ca(OH)2

•

Recalled at 3, 6, and 12 months

•

2 Ca(OH)2 failures at 6 & 12 months •

•

persistent periradicular inflammation

No MTA failures

384

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MTA Apexification Case Series •

57 permanent teeth, open apices

•

Single appointment MTA tx followed by gutta percha obturation

•

Blinded evaluation of films with >2 yrs f/u

•

95% of apical lesions demonstrated complete or progressive healing

•

Apical closure seen in 26% Simon et al 2007

•

Pulpal Revascularization of Immature Necrotic Permanent Teeth Assumption: •

•

Goal: •

•

apical portion of pulp may still be vital encourage this vital tissue to migrate coronally

Procedure: • •

disinfect root canal place triple antibiotic paste (ciprofloxacin, metronidazole, cefaclor)

385

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Pulpal Revascularization of Immature Necrotic Permanent Teeth •

Procedure, cont’d • • • •

•

remove paste after several weeks induce bleeding by stimulating tissue beyond apex allow clot to reach CEJ cover with MTA, restore

Resulting clot acts as scaffold to aid growth of new tissue in canal

Pulpal Revascularization of Immature Necrotic Permanent Teeth

386

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Pulpal Revascularization of Immature Necrotic Permanent Teeth

Expect continued root lengthening and thickening Pulp responsive to cold stimulus

387

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388

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Oral Pathology and Oral Medicine Andrew L. Sonis, D.M.D. Senior Associate in Dentistry Children’s Hospital, Boston Clinical Professor Harvard University School of Dental Medicine Private Practice Newton, Massachusetts

Correction in manual: p. 73 & Alveolar bone: & Should be Intramembranous bone formation, not Endochondral bone formation

389

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Developmental variations of normal oral structures

Epstein’s Pearls

&Epithelial inclusion cyst &Palatal midline

390

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Bohn’s Nodules

&Buccal and lingual aspect of alveolus &Ectopic mucous glands

Dental Lamina Cysts

&Crest of the alveolus &Remnants of dental lamina

391

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Hyperplastic foliate papillae &Lateral border of tongue &Easily traumatized &Normal lymphoid tissue

Fordyce granules & Ectopic sebaceous glands in oral mucosa & Elevated yellowish nodules & Maybe discrete or confluent & Common sites: buccal mucosa, upper lip

392

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Median rhomboid glossitis & ? Result of anomalous vascularity vs. persistence of tuberculum impar & Usually asymptomatic, but may cause soreness/burning & Surface flat or slightly raised & Color varies from pale pink or whitish to bright red & Candidial infection present ~ 40%

Fissured tongue & Rarely seen before age 4 years & ? Genetic (A.D.) & 3-5% frequency, but higher in mentally retarded population & Maybe associated with Melkersson-Rosenthal syndrome

393

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Leukoedema & Most commonly seen in blacks & Grayish-white thickening of buccal mucosa & Usually bilateral & Extensive intracellular edema of epithelium

Idiopathic osteosclerosis & Well-defined radiopacity in the toothbearing area of jaw & No surrounding radiolucent space & Not typical of any other condition & Mandibular premolar/molar area most common & Maybe related to root apex, but normal PDL

394

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Stafne bone defect &Cyst-like radiolucent area near angle of mandible &Indentation of bone containing extension of submandibular gland

Bifid tongue & Developmental malformation & May coexist with orofaciodigital syndrome & Complete form requires surgical reconstruction

395

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Bifid Uvula

&Minor expression of cleft palate &Must r/o sub mucous cleft &May require surgical correction

Macroglossia

396

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Discrete Swellings or Lumps/Bumps &Congenital &Inflammatory &Traumatic &Neoplastic &Others

Lingual thyroid & Redundant thyroid tissue in tongue & Hypothyroidism~20 % & ~70% lack normal thyroid tissue in neck

397

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Lingual thyroid & Redundant thyroid tissue in tongue & Hypothyroidism~20 % & ~70% lack normal thyroid tissue in neck

Vascular Malformations &Present at birth &Become clinically evident in late infancy/early childhood &May increase in size following trauma, infection, or endocrine changes &~35% associated with skeletal changes

398

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Lymphangioma &Diffuse vs. discrete &Tongue most common site &Surface often papillary or vesicular &Tx: surgical excision

Hemangioma & Common vascular tumor of infancy & Usually appear early in infancy, grow rapidly until age 6-8 mos., then slowly involutes & Blanch on pressure & Generally do not involve the adjacent skeletal tissue & Tx: watch and wait

399

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Hemangioma: Indications for Treatment &Kasabach-Merritt syndrome with severe thrombocytopenia (<40,000) &Lesions interfering with function &Recurrent bleeding, ulceration, infection &Rapidly growing lesion that causes facial distortion

Infection/abscess & Uncommon, but may follow traumatic injury & May represent secondary infection of neoplasm/cyst & Tx: remove source of infection/antibiotics

400

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Tongue pyogenic granuloma & Common reactive lesion & Painless, nodule, red lesion & Typically pedunculated with ulcerated surface & Tx: surgical excision

Tongue trauma due to neurocomatose chewing

401

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Tongue trauma: Riga-Fede syndrome &Chronic trauma from primary incisors &Typically ulcerated lesion on tip of tongue &Tx: smooth incisal edges

Fibroma & Most common tumor of oral mucosa & Often the result of chronic trauma & Typically painless, firm, sessile or pedunculated & Tx: surgical excision

402

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Papilloma & Human papilloma virus & Exophytic, well circumscribed & Usually pedunculated with either finger-like projections or cauliflower surface & R/O condyloma acuminatum & Tx: surgical removal

Neurofibroma & Rare in childhood & Tongue and buccal mucosa commonly affected & Maybe solitary or multiple (neurofibromatosis) & Tx: surgical excision

403

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Neurofibroma & Rare in childhood & Tongue and buccal mucosa commonly affected & Maybe solitary or multiple (neurofibromatosis) & Tx: surgical excision

Neurofibromatosis & A.D. ( ~50% spontaneous mutations) & Peripheral form most common ~90% & ~70% have oral involvement & Café-au-lait spots, subcutaneous neurofibromas, Lisch nodules

404

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Neurofibromatosis & A.D. ( ~50% spontaneous mutations) & Peripheral form most common ~90% & ~70% have oral involvement & Café-au-lait spots, subcutaneous neurofibromas, Lisch nodules

John Merrick: The Elephant Man

405

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Granular-cell Tumor & Uncommon benign lesion & Tongue most common site (25%) & Typically solitary, asymptomatic, welldefined, sessile lesion & Tx: surgical excision

Tongue Foreign Body

Fractured palatal cusp

406

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Exophytic Lesions in BMT

Diffuse Swelling of the Tongue

&Congenital &Inflammatory &Traumatic &Others

407

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Just a “BIG” Tongue

Positive Gorlin sign

Ehlers Danlos Syndrome & Collagen defect (procollagen) & Classic form: & & & &

Loose jointedness Fragile, bruisable skin Laxity of skin “cigarette paper” scars

& Dental: oral bleeding, periodontal disease, delayed healing

408

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Ehlers Danlos Syndrome

bruisability

Loose jointedness

Down syndrome & Chromosomal disorder: trisomy 21 & 1:800 births average & Commonest identifiable cause of intellectual disability & Risk increases with maternal age

409

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Maternal Age and Risk of Down Syndrome

Medical Conditions Associated With Down Syndrome

& Congenital heart disease ~50% & ECD, VSD, TOF

& Gastrointestinal anomalies ~15% & & & &

Tracheoeosophageal fistula Pyloric stenosis Duodenal atresia Celiac disease

& Increased incidence of ALL (20X non-DS) & Mental retardation

410

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Dental conditions associated with Down syndrome

& Relative macroglossia & Microdontia & Oligodontia & Class III malocclusion & Open-mouth posture & Fissured tongue & Decreased caries rate (historical)

& Increased periodontal disease & Delayed eruption and over-retained teeth & Atypical root morphology & Abnormal palate & Enamel hypoplasia

Hypothyroidism (Cretinism) & Short stature & Mental retardation & Delayed eruption & Enamel hypoplasia & Generalized edema & Tx: replacement therapy

411

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Hypothyroidism (Cretinism) & Short stature & Mental retardation & Delayed eruption & Enamel hypoplasia & Generalized edema & Tx: replacement therapy

Mucopolysaccharidoses & Hurler’s syndrome(prototype) & Progressive infiltration of tissues by mucopolysaccharides & Coarse facies, large head & Spacing of teeth & Tx: bone marrow transplantation

412

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Cystic Hygroma & Large diffuse lymphangioma & Extends from tongue into neck & May cause dysphagia or respiratory embarrassment & Tx: plastic surgery

Cystic Hygroma

413

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Cystic Hygroma

Cystic Hygroma

414

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Cystic Hygroma

Inflammatory Causes of Diffuse Tongue Swelling & Infection & Allergic reaction/irritation & Ludwig’s angina (rare in children)

415

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Multiple Endocrine Neoplasm, type 2B &Oral mucosal neuromas &Medullary cell carcinoma of the thyroid &Pheochromocytoma

Multiple Endocrine Neoplasm

416

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Angioedema & Allergic form maybe precipitated by drugs, foods, etc. & Hereditary form A.D. & Most are idiopathic & Tx: & Allergic formantihistamines & Hereditary form: androgens

Beckwith-Wiedeman syndrome & Macroglossia & Omphalocele or umbilical hernia & Cytomegaly of adrenal cortex & Post-natal somatic gigantism & Severe hypoglycemia & Neoplasms (nephroblastoma most common) & Very prone to OSA

417

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Indications for Tongue Reduction &Airway difficulty &Speech difficulty &Dentoalveolar protrusion &Esthetics &Drooling &Recurrence of openbite/bimaxillary protrusion/spacing

Surgical tongue reduction

418

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Common Causes of a Sore Tongue &Ulceration &Geographic tongue &Median rhomboid glossitis &Foliate papillitis

Common Causes of a Sore Tongue &Ulceration &Geographic tongue &Median rhomboid glossitis &Foliate papillitis

419

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Common Causes of a Sore Tongue &Ulceration &Geographic tongue &Median rhomboid glossitis &Foliate papillitis

Glossitis & Generalized erythema and depapillation & Anemia & Candidiasis & Vitamin B deficiency & Radiotherapy & Depression & Diabetes & Hypothyroidism

420

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Sublingual Swelling/Mass of the Tongue & Trauma & Ranula & Abscess & Hemorrhage & Salivary gland infection & Dermoid cyst & Salivary gland tumor & Other

Ranula & Mucous retention & Typically painless & Dome-shaped, soft swelling of normal or blue color & Involves submaxillary or sublingual gland & Tx: excision or marsupialization

421

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Sublingual Dermoid Cyst

Sublingual Dermoid Cyst

422

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Sublingual Dermoid Cyst

Cheeks/Buccal Mucosa

423

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Trauma &Acute or chronic mechanical injury &Dx based on history and clinical findings &Generally heals in 7-10 days &Tx: symptomatic

Candidiasis & Several forms:

& Acute pseudomembranous & Hyperplastic & Erythematous & Common oral organism & Newborns may acquire infection from mother & Increased susceptibility with long-term antibiotics, corticosteroids, immunosuppression & Tx: nystatin, chlortrimazole, fluconazole, amphotericin B

424

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Candidiasis (Erythematous form)

Candidiasis (hyperplastic form)

425

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Nystatin (topical) & Neonate: 100,000 U PO qid & Continue 48h after resolution

& Infant: 200,000 U PO qid & Continue 48h after resolution

Fluconazole (systemic) &Loading dose: 6mg/kg PO x 1 &3mg/kg qd x 14 days &Be aware of drug interactions & Budesonide & Theophylline & Erythromycin

426

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White Sponge Nevus & A.D. & Buccal mucosa, tongue, floor of mouth & Symmetrical, bilateral white thickened plaques & Lesions maybe present at birth

Frictional Keratosis/Cheek Biting & Hyperkeratosis secondary to irritation & Smokeless tobacco products & White hyperkeratotic lesions & Early changes erythematous & Snuff > chewing

427

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Lupus Erythematosus & Immunologically-mediated disorders involving connective tissue & Discoid form (rare): & Skin disorder & ~20% have oral involvement & Systemic form (more common in children): & Arthralgia and rashes common & Affects many organ systems & Stomatitis common (3040%) & Tx: steroids

Systemic form

Lupus Erythematous

428

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Lupus Erythematous

“Moon Facies”

Contact Dermatitis: Two Major Types & Irritant & I.e. harsh soaps, chemicals: direct toxic effect upon contact with mucosa/skin & Allergic contact dermatitis: T-cell mediated immune reaction requiring sensitization to specific antigen

429

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Burns (thermal, chemical) & Common & White appearance due to necrotic tissue & Associated with a number of chemicals, i.e., ASA, formocresol, phosphoric acid, phenol, etc.

Chemical Burn

Thermal Burn

“Pizza Palate”

430

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Lip Lesions

Causes of Angular Stomatitis & Candidiasis & Common finding in HIV infection

& Staphylococcal, streptococcal, or mixed infections & Nutritional deficiencies & Crohn’s disease & Anemia

431

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Crohn’s Disease & Chronic inflammatory granulomatous disease & Affects entire G.I. tract (mouth to anus) & Etiology unknown, likely autoimmune & Oral lesions ~30% & Facial swelling & Ulcerations & Mucosal tags & Tx: antibiotics; 5-ASA; corticosteroids

Crohn’s Disease: mucosal tags

Cobblestone appearance

432

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Oral concerns in patients with inflammatory bowel disease & Increased risk of aphthous ulcers & Increased risk of periodontal disease & Steroid therapy & Patient maybe immunosuppressed & Drug therapy may cause gingival hyperplasia (cyclosporin)

When does adrenal-pituitary axis suppression occur in prolonged steroid treatment?

& Pharmacological doses of steroids used for < 10 days & Relatively small risk of permanent adrenal insufficiency & Typically full recovery in 6-12 months

& Daily use > 30 days & High risk of transient or permanent adrenal suppression

& Alternative day & Very low risk

& Inhaled steroids & Essentially no risk

433

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Who Needs Steroid Bump/Supplement? &Patients under stress &Fever > 101º &Surgery, I.e. third molar extractions &General anesthesia &Fractures &Prolonged fasting/vomiting

Causes of Lip Ulcerations/Vesicles/Blisters & Herpes simplex & Burns & Herpes zoster & Erythema multiforme & Epidermolysis bullosa & Impetigo & Allergic cheilitis

434

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Herpes simplex &Herpes labialis & Reactivation of HSV & Recurrent & Antiviral agents of limited value

Herpes labialis

1 week f/u

435

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Penciclovir (Denavir)

Denavir Promo

436

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Burns & Maybe electric, thermal, chemical & Treatment directed at preventing contraction of orafice

Varicella/Zoster & Varicella zoster virus (chicken pox) & Crops of pruritic vesicles on skin and mucous membranes & Vesicles may precede fever & Begins on trunk and spreads to limbs/face

& Infectious 24 hrs. before to 6-7 days after vesicles appear & Incubation period may last up to 20 days & Resolves in 7-10 days & Tx: palliative and supportive

437

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Herpes Zoster

Erythema Multiforme & Erythematous macules, papules, bullae, and erosions & Possible allergic etiology (drug reaction) & Target lesions & May have ocular, genital lesions (Stevens-Johnson syndrome) & Tx: palliation; steroids

438

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Erythema Multiforme (StevensJohnson syndrome)

Epidermolysis Bullosa &Hereditary vesiculobullous disease of skin and mucous membranes &E.B. simplex: most common form & A.D.

&Junctional E.B.: several subtypes & A.R.

&Dystrophic E.B. & Dominant form & Recessive form

439

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Epidermolysis Bullosa

Dystrophic EB-dominant form

Epidermolysis Bullosa

Dystrophic EB- dominant form

440

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Epidermolysis Bullosa

Dystrophic EB-recessive form

Impetigo &Most commonly caused by: & staphylococcus aureus & beta hemolytic strep

&Tx: & Localized: topical antibiotics & Widespread: systemic antibiotics

441

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Allergic cheilitis & Maybe due to contact irritation or true allergy & Tx: remove irritant or allergen

Causes of Diffuse Swelling of Lips & Edema secondary to trauma & Angioedema & Crohn’s disease & Cheilitis granulomatosis & MelkerssonRosenthal syndrome & Lymphangioma & Hemangioma

442

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Hemangioma

7 months

12 years

5 years

Vascular malformation

S/p laser surgery

443

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Causes of Localized Swellings of the Lips & Mucoceles & Tumors & Neuroma & Neurofibroma

& Cysts & Abscesses & Insect bites & Hematomas

Causes of Lip Crusting/Desquamation & Dehydration & Febrile illness & Chemical/allergic cheilitis & Mouth-breathing & Actinic cheilitis & Erythema multiforme & Psychogenic & Drugs

444

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Soft Tissue Lesions in the Newborn/Infant

Vascular Malformations &Lymphangioma &Capillary malformation & Port wine stain

&Sturge Weber syndrome &Venous malformation & “cavernous hemangioma”

&Arterial malformation &Combined

445

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Capillary Malformation:Port Wine Stain

Capillary Malformation:Port Wine Stain

446

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Sturge Weber Syndrome & Venous angiomatosis of leptomeniges & Ipsilateral facial angiomatosis & Ipsilateral gyriform calcifications of cerebral cortex & MR & Seizures & Hemiplegia & Ocular defects & Telangiectasias

Sturge Weber Syndrome

447

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Vascular Tumors &Hemangioma &Treatment modalities: & Steroids & Interferon & Pulsed dye laser & Chemotherapeutic agents & Embolization & Surgery

Congenital Epulis & Firm pedunculated mass arising from alveolus at birth & Maxillary lateral and canine region most common & Females>males & Maxilla>mandible & Tx: surgical excission

448

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Congenital Epulis

Congenital Epulis

449

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Melanotic Neuroectodermal Tumor of Infancy & Maxilla>mandible & Destructive lesion & Submucosal pigmentation (may appear blue clinically) & # urinary VMA & 15% may recur & Tx: radical excision

Melanotic Neuroectodermal Tumor of Infancy

450

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Hemifacial Hypertrophy & Unilateral oral and facial enlargement & Usually evident at birth & Involves hard and soft tissues & Teeth may exfoliate prematurely & MR: 25% & Increased incidence of embryonal tumors & Tx: cosmetic surgery

Hemifacial Microsomia & Etiology unknown & Unilateral microtia, macrostomia, and failure of formation of mandibular ramus and condyle & 50% have cardiac pathology (PDA, VSD) & Tx: orthognathic surgery

451

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452

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453

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Dwarfism

454

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Seven major cateogories of causes of short stature 1. 2. 3. 4. 5. 6. 7.

Genetic Constitutional delay Chronic disease Chromosomal/syndromic Endocrine Psychosocial Intrauterine

Achondroplasia & 80% sporatic mutations, A.D. & 1/20,000 live births & Short limbed dwarfism & Enlarged head, depressed nasal bridge & Short, stubby, trident hands & Lordotic lumbar spine & Prominent buttocks & Protuberant abdomen

455

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Hypopituitarism & Well proportioned body & Fine, silky hair, wrinkled atrophic skin & Hypogonadism & Delayed eruption /exfoliation & Malocclusion common due to small dental arches & Panhypopituitarism may lead to other systemic problems

Causes of Hypopituitarism & Tumors & Pituitary & Parasellar & Suprasellar (hypothalamic) & Radiation & Pituitary apoplexy

& Infiltrative diseases & Granulomatous diseases & Infection & Miscellaneous

456

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Mucopolysaccharidoses

Nutritional

457

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Chrondroectodermal Dysplasia (Ellis van Crevald syndrome) &Dwarfism &Polydactaly &Ectodermal dysplasia(hidrotic) affecting nails and teeth &Multiple frenae &Cardiac defects: 50%

Chondroectodermal Dysplasia

Nail dystrophy/ Spade-shaped hand

polydactaly

458

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Chondroectodermal Dysplasia

Hallerman-Streiff syndrome (Oculo-mandibulo-dyscephaly) & Dyscephaly & Hypotrichosis & Microphthalmia & Cataracts & Beaked nose & Micrognathia & Short stature & May have supernumerary teeth/natal teeth

459

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Syndromes Characterized by Senile-like Appearance &Progeria &Werner syndrome &Cockayne syndrome &RothmundThomson syndrome

Hypothyroidism & Large posterior fontanel & Macroglossia & Hypothermia & Lethargy & Hypotonia & Bradycardia & Delayed growth and skeletal maturation

460

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Turner’s syndrome & 45X karyotype & 1/8000 & Females only & Near normal IQ & Sterile & Coarctation of aorta most common cardiac defect & Webbed neck & Enamel hypoplasia

Osteogenesis Imperfecta & Type I: mildest form & Associated with blue sclera; type IBdentinogenesis imperfecta

& Type II: perinatally lethal; severe fragility of connective tissues; multiple in utero fractures & Type III: progressive deforming; severe fragility; usually associated with in utero fractures & Type IV: similar to type I but more severe & Type IVB-dentinogenesis imperfecta

461

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Osteogenesis Imperfecta

Osteogenesis Imperfecta Blue Sclera

462

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Osteogenesis Imperfecta

Dentinogenesis Imperfecta

Self-Mutilation &Common in children with MR/psychological problems/autism &Usually due to repeated trauma

463

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Autism &Profound withdrawal &Obsessive desire for preservation of sameness &Skillful relation to inanimate objects &Retention of intelligent, pensive physiognomy &Language development not understandable &Often self-abusive, self-stimulating

Congenital Indifference to Pain &Autosomal recessive &Frequent scarring of face with mutilations of lips, tongue, arms, legs &Mild mental retardation

464

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Congenital Indifference to Pain

Lesch Nyhan syndrome & X-linked recessive & MR & Spastic CP & Choreoathetosis & Bizarre self-mutilating behavior & Absence of hypoxanthineguaninephosphoribosyltransferase

465

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Erythematous Gingiva

&Gingivitis &Periodontitis

Characteristics of Gingivitis in Children & Most common periodontal infection in children and adolescents & Generally increases with age, eruption, puberty & Rounded gingival margins accentuate inflammatory changes; tissues may become fibrotic & Generally reversible with improved oral hygiene & Does not occur to same degree as in adults with comparable plaque

466

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Systemic Factors influencing Gingivitis - Endocrine System & Puberty-associated, menstrual cycleassociated, pregnancy-associated & Presence of steroid hormones (esp. estrogen, progesterone) may amplify inflammatory changes in gingiva & Plaque is generally non-specific

Periodontitis & Prevalence of destructive disease in children & Age 5-11 years: 1-9% & Age 12-15 years: 1-46%

& Clinical attachment loss precedes radiographic bone loss & Disease threshold CEJ-ABC > 2 mm in primary dentition & Loss of lamina dura

467

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Types and characteristics of periodontal disease in children & Aggressive periodontitis & Common characteristics of localized and generalized forms: & Primary findings: $ Rapid bone loss $ Familial aggregation: (?) genetic predisposition

& Secondary findings: $ Phagocyte abnormalities $ Hyper-responsive macrophage phenotype $ Reports of disease being self-limiting

Localized Aggressive Periodontitis &Prevalence in U.S. & Overall: 0.3% &African Americans: 10% &Hispanics: 5.5%

468

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Localized Aggressive Periodontitis & Interproximal attachment loss on at least 2 permanent molars and incisors with attachment loss on no more than two additional teeth & No evidence of systemic disease

Localized Aggressive Periodontitis & Radiographic signs & vertical bone loss around molars & horizontal bone loss around incisors & rate of progression 3-5x times adult periodontitis (5 microns/day)

469

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Localized Aggressive Periodontitis & Etiology & genetic basis?; familial distribution & Actinobacillus actinomycetemcomitans and bacteroides –like species & depressed neutrophil chemotaxis in ~70% & possible defect in phagocytosis

LAP Diagnosis & History and clinical findings & & & &

Medical history Familial pattern Ethinicity Loss of attachment pattern

& Radiographic findings & Pattern of bone loss

& Microbiologic findings & DNA probing

470

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LAP Diagnosis & History and clinical findings & & & &

Medical history Familial pattern Ethinicity Loss of attachment pattern

& Radiographic findings & Pattern of bone loss

& Microbiologic findings & DNA probing

LAP Diagnosis & History and clinical findings & & & &

Medical history Familial pattern Ethinicity Loss of attachment pattern

& Radiographic findings & Pattern of bone loss

& Microbiologic findings & DNA probing

471

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LAP Diagnosis & History and clinical findings & & & &

Medical history Familial pattern Ethinicity Loss of attachment pattern

& Radiographic findings & Pattern of bone loss

& Microbiologic findings & DNA probing

Treatment: Surgical and nonsurgical root debridement with antimicrobial therapy & Scaling, curettage, root planing & Antibiotic therapy & & & &

tetracycline, doxycycline amoxicillin metranidazole metranidazole + Augmentin

& Periodontal surgery & Regenerative techniques & root conditioning, composite graft, ePTFE membranes

472

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Generalized Aggressive Periodontitis & Prevalence in U.S. & Overall: 0.15% & Higher in males and African Americans

& Generalized attachment loss including at least 3 teeth that are not 1st molars

GAP & Considered a disease of adolescents and young adults & Marked periodontal inflammation with heavy plaque and calculus & Subgingival bacterial cultures typically nonmotile, facultative, anaerobic gram (-) rods & Suppressed neutrophil chemotaxis

473

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GAP - Radiographic Signs

Generalized Aggressive Periodontitis & Treatment & surgery & scaling, root planing, curettage & Antibiotics & Does not always respond to conventional mechanical and antibiotic therapy & Culture and sensitivity maybe helpful in refractive cases

474

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c.c.: premature loss of primary incisors & 3 y.o Caucasian male is referred by pediatrician for consultation with c.c. of premature loss of primary incisors & This is the patient’s first dental visit

History of Present Illness & Mother noticed teeth becoming loose several months ago & 5 days ago teeth spontaneously exfoliated & Mother denies any history of trauma & Mother presents primary incisor which appears grossly normal with age appropriate root length

475

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Past Medical History & Prenatal history: unremarkable & Family history: unremarkabale & Hospitalizations: Patient sustained broken leg at age 30 months following a “minor fall” & Meds: none & ROS: wnl & NKA & Childhood illnesses: 2 bouts of O.M.

Clinical findings: & Extra-oral soft tissues WNL & Intra-oral soft tissues WNL & Missing primary incisors & 2+/3 mobility of remaining incisors & No mobility of remaining primary teeth

476

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Potential causes of premature loss of primary teeth & Trauma & Genetic/ hereditary & Neoplasms & Infectious & Miscellaneous

Trauma & Accidental & Psychiatric/self-abuse & Iatrogenic & Radiotherapy & Intubation

& Child abuse

477

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Genetic & Acatalasia & Chediak-Higashi syndrome & Chronic neutropenia & Dentin dysplasia & Down syndrome & Hypophosphatasia & Hypophosphatasia vitamin D resistant rickets & Lesch-Nyhan syndrome & Papillon-Lefévre syndrome

Neoplasms & Lymphoma & Leukemia & Langerhans’ cell histiocytosis & Soft and hard tissue neoplasms (benign and malignant)

478

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Infectious & Dental abscess & Osteomyelitis & Periodontitis

Miscellaneous & Acrodynia & Odontodysplasia & Vitamin C deficiency & Leukocyte adhesion deficiency-1

479

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Differential Diagnosis & Hypophosphatasia & TNSALP & Urinary phosphoethanolamine

& Papillon-LeFévre syndrome & Examine palmar/plantar surfaces for hyperkeratosis

& Periodontitis & DNA probing

Congenital Causes of Erythematous Gingiva & Hereditary hemorrhagic telangiectasia & AD & Mucosal and cutaneous telangiectases & May result in repeated bleeding episodes

& Sturge Weber syndrome

480

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Hereditary Hemorrhagic Telangiectasia

Palatal telangiectases

Acquired Causes of Erythematous Gingiva & Trauma & Physical, chemical, radiation, thermal

& Drugs: chlorhexidene, cinnamonaldehyde & Infectious: candidiasis & Desquamative gingivitis & Leukemia

481

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Causes of Gingival Bleeding & Localized disease & & & & & &

& Systemic disease & & & & & &

Periodontal disease Chronic gingivitis Chronic periodontitis ANUG HIV gingivitis HIV periodontitis

& & & &

Clotting defects Hepatobiliary disease Hemophilias Von Willebrand’s disease Vitamin K deficiency Lymphoproliferative disorders ITP Hereditary hemorrhagic telangiectasia Ehlers-Danlos syndrome Scurvy

Causes of Gingival Bleeding (cont.) &Drugs & Anticoagulants & NSAID &ASA &Non-ASA & Cytotoxics & Sodium valproate

482

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Generalized Gingival Enlargement: Congenital &Gingival fibromatosis &Mucopolysaccharidoses

Generalized Gingival Enlargement: Acquired & AML & Aplastic anemia & Drugs & Phenytoin & Cyclosporin & Calcium-channel blockers & Sodium valproate (rare) & Tranexamic acid (rare)

& Scurvy

483

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Acute Myelogenous Leukemia

Pre-chemotherapy

Post-chemotherapy

Localized Gingival Enlargement: Congenital & Fabry’s disease & Cowden’s disease & Tuberous sclerosis & Focal dermal hypoplasia & Sturge-Weber syndrome & Congenital granular cell tumor

Cowden’s Disease

484

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Tuberous Sclerosis & A.D. & Seizures (90%) & MR (60%) & Angiofibromas of face (70%) & May involve oral mucosa

& Enamel defects

Localized Gingival Enlargement: Acquired & Heck’s disease & Lymphoma & Histiocytosis & Peripheral giant cell epulis & Pyogenic granuloma & Peripheral ossifying fibroma & Papilloma & Crohn’s disease & Neoplasms

Pyogenic granuloma Peripheral Giant Cell Epulis

485

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Peripheral Ossifying Fibroma

Initial presentation

Relapse 2y later

Fibro-osseous lesions

486

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Fibro-osseous lesions

Facial Swelling/Enlargement-Hard Tissue: Congenital &Albright’s syndrome &Cherubism &Hemihypertrophy

487

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Albright’s Syndrome & Polyostotic fibrous dysplasia & Abnormal skin pigmentation & “coast of Maine” café-au-lait spots

Kennebunkport

& Endocrine dysfunction & Precocious puberty

& X-ray: ground glass

Albright’s syndrome

Ground glass

“Chinese characters”

488

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Cherubism & A.D. & Bilateral fullness of cheeks & Hypertelorism & Irregularly spaced 1º dentition & Giant cell histology & X-ray: multilocular radioluncencies

Cherubism

Multilocular radioluncencies

Giant cell histology

489

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Facial Swelling/Enlargement-Hard tissue : Acquired/Inherited

&Fibrous Dysplasia &Sickle cell anemia &Thalassemia &Neoplasms

Monostotic Fibrous Dysplasia

Sickle Cell Anemia

Hair on end

490

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Neoplasm: Neuroblastoma

“racoon eyes” Periorbital ecchymosis

Obstruction of palpebral vessels

Facial Swelling: Inflammatory &Oral infections &Cutaneous infections &Insect bites Poison Ivy

491

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Facial Swelling: Inflammatory

Odontogenic Infection

Facial Swelling: Traumatic &P/O edema/hematoma &Traumatic edema/hematoma &Surgical emphysema

492

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Facial Swelling: Immunologic

&Allergic angioedema &HANE

Facial Swelling: Immunologic

&Allergic angioedema &HANE

493

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Facial Swelling: Endocrine/Metabolic & Systemic corticosteroids & Cushing’s disease/syndrome & Myxedema & Acromegaly & Obesity & Nephrotic syndrome

Facial Swelling: Others & Cysts

Most common cause of lumps in children

& Nasolabial cyst & Soft tissue cyst & Forms deep to nasolabial fold & May cause obliteration of nasolabial fold & Tx: surgical excision

& Vascular malformations & Vascular tumors & Melkersson-Rosenthal syndrome & Crohn’s disease

494

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Nasolabial Cyst

Nasolabial Cyst

495

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Facial Swelling: Major Salivary Glands: Inflammatory & Mumps & Recurrent parotitis & Sjögren’s syndrome & Ascending sialadenitis & Recurrent sialadenitis & Sarcoidosis & Actinomycosis

Facial Swelling: Major Salivary Glands: Neoplasm

Pleomorphic adenoma

496

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Facial Swelling: Major Salivary Glands: Others & Duct obstruction & Sialosis & Parotid & Submandibular & Mikulicz disease & Amyloidosis & HIV disease

Facial Swelling: Major Salivary Glands: Others & Duct obstruction & Sialosis & Parotid & Submandibular & Mikulicz disease & Amyloidosis & HIV disease

497

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Facial Swelling: Major Salivary Glands: Others & Duct obstruction & Sialosis & Parotid & Submandibular & Mikulicz disease & Amyloidosis & HIV disease

Facial Swelling: Major Salivary Glands: Others & Duct obstruction & Sialosis & Parotid & Submandibular & Mikulicz disease & Amyloidosis & HIV disease

498

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

HIV Disease

&Bilateral parotid enlargement

Facial Swelling: Major Salivary Glands: Drug associated & Chlorhexidene & Phenylbutazone & Iodine compounds & Thiouracil & Catecholamines & Sulphonamides & Phenothiazines & Methyldopa

499

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Intraoral Ulcerations

Traumatic & Very common & Usually caused by accidental biting, hard foods, appliances, etc. & Less common causes: child abuse, recurrent bouts of severe coughing, oral sex

500

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Neoplastic &Carcinoma &Histiocytosis &Other malignancies Lymphoma

Recurrent Aphthous Stomatitis & Isolated & Behçet’s syndrome & MAGIC syndrome & Mouth, genital lesions/inflamed cartilage

& Sweet’s syndrome & Acute febrile neutrophilic dermatosis

& PFAPA & Periodic Fever/Aphthous ulcers/Pharyngitis/Adenitis

501

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Recurrent Aphthous Ulcers &Etiology unknown &Predisposing factors, I.e. stress &Involves “unbound” mucosa &Tx: palliative

& Minor: most common & Shallow, round ulcer & Erythematous halo & 7-10 day duration

& Major: less common & Deep, large ulcers & 3-6 week duration

& Herpetiform: rare & Clusters of small ulcers & 1-2 week duration

Apthous Ulcers: treatment modalities

502

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Behçet’s Syndrome & Etiology unknown & Rare in children < 5 y & Males > females (5:1) & Oral, genital, ocular, and skin lesions & Mucosal lesions similar to aphthous ulcers & Tx: steroids

Behçet’s Syndrome

503

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Systemic Disease: Cutaneous & Erosive lichen planus & Pemphigus vulgaris & Mucous membrane/bullous pemphigoid & Erythema multiforme & Dermatitis herpetiformis & Epidermolysis bullosa

Pemphigus Vulgaris

Systemic Disease: Gastrointestinal &Crohn’s disease &Chronic inflammatory granulomatous disease &Affects entire GI tract &Etiology unknown, likely autoimmune &Oral lesions (~30%) &Tx: antibiotics, 5-ASA, corticlsteroids

504

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Systemic Disease: Connective Tissue Disease &Lupus erythematosus &Reiter’s syndrome &Mixed connective tissue disease &Felty’s syndrome Systemic Lupus Erythematosus

Oral infectious disease &Herpetic gingivostomatitis &Hand, foot, and mouth disease &Herpangina &Acute necrotizing ulcerative gingivitis

505

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Herpetic gingivostomatitis & HSV type1 typically & Oral ulcers, gingivitis, fever, lymphadenopathy & Painful & Tx: palliative and supportive

Hand, Foot, and Mouth Disease & Cocksackie virus & Epidemic & Fever, malaise, lymphadenopathy & Vesicles and ulcerations intraorally and on hands, arms, feet, legs & Duration 7-10 days & Tx: supportive and palliative

506

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Hand, Foot, and Mouth Disease

Herpangiana & Cocksackie virus & Multiple vesicular lesions involving tonsillar pillars, uvula, soft palate & Vesicles rupture leaving ulceration & Malaise, fever & Most common in summer months & Tx: supportive and palliative

507

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Acute Necrotizing Ulcerative Gingivitis & Fusospirochetes & Rare in children & Necrosis, ulceration, punched out papillae & Sore, bleeding gingiva & Foul breath & Tx: oral hygiene, topical and/or systemic antibiotics

Systemic Disease: Infective (cont.) & Histoplasmosis & Coccididioidomycosis & Blastomycosis & HIV & Gram-negative infection

& Atypical mycobacterium infection & Syphilis & Aspergillosis & Cryptocococcosis & Leishmaniasis & Tularemia & Lepromatous leprosy & Paracoccidiodomycosis

508

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Systemic Disease: Drugs

&Cytotoxics &Methotrexate &5-FU

Systemic Disease: Others & Wegener’s granulomatosis & Midline lethal granuloma & Histiocytosis & Noma Noma

509

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Histiocytosis (Langerhans Cell Histiocytosis) & Variety of disorders of mononuclear phagocytes & Acute disseminated & Infants

& Chronic & Skull lesions & Diabetes insipitus & Exopthalamus

& Acute localized & Limited to bone

Histiocytosis

510

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Generalized Pigmentation Vitiligo

Racial &No direct correlation between skin color and oral pigmentation &Typically seen only on gingiva

511

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Food/Drugs &Carotenemia &Antimalerial drugs &Minocycline &Doxorubicin Carotenemia

Food/Drugs &Carotenemia &Antimalerial drugs &Minocycline &Doxorubicin Minocycline

512

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Endocrinopathies &Addison’s disease &Nelson’s syndrome &Ectopic ACTH production Addison’s Disease

Others & Pigmentary incontinence & Albright’s syndrome & Hemochromatosis & $-thalassemia & ACTH therapy & Biliary atresia & Heavy metals

Biliary Atresia

513

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Localized Pigmentation & Ecchymoses & Ephelis & Melanoma & Melanoacanthoma & Melanotic macule & Nevus & Peutz-Jeghers syndrome & Kaposi’s sarcoma

& Neurofibromatosis & Neuroectodermal tumor & Tattoos & Epithelioid angiomatosis & Smoker’s melanosis & Acanthosis nigricans

Localized Pigmentation & Ecchymoses & Ephelis & Melanoma & Melanoacanthoma & Melanotic macule & Nevus & Peutz-Jeghers syndrome & Kaposi’s sarcoma

& Neurofibromatosis & Neuroectodermal tumor & Tattoos & Epithelioid angiomatosis & Smoker’s melanosis & Acanthosis nigricans

514

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Peutz-Jeghers Syndrome &A.D. &Perioral and intraoral pigmentation &Intestinal polyposis &Tx: intestinal polyps may occasionally require surgical intervention

Peutz-Jeghers Syndrome

515

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Soft Tissue Neck Mass/Swelling

Cervical Lymph Nodes: Inflammatory &Lymphadenitis &Glandular fever syndromes &Mycotic infections &Other infections

516

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

When to consider biopsy of lymph node: &? of malignancy, i.e. fixed node &Suspected atypical mycobacterium &Failure to respond to antimicrobials &After 3 months of observation with either no change or increase in size

Cervical Lymph Nodes: Neoplasms &Primary malignancy & Hodgkin’s disease & Leukemia & Lymphoma

&Secondary malignancy

Hodgkin’s Disease

517

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Cervical Lymph Nodes: Others &Connective tissue disease &Drugs &Mucocutaneous lymph node syndrome

Mucocutaneous lymph node syndrome (Kawasaki’s disease)

Salivary Glands &Mumps &Tumors &HIV &Sjögren’s syndrome &Sarcoidosis &Sialadenitis &Sialosis

518

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Side of Neck Swelling/Mass &Actinomycosis &Branchial cleft cyst &Parapharygeal cellulitis &Pharyngeal pouch &Cystic hygroma &Carotid body tumor

Middle of Neck Swelling/Mass & Submental lymphadenopathy & Thyroglossal duct cyst & Ectopic thyroid & Thyroid tumor & Plunging ranula & Ludwig’s angina & Dermoid cyst

Thyroglossal Duct Cyst

519

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Palatal Lesions/Malformations

Cleft Palate & Isolated (with and without cleft lip) & Associations (reported with > 100 syndromes) & Pierre-Robin sequence & Cleidocranial dysplasia & Down syndrome & Mandibulofacial dysplasia & Orofaciodigital syndrome & Apert’s syndrome & Crouzon’s syndrome

520

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Cleft Palate

Pierre-Robin Sequence &Glossoptosis &Micrognathia &Cleft palate &15-25% cardiac defect

521

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Cleidocranial Dysplasia & Brachycephaly & Frontal and parietal bossing & Depressed nasal bridge & Delayed closure of sutures and fontanels & Wormian bones

& Supernumerary teeth

& Clavicular defect & Delayed or failure of exfoliation of 1º teeth & Delayed eruption of 2º teeth & Highly arched palate often with submucous or complete cleft & Roots lack layer of cellular cementum

Cleidocranial Dysplasia

522

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Cleidocranial Dysplasia

Wormian bones

Multiple unerupted teeth

Mandibulofacial Dysostosis (Treacher Collins Syndrome) & Defect of 1st branchial arch/pouch/groove & Microtia/malformed ears & Hypoplastic midface & Downward sloping palpebral fissures & Coloboma & Hypoplastic mandible

& 30% cleft palate

523

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

524

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Orofaciodigital Syndrome & Type 1 most common form & X-linked dominant trait & MR

& Oral findings: & Multiple hyperplastic frenae & Bifid/multilobed tongue & Hypodontia (mandibular lateral incisors) & Supernumerary teeth & Cleft palate

525

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Orofaciodigital Syndrome

“Copper-beaten Skull” &Craniosynostosis & Apert’s syndrome & Crouzon’s syndrome & Pfeiffer’s syndrome

526

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Apert’s Syndrome & Syndactaly & Shallow orbits, ocular hypertelorism & Parrot nose & 30% cleft palate & Mental retardation & Crowded dentition & V-shaped maxilla & Class III with openbite

Apert’s Syndrome

Syndactaly

527

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Crouzon’s Syndrome & Brachycephaly & Maxillary hypoplasia & Ocular hypertelorism & Parrot nose & Crowded dentition & V-shaped maxillary arch & Exopthalamus

528

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

529

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Palatal Swelling/Lump: Developmental &Unerupted tooth &Torus palatinus &Cysts

Palatal Swelling/Lump: Inflammatory &Abscess &Cyst &Papillary hyperplasia &Sarcoidosis

530

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Palatal Swelling/Lump: Neoplasm & Minor salivary gland tumor & Fibroma & Kaposi’s sarcoma & Papilloma & Neuroma & Neurofibroma

Kaposi’s sarcoma

Halitosis & Oral sepsis & Food impaction & Chronic dental/periodontal sepsis & ANUG & Dry socket & Pericoronitis & Xerostomia & Oral ulceration

531

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Halitosis: Nasopharyngeal Disease

& Foreign body & Sinusitis & Tonsillitis & Neoplasm

Halitosis: Nasopharyngeal Disease

& Foreign body & Sinusitis & Tonsillitis & Neoplasm

532

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Volatile Foodstuffs

&Garlic &Onions &Highly spiced foods

Drugs & & & & & & & & & & &

Solvent abuse Alcohol Smoking Choral hydrate Nitrates/nitrites Dimethyl sulphoxide Disulphiram Cytotoxic drugs Phenothiazines Amphetamines Paraldehyde

533

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Radiographic Key Concepts

See what’s under the surface…

Radiographic Description and Interpetation 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12.

Shape Size Anatomic location Degree of lucency or opacity Recognizable structure(s) Single or multiple Unilocular or multilocular Quality of border Cortical involvement Lamina dura PDL Root resorption VCU School of Dentistry, Dept. of Oral Pathology

534

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Differential Diagnosis of Radiographic Lesions 1. Benign and Neoplastic Lesions 2. Inflammatory Lesions 3. Aggressive and Malignant Lesions

Benign Cystic and Neoplastic Lesions & Uncommon occurance & Non-tender to palpation & Slow growing (months to years) & Localized expansion & Surrounding mucosa normal & Usually etiology unknown & No systemic involvement & May interfere with tooth eruption & Subtle facial asymmetry

535

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Radiolucent lesions & Pericoronal location & Unilocular & Eruption cyst & Dentigerous cyst & Unicystic ameloblastoma

& Multilocular & Odontogenic keratocyst $ Basal cell nevus syndrome

& Ameloblastic fibroma

Eruption Cyst & Follicular cyst involving soft tissue & Most frequently involves 1º dentition/permanent molars & Bluish, painless swelling over erupting tooth & Tx: typically none necessary as cysts spontaneously rupture & Typically don’t interfere with eruption

536

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Dentigerous Cyst & Surrounds crown/attached to neck of unerupted tooth & Cystic enlargement of dental follicle & Usually asymptomatic & Tx: surgical enucleation

Ameloblastoma (Unicystic) & Most common primary tumor of jaws & 80% in molar/ramus area of mandible & Frequently contain tooth & May mimic dentigerous cyst & 10% recurrance rate & Tx: surgical excession

537

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

538

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

539

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

540

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Odontogenic Keratocyst & Most often found in mandible & Bone expansion uncommon & Pain, discharge, or paresthesia uncommon & Tx: “vigorous” enucleation & Recurrence not uncommon

541

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Common Findings in Basal Cell Nevus Syndrome & & & & & & & & & &

Enlarged occipitofrontal circumference Mild ocular hypertelorism Multiple basal cell carcinomas Odontogenic keratocysts of the jaws Epidermal cysts of skin Palmar and/or plantar pits Calcified falx cerebri Rib anomalies Spina bifida occulta of cervical or thoracic vertebrae Hyperpneumatization of paranasal sinuses

Basal Cell Nevus Syndrome

542

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Ameloblastic Fibroma & Slow growing benign tumor & Usually asymptomatic & Posterior mandible most common site & Tx: conservative excision & Note: ameloblastic fibrosarcomas have arisen in ameloblastic fibromas

Peripheral or central location & Unilocular & & & &

Traumatic bone cyst Nasopalatine duct cyst Globulomaxillary cyst Median palatal cyst

543

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Traumatic Bone Cyst & Mandible most common site & Usually asymptomatic w/o expansion & Teeth are vital & Tx: surgical intervention

Traumatic Bone Cyst pretreatment

Post-treatment

544

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

• 16yo M • Incidental finding of radiolucent lesion in posterior mandible • Healthy

545

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

546

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

547

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Traumatic bone cyst •First described by Lucas in 1929 •Hemorrhagic bone cyst, solitary bone cyst, unicameral bone cyst, extravasation cyst, idiopathic bone cavity •Pathogenesis not understood – Trauma • Intraosseous hematoma'enzymatic clot liquification leads to bone resorption… • subperiosteal hematoma compromises blood supply'osteoclastic bone resorption Xanthanaki AA, Konstantinos CI, et al. Traumatic bone cyst of possible iatrogenic origin: Case report and review of the literature. Head and Face Medicine. 2006; 40:1-5.

Nasopalatine Duct Cyst &Derived from epithelium of nasopalatine duct &May perforate labial plate &Teeth are vital

548

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Nasopalatine Duct Cyst

Globulomaxillary Cyst & Originally thought to occur due to epithelial entrapment & Most likely radicular cyst & May cause displacement of teeth & Tx: surgical enucleation

549

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Globulomaxillary Cyst

Median Palatal Cyst & Fissural cyst & Epithelial entrapment & Maybe confused for posteriorly positioned nasopalatine duct cyst & Firm of flucuant swelling of midline of hard palate & Tx: surgical excision

550

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Median Palatal Cyst

Unilocular when small/multilocular when large & Central giant cell granuloma & Aneurysmal bone cyst & Central hemangioma & Odontogenic myxoma & Cherubism

551

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Central Giant Cell Granuloma & Painless swelling sometimes causing displacement of teeth & Posterior mandible most common site & Tx: curettage & R/O other jaw lesions with giant cell histology

J.L. & 4 yo male & Otherwise healthy & Left mandibular swelling & No pain or paresthesia

552

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

553

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

554

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

555

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

556

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Aneurysmal bone cyst & Eccentric ballooning of mandible & 50% associated with pain & Associated with concurrent lesion

Aneurysmal bone cyst & Eccentric ballooning of mandible & 50% associated with pain & Associated with concurrent lesion

557

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

HS 6 yo female

558

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

559

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Central hemangioma & Vague margins & Gingival bleeding, bruit, pulsation & Tooth mobility & Potentially life threatening

560

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Odontogenic myxoma & Faint radiopaque striations & Posterior mandible & Moderate recurrance rate

A.L.

561

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

562

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

563

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

564

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Cherubism & Bilateral & “Burns out” over time

565

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

A.B. & Painless midface swelling & 4yo F & Healthy

2005

2005

566

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

567

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

2005

2007

2005

2007

568

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Mixed radiolucent-radiopaque & Pericoronal location & Calcifying odontogenic cyst & Adenomatoid odontogenic tumor & Ameloblastic fibro-odontoma

& Periapical or central location & Central ossifying fibroma & Juvenile ossifying fibroma

Calcifying Odontogenic Cyst & Affects both maxilla and mandible & Painless swelling/ may expand & Radiographic: may contain scattered radiopacities & 25% associated with odontoma & Tx: surgical excision

569

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Adenomatoid Odontogenic Tumor & 90% appear before 30 y & 60% form in anterior maxilla & 75% associated with unerupted tooth (canine) & Radiographic: may contain faint radiopaque foci & Tx: surgical excision

Adenomatoid Odontogenic Tumor & 90% appear before 30 y & 60% form in anterior maxilla & 75% associated with unerupted tooth (canine) & Radiographic: may contain faint radiopaque foci & Tx: surgical excision

570

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Ameloblastic Fibro-odontoma & Most often found in children & Typically asymptomatic and discovered radiographically & Most frequently associated woth unerupted tooth

571

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

572

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Periapical or Central Location & Central ossifying fibroma & Juvenile ossifying fibroma

573

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Central ossifying fibroma & Maybe unilocular or multilocular & Progresses from radiolucent to radiopaque

Juvenile ossifying fibroma & Multilocular & Maxilla>mandible & Aggressive

574

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

DR 8yo male

575

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

576

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

577

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Radiopaque & Pericoronal location & Odontoma

& Periapical or central location & Fibrous dysplasia & Cementoblastoma & Osteoblastoma

& Peripheral location & Torus/exostosis & Osteoma

578

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Radiopaque: pericoronal location Odontoma & Compound & Small separate denticles (tooth-like) & Anterior maxilla

& Complex & irregular mass of hard and soft dental tissues & Morphology grossly distorted

& May interfere with tooth eruption & Tx: surgical enucleation

Complex odontoma

Radiopaque: periapical or central location Fibrous dysplasia & Non-neoplastic condition & Maybe multifocal & Maxillary premolar/ molar region & Progresses from radiolucent to radiopaque & “Ground glass” appearance

& Poorly defined margins & Expansile, but “burns out” with time

579

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Radiopaque: periapical or central location Fibrous dysplasia & Non-neoplastic condition & Maybe multifocal & Maxillary premolar/ molar region & Progresses from radiolucent to radiopaque & “Ground glass” appearance

& Poorly defined margins & Expansile, but “burns out” with time

Radiopaque: periapical or central location Fibrous dysplasia & Non-neoplastic condition & Maybe multifocal & Maxillary premolar/ molar region & Progresses from radiolucent to radiopaque & “Ground glass” appearance

& Poorly defined margins & Expansile, but “burns out” with time

580

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

C.B. & 6 yof & 1 yr s/p dental extraction LUQ, ? Mesial drift of molar & Painless swelling in palate, expanding rapidly & PMH: s/p laser ablation of L temporal hemangioma & Alls: Latex, tape & FH: Brother with von Willebrand

581

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

582

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

583

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

584

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Cementoblastoma & Cementum-like tissue resorbs/fuses with root & 50% patients > 20 yrs & 75% form in mandible & Usually molar or premolar & Expansion/pain common

& Tx: extraction/removal of tooth and mass

585

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Osteoblastoma & Posterior mandible & Progresses from radiolucent to radiopaque & Pain common & Vital tooth & May demonstrate “sunburst” appearance

Radiopaque: peripheral location Torus/exostosis & Non-neoplastic & Rare before age 10 y & May interfere with appliance therapy

586

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Radiopaque: peripheral location Torus/exostosis & Non-neoplastic & Rare before age 10 y & May interfere with appliance therapy

Osteoma/Gardner’s syndrome & A.D. & Multiple osteomas & Epidermoid/dermoid cysts (50-60%) & Multiple polyposis of large intestines with high malignant potential & Multiple supernumerary/impacted teeth

587

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Gardner’s Syndrome

Inflammatory lesions & Common & Tender or painful to palpation & Rapid enlargement (days to weeks) & Diffuse or localized enlargement & Red, tender, swollen mucosa & Fluctuates in size

& Drainage, sinus tract formation & Cause is often apparent & Mobile, non-vital tooth & Systemic involvement occurs with advanced infection & Trismus, occasional paresthesia & Regression with treatment of source

588

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Localized lesions & Periapical location & Radiopaque & Focal sclerosing osteomyelitis

& Radiolucent & Periapical abscess & Periapical granuloma & Periapical cyst

Focal sclerosing osteomyelitis & Chronic pulpal disease & Non-expansile & Posterior mandible & Well-defined margins

589

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Periapical abscesses associated with Dentin Dysplasia, type I & Amber colored crowns & Obliteration of pulp chamber & Poor root formation & Periapical radiolucencies around malformed roots

Periapical Granuloma & Chronic infection & Flare-ups common & Unilocular, distinct margins & Non-vital tooth

590

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Periapical Cyst & Tender? & Well-defined margin & Non-vital tooth & Granuloma develops into cyst

& Maybe expansile & May cause displacement of unerupted tooth & Variation: lateral radicular cyst

Lateral Radicular Cyst

&Forms at side of necrotic tooth as result of lateral canal

591

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Pericoronal location: Paradental Cyst & Inflammatory cyst & Most frequently associated with partially erupted third molars & Mandibular buccal infected cysts & Buccal aspect of 1st molars in children & Pain/swelling & Tx: enucleation

Peripheral cortex location: Traumatic osteoma & Radiopaque & History of facial trauma & Inferior border of mandible & Maybe associated with jaw fracture & Irregular or sunburst appearance

592

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Diffuse lesions & Radiolucent/infectious etiology & Acute osteomyelitis

& Mixed radiolucent/radiopaque/infectious etiology & Chronic diffuse sclerosing osteomyelitis & Chronic osteomyelitis with prolerative periostitis (Garre’s osteomyelitis)

& Mixed radiolucent/radiopaque/idiopathic & Infantile cortical hyperostosis

Mixed radiolucent/radiopaque/infectious etiology: Chronic diffuse sclerosing osteomyelitis & Chronic dental infection & Indistinct borders & Mottled bone pattern & Sequestrum common & May result in ankylosis & Posterior mandible

593

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Chronic osteomyelitis with proliferative perostitis & Chronic dental infection & Diffuse, expansile & Indistinct margins & Mottled bone pattern & “Onion skin” appearance & Posterior mandible

Proliferative periostitis

Mixed Radiolucent/radiopaque/idiopathic: Infantile cortical hyperostosis Inherited disease (A.D.) Onset prior to 6 m of age Tender, soft tissue swelling Febrile Lymphadenopathy Bilateral mandibular involvement & “Onion skin” appearance & Spontaneous resolution & & & & & &

594

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Aggressive and Malignant Lesions & Uncommon or rare & Maybe tender or painful & Moderate to rapid growth (days to weeks to years) & Diffuse enlargement & May have multifocal distribution & Mucosa red, ulcerated & Lymph nodes firm and fixed

Vital, mobile teeth Extrusion of teeth Progressive increase in size No apparent cause or source & Systemic involvement common & Frequent paresthesia/anesthesia & Trismus with advanced disease & & & &

Unifocal and radiolucent & Benign & Neuroectodermal tumor of infancy & Desmoplastic fibroma of bone & Localized histiocytosis (Eosinophilic granuloma)

& Malignant & Central sarcoma of bone & Primary soft tissue malignancies adjacent to bone

595

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Neuroectodermal tumor of infancy & Anterior maxilla & Poorly defined margins & Expansile & May displace developing teeth/tooth buds & Pigmented surface & Recurrence moderate to high

Desmoplastic fibroma of bone & Maybe multilocular & Poorly defined margins & Expansile & “Floating” toothbuds & Soft tissue extension & High recurrence rate

596

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Localized histiocytosis (eosinophilic granuloma) & Maybe multifocal & Punched radiolucencies & Usually non-expansile

& “Floating” teeth & Often soft tissue involvement

Central sarcomas of bone & Body of mandible & Paresthesia & Unilocular or multilocular & Cortical perforation

597

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Primary soft tissue malignancies adjacent to bone & Well to poorly defined margins & “Cupped” out appearance & Fine “ground glass” appearance

Primary soft tissue malignancies adjacent to bone & Well to poorly defined margins & “Cupped” out appearance & Fine “ground glass” appearance

598

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Unifocal and mixed radiolucent-radiopaque & Ewing’s sarcoma & Osteosarcoma & Mesenchymal chondrosarcoma

Ewing’s sarcoma & Posterior mandible and ramus & Painful expansion & Febrile & Leukocytosis & “Moth-eaten” appearance & Periosteal proliferation

599

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Multifocal and radiolucent & Disseminated histiocytosis & Burkitt’s lymphoma & Leukemia (AML) & Metastic disease

Disseminated histiocytosis & Multiple organ involvement & Pain & Lymphadenopathy & Gingival involvement & Premature exfoliation of teeth & “Floating” teeth appearance

600

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Disseminated histiocytosis & Multiple organ involvement & Pain & Lymphadenopathy & Gingival involvement & Premature exfoliation of teeth & “Floating” teeth appearance

E.D. •PMH: normal development •E/O: •Slight mand asymmetry •Palpable, nontender mass left preauricular area •I/O: •palpable mass left ramus •normal dentition

601

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

602

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Burkitt’s lymphoma & Posterior maxilla and mandible & Single or multiple quadrants & Painful swelling & First signs often tooth mobility & “Moth eaten” or multilocular radiocency & Periosteal bone formation

603

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Leukemia (AML) & Widespread involvement & Occasional gingival enlargement due to leukemic infiltrates & Loss of lamina dura & Diffuse, poorly defined radiolucency & Occasional periosteal bone formation

604

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

605

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Differential Diagnosis & Leukemic infiltrate & Ewing’s Sarcoma & Primary malignancy (NH Lymphoma) & Langerhans Cell Histiocytosis (E.G.) & Giant Cell Granuloma/Tumor

606

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Metastic disease & Posterior mandible & Poorly defined radiolucency & Soft tissue extention common & paresthesia

607

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Metastic disease & Posterior mandible & Poorly defined radiolucency & Soft tissue extention common & paresthesia

608

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.



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612

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Etiology, Epidemiology, and Prevention of Dental Disease in Children Current Concepts and Recent Evidence Dr. Steve Adair Medical College of Georgia

Definition Dental caries is a dietary carbohydratemodified bacterial infectious disease with saliva as a critical regulator.

It is the most common chronic infectious disease of childhood. Caries is a disease process, as is “diabetes.”

613

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Non-specific Plaque Hypothesis •

Microorganisms in dental caries first observed by van Leeuwenhoek in 1683

•

W.D. Miller – University of Berlin 1890 – considered all bacteria in mouth were potentially cariogenic – hence, non-specific plaque theory

•

Acid production by bacteria considered responsible for breakdown of tooth

“Miller time”

Specific Plaque Hypothesis •

1924 – Clarke isolated a streptococcus species from a cavity in a child

•

The bacteria were more oval than round – Clarke named it Streptococcus mutans for “mutation”

614

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Mutans streptococci •

1960 – Keyes “rediscovered” S. mutans

•

He demonstrated that: • specific microorganisms were responsible for caries • caries was transmissible

•

Responsible bacteria were found to comprise seven distinct species – only mutans and sobrinus are associated with caries in humans

Characteristics of MS •

Ecological niche: human oral cavity

•

Cariogenic properties • ability to produce acid (acidogenicity) • ability to withstand acid conditions (aciduricity) • adherence to teeth

615

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Characteristics of MS •

Metabolism yields: • acids, primarily lactic, from a variety of sugars • extracellular polyglucose, called glucan

•

MS is responsible for initiation of caries

•

MS is a necessary, but not solely sufficient, factor for dental caries

Acquisition of MS - “Classic” Data •

MS colonize oral cavity after eruption of teeth – require hard, nondesquamating surface

•

Window of infectivity relies on virgin tooth surfaces for initial colonization

•

Second window may open when permanent dentition erupts

616

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Acquisition of MS by Infants •

MS is poor competitor for colonization – once stable biofilm is in place, ability for MS to colonize is reduced

Birth S mitis 1

S sanguis 8

11

25%

S mutans

19

26

75%

33 m

Infants who acquire S sanguis early may acquire less MS. Those who acquire MS early may be at higher risk for caries.

Transmission of MS Transmission may be direct or indirect • Source is usually mother • Vertical transmission • Fidelity >70% •

617

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

More Recent Data •

Transmission may occur at birth

•

Fissures of tongue may be ecological niche

•

Early MS acquisition associated with Bohn’s nodules and high maternal levels

•

Horizontal transmission may occur within or outside of the family

Acquisition of MS •

50% of infants are infected by 6 months

•

By 24 mo, 84% harbor MS

•

Mean age of MS colonization - 15.7 mo in dentate infants Wan et al 2003

618

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Acquisition of MS •

Factors associated with colonization • sweetened fluids taken to bed • frequent sugar exposure • snacking • sharing of foods with adults • maternal MS levels > 105 cfu/mL saliva

Wan et al 2003

Acquisition of MS •

Factors associated with non-colonization • toothbrushing • multiple courses of antibiotics

Wan et al 2003

619

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

More Evidence of Early Transmission

•

Li et al 2005 156 primigravid women

•

127 vaginal deliveries; 29 C-sections

•

Followed for 4 years for S mutans colonization

More Evidence of Early Transmission •

S mutans detected in 35% of children

•

Mean age of acquisition 22.3 mos

•

C-section infants acquired S mutans at earlier age: 17 vs 29 mos

•

100% fidelity for C-section group

•

Earlier colonization by competing strains in vaginally-delivered infants?

620

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Prevention of Transmission •

Söderling et al 2000

•

169 mothers with high MS levels during pregnancy

•

Three groups: • xylitol gum (65% w/w) 2-3 x/day starting at 3 mo • chlorhexidine varnish at 6, 12, 18 months • fluoride varnish at 6, 12, 18 months

Percent of Children Infected Age (years)

Mothers treated with Xyl

CHX

F Varnish

2

10%

28%

48%

3

28%

37%

65%

6

52%

87%

84%

Söderling et al 2001

621

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Other Microorganisms !

Lactobacilli sp. ! found in large numbers in some children ! considered opportunistic, not initiators ! numbers in cavity increase after DEJ invaded ! lactobacilli are good indicators of total carbohydrate intake

Other Microorganisms •

Li et al 2007 • children with S-ECC have less microbial diversity/complexity in biofilm compared to caries-free children

•

de Carvalho et al 2006 • frequency of C albicans higher in children with ECC than in children with non-ECC caries, or those who were caries-free

622

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Etiology - Diet !

Hopewood House (Australia) 1947 - 52

!

Vipeholm (Sweden) 1945 – 52

! diets devoid of sugar and white flour ! extremely low dental caries prevalence

! effects of frequency of sugar consumption ! effects of consistency (retentiveness) of sugar ! sugar at meals vs. in between meals

Lessons from Vipeholm •

Sugar consumption at meals – slight increase in caries

•

Sugar between meals – marked increase in caries

•

Sugar in sticky candies – greatest caries activity

•

Increased caries risk from increased frequency of ingestion

•

Caries activity differs among individuals

•

Caries activity declines with withdrawal of sugar-rich foods

623

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Sucrose •

Glucose + fructose

biofilm bacteria

metabolized by

fructan

+

glucan

Glucan From sucrose only

•

Water soluble

•

Extracellular “glue”

•

Enables adhesion to tooth • reduced susceptibility to mechanical disruption

•

Inhibits diffusion properties of biofilm • reduces buffering capacity of saliva • inhibits transport of acid away from tooth

624

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Fructan •

Produced extracellularly

•

Water soluble

•

May be used by MS as energy source

From fructose only

Biofilm •

Dental plaque now viewed as dynamic biofilm • maintains its own microenvironment

•

Influences oral health • negatively: acid attack, periodontal disease • positively: fluoride reservoir, protects against colonization by more pathogenic bacteria

625

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Role of Other Sugars •

Fructose and glucose are as effective as sucrose in vitro in their ability to cause a pH drop

•

In animal studies, fructose is nearly equal to sucrose in cariogenicity

•

Raw starch causes only a small drop in biofilm pH

Role of Refined Starch •

Soluble starch and refined starch can be broken down by salivary amylase into sugars

•

These refined carbohydrates cause a variable pH drop that may be as large as that caused by sucrose

626

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Biofilm pH after Sucrose Ingestion Stephan curve

7.0

Remineralization 6.0 pH

Demineralization 5.0

4.0

1

10

30

45

60

Minutes

Stephan Curves 7

6.5 Caries Resistant

6

Caries Susceptible

5.5

5 0

5

10

15

20

627

25

30

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Other Dietary Factors 7.0

Frequency of ingestion

6.0 pH 5.0

Refined CHO ingestions

4.0

1

10

30

45

60

Minutes

Other Dietary Factors !

Retentiveness/clearance

!

pH

!

Salivary stimulation

!

Fat content - protective

!

Inability of MS to metabolize (sugar alcohols)

!

Difficult (futile?) to categorize “good” vs. “bad” foods

628

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Protective Food Factors

Ca, PO4, casein, proteose peptones

similar to milk, fat salivary stimulation, CPP-ACP

gustatory stimulus, fat

flavonoids, antibacterial actions

masticatory stimulus

Carbonated Beverages •

Two studies using data from NHANES III

•

Heller et al 2001: found no relationship between soft drink consumption and DMFS in persons <25 years old, or dfs in those <12

629

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Carbonated Beverages •

Sohn et al 2006

•

Children identified as “high carbonated soft drink” users had significantly higher dental caries experience in primary dentition than did those in “high milk,” “high water,” and “high juice” groups

Sugar Consumption and Caries Risk •

Relationship between sugar consumption and caries (number of papers) • strong: 2 • moderate: 16 • weak: 18

•

Relationship is much weaker in modern age of fluoride exposure

•

Controlling sugar intake justifiable part of caries prevention, but maybe not always most important part of prevention program Burt and Pai 2001

630

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Etiology – Host Factors !

Tooth factors

!

Saliva

! ! ! ! ! ! ! ! !

quality of enamel presence/depth of pits and fissures hypoplasia fluoride exposure mineral content pH flow rate buffering capacity (carbonate, phosphate) antimicrobial components, fluoride

Antimicrobial Components •

Lysozyme: Gram-pos bacteria

•

Lactoferrin: Gram-pos and Gram-neg

•

Peroxidase: antimicrobial activity

•

Agglutinins: agglutination/aggregation

•

Secretory IgA: inhibition of adhesion

•

IgG: enhancement of phagocytosis

•

IgM: enhancement of phagocytosis?

631

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Saliva !

Flow rate reduced by:

!

Increased by:

! medications (antihistamines, antiasthmatics, antidepressants, others) ! disease (degenerative, metaplastic) ! dehydration ! radiation ! age ! gustatory stimulants (sugar-free candy) ! masticatory stimulants (s-f chewing gum)

Caries Factors Dietary intake of refined CHO

Oral flora – principally MS Caries

Host factors

632

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The Caries Balance Protective Factors • Saliva flow and components • Fluoride - remineralization • Antibacterials:chlorhexidine, xylitol, new?

Pathological Factors Acid-producing bacteria • Frequent eating/drinking of fermentable carbohydrates •Sub-normal saliva flow and function

No Caries

Caries

Courtesy of Dr. John Featherstone, UCSF

Modifying Effects Stress Genetics

Diet

Oral flora Culture

Caries

General health Host factors

Race / ethnicity

Healthcare delivery system

Behavior/education Socioeconomic status

633

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Shifts in Caries Presentation •

19th vs 20th/21st centuries • 19th century - disease of affluence • 20th/21st century - disease of poverty

•

1900-1950 - pandemic • presumption of caries inevitability • dental disease was among highest causes of time lost at work/school • could not target preventive efforts

Shifts in Caries Presentation •

1950-1970s - era of fluoridation • 50% reductions in caries • ~70% of US population on naturally- or artificially-fluoridated water supplies • preventive efforts could be targeted to non-fluoridated communities - still a broad target (population strategy)

634

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Epidemiology of Caries •

1970s - present • NIDR documented decline in caries prevalence Mean DMFT

Age

1963-70

1971-74

6-11 12-17

1.4 6.2

1.7 6.2

1979-80 1986-87 1.1 4.6

0.71 3.35

Shifts in Ethnic/SES Distribution !

80% of caries is in 20-25% of the population

!

Disproportionately more caries found in lower SES groups

!

Disproportionately more caries in minority groups - native Americans, African-Americans, Hispanics

!

Access to care is a problem for many of these children

635

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Recent Data - NCHS •

Prevalence of dental caries in primary teeth increased from ~40% during 1988-94 to 42% during 1999-2004

•

Among children 2-5, prevalence of primary tooth caries increased from ~24% to 28%

•

Caries rates in children 2-11 still greater for lower SES groups Dye et al 2007

The Caries Process •

Epidemiology

if one tooth erupted every year of life

dmf/DMF

Birth

age Caries is “steady-state” disease

636

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The Caries Process •

root surfaces

Epidemiology

permanent crowns dmfs/ DMFS

Birth

primary

age Expression is variable over time

Histopathology of Caries •

Demineralization - remineralization dynamic process, constant, not on/off

637

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Histopathology of Caries Zones of early lesion surface (5-10% mineral loss) body – 60% loss translucent zone – 5-10% loss normal enamel

Histopathology of Caries

White spot lesion Radiographic

638

Histologic

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Histopathology of Caries Remineralization is possible as long as enamel surface is intact

Remineralization is accelerated if there is sufficient ambient fluoride; remineralization of deep lesions in enamel and dentin is experimentally possible (ten Cate 2001)

Primary Tooth Considerations More rapid caries progression (less mineral) • Thinner enamel and dentin •

•

Relatively larger pulp

•

Flat contacts

•

Caries sequence • lower molars, upper molars, anteriors

•

2nd molars more susceptible than 1st

639

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Medical Approach to Caries Management !

Characteristics of caries that enable a medical approach ! diet-dependent infectious disease ! biphasic (demin-remin) ! threshold for expression ! external interface disease ! site specific and symmetric ! steady state phenomenon with variable expression over time (eruption)

Medical Approach to Caries Management •

Principles • reorient management from treatment of cavities (disease) to management of caries (process) • surgical approach problematic when applied to dynamic process • better to treat cause rather than manifestation of disease

640

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Medical Approach to Caries Management •

Strategy • determine child’s current caries experience • estimate risk for future caries • develop plan to address current problem and prevent future disease

•

Goal • minimize lifelong caries experience while using least intervention consistent with level of risk

Medical Approach to Caries Management Historical approach: Diagnosis No cavities

Cavities Treatment

Maintenance (“Recall”) Health

641

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Medical Approach to Caries Management Diagnosis Caries-

Caries+

Cavity+ Cavity-

Cavity+ Cavity-

Treat Caries Treat Cavity Maintenance Health

Medical Approach to Caries Management Classification: Findings

Status Group

Caries+ Cavity+

Manifest disease

Caries+ Cavity-

Premanifest disease

Caries- Cavity+

Postmanifest/arrested

Caries- Cavity-

Inactive disease

642

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Management of Status Groups •

Manifest disease: arrest and restore; caries removal; sequential cultures; anticipatory guidance; restoration

•

Premanifest disease: arrest process

•

Postmanifest disease: maintain suppression of process; restore lesions

•

Inactive disease: anticipatory guidance

Interim Therapeutic Restorations

Lesions in young patient

643

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Interim Therapeutic Restorations Caries removal – no local anesthesia

Lesions in young patient

Interim Therapeutic Restorations Caries removal – no local anesthesia

Lesions in young patient

Lesions restored

644

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Rationale for Earlier Initial Visits !

Health supervision, not disease treatment

!

Old model: caries inevitable; treat effects of disease, then institute preventive (suppressive) care; OK to start at age 3 (can’t manage behavior any earlier)

!

New model: examine early; risk assessment; anticipatory guidance; true prevention

!

Early identification/intervention are cost effective (Savage et al 2003)

Rationale for Earlier Initial Visits •

Further support: • acquisition of MS as early as birth • recognition of ECC - BBTD, nursing caries, rampant caries • feeding management • risk assessment for fluorosis • non-nutritive sucking • trauma prevention; early ID of abuse/neglect • anticipatory guidance for growth and development

645

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Initial Evaluation •

ADA, AAPD, AAP, AGD, others support initial evaluation by 1 year of age

Knee-to-Knee Exam

Positive reinforcement for caregiver; use toothbrush to facilitate exam

646

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Anticipatory Guidance •

Developmentally paced information

•

Provides practical, developmentallyappropriate health info to parents

•

Alerts parents to impending changes

•

Teaches parents their role in maximizing child’s developmental potential, identifies special needs

Dental Home !

Modeled after AAP’s medical home

!

Accessible, family-centered, continuous, comprehensive, coordinated, compassionate, culturally competent

!

Early prevention; emergency care

!

Coordinates specialty care

!

Individualized recall programs

647

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Early Childhood Caries (ECC) Defined as presence of >1 dmf surfaces in any primary tooth in a child <71 months old

Early Childhood Caries (ECC) !

Distinguishing characteristics of ECC:

! ! ! !

distinctive pattern of decay many teeth may be affected caries develops rapidly caries develops in tooth surfaces normally at low caries risk

648

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Early Childhood Caries •

Prevalence: • no accurate data on national prevalence • 1-70% reported, depending on criteria/definition, sample characteristics • probably ~3-6% in US, and costly to manage

Implications of ECC !

Higher risk for caries in permanent dentition

!

Expensive to treat ! >$1000/child ! may require GA or deep sedation

!

Associated with malnutrition, retardation of growth (Acs et al 1992; Clarke et al 2006)

!

Dental care under GA significantly improves: o o

OHRQoL impact of the disease on the family (Malden et al 2007)

649

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Caries Risk Assessment •

A systematic evaluation of the presence and intensity of etiologic and contributory disease factors

•

The assessment is designed to provide an estimation of disease susceptibility, and an aid to targeting preventive and treatment strategies

Salivary Assays •

CRT system assays LB and MS

MS in biofilm/saliva of young caries-free children appears to be associated with a considerably increased caries risk. Thenish et al 2006

650

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Cariostat Caries Activity Test •

Predicts caries risk of 3½ year olds based on test results at 18 months and 2 years

•

Changes that were effective in reducing caries risk: • lower sucrose intake • toothbrushing by parents

•

Cariostat not yet available in US Nishimura et al 2008

Demographic Data !

Age ! MS transmission? ! expected dental development

!

Race/ethnicity

!

Socioeconomic status

!

Maternal education level - strong caries predictive value in 1-year-olds (Grindeford et al 1993)

651

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Other Clinical Data •

Maternal age

•

Maternal DMF

•

Maternal gingivitis

•

Parental smoking

•

Consumption of candy

•

Sweetened beverages

•

Visible biofilm on maxillary anterior teeth

Medical History !

Prenatal/perinatal history ! low birth weight/hypoplastic defects

!

General health ! growth lags: children with ECC were in lowest 10th percentile for weight (Acs et al 1992)

! asthma (?) ! medications

652

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Overweight / Obesity •

Not significantly associated with increased caries risk in all studies

•

NHANES III and NHANES 1999-2002 • no evidence that overweight children are an increased risk for caries

•

Significant association between high weight and caries frequency found in primary and permanent dentitions of German schoolchildren

Behavioral Factors •

Oral hygiene • gingivitis - marker for home care • biofilm accumulation rates

•

Infant feeding patterns/diet • breast/bottle patterns • amount/frequency of fermentable carbohydrates • adhesiveness, pH, protective factors

653

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Nursing Caries - Bottle Use •

Distinct patterns of cavities

•

Relationship with bottle contents not certain in all studies

•

Nursing bottle used by 95% in U.S. 6 mo to 5 years

•

Almost 20% have been put to bed with bottle

•

>8% ages 2-5 years continue to use bottle

Nursing Caries - Bottle Use Many children continue to use bottle at ages 2-3 • Working mothers tend to bottle feed longer • Working parents may engage in more bottle use •

654

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Nursing Caries - Role of Milk •

Recent animal and in vitro studies suggest that milk/components are not cariogenic

•

Does not cause appreciable drop in pH

•

May aid in remineralization

•

May support/promote growth of cariogenic bacteria

Nursing Caries - Role of Formula !

Some common formulas are as cariogenic as sucrose (Erickson et al 1998)

!

Sucrose is an ingredient in some infant formulas; also lactose, glucose

!

Rinsing with formula reduces biofilm pH significantly (Sheikh and Erickson 1996)

!

Others have found that formulas cause less caries than sucrose in lab animals

655

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Role of Breast Milk !

Case reports suggest ECC related to prolonged, ad lib breastfeeding

!

Erickson et al (1999): does not cause pH drop, supports bacterial growth, deposits Ca and P, poor buffer, does not cause demineralization alone; but with 10% sucrose causes dentinal caries

Role of Breast Milk •

Exclusive breastfeeding is associated with: • older mothers • urban residence • higher education level • higher income

656

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Systematic Review – Valaitis et al 2000 •

Quality of studies • • • •

0 strong 3 moderately strong 9 weak 16 very weak

•

Lack of methodological consistency

•

Moderately strong studies suggest that breastfeeding >1 yr and at night after eruption of teeth may be associated with ECC

Secondary Data Analysis •

NHANES 1999-2002 data • 1576 children ages 2-5

Those breastfed >1 year more likely to have ECC (33%) than those breastfed 1 year (22%) • After adjusting for confounding variables, no association seen between breastfeeding or bf duration and risk for ECC •

Iida et al 2007

657

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Randomized Trial – Kramer et al 2007 13,889 Belarusian mother/child dyads • No evidence of beneficial or harmful effects of •

• prolonged breastfeeding • exclusive breastfeeding

on dental caries in early school age children • Prolonged/frequent breastfeeding may be associated with other factors that increase caries risk

Nursing Caries - Bottle Use •

Fruit juices • low pH • fermentable carbohydrates • enhance demineralization by oral bacteria • use of sweetened beverages in bottle may lead on increased mutans strep colonization (Mohan et al 1998)

658

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AAPD Caries-Risk Assessment Tool (CAT) - Caveats •

“Snapshot” – should be used periodically

•

Can be used by dental and non-dental personnel – does not render a diagnosis

•

Treatment decisions are to be made by dentist

•

Radiographic and microbiologic testing are not essential for use of CAT

659

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Shifts in Preventive Strategies •

Old paradigm: • primary - suppression of disease • secondary - reparative procedures • tertiary - prosthetic procedures

•

New paradigm: • primary - truly preventive/pre-emptive • secondary - suppression of process below threshold • tertiary - limit extent of lesion prior to restoring

Prevention Pharmacotherapeutics •

Fluoride

•

Xylitol

•

Chlorhexidine

•

Other Antimicrobials

•

Remineralizing Agent

660

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Fluoride: Mechanisms of Action !

Topical (most important) ! inhibits demineralization ! promotes remineralization

!

Antibacterial (somewhat important)

! disrupts enzyme systems (enolase) ! reduces acidogenesis, extracellular polysaccharide

!

Systemic (not very important/no effect)

! improves enamel crystallinity, reduces acid solubility ! improves tooth morphology (?) ! recirculates through saliva

Dietary Fluoride Supplements •

Rationale: • to provide a systemic dose of F equivalent to that ingested by children who consume optimally-fluoridated water

•

Questions: • How much F is ingested by children in OF communities? • How effective is a single daily dose? High dose-low frequency vs. low dose-high frequency

661

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Effectiveness of F Supplements •

Primary teeth: • 22-80% reduction in defs • 40-93% reduction in deft

•

Permanent teeth: • 20-80% reduction in DMFS • 16-36% reduction in DEFT

•

Level of evidence is poor for some studies

Supplementation Goals •

Determine the proper dosage

•

Select proper supplement

•

Write the prescription

•

Educate parent and patient

662

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Current Supplementation Schedule Drinking Water F Level (ppm) Age

0<0.3 0.3 - 0.6

>0.6

6 mo<3 yr

0.25*

0

0

3 < 6 yr

0.50

0.25

0

6 to at least 16 yr

1.00

0.50

0

*mg F ion per day Safety tip: Prescribe <120 mg F ion at one time for a family

Supplemental Fluoride Issues •

Fluorosis

•

Prenatal fluoride

•

Breastfeeding

•

Bottled water

•

Water filtration systems

•

Water analysis

•

Inappropriate prescriptions

663

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Fluoride Dentifrices

Fluoride Dentifrices •

High dose - low frequency regimen

•

Best vehicle for topical F application

•

Current formulations: • NaF and MFP: 1000, 1500 ppm F • 1 g of 1000 ppm F = 1 mg F ion

664

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Systematic Reviews !

Pooled prevented fraction – 24% (Cochrane); 25% (Twetman)

!

Effect was increased with ! ! ! !

!

higher baseline caries rates higher fluoride concentration higher frequency of use supervised brushing

Little information concerning primary dentition

Issue: Retention of Dentifrice % dentifrice retained

60

(Data compiled from several studies)

50 40 30 20 10 2

4

Age

665

7

10

13

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Dentifrice Recommendations !

Use fluoridated toothpaste beginning at ~1-2 yr based on risk assessment

!

Use “smear” or “pea-sized” amount

!

Parents should supervise loading of brush and brushing

!

Avoid highly abrasive dentifrices

NaF Mouthrinses •

OTC preparations • 0.05% (~225 ppm) - daily

•

Rx preparations: • 0.05% NaF/APF (~225 ppm) - daily • 0.2% (~900 ppm) – weekly

Omni CaviRinse

666

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SnF2 Mouthrinses 0.044% (~100 ppm F) in acidulated phosphate solution • 0.63% diluted to 0.1% (~250 ppm F) •

Fluoride Mouthrinses !

Indications ! orthodontics (?) ! radiation therapy ! prosthetics

!

No proven additional efficacy in healthy children demonstrated when fluoridated dentifrice is used

667

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Effectiveness – F Mouthrinses •

Cochrane Review meta-analysis • DMFS pooled prevented fraction: 26%

•

No association with: • higher baseline DMFS, background F exposure, rinsing frequency, F concentration

Effectiveness – F Mouthrinses •

Twetman et al 2004 • limited evidence (PF=29%) for individuals with limited fluoride exposure • inconclusive for individuals exposed to other sources of fluoride (eg, toothpaste)

•

Long-term use of F mouthrinse associated with reduced salivary levels of MS (Kaneko et al 2006)

668

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F Retention from F Mouthrinse Age Volume of Rinse (years)

Rinse Time (s)

Mg F Retained

3

5 mL 5 mL

30 60

0.38 0.41

4

5 mL 5 mL

30 60

0.25 0.35

5

7 mL 10 mL

30 60

0.27 0.32

Self-Applied Fluoride Gels •

High dose - variable regimen

•

Designed for custom tray use • rampant caries • orthodontic patients • special-needs patients • post-radiation • impaired salivary flow • high susceptibility to caries

•

Now used in brush-on technique

669

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Effectiveness of Self-Applied Gels Community

Preparation

Application Frequency

% DMFs Reduction

Optimally fluoridated

APF

3x/week (total 225) 3x/week (total 162)

19% 15% (dfs)

Fluoride deficient

APF NaF

5x/week (total 245) 5x/week (total 245)

75% 80%

No controlled trials with SnF2

Professionally-Applied Fluoride •

Gels • NaF 2% - 9000 ppm F • APF 1.23% - 12,300 ppm F

•

Foam • APF 1.23%

•

Varnish • 2.26 % F = 22,600 ppm F

670

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Fluoride Foam and Varnish !

Fluoride varnish (22,600 ppm)

! Duraflor, Duraphat, Cavity Shield ! approved for use in US as cavity varnish (liner) or desensitizing agent ! used since early 1960s in Europe ! typical use 0.2 - 0.5 mL = 5 - 11 mg F ! topical use is “off-label,” but legal

Effectiveness –Gels/Foam •

Cochrane Reviews meta-analysis • DMFS pooled prevented fraction: 28%

•

Marinho et al 2003 • DMFS prevented fraction: 21%

671

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Effectiveness - Varnish Prevented fraction in meta-analyses:

•

• Cochrane: 46% • Petersson: 30%

No significant association with

•

• baseline caries • background exposure to F

Inconclusive evidence for effect in primary dentition

•

Effectiveness Against ECC •

Weintraub et al JDR 2006

•

Randomized controlled trial

•

3 study groups, ages 6-44 months at start • counseling only – control • counseling with FV 1x/year (2 intended applications • counseling with FV 2x/year (4 intended applications

672

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Effectiveness Against ECC •

Caries incidence of counseling-only group compared to: • FV 1x/year: OR 2.2 • FV 2x/year: OR 3.77

•

Significant protective effect of FV vs. early childhood caries

•

No adverse events reported

Fluoride Prophylaxis Pastes •

Caries reductions probably 0%

•

Will remove F-rich enamel - should replace with topical F treatment

•

Not necessary for topical F deposition from F gel/foam/varnish, but use as necessary to remove biofilm and stain

•

Use low abrasive, light pressure

673

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

White Spot Lesion Avoid use of prophy paste on white spot lesions

ADA Recommendations for Professionally-Applied Topical Fluoride (2006) •

Under age 6 • low caries risk: possibly no benefit from topical F • moderate risk: F varnish q 6 mo • high risk: F varnish q 3-6 mo

674

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ADA Recommendations for Professionally-Applied Topical Fluoride (2006) •

Ages 6-18 • low caries risk: possibly no benefit • moderate risk: F varnish or gel q 6 mo • high risk: F varnish or gel q 6 mo • F varnish or gel q 3 mo may provide additional protection

Acute Fluoride Toxicity •

Mechanisms of toxicity • corrosive action on stomach lining • affinity for calcium - tetany • enzyme inhibition

•

Toxic doses • “certainly lethal dose” - 32-64 mg F/kg • lethal pediatric dose - 15 mg F/kg • “probably toxic dose” - 5-8 mg F/kg

675

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Treatment of Fluoride Ingestion •

<8 mg F/kg: give milk; observe > 6 hours; refer if symptoms develop

•

>8 mg F/kg: induce vomiting (if recent ingestion), followed by milk; refer immediately

•

Unknown ingestion: if asymptomatic, give milk, observe >6 hours, refer if symptoms develop; if symptomatic, give milk and refer immediately

Xylitol !

5-carbon sugar alcohol (also sorbitol, mannitol, erythritol)

!

Looks/tastes/relative sweetness same as sucrose (40% fewer calories)

!

Found in plants, esp. birch trees, grasses, fruits, vegetables

!

Oral intake shown to be safe in long term human studies

676

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Xylitol Properties • • • • •

Reduced acid production in biofilm Reduction in amount of biofilm Reduced adherence of biofilm Reduced numbers of MS No accommodation by MS to xylitol

Xylitol Properties •

Accumulates intracellularly in MS, inhibits growth

•

Long-term intake has selective effect for MS that are less adherent to teeth

•

Osmotic diarrhea at high doses (>200 g/day)

677

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Stephan Curves

Fugleman et al 1977

Milgrom et al JDC 2006 •

MS dose response to xylitol chewing gum

•

4 study groups based on daily xylitol dose • placebo - 9.8 g sorbitol and 0.7 g maltitol • 3.44, 6.88, or 10.32 g xylitol

•

Each group chewed 3 gum pellets 4x/day

•

Randomized controlled trial

678

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Log MS CFU/mL

Milgrom et al 6-Month Data

placebo 10.32 g/d 3.44 g/d 6.88 g/d

Xylitol Dose (g/day)

Over the Counter Xylitol, mannitol, aspartame $.10-.15/piece 1.5g xylitol/piece Cost per 7g dose: $.50-.75 For xylitol content & cost of other products, see Ly et al Pediatr Dent 2006;28:154-63.

679

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Other Xylitol Gums

Percentage of xylitol is proprietary information; percentage may vary; No data to support the caries-inhibitory potential of OTC U.S. chewing gums

Use of Xylitol Gums •

Chew 20-30 minutes 2-3 times/day (a total of >7g/day)

•

Chewing immediately after meals especially helpful – salivary buffering

•

Use with mothers of infants to reduce MS transmission?

680

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Chlorhexidine •

Available in U.S. as chlorhexidine gluconate oral rinse 0.12% • Peridex (Omni) • PerioGard (Colgate) • GUM (Butler) alcohol-free

•

Available in Europe as 0.2% rinse, 1% gel, 3% varnish

Chlorhexidine •

More effective against MS than lactobacilli or S. sanguis - thus selective for anticaries effect

•

Can reduce biofilm and salivary MS concentrations to low/nondetectable levels

•

Shown to be effective in high-risk subjects

•

Professionally-applied gel and varnish more effective than mouthrinse use at home

681

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Chlorhexidine Meta-analyses •

Prevented fraction: 46% (van Rijkom et al 1996)

•

No significant influence for variables: • application method, application frequency • caries risk, fluoride regime, caries diagnosis, tooth surface

•

CHX mouthrinse has short-term effect; gel and varnish have larger effects (Ribeiro et al 2007)

Chlorhexidine !

Use in high-caries risk patients (Featherstone) ! rinse with 1 - 2 tsp one minute per day for one week ! repeat every 3 months as needed ! can be used more frequently (one week per month) in more resistant children ! brush or swab onto the teeth of young children to avoid ingestion

682

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Chlorhexidine •

Disadvantages • staining of teeth • taste disturbances • recolonization by MS within weeks of discontinuation

•

Still considered one of the most efficient tools in caries management in high risk patients

Other Antimicrobials !

Povidone-iodine 10% (Betadine)

!

Mouthrinses containing essential oils (Fine et al 2000; Zhang et al 2004) Cetylpyridinium chloride, triclosan, sanguinaria extracts, hexetidine, enzymes, metal ions, others

!

! broad spectrum topical iodophor microbicide ! topical use reduces risk for ECC (Lopez et al 1999)

683

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

CPP – APP: Recaldent •

Calcium phosphopeptide – amorphous calcium phosphate

•

Ca and PO4 ions stabilized into nanoclusters by CPP – milk-derived protein

•

Available as MI Paste and MI Paste Plus • Tooth Mousse in Europe, Australia

CPP - ACP Soluble Ca and PO4 do not concentrate in plaque or localize at tooth surface • CPP stabilizes Ca and PO4 along with F at tooth surface – binding to pellicle and plaque •

CPP – ACP bound to Mutans strep in plaque

684

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CPP – ACP: In vivo, in vitro, in situ studies •

Demonstrated anticariogenicity in rat (in vivo)

•

Inhibition of demineralization / promotion of remineralization seen in several in vitro studies

•

Promotion of remineralization of subsurface lesions seen in in situ studies

•

Incorporation in chewing gum produced remineralization in in situ models

CPP – ACP Human Trials •

Increases in levels of Ca and PO4 in supragingival plaque with mouthrinse

•

CPP – ACP chewing gum slowed proximal caries progression and remineralized more lesions compared to placebo – radiographic assessment

685

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CPP – ACP Human Trials •

RCT showed CPP-ACP more effective than F mouthrinse in remineralizing post-ortho white spot lesions

•

Multiple case reports • treatment of fluorosis • reversal of early lesions • stabilization of lesions

CPP - ACP •

Quality of existing studies: good

•

Need more human trials

•

Promising

686

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Remineralizer – CPP-ACP •

Can be applied by prophy cup, custom tray, finger

•

Also available in chewing gums

•

MI Paste Plus • contains fluoride in 5:3:1 formulation (5 Ca, 5 PO4, 1 F)

Managing Occlusal Surfaces of Young Permanent Teeth !

Pit and fissure decay ! occlusal surfaces comprise 12.5% of total surface area ! comprise 50-80% of decay in ages 5-17

!

Less decline of pit and fissure caries in recent years - relative F effectiveness

!

Relative increase in occlusal caries in recent years

687

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Pits and Fissures Photomicrograph of toothbrush bristle and molar fissure

Photomicrograph of molar fissure pattern

Effectiveness of Sealants •

Systematic review • relative caries risk reduction on permanent 1st molars: 33% • effect was dependent on retention • incomplete evidence for permanent 2nd molars, premolars, primary molars, and glass ionomer cements Mejare et al 2003

688

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Effectiveness of Sealants •

Cochrane Review

•

After 4.5 years, sealed permanent molars of children ages 5-10 had caries reductions in over 50% of occlusal surfaces

•

Caries reductions ranged from 86% at 12 months to 57% at 48-54 months

Sealant Types ! ! ! ! ! ! ! !

Self-cure vs. light cure Filled vs. unfilled Fluoride containing Radiopaque Clear vs. opaque White, tinted, color-changing GIC, flowable composite, bonding agent, bonded amalgam Self-etching

689

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

ADA Recommendations (2008) •

Resin-based sealants first choice (high level of evidence)

•

GIC sealants may be used when moisture control is an issue (high level of evidence, but low strength of recommendation)

•

Hiiri et al 2006: • sealants provide better protection than fluoride varnish

ADA Recommendations (2008) •

Use of compatible 1-bottle agents (primer/adhesive) may be used between etching/sealant to enhance retention (mod high level of evidence)

•

Use of self-etching bonding agents may provide less retention than standard etching procedure (mod high level of evidence)

•

Borsatto et al 2007 • Er:YAG laser may improve sealant bond strength to primary teeth, but only if enamel is etched subsequently

690

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Concerns •

Sealing over decay • proven effective in arresting lesion

•

Systematic review (Griffin et al 2008) • sealing non-cavitated caries in permanent teeth effective in reducing caries progression

•

Routine mechanical preparation of enamel not recommended (ADA; mod high level)

ADA Recommendations for Use of Sealants (2008) •

Primary teeth • when tooth and/or patient is at risk for caries • low level of evidence

•

Permanent teeth (children/adolescents) • when tooth and/or patient is at risk for caries • high level of evidence

•

Placement over non-cavitated lesions • high level of evidence

•

Use 4-handed technique when possible • low level of evidence

691

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Fissure Diagnosis • •

•

Use care with explorer Probing can convert non-cavitated occlusal lesion into cavitated lesion (Künisch et al 2007) Use • air • visual exam • diagnostic aids (eg, QLF)

692

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

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Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Constance M. Killian, D.M.D.

Special Needs Definition of Persons with Special Health Care Needs: Individuals with a 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.

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Special Needs

General Considerations • May cause limitations in performing daily selfmaintenance • Persons with SHCN are at increased risk for oral disease • Disability impacted by severity of disease

Special Needs

Epidemiology The numbers are increasing... Nearly 1 in 5 Americans older than 5 years have a disability Nearly 2.6 million children ages 5-15 years have a disability

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Special Needs

Epidemiology Causes of Disability • Extreme pre-term birth (< 26 weeks) • Congenital disorders • Acquired disorders – accidents, diseases

5

Special Needs

Changing Patterns • History of care in institutions • Increasing numbers of children with

intellectual, physical, or developmental disability are surviving into adulthood

What does this mean to you?

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Special Needs

Healthy People 2010 Goal: To decrease to zero the number of persons under 21 years of age in congregate care facilities by the year 2010

Special Needs

Trends As more children with SHCN are living at home, they become part of the patient population in private practice

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Special Needs

Families of Children with SHCN Parents of these children are overwhelmed • • • •

Complex medical conditions Daily maintenance tasks No respite Complicated family dynamics

Special Needs

Principles of Providing Care Get to know the patient Get to know the patient’s family • Family circumstances • Experiences with medical/dental care

Get to know the patient’s condition • Thorough medical history

• Consultation with physician – get it in writing • Use internet/other resources

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Special Needs

Principles of Providing Care Be prepared !Communicate with caregiver !Plan for emergencies !Staff training

Special Needs

Principles of Providing Care • Listen and learn • Be flexible • Think multi-disciplinary when

treatment planning

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Special Needs

Principles of Providing Care • Be an educator • Discuss impact of medical condition on patient’s oral care • Establish dental home • Provide an atmosphere of increased awareness for all parents

Be Inclusive

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Special Needs

Principles of Providing Care

Your office can be the great equalizer

Special Needs

Principles of Providing Care Remember that “Attached to every tooth there is a person” Look beyond the condition to see the unique personality, needs and special gifts of each patient

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Asthma

Asthma Features • Chronic condition of respiratory system • Airway has increased responsiveness to stimuli • Characterized by wheezing, dyspnea, coughing and airflow obstruction • Prevalence is increasing – currently 7-10% of children • One of leading causes of hospitalizations • High costs - $ and lost work/school

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Asthma

Triggers • Allergens: dust mites, pollen, animals • Cigarette smoke (including second hand), ozone

Asthma

Pathogenesis Exposure to a trigger Mast cell degranulation Bronchoconstriction Decrease in expiratory airflow Progressive shortness of breath – wheezing, cough • Airway inflammation • Bronchial hyper-responsiveness • • • • •

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Asthma and the Airway

Asthma and the Airway

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Asthma

Classification • Mild • No night symptoms • Tolerates exercise • Wheezing < 2 days/wk

• Moderate • Some night symptoms • Limited exercise tolerance • Wheezing 2-5 days/wk

• Severe • Frequent night symptoms • Poor tolerance to exercise • Wheezing daily

Asthma

Goals of Therapy ! Reduce symptoms ! Maintain pulmonary function ! Prevent acute attack ! Avoid effects of medications

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Asthma

Medications

• Asthma therapy should be flexible and based on changes in symptoms • Albuterol – B2 agonist – Bronchodilator – relaxes bronchial smooth muscle – Used as rescue inhaler – Examples: Proventil, Ventolin

Asthma

Medications • Corticosteroids • Anti-inflammatory • Immunosuppressive • Maintenance medication • May be inhaled •

Fluticasone (Flovent), Budesamide (Pulmicort)

• May be systemic •

Prednisolone

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Asthma

Risks of Inhaled Corticosteroids • Overall low risk • Suppressed adrenal function • Decreased bone density • Increased risk for cataracts • Growth retardation • Control risks by reducing dose to minimal dose

that is effective

Asthma

Newer Classes of Medications • Long-acting B2 agonists (12 hour activity): bronchodilators • LTRA – Leukotriene receptor antagonists –decrease or block leukotrienes • Montelukast (Singulair )

• Anti IgE agents

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Asthma

Compliance with Medication

Compliance is critical, but especially with adolescents: the greatest number of asthma deaths occurs in ages 10-14

Asthma

Relevant Oral Findings • Decreased salivary flow • Increase in dental caries • Dental erosion • Increased calculus • Increased gingivitis

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Asthma

Relevant Oral Findings

Dentofacial findings • High palate • Increased anterior face height • Increased overjet • Greater incidence of posterior

crossbite

Asthma

Relevant Oral Findings

• Evidence of steroid use • Candidiasis • Tongue enlargement • Pharyngeal irritation

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Asthma

Dentistry and the Patient with Asthma What to Ask… • • • • • • • • •

Medications used Triggers Last asthma attack Frequency of attacks Ever hospitalized for attack? Last visit to ED for asthma History of needing mechanical ventilation Recent use of oral steroids How often is inhaler used/refilled - >1 canister/month?

Asthma

Dental Treatment and Asthma Dental treatment can result in 15% decreased lung function • Dental treatment can provide triggers… • • • • •

Prolonged supine position Position of dental instruments Tooth dust Sealant materials Aerosols

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Asthma

Dental Management of Asthma Patients • Confirm patient has taken medication • Have patient bring inhaler • Avoid triggers as much as possible • Use rubber dam

Asthma

Adjunctive Therapy for Dental Care • Nitrous oxide appropriate with mild/moderate

asthma • Sedation: avoid narcotics, barbiturates • Be prepared to rescue patient

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Asthma

Management of Acute Asthma Attack • • • • • • •

Discontinue treatment Remove everything from mouth Position patient for comfort Apply pulse oximeter B2 rescue inhaler Oxygen If O2 < 91%, struggling to breathe • Epinephrine 0.01mg/kg • Call 911

Congenital Heart Disease

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Congenital Heart Disease Incidence of Congenital Heart Disease is 8-10 per 1,000 live births

Congenital Heart Disease

Heart Murmurs • Related to increased blood flow velocity

across valve • Common – present in 80% of all children • Systolic murmurs may be innocent • Diastolic murmurs and continuous

murmurs are abnormal

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Anatomy of the Heart

Congenital Heart Disease

Cardiac Defects

Increased pulmonary blood flow • L to R shunt: ASD, VSD, PDA, AV

Canal • Increase in pulmonary blood flow at

expense of systemic circulation • Appears as CHF over time

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Anatomy!of!the! Heart:!Increased! Pulmonary!Flow Example:!VSD

Congenital Heart Disease

Cardiac Defects Decreased pulmonary blood flow • R to L shunt: Less blood to lungs • Example: Tetrology of Fallot • Patients appear cyanotic • High risk of endocarditis

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Decreased! Pulmonary!Flow Example:!Tetrology of!Fallot 1.!!Pulmonary!stenosis 2.!Right!ventricular!!! hypertrophy 3.!Overarching!aorta 4.!VSD

Congenital Heart Disease

Cardiac Defects Obstructive defects • Anatomic narrowing: coarctation of aorta,

aortic stenosis, pulmonic stenosis • Valvular, subvalvular or supravalvular • Appears as CHF over time

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Congenital Heart Disease

Cardiac Defects

• Primary pump failure • Dilated cardiomyopathy • Hypertrophic cardiomyopathy : can result in syncope, sudden death

Congenital Heart Disease Cardiac Defects Hypertrophic Cardiomyopathy • Thickening of cardiac muscle • Most often affects ventricular septum

48

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Congenital Heart Disease

Cardiac Defects Congestive Heart Failure Management with medications

• Remove accumulated fluid – e.g. diuretics • Improve cardiac function – e.g. digoxin • Improve tissue oxygenation- e.g. warfarin to increase PT • Reduce demands on heart – ACE inhibitors to decrease BP

Management with surgery

Congenital Heart Disease

Management of Cardiac Conditions • Valve stenosis: corrected by balloon valvuloplasty • Condition improves as leaflets of valve are separated • Valve is able to open

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Congenital Heart Disease

Management of Cardiac Conditions Open heart surgery • ASD/VSD repair – patch closure • Shunts • Valve replacement

Congenital Heart Disease

Management of Cardiac Conditions Valve Replacement: Bioprosthetic valves • Porcine, bovine, human • Benefits – No need for anticoagulants – Good hemodynamics

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Congenital Heart Disease

Management of Cardiac Conditions Valve Replacement: Mechanical valves • Doesn’t grow with patient • Need anticoagulants • Readily available, replacements available

Mechanical and Tissue Heart Valves

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Congenital Heart Disease

Oral Care for Cardiac Patients • Medical history • • • • • • •

Type of defect Hospitalizations – when, why Surgery – when, type Medications Any prosthetic valves Any limitations on activities Hypertension

Congenital Heart Disease

Oral Care for Cardiac Patients Oral findings • Increased caries • Poorer oral health than siblings • Increase in untreated caries in cases of

severe CHD • Gingival bleeding

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Congenital Heart Disease

Infective Endocarditis (IE) • Low incidence in general population • Less frequent in children • Microbial infection – affects valves, muscle, defects • Strep viridens most common microorganism ! Symptoms – may appear as other infection ! Fatigue, fever, rash, anorexia ! 7-14 day typical incubation period, but may take up to 4 weeks

Congenital Heart Disease

Sequence of Events in IE • Clinical manifestations of IE related to host’s immune response: immune cells, platelets and fibrin sent to site of cardiac defect/valve • Formation of non-bacterial thrombotic endocarditis (NBTE) at site of defect/valve • Bacteremia • Bacteria adhere to NBTE & proliferate there, forming “vegetations” • Vegetations may break off and enter circulation

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Congenital Heart Disease

Risk of Transient Bacteremia • Dental procedures – done infrequently – Extraction: 10-100% – Perio surgery: 36-88% – Scaling/Root planning: 8-80% – Teeth cleaning: 40% – Rubber dam placement: 9-32%

! Routine daily procedures – done much more often – Toothbrushing/flossing: 20-68% – Toothpicks: 20-40% – Chewing food: 7-51%

Congenital Heart Disease

Risk of Transient Bacteremia Antibiotic Prophylaxis against Infective Endocarditis: 2007 AHA Guidelines

A Change in Emphasis

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Congenital Heart Disease

Summary of Changes – See Appendix • Bacteremia resulting from daily activities is more likely to cause IE than that of dental procedures • Maintenance of optimal oral health and hygiene may reduce the incidence of bacteremia from daily activities • Only very small number of IE cases might be prevented by AP, even if 100% effective

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Congenital Heart Disease

Summary of Changes – See Appendix AP only recommended for cardiac conditions associated with the highest risk of adverse outcome from endocarditis (See Appendix): • Prosthetic heart valve • Previous infective endocarditis • Congenital heart disease – limited to: – Unrepaired cyanotic CHD – Completely repaired congenital heart defect : AP needed during first 6 months after procedure – Repaired CHD with residual defects • Cardiac transplantation recipients who develop cardiac valvulopathy

Congenital Heart Disease

Summary of Changes – See Appendix • AP recommended for procedures that

involve manipulation of gingival tissues or periapical region of teeth or perforation of oral mucosa only for high risk patients

• AP recommended for procedures on

respiratory tract or infected skin, skin structures, or musculoskeletal tissue only for high risk patients

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Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Congenital Heart Disease

Considerations for Antibiotic Prophylaxis ! See Appendix for specific recommendations ! Single dose one hour pre-op ! Patient already on antibiotic ! Patient taking parenteral antibiotic therapy

Genetics and Congenital Disorders

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Genetics and Congenital Disorders

General Considerations Role of the Pediatric dentist • Be familiar with molecular basis for disease • Recognition of the clinical expression • Be a source of information for oral health care issues

Genetics and Congenital Disorders

Principles • Understand the disorder and its dental

implications • Consult with medical colleagues • Provide information • Develop short-term and long-term plan for oral health of the patient

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Genetics and Congenital Disorders

Diagnosis of Genetic Disorders Phenotype/Genotype and the Human Genome • Diagnosis previously made solely by identification of dysmorphic features, pattern recognition (phenotype) • Human genome project allows for identification by genetic findings (genotype) • Relationship between phenotype and genotype is not always straightforward

Genetics and Congenital Disorders

Diagnosis of Genetic Disorders Genetic disorder may result from spontaneous mutation with no familial inheritance pattern

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Genetics and Congenital Disorders

Clinical Application Molecular genetics of a syndrome • Identify syndrome w/familial pattern • In-depth family history • Linkage studies to sequence gene in

affected/unaffected family members • Identify and positionally clone the mutation • Determine the function of the gene and understand how mutation alters this function

Genetics and Congenital Disorders Identification of Dysmorphic Features • Pediatric dentist can provide information to other professionals to aid in diagnosis of genetic disorder • Pediatric dentist can consult various online sources for information about inheritance of specific syndromes – National Center for Biotechnology Information – Online Mendelian Inheritance in Man – National Human Genome Research Institute

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Genetics and Congenital Disorders

Clinical Application Treatment will primarily be determined by the clinical features and patient’s needs: • • • •

Behavioral Physical features Medical aspects Multidisciplinary approach to dental care – think about orthodontic issues early on and incorporate care into overall treatment plan

Genetics and Congenital Disorders

Modes of Inheritance Single Gene Inheritance: caused by mutation in a single gene Chromosomal anomalies ! Autosomal Dominant Transmission ! Autosomal Recessive Transmission ! X-linked Recessive Transmission !

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Genetics and Congenital Disorders

Modes of Inheritance Multifactorial Inheritance: caused by interaction between genetic and environmental factors • •

Cardiovascular disease Diabetes

Genetics and Congenital Disorders

Chromosomal Anomalies • Defect in the chromosome can result in ! Extra copies of chromosome– Trisomy 21 ! deletion of chromosome – 22q11.2 ! translocation of part of a chromosome

• Multiple physical defects • Mental/developmental delay

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Chromosomal Anomalies

Down Syndrome

• Trisomy 21 – chromosomal sporadic mutation

Down Syndrome

Characteristic Physical Features • Hypotonia • Mental deficiency – varying degrees • Increased incidence of cardiac defects • Increased incidence of hypothyroidism • Increased incidence of ALL

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Down Syndrome

Dental/Craniofacial Features • Small ears • Inner epicanthal folds • Up-slanting palpebral fissures • Relative macroglossia, fissured tongue • Class III orthognathic tendency • Microdontia • Hypodontia • Decreased risk for dental caries • Increased risk for periodontal disease

Down Syndrome

Periodontal Disease in Down Syndrome • Prevalence: 50-90% , all under age 30 • Prevalence increases with age • Primary dentition involved in 36%

patients • Greater in Down than in general population • Lower prevalence for Down at home • Higher prevalence of ANUG in institutionalized Down

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Down Syndrome

Periodontal Disease in Down Syndrome Mechanism of Periodontal Disease in Down Syndrome • Calculus not remarkable • Bacteria not different from other MR • Pathogens colonize earlier than in non-Down • Vasculature: abnormal capillary fragility • B-Cells normal • T-Cells dysfunctional: may have diminished

ability to recognize and respond to specific antigens

Down Syndrome

Plan for Dental Treatment If considering sedation or general anesthesia, consider specific issues related to patient’s medical condition • Atlanto-axial instability • Bradycardia • Airway challenges

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Genetics and Congenital Disorders

Autosomal Dominant Tranmission • Gene responsible for phenotype located on one of 22 pairs of autosomes • Expressed in individuals who have just one copy of the mutant allele • Males/Females equally affected • Offspring of affected individuals have 50% chance of inheriting mutant allele

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Autosomal Dominant Transmission

Dentinogenesis Imperfecta Type 2 • Physical findings normal (differs from OI –

DI Type 1) • Family usually aware of condition & its consequences • Early consultation to prepare for future needs

Autosomal Dominant Transmission

Dentinogenesis Imperfecta Type 2 Dental Findings • Primary and permanent dentition affected • Teeth blue-gray/brown • Teeth susceptible to severe wear • Pulpal obliteration/dental abscesses

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Autosomal Dominant Transmission

Dentinogenesis Imperfecta Type 2 • Plan for dental treatment: Primary Dentition ! SSCs when molar wear is evident ! Pulp therapy/extractions as needed • Plan for dental treatment: Permanent Dentition • Possible bleaching • Composite veneers • Full coverage crowns • Endodontic therapy

Genetics and Congenital Disorders

Autosomal Recessive Tranmission • Gene responsible is located on one of 22 autosomes • Expressed only in individuals who have both copies of the mutant allele • If only one copy of mutant allele is present, individual is an unaffected carrier • Males/females equally affected • If 2 carriers mate, resulting offspring have: ! 25% chance of being unaffected ! 25% chance of being affected w/ expression ! 50% chance of being unaffected carrier

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Autosomal Recessive Transmission

Cystic Fibrosis Epidemiology • 1/3,200 live Caucasian births • 2-4% of Caucasians are carriers • Chronic progressive disease • Shortened life expectancy

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Autosomal Recessive Transmission

Cystic Fibrosis • Mechanism of CF • Abnormal CFTR protein • Abnormal ion transport • Decreased secretion of chloride • Increased absorption of sodium • Exocrine glands produce thick sticky secretions • Lungs, intestine, reproductive epithelium most affected

Autosomal Recessive Transmission

Cystic Fibrosis Diagnosis of CF • 10% detected at birth, most detected in

first 3 years of life • Genetic testing • Sweat chloride test for diagnosis

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Autosomal Recessive Transmission

Cystic Fibrosis Symptoms of CF • • • • • • • •

Salty tasting skin 2-5 times normal amount of Na, Cl, K in sweat Failure to gain weight Abnormal bowel movements Recurrent wheezing, cough Recurrent pneumonia Nasal polyps Clubbing of fingers and toes

Autosomal Recessive Transmission

Cystic Fibrosis Respiratory Complications of CF Chronic lung disease ! Bronchiectasis – form of COPD ! Pneumothorax – collapse of lung ! Hemoptysis – coughing up blood ! Cor pulmonale- right side heart enlargement

secondary to pulmonary dysfunction ! Clubbing

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Autosomal Recessive Transmission

Cystic Fibrosis Respiratory Treatments of CF Airway clearance techniques • Chest physiotherapy 1-3 times/day • Mechanical vest – no assistance needed • Flutter device – resembles pipe

Compliance is most difficult in adolescents – allowing for independence is the key

Respiratory therapies for Cystic Fibrosis

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Autosomal Recessive Transmission

Cystic Fibrosis Respiratory Treatments of CF • Exercise – Improves cardiovascular fitness and muscle strength – Loosens mucous, stimulates coughing • Aerosols – Bronchodilators – Mucolytics - (Pulmozyme) – Decongestants – Antibiotics – (Tobramycin) • Oral antibiotics

Autosomal Recessive Transmission

Cystic Fibrosis Digestive System and CF ! Pancreatic enzymes blocked in duct ! 90% patients affected ! Malabsorption of fat and protein

Poor weight gain – High fat stools – Abdominal pain, excess gas –

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Autosomal Recessive Transmission

Cystic Fibrosis Management of Digestive System ! Pancreatic enzyme supplements ! Vitamins - fat-soluble A,D,E,K ! Iron ! Increase caloric intake to 120-150%

RDA

Autosomal Recessive Transmission

Cystic Fibrosis Oral Findings in CF ! Increased enamel defects ! Decreased caries ! Increased calculus ! Salivary pH elevated ! Gingivitis ! Potential for mouthbreathing/malocclusion

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Genetics and Congenital Disorders

X-Linked Recessive Transmission • Mutation located on gene affecting the X chromosome • Females typically carriers •

If mother is carrier, daughter 50% chance of being carrier

• Males • •

If mother is carrier, son has 50% chance of inheriting defective gene and expressing disease All daughters of affected males are carriers

Common examples: Ectodermal dysplasia, Hemophilia

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X-Linked Recessive Transmission

Ectodermal Dysplasia Genetic Features • X-linked recessive, autosomal dominant,

autosomal recessive

• Many forms of ED that can affect one or

more of ectodermally derived tissues

Characteristic physical features • Sparse hair • Dry skin • Absence of sweat glands – heat

intolerance

• Normal mental status

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Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

X-Linked Recessive Transmission

Ectodermal Dysplasia Dental/Craniofacial features • Hypodontia to complete

anodontia of primary and permanent teeth

• Dental agenesis results in

underdevelopment of alveolar ridges

Ectodermal Dysplasia

Long-term Prosthetic Plan Long-term prosthetic plan • • • •

Dentures Bone-grafts, implants Orthognathic implications Psychosocial implications as child matures

Resource information: National Foundation for the Ectodermal Dysplasias

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Coagulation Disorders

Coagulation Disorders Process of Hemostasis • Primary: Platelet aggregation – – – –

Injury causes platelets to aggregate Release of vWF and collagen fibers from endothelium Platelets adhere to subendothelial matrix-vWF-collagen Vasoconstriction occurs

• Secondary: Coagulation Cascade – – –

Extrinsic pathway activated when injury exposes blood to Tissue Factor Intrinsic pathway produces factor X Common pathway generates thrombin

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The Cascade of Coagulation

Coagulation Disorders

Fibrinolysis How is the clot removed? • Plasmin dissolves fibrin clot • Plasmin is regulated by antiplasmin and

plasminogen activator inhibitor

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Coagulation Disorders

Medical History Pursue all positive responses to “bleeding problems” • • • • • • • • • • •

Age of onset Type of bleeding Spontaneous or induced How long does bleeding continue? How does bleeding stop? Any problems with surgery or venipuncture Current medications Overall health – liver disease, etc. Family history History of blood or plasma transfusions Inhibitor status

Coagulation Disorders

Anticoagulant Medications • Aspirin • NSAID • Warfarin (Coumadin) – inhibits

production of Vit K-dependent factors

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Coagulation Disorders

Screening Lab Tests • PT – Extrinsic Path: tests for Factors VII, X, V, thrombin, fibrinogen • PTT –Intrinsic Path: tests for Factors VIII, IX, X, XI, V, thrombin, fibrinogen • Platelet count: platelet phase • Platelet function: platelet phase • Bleeding time: platelet phase, vascular

Coagulation Disorders

Patients at Moderate Risk for Bleeding • Family history • Abnormal bruising • Liver disease • ASA/NSAID use

–Juvenile rheumatoid arthritis

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Coagulation Disorders

Management of Moderate Risk Patients • Detailed medical history • Physician consult • Lab tests: PT, PTT, Platelet function, Platelet count • Optimize patient’s hematologic condition pre-op

Coagulation Disorders

Patients at High Risk for Bleeding • Known bleeding disorder • Taking oral anticoagulants – anti-Vit K (Coumadin) – Thrombotic disease – Factor V Leiden thrombophilia – Cardiac arrythmia • Use of heparin in last four hours

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Coagulation Disorders

Management of High Risk Patients • Consult with hematologist • Lab tests: PT, PTT, Platelet function,

Platelet count • Have patient optimized pre-op • Plan for post-op management

Coagulation Disorders

Dental Procedures and Risk of Bleeding Low • Supragingival restorations or prophylaxis • Infiltration anesthesia

Intermediate • • • •

Subgingival restoration Single extraction Endodontic treatment Nerve blocks

High • Multiple extractions • Periodontal surgery • Gingival curettage

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Coagulation Disorders Primary Defect • Defects in platelet number/function • Von Willebrand Disease

Clinical manifestations • • • • •

Longer bleeding time Bleeding from superficial and deep cuts Petechiae Small, multiple ecchymoses Spontaneous bleeding

Coagulation Disorders

Type of Defect Secondary defect • Defect in the Coagulation pathway • Hemophilia A & B

Clinical manifestations • No significant bleeding after superficial cuts • Significant bleeding after deep cuts • No petechiae • Large, wide-spread ecchymoses • Hematoma, Hemarthrosis • Spontaneous bleeding

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Coagulation Disorders

von Willebrand Disease • • • • • • • •

Autosomal dominant inheritance Most common inherited coagulation disorder vWF may be deficient or defective Often detected after prolonged bleeding episode Low levels of vWF Low levels of factor VIII Prolonged bleeding time Abnormal platelet function test

Coagulation Disorders

von Willebrand Factor What is von Willebrand Factor? • Plasma protein produced in endothelial cells of vessels • Functions as a bridge between platelets and injury site in vessel – helps in platelet plug formation • Protects factor VIII from quick degradation

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Coagulation Disorders

Management of von Willebrand Disease Patients with von Willebrand may respond to desmopressin (DDAVP) • Synthetic peptide • For mild hemophilia A or vWD • Causes rapid release of factor VIII and vWF • 30-45 minutes to take effect • IV or subcutaneous injection • Stimate – nasal spray

Coagulation Disorders

Management of von Willebrand Disease Amicar (e-aminocaproic acid) effective for all types in stabilizing clot • Antifibrinolytic – inhibits activation of

plasminogen to plasmin • 2 hours to peak effect • Give IV or PO: 50mg/kg q6h until healed (usually 7 days) • May be given alone or with DDAVP

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Coagulation Disorders

Thrombocytopenia • Insufficient number of platelets • May be due to low production of platelets – Aplastic anemia – Cancer in bone marrow • May be due to increased breakdown of platelets – Idiopathic thrombocytopenic purpura (ITP) – Drug-induced immune thrombocytopenia

Coagulation Disorders

Thrombocytopenia Clinical manifestation ! Bruising ! Epistaxis, gingival bleeding ! Petechiae

Lab tests & findings ! CBC – low platelets ! PTT, PT - normal

Consult with physician prior to any procedures likely to induce bleeding

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Coagulation Disorders

Hemophilia • X-linked recessive inheritance • 1/3 cases – new mutations • Hemophilia A – Factor VIII – most

common (85%) • Hemophilia B – Factor IX (15%)

Coagulation Disorders

Hemophilia Classification of severity of hemophilia

• Hemophilia A Severe - < 1% Factor activity (70%) • Moderate 1-5% Factor activity (15%) • Mild >5% Factor activity (15%) Hemophilia B • Severe - < 1% Factor activity (50%) • Moderate 1-5% Factor activity (30%) • Mild >5% Factor activity (20%) •

•

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Coagulation Disorders

Hemophilia Bleeding with hemophilia • Normal platelet plug forms • Delayed formation of fibrin clot • Types of bleeding – Deep bleeding into joints or muscles – Increased bleeding from open wounds

Coagulation Disorders

Hemophilia - Complications Inhibitors • Antibodies that block activity of clotting factors – 15% of severe hemophilia A patients – 2.5% of hemophilia B patients

• Emerge after variable number of factor exposures • Treatments – High dose of clotting factor – Bypassing agents – Efforts to induce immune tolerance

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Coagulation Disorders

Hemophilia - Complications • Arthropathy • Bleeding into CNS or

airway • HIV infection • Hepatitis

Coagulation Disorders

Hemophilia - Treatment General Prophylaxis ! Goals

Decrease joint disease – Decrease hospitalizations – Decrease time lost from school or work ! Use clotting factor 2-3 times/week ! Prevent bleeds –

! Possible need for indwelling catheter for young patients

! High cost - $100,000/year

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Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Coagulation Disorders

Hemophilia - Treatment Management of coagulation disorders • Replacement with recombinant factors VIII and IX

Evolution of Factor VIII

Coagulation Disorders

Hemophilia - Treatment Management of coagulation disorders: DDAVP • Synthetic analogue of vasopressin that causes a rise in levels of Factor VIII and vWF • Peak levels obtained ~ 1 hour post-administration

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Coagulation Disorders

Hemophilia - Treatment Management of coagulation disorders: Antifibinolytics • Prevent clot dissolution • Amicar: e-aminocaproic acid • Cyklokapron: tranexamic acid Aminocaproic Acid (Amicar)

Coagulation Disorders

Hemophilia & Dental Treatment Pre-treatment planning for dental treatment • • • • • • • • •

Consult hematologist Type and severity of hemophilia Medications Type of treatment for bleeding disorder Contact info for hemophilia treatment center Inhibitor status Infectious disease status History of joint replacement? Venous access device present?

768

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Coagulation Disorders

Hemophilia & Dental Treatment Management of hemorrhage • Need to have Factor level to achieve/maintain

clot • Goal: 30-40% of normal • 1 unit factor VIII/kg = 2% increase in Factor VIII

level • 1 unit factor IX/kg = 1% increase in Factor IX

Hemostasis

769

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Coagulation Disorders

Hemophilia & Dental Treatment Local measures for hemorrhage control • Pressure • Sutures – absorbable if possible • Collagen sponge – increases platelet aggregation • Gelfoam – absorbs blood, forms matrix • Bone wax • Thrombin – helps conversion of fibrinogen to fibrin • Electrocautery • Epinephrine – re-bleeding likely to occur

Coagulation Disorders

Hemophilia & Dental Treatment Dental management of patients with hemophilia Focus on prevention – caries, gingival tissues Consultation with hematology team Plan for management of hemophilia Plan for all dental treatment in one visit Fabricate splints for extractions Local measures: collagen, gelfoam, topical thrombin, soft diet – 10 days • Management of break-through bleeding • Management of liver clot from slow bleed • • • • • •

770

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Coagulation Disorders

Thrombotic Disorders Acquired • • • •

Short-duration Pregnancy Surgery Immobilization

Inherited • Related to impaired function of protein C-

anticoagulant system

• Factor V Leiden – Incidence 5% in North America – Results in increase in prothrombin

Coagulation Disorders

Thrombotic Disorders Management Acute • Heparin for several days, followed by Warfarin for 3-6 months Long-term • Anti-coagulant therapy

771

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Sickle Cell Anemia Sickle Cell Disease • Autosomal recessive hemoglobin defect • Genotype determines symptoms – Heterozygote: HbA and HbS • 8-10% African Americans • Sickle cell trait – Homozygote: HbSS • 1 in 500 African Americans

Sickle Cell Anemia

Diagnosis • Blood sample collected • RBCs are exposed to deoxygenating agent • Sickling of cells occurs if trait or disease is present – Homozygous – rapid rate of sickling; almost all red blood cells involved – Electrophoresis confirms diagnosis

772

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Sickle Cell Anemia

Hemoglobin S

Sickle Cell Anemia

Hemoglobin S Sensitive to O2 demands and supply • Systemic disease • Dehydration • Exposure to cold • Rigorous exercise • Infection • Acidosis • Stress

773

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Sickle Cell Anemia

Medical Findings • Anemia due to decreased survival of • • • •

sickled RBC’s Chronic anemia: HbG 6-9 g/dl; Hct – 20 Delayed growth and puberty Susceptibility to sepsis Bone pain – sickled RBC trapped in bone sinusoids

Sickle Cell Anemia

Medical Findings • Hand/foot syndrome – when small vessels blocked • Chest syndrome – Sickled RBC block circulation in alveoli – Severe pain, cough, fever, dyspnea • Abdominal pain – Liver, spleen, kidney damage • Aplastic crisis • Thrombotic crisis

774

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Sickle Cell Anemia

Morbidity/Mortality • Pneumococcal infections –

early treatment with antibiotics decreases incidence • Morbidity related to blockage of various organs • Life expectancy: late 40s

Sickle Cell Anemia

Medical Management of Patients ! Early diagnosis ! Avoid sickling-inducing conditions –Dehydration –Acidosis –Cold exposure ! Blood transfusions regularly

775

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Sickle Cell Anemia

Crisis Management • Bed rest to decrease oxygen use • Hydration • Electrolyte replacement • Analgesics • Transfusion to treat anemia • Antibiotics

Sickle Cell Anemia

Oral Findings • • • • • • • •

Pale mucosa Enamel hypoplasia Dental or jaw pain (from infarcts) Delayed eruption Pulp calcifications Mandible – decreased trabeculae Class II – protrusive maxilla Decreased caries when taking antibiotics

776

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Sickle Cell Anemia

Dental Management of Patients • • • • • • • •

Prevention of dental disease Antibiotic prophylaxis – uncertain value AM appointments – keep brief Local anesthesia with vasoconstrictor is okay N2O – minimum of 50% O2 to avoid hypoxia Acetaminophen for pain Considered ASA III Avoid elective surgery – treat infections vigorously

Diabetes

777

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Diabetes

Type I (Insulin-Dependent) Diabetes • Destruction of pancreatic beta cells leads to absolute insulin deficiency • Most common form of pediatric diabetes: 70% • Peak onset – Girls: 10-12 years – Boys 12-14 years • Causes – Genetic, environmental, autoimmune factors

Diabetes

Symptoms of Type I Diabetes • • • • • •

Frequent urination Extreme increase in appetite and thirst Weight loss Fatigue Weakness Symptoms develop over a short period of time

778

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Diabetes

Type II (Non-Insulin-Dependent) Diabetes • 30% of pediatric diabetes • Increasing incidence in children &

adolescents • Body doesn’t use insulin properly • Risk factors – major one is obesity

Diabetes

Symptoms of Type II diabetes • • • • • • • •

Increased appetite and thirst Increased urination Fatigue Blurred vision Dry, itchy skin Tingling or numb extremeties Nonhealing skin infections Acanthosis nigricans – cutaneous marker of insulin resistance – at nape of neck

779

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Diabetes

Medical Treatment Goals • Eliminate hyperglycemia symptoms • Stabilize blood glucose • Restore normal body weight • Prevent long-term complications

Diabetes

Management of Type I Diabetes • Frequent glucose monitoring (4 times/day or more) • Diet • Medications – injected insulin • Insulin pump • Pancreatic islet cell transplant

780

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Diabetes

Management of Type II Diabetes • • • • •

Weight loss Small, frequent meals Exercise Daily glucose monitoring Medications – Oral hypoglycemics

– Injected Insulin • Long-term compliance difficult

Management of Diabetes

781

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Diabetes

Diet Management Glycemic Index Goal is to eat low-to medium GI foods Refined grains, potatoes, sucrose - high GI Non-starchy vegetables, fruits, legumes, nuts - low GI • Fat and protein have minimal effect on blood glucose • • • •

Diabetes

Oral Findings • Increased incidence of periodontal • • • •

disease Prolonged infections Xerostomia Delayed wound healing Altered sensations: numbness, burning, taste

782

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Diabetes

Periodontal Disease and Diabetes • More gingival bleeding in diabetic children than in healthy counterparts • Diabetic children: lifelong increased risk of PD • Plaque Index not correlated with Gingival Index • Level of diabetic control is more important than plaque control in the severity of the gingival inflammation • Good metabolic control helps address periodontal considerations

Diabetes

Periodontal Disease and Diabetes Mechanism of periodontal changes • Early acute inflammatory response • HgA1C elevated • HgA1C levels positively correlate with

gingival bleeding levels – this implies a relationship between periodontal microvasculature and metabolic control

783

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Diabetes

Dental Management of Patients AM appointments best Normal insulin dose + normal meal Ask about history of hypoglycemia Bring glucometer to appointment, check pre-op • Have source of glucose available • • • •

Diabetes

Dental Management of Patients Prevention is to be maximized • Incorporate periodontal exam/screening into

routine care

• Discuss relationship between glycemic

control and periodontal disease

• Manage infections aggressively: consider

antibiotics

784

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Diabetes

Hypoglycemia Symptoms • Mild: hunger, weakness, increased pulse,

sweating

• Moderate: incoherence, uncooperativeness,

belligerence

• Severe: LOC, tonic or clonic movements,

hypotension, hypothermia

Diabetes

Hypoglycemia Management • Treat immediately – Don’t wait • Administer glucose in some form • Retest blood sugar • Repeat in 15 minutes if symptoms don’t

improve

785

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Diabetes

Long-Term Complications Caused by chronic hyperglycemia • • • • • • •

Retinopathy Nephropathy Neuropathy Peripheral vascular disease Hypertension Atherosclerosis Coronary artery disease

Gastro-Esophageal Reflux Disease

786

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Gastro-esophageal Reflux Disease

GERD Malfunctioning or weak LES Hiatal hernia Incidence: 5-7% of population Symptoms + tissue damage: esophagitis, erosive GERD • Symptoms + no tissue damage: non-erosive GERD • • • •

Anatomy of GERD

787

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

GERD

Symptoms ! Chronic heartburn ! Acid regurgitation ! Belching ! Painful swallowing ! Chronic sore

throat ! Laryngitis ! Sour taste

GERD

Untreated • • • • • • • •

Persistent discomfort Burning/scarring of esophagus Malignant transformation Apnea Chronic cough Asthma Recurrent pneumonia Poor weight gain

788

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

GERD

Diagnosis • • • • • • •

History 2 week trial of medication pH monitoring of esophagus Barium swallow – upper GI series Endoscopy Ultrasonography Laryngoscopy

GERD

Oral Signs/Symptoms • Difficult or painful swallowing • Gingival inflammation • Enamel erosion – Maxillary palatal surfaces affected first – Loss of hard tissue by chemical process

789

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

790

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

GERD

Treatment Lifestyle modification • Upright until meal digested • Decrease portion size • Restrict food choices • No exercise after meals • Reduce body weight

GERD

Treatment

Avoid foods that aggravate GERD • Caffeine-containing sodas • Chocolate • Peppermint • Spicy foods • Acidic foods • Fried, fatty foods • Alcohol

791

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

GERD

Treatment Medications • Antacids – neutralize stomach acid • Foaming agents – cover stomach contents • Proton pump inhibitors – impede acid production • Prokinetics – strengthen sphincter

GERD

Treatment Surgery • Fundoplication – 90% cure rate • Stretta procedure: electrosurgery- induced scarring of GEJ • Endocinch procedure: sutures to reduce LES opening • Enteryx procedure: inject polymer into LES

792

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

GERD

Dental Considerations • Children with GERD have increased risk of erosion • Higher salivary micro-organism colonization in GERD children increases caries risk • Consider evaluation for GERD when dental erosion is present in asymptomatic children

Seizure Disorders

793

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Seizure Disorders

General Considerations • Epilepsy = 3 or more recurrent seizures • Affects 1% of general population • Majority: no identifiable etiology • Involves spontaneous uncontrollable

excessive discharge of cerebral neurons

Seizure Disorders

Seizure Classification New terminology • • • •

Partial: simple or complex (40%) Generalized: convulsive or nonconvulsive (40% ) Unclassified Status epilepticus – seizure lasting > 30 minutes

794

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Generalized seizure

Partial seizure

Seizure Disorders

Partial Seizures - Simple • Originate from localized area of brain • Patient remains conscious • Motor, autonomic, sensory, or psychic symptoms – Localized muscle twitching – Localized numbness or tingling – Chewing, smacking lips – Flashes of light – Feeling of dissociation from body

795

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Seizure Disorders

Partial Seizures - Complex • • • •

Originate from localized area of brain May be preceded by aura 1-2 minute loss of consciousness Motor, autonomic, sensory, or psychic symptoms – – – – –

Localized motor activity Paresthesia Overwhelming sense of fear Visual disturbances Distorted perceptions

• Confusion continues 1-2 minutes postictal

Seizure Disorders

Generalized Seizures • Involve entire brain • Classified by presentation ! Absence ! Myclonic ! Tonic-Clonic ! Atonic ! Clonic ! Tonic

796

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Seizure Disorders

Generalized Seizures • Absence seizures (formerly termed petit mal) ! 10-30 second LOC ! Brief eye or muscle fluttering ! Sudden stop of activity ! Onset generally 4-10 year ! 50% develop tonic-clonic seizures at puberty ! Misdiagnosed as behavior or learning problems

Seizure Disorders

Generalized Seizures Tonic-Clonic seizures (formerly termed grand mal) ! Aura - hours to days before seizure ! LOC leads to falling ! Tonic phase: muscle rigidity for 10-20 seconds ! Clonic phase: 2-5 minutes of muscle contractions ! Urinary and/or fecal incontinence ! Postictal period 10-30 minutes ! Full recovery – 3 hours

797

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Seizure Disorders

Other Generalized Seizures Atonic: brief loss of muscle tone May/may not lose consciousness ! Many injuries from falls !

Clonic: contraction/relaxation Tonic: persistent contractions

Seizure Disorders

Unclassified Seizures • Neonatal seizures • Severe myoclonic epilepsy in infancy • Febrile convulsions • Special syndromes

798

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Seizure Disorders

Seizure History Questions to ask ! Age of onset ! Type ! Duration ! Triggers ! Frequency – date of last seizure ! Medications and compliance ! Control – date of last hospitalization for seizure ! Diet

799

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Seizure Disorders

Medical Management Anti-convulsive medications Ketogenic diet – used for difficult-to-control seizures ! High in fat (3:1 ratio of calories) ! Adequate in protein ! Low in carbohydrate ! Vitamin/mineral supplements indicated ! Avoid liquid and chewable medications – contain

carbohydrates

800

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Seizure Disorders

Medical Management Surgery Hemispherectomy ! Vagus nerve stimulator ! Section corpus callosum !

Alternative /Complementary medicine

Seizure Disorders

Medical Management Medications • Comprehensive descriptions in Manual • Choice of medication based on type of seizure • Medications may be changed based on patient response • Basic principles • Consult with physician/neurologist • Know medication actions • Know medication interactions • Know medication side effects

801

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Seizure Disorders

Medical Management Medications Common side effects of seizure medications • Lethargy • Dizziness • Ataxia • Potential for drug interactions

Some dental effects of seizure medications • Xerostomia (Tegretol, Neurontin) • Gingival bleeding (Depakene) • Gingival hyperplasia (Dilantin)

Seizure Disorders

Medical Management Medications Dilantin-induced gingival hyperplasia

802

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Seizure Disorders

Medical Management Medications Dilantin-induced Gingival Overgrowth • Prevalence of gingival enlargement: 50% • Overgrowth is fibroepithelial in nature • Increase in plaque and inflammation related to increase in dilantin-induced gingival overgrowth

Seizure Disorders

Dental Considerations for Patients • Consider anxiety management • Caution with sedation due to effects of medications • Schedule when well-rested • Make sure medications were taken • Be aware of medication side effects • Be prepared to manage seizure

803

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Seizure Disorders

Seizure Management • • • • • •

Note time that seizure begins Stay calm Move onlookers away Position patient to prevent injury Post-ictal airway support Seizures > 5 minutes, activate EMS: Status epilepticus

Attention Deficit Hyperactivity Disorder ADHD

804

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Attention Deficit Hyperactivity Disorder

ADHD Components of attention ! Focus: ability to spotlight ! Shift: flexibility ! Sustenance: vigilance

over time

Prefrontal brain functions ! Maintain attention ! Self-regulate impulsivity ! Delay gratification

ADHD

Diagnosis ADHD not considered a developmental disorder • Psychiatric diagnosis • Incidence 6-16% • Serious and persisting difficulties

Inattention – Hyperactivity – Impulsivity –

805

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

ADHD

Possible Etiologies of ADHD • Genetic predisposition • Brain size – 3 to 4% smaller in ADHD • System dysfunctions !

Neurotransmitter deficiencies

• Environmental toxins • Severe head injury • History of childhood cancer

ADHD

Effects of ADHD • Psychological impact • Education • Occupational adjustment • May be underachievers • May develop significant social/psychiatric

dysfunction

806

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

ADHD

Common Behaviors and Symptoms Inattentive

ADHD

Common Behaviors and Symptoms

Hyperactivity

807

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

ADHD

Common Behaviors and Symptoms

Impulsivity

AHDD

Diagnosis of ADHD Behaviors of inattention, impulsivity, hyperactivity must: ! Occur in more than one setting (home/school) ! Be more severe than in other children same

age ! Start before 7 years of age ! Continue for >6 months ! Make it difficult to function in various settings

808

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

ADHD

Types of ADHD • Inattentive only (formerly ADD) • Hyperactive/Impulsive • Combined Inattentive/Hyperactive/Impulsive

ADHD

Co-existing Conditions (Comorbity) Oppositional defiant disorder/Conduct disorder (35%) Depression (18%) Anxiety disorders (25%) Learning disabilities

809

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

ADHD

Childhood Impairments • Poor schoolwork completion • Increased learning disabilities • Conduct problems • Peer rejection • Conflict with parents and teachers • Low self-esteem • Poor coordination

ADHD

Adolescent Impairments • • • • • • • •

Failed a grade Increased dropout rate School suspensions Serious antisocial behavior Alcohol or drug use Serious auto accidents Low self-esteem Trouble keeping friends

810

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

ADHD

Safety Concerns ADHD – requires close supervision

ADHD

Treatment of ADHD: Medical/Behavioral • Treatment plan as for other chronic conditions • Long-term management: Set goals, assess outcomes • Teamwork – Doctors, teachers, parents, caregivers, etc. • Medications • Behavior therapy • Parent training • Counseling

811

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

ADHD

Medications Dosages not based solely on weight, but also on patient response to medication

ADHD

Medications - Stimulants Methylphenidate (Ritalin, Concerta) • • • • • • •

Non-amphetamine CNS stimulant Xerostomia Tachycardia Nervousness Anorexia Insomnia Potentiates arrythmogenic effects of tricyclic antidepressants (TCAs)

812

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

ADHD

Medications - Stimulants Dextroamphetamine (Adderall) • • • • • • • • •

Amphetamine CNS stimulant Xerostomia Altered taste Bruxism Hypertension Nervousness, insomnia Anorexia Potentiates arrythmogenic effects of TCAs Meperidine contraindicated

ADHD

Medications – Non-stimulants Amoxetine HCL (Strattera) •

• • • • •

Selective nor-epinephrine reuptake inhibitor Xerostomia Anorexia Fatigue Elevated BP Avoid levonordefrin

813

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

ADHD

Medications – Non-stimulants Clonidine (Catapres) • • • • • •

Anti-hypertensive Xerostomia Dysphagia Sialadenitis Potentiates CNS depressants Cardiac arrythmias

ADHD

Medications – Trends • Between 1991 and 1995, use of stimulants in 2-4 year old children tripled • Use of these medications in children < 6 yrs is “off-label” • Questions of efficacy and safety • Difficult to assess changes in developing personality due to psychotropic drugs • Questionable validity of diagnosis of ADHD, mood disorders in very young children

814

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

ADHD

Behavioral Therapy • Positive reinforcement: reward desired behavior • Time out: remove access to activity due to unwanted behavior • Response-cost: withdraw rewards due to unwanted behavior • Token economy: child receives tokens when displaying desired behavior; tokens later exchanged for meaningful object/privelege

ADHD

Additional Behavioral Therapies • Keep child on a schedule • Cut down on over-stimulating distractions • Provide an organized environment • Reward positive behavior • Set small, attainable goals • Limit choices • Use calm discipline

815

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

ADHD

Dental Management of Patients Behavioral aspects ! Know definitive diagnosis and treatment plan

for patient

! Use behavioral approaches that reinforce

those being used in long-term management plan

! Immediate positive reinforcement ! Short appointments ! Don’t treat on drug holidays

ADHD

Dental Management of Patients • Increased bruxism • Involve parent in oral hygiene • Remember that patient has ADHD • Update history/progression of ADHD

since last dental visit

816

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

ADHD

Dental Management of Patients • Look up medications – side effects • Increased risk of dental trauma • •

Poor coordination Impulsivity

Developmental Disabilities

817

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.



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819

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Steven M. Adair, DDS, MS Medical College of Georgia

•

Dental lamina

•

Bud stage

•

Cap stage

•

Bell stage

•

Advanced bell stage

•

Hertwig’s epithelial root sheath

820

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Initiation - seen at 37-42 days in utero • dental lamina inductive activity • anomalies: tooth number

•

Proliferation • bud, cap, early bell, late bell stages • anomalies: size, proportion, number, twinning

821

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Histodifferentiation • cap, early and late bell stages • differentiation of odontoblasts and ameloblasts • anomalies: AI type I (hypoplastic), AI type IV, dentinogenesis imperfecta

•

Morphodifferentiation • bud, cap, early and late bell stages • basic form and relative size established; DEJ outline established • anomalies: size and shape

822

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

o

Apposition • matrix deposition for hard tissues • anomalies: enamel hypoplasia, dentinal dysplasia, hypercementosis, enamel pearls

•

Mineralization and Maturation • occurs in immediate and maturation phases • removal of H2O/organic material, add’l mineralization • outward from DEJ, from incisal to cervical • anomalies: AI II, III, IV, fluorosis, interglobular/sclerotic dentin and localized hypomineralization

823

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Lines of apposition and maturation seen via tetracycline staining

•

Incidence 0.3-3%; males 2:1 females

•

Permanent dentition 5:1 primary dentition

•

90—98% in maxilla

824

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Supplemental

“normal” morphology

Supplemental permanent?

Supplemental primary incisor

825

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•Rudimentary

conical tuberculate molariform

826

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

827

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

828

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Apert

•

Cleidocranial

•

Down

•

Sturge-Weber

•

Orofaciodigital syndrome I

dysplasia •

Gardner

•

Hallerman-Strief

•

Crouzon

•

Cleft lip and palate

•

Incidence 1.5-10%, excluding 3rd molars (0.09-0.4% for primary dentition)

•

Frequency: 3rd molar, mandibular 2nd premolar, maxillary lateral incisor, maxillary 2nd premolar

•

Significant correlation b/t missing primary tooth and missing permanent successor

•

Familial tendency

829

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Problems may arise from

• • • •

failure of induction abnormality of lamina insufficient space physical obstruction of lamina

830

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Bilateral

831

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Missing primaries

No (?) permanent teeth

•

Ectodermal dysplasia

•

Incontinentia pigmenti

•

Crouzon

•

•

Achondroplasia

Orofaciodigital syndrome I

Chondroectodermal dysplasia

•

•

Hallerman-Strief

•

Reiger

•

Extremely talented/rich former NBA players

•

Seckel

Other ectodermal organs sometimes affected: salivary glands, skin (sweat glands), hair, nails – not part of ectodermal dysplasia

832

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

True generalized • small/large teeth in normal jaws

•

Relative generalized

• normal or slightly small teeth in large jaws • normal or slightly large teeth in small jaws

•

Single tooth macrodontia rare • rule out fusion, gemination

•Frequency –lateral incisors –second premolars –third molars

True localized

833

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Barrel-shaped lateral Peg lateral on right, missing lateral on left

Microdont molars and 3 premolars

Relative generalized

834

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Ectodermal dysplasia

•

Chondroectodermal dysplasia

•

Hemifacial microsomia

•

Down syndrome

•

Crouzon

•

Hemifacial hypertrophy; accelerated eruption on affected side

•

Crouzon

•

Otodental syndrome • macrodontia of posterior teeth • globodontia, molar fusion

835

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Photos courtesy of Dr. Lourdes Santos-Pinto

836

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Gemination • incidence ~0.5%; more common in primary dentition • may retard eruption of permanent successor • clinical diagnosis: extra crown (assumes normal complement of other teeth)

837

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Single pulp canal; extra crown (depends on clinical appearance)

•

Twinning • complete cleavage of single bud • mirror image “supernumerary” tooth

838

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Fusion • incidence roughly 0.5%, more common in primary dentition • union by dentin; separate pulp chambers/canals • may retard eruption of permanent successor • clinical diagnosis: normal complement of crowns (unless fusion with supernumerary)

839

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Concrescence • fusion occurs after root formation complete • etiology: trauma?, crowding? • may occur pre- or post-eruption

840

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Dens-in-dente (dens invaginatus)

•

Dens evaginatus (talon cusp)

•

Taurodontism

•

Dilaceration

•

“Tooth within a tooth”

•

Incidence 1-7.7%; rare in African-Americans

•

4 classes

crown only

841

part of root

entire root

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Maxillary lateral most affected; both dentitions

•

Etiology: invagination of inner enamel epithelium

•

Hertwig’s epithelial root sheath involved in severe cases

•

Treatment • • • •

conventional RCT MTA/RCT combined RCT/surgery intentional replantation

842

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

3 types:

•

• I – talon • II – semi-talon • III – trace talon

•

Incidence 1-8%

•

Higher in some racial groups

•

77% occur in permanent teeth

•

94% are maxillary incisors

•

55% are lateral incisors

•

May be uni- or bilateral

•

65% in males

843

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Evagination of enamel epithelium

•

Pulp tissue within extra cusp

•

Seen in lobodontia (“wolf teeth”)

•

Failure of proper invagination of Hertwig’s epithelial root sheath

•

“Bull’s teeth”

•

Incidence 0.5-5.6%; higher in some groups

•

Genetic advantage to groups that use teeth as tools (?)

844

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Klinefelter

•

Trichodento-osseous

•

Orofaciodigital II (Mohr)

•

Ectodermal dysplasia (hypohidrotic)

•

Amelogenesis imperfecta type IV

•

Down syndrome

•

Etiology: trauma, especially intrusion injuries to primary dentition

•

Syndrome with dilaceration: lamellar ichthyosis

845

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Enamel defects • amelogenesis type I • amelogenesis type IV (discussed under Maturation)

•

Dentin defects • dentinogenesis types I, II, III

846

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Heritable enamel defect

•

Reported incidence varies from 1:14,000 to 1:4000

•

Multiple inheritance patterns

•

4 major types (Witkop), 14 subgroups

•

Distinguished from other enamel defects: • confined to distinct patterns of inheritance • occurs apart from syndromic, metabolic, or systemic conditions

•

Insufficient quantity of enamel (matrix)

•

Both dentitions affected

•

Most subgroups autosomal dominant

•

Most frequently reported type (?)

Anterior openbite in 44% “vertical dysgnathia”

847

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

848

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

849

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Heritable defect of predentin matrix • normal mantle dentin • amorphic and atubular circumpulpal dentin

•

Incidence 1:8000

•

Three types as defined by Shields

850

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Mantle: outer layer of primary dentin Primary: develops before and up to root completion (Circumpulpal = primary – mantle)

Secondary: develops after root completion

Tertiary: develops in response to trauma/caries Predentin: innermost layer

•

Occurs with osteogenesis imperfecta (IB & IVB)

•

Dental manifestation of type I collagen defect

•

Primary teeth more severely affected

•

Permanent teeth - central incisors and 1st molars

851

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Least severe form

•

Amber translucence

•

Periapical radiolucencies, alveolar abscesses

•

Autosomal dominant

•

Rapid attrition

•

Pulpal obliteration – occurs soon after eruption of prior to eruption

•

Degree of expressivity is variable intra- and interpatient

•

Bulbous crowns, short roots

•

Occurs alone - no osteogenesis imperfecta

•

Attributed to mutations of DSPP gene

•

Nearly complete penetrance; more consistent expressivity w/in a family

852

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Both dentitions equally affected

•

Same characteristics as DI-I

•

Irregular or tubular pattern

•

Autosomal dominant

•

Rare; most severe; Brandywine triracial isolate

•

Bell-shaped crowns, opalescent hue

•

Shell teeth (esp. primary teeth, short roots, enlarged pulp chambers), only mantle dentin

•

Rapid wear of primary and permanent teeth

•

Permanent pulps obliterated; multiple pulp exposures in primary teeth

•

Regular tubules

•

Enamel pitting

853

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Enamel hypoplasia • systemic • local

•

Enamel pearls

854

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Physiologic • developmental, ingestional

•

Infectious

•

Traumatic

•

Iatrogenic Jorgenson & Yost

•

Potential marker for celiac disease

•

Predominant locations: • upper/lower • primary/permanent • centrals/laterals

•

55% of celiac patients vs 18% of controls

Bossu et al 2007; Wierink et al 2007

855

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Cells of epithelial root sheath may remain attached to dentin

•

May differentiate into ameloblasts and produce enamel

•

Enamel pearls may contain dentin and pulp

•

Dentin dysplasia - 2 types (Shields)

•

Regional odontodysplasia

•

Others

856

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Short, blunted roots, or rootless

•

Obliterated pulp chambers

•

Multiple periapical radiolucencies

•

Severe mobility and malalignment

•

Autosomal dominant - root sheath problem

•

Prevalence 1:100,000

“rootless” teeth

857

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Coronal and root dentin dysplasia

•

Primary teeth affected

•

Amber color - looks like DI-II

•

Permanent teeth appear normal clinically, but demonstrate thistle-tube shaped pulps, multiple pulp stones

•

Characteristics of DI-II sometimes seen

Kim & Summer 2007

858

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

•

• •

•

•

“Ghost teeth” - localized arrest in tooth development Thin enamel, diffuse shell appearance Large pulps, little dentin Affects primary and/or permanent dentitions 80% involve central incisors No known etiology or inheritance pattern

859

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

860

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Vitamin D-resistant rickets

•

Ehlers-Danlos syndrome

•

Hypoparathyroidism

•

•

Pseudohypoparathyroidism

Epidermolysis bullosa

•

Osteogenesis imperfecta

•

Albright’s hereditary osteodystrophy

•

Hypercementosis

•

Hypophosphatasia - 4 types • little cementum produced (controversial) • autosomal recessive • early exfoliation of primary teeth (little or no resorption)

•

Epidermolysis bullosa

•

Cleidocranial dysplasia

861

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Hypophosphatasia

Cleidocranial dysplasia

•

Enamel hypomineralization - systemic and local

•

Hypomineralized permanent first molars

•

Amelogenesis imperfecta type III

•

Enamel fluorosis

862

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

See etiologies for enamel hypoplasia previously discussed – similar etiologies

•

Hypomineralization of 1-4 permanent first molars

•

Frequently assoc w/ affected permanent incisors

•

Prevalence 4-25% (Europe)

•

Varies with birth cohorts, suggesting potential environmental factors

863

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Called “cheese molars” by the Dutch

•

Possible problem with ameloblast function and/or mineral uptake

•

Associated with • • • • • •

febrile illness confounding factors antibiotics nutritional deficiencies preterm birth dioxin compounds in breastmilk others – see manual; William et al 2006

864

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Most common type (?)

•

Deficit in mineralization of normal matrix

•

Normal thickness, but soft; yellow to yellow-brown

•

Pronounced thermal sensitivity

•

Reduced radiographic distinction between enamel and dentin

•

Anterior openbite in 64% (Rowley et al)

•

High calculus formation (rough enamel)

•

Delays in eruption

•

Inheritance patterns: autosomal dominant and recessive

865

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Defect of mineralization (subsurface)

•

Thin, paper white opaque lines corresponding to perikymata

•

Entire surface chalky white

•

Porosity leads to staining

•

Pitting, enamel loss in severe cases

866

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

• •

Amelogenesis imperfecta type II Amelogenesis imperfecta type IV

867

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Normal enamel thickness, but undermineralized, low radiodensity

•

Less severely hypomineralized than hypocalcified type

•

Brown, porous surface, soft, chips away (rather than wears away)

•

Persistence of organic content

•

X-linked recessive

•

Subgroups • pigmented - autosomal recessive • X-linked recessive • snow capped - autosomal dominant?

868

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Brown, porous surface

• •

• •

Distinct from trichodento-osseous syndrome Mottled yellow-brown enamel with pits

Molars are taurodont Subgroups

• hypomaturation-hypoplastic • hypoplastic-hypomaturation • both autosomal dominant

869

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Blood-borne pigments • • • •

porphyria: purplish-brown bile duct defects: green neonatal hepatitis: black, gray Rh incompatibility: blue-green, brown • anemias: gray • dental trauma: red, gray, black

870

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Trauma

•

Hypoplasia/hypocalcifi-cation disorders • amelogenesis imperfecta

•

Dentinogenesis imperfecta • dental caries • enamel and dentin dysplasias

•

Systemic fluoride

•

Mechanisms of tooth bleaching • H2O2 oxidizes wide variety of organic / inorganic compounds that cause staining • bleaching can occur in solution or on a surface • mechanisms of H2O2 bleaching not well understood

871

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Mechanisms of tooth bleaching

• peroxide diffuses into / through enamel to reach dentin and pulp • levels of peroxide in pulp insufficient to inactivate pulpal enzymes • color changes occur throughout dentin

•

Type of bleach • hydrogen peroxide • carbamide peroxide • adduct of urea & H2O2 breaks down on contact with water into those components • 10% carbamide peroxide = 3.6% hydrogen peroxide

• sodium percarbonate • used in silicone polymer that is painted onto teeth •

Concentration of bleaching agent

•

Time

872

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Temperature • rise of 10º C doubles rate of reaction

•

Light • halogen, plasma arc, lasers, LEDs • light source may energize stain to accelerate bleaching process, but actual effect is controversial

•

Type of stain • eg, tetracycline

•

Effect of plaque and pellicle • appear to be minimal

•

In-office procedures • internal bleaching (incl. “walking bleach”) for endodontically treated teeth • external bleaching: 25-38% carbamide peroxide with / without heat / light

•

Vital nightguard bleaching • 10% carbamide peroxide in custom trays

•

OTC products • bleaching strips, paint-on gels, userfabricated or user-modified trays

873

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Transient tooth sensitivity • reduce duration / frequency of bleaching sessions • use desensitizing toothpaste • discontinue bleaching (rare)

•

Gingival irritation • usually caused by improperly made tray

•

Use of acidified pumice • manual or handpiece-driven rubbing

•

Can remove stains if discoloration is less than a few tenths of a mm deep • cannot know depth of stain until microabrasion is attempted

874

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Best for isolated brown or white areas in otherwise normal enamel (eg, fluorosis)

•

If combined with bleaching, generally attempt microabrasion first

•

Microabrasion followed by bleaching can improve tooth discoloration prior to composite or other veneer

•

Generally contain abrasives designed to remove surface stains

•

Some contain peroxide bleaching agents

•

No evidence of efficacy for internal stains

875

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

• • •

Root growth Hydrostatic pressure Bone remodeling

•Periodontal ligament traction •Connective tissue proliferation at pulp apex

•

Hormonal control (growth and thyroid) • circadian rhythms in eruption reflect rhythmic activity of PDL • more eruption seen in evening during sleep • corresponds to release of growth hormone factor

876

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Children with height for age deficits at 6 months • fewer pairs of erupted primary teeth at 6 & 12 mos • less likely to have some permanent molars erupted at age 6

•

Physical control • teeth undergo periods of eruption and intrusion

•

Most favorable in primary dentition: ABDCE

•

Most favorable in permanent dentition Maxilla: 6 1 2 4 5 3 7 8 Mandible: 6 1 2 3 4 5 7 8

•

Sequence more important than timing

877

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Genetic • strong correlation in twin studies • AfrAmer earlier than whites (?) • females ahead of males

•

Environmental • low birth weight/prematurity delays eruption • nutrition – little/no effect • SES – may hide confounding variables

•

Systemic • high correlation with hypopituitarism and hypothyroidism • low correlation with growth hormone production

•

Root development

•

Amount of overlying bone

•

Presence of infection

•

Timing of primary molar loss: • before age 5/prior to crown completion - delays premolar • after age 8/after crown completion - accelerates premolar

878

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Erupt prior to 3 months of age

•

Natal – present at birth

•

Neonatal – present w/in first 30 days

•

Natal 3:1 neonatal

•

Incidence 1:716-3500

•

Positive family hx 1518%

•

90% are true primary teeth

•

Etiology unknown

•

Most are poorly formed

•

Most may exfoliate early (?)

879

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

880

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

biting, drooling

•

gum rubbing, sucking

•

irritability, wakefulness

•

ear rubbing, facial rash

Macknin et al 2000

881

#

decreased appetite for solid foods

#

mild (<102) temperature elevation

#

no combination could predict teething

#

symptoms occurred in <35% of infants

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Wake et al Pediatrics 2000

•

Did not confirm strong associations between tooth eruption and a range of teething symptoms

•

Stated that weak associations may exist

•King et al. 1992 –HSV-1 found in 9 of 20 infants with teething difficulties

•Other studies have implicated HHV-6

882

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

No evidence available to suggest signs/symptoms specific to teething to allow confident diagnosis without excluding other organic pathology

•

Tighe & Roe 2007

•

Local causes • • • •

•

trauma impaction ankylosis supernumeraries

Systemic causes

• syndromes • hypothyroidism, hypopituitarism

•

Genetic conditions

883

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Malfunction of eruption mechanism causes nonankylosed tooth to fail to erupt

•

Teeth can partially erupt

Frazier-Bowers et al 2007

•

Only posterior teeth affected

•

Result is posterior openbite

•

Type 1: eruption failure occurs at/near same time for all teeth in affected quadrant

884

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Type 2: gradient in time of failure; some further development of teeth posterior to affected tooth

•

Rarely symmetric, frequently unilateral

•

Can affect any or all quadrants

•

Abnormal or lack of response to orthodontic force

•

Non-ankylosed tooth with PFE likely to become ankylosed when force applied

Frazier-Bowers et al 2007

•

Local causes • loss of primary predecessor

•

Systemic causes • hyperthyroidism • syndromes • others: see Table

885

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

• •

•

•

Diseases of bone Diseases of periodontium Diseases of metabolism Deviations of growth

• •

•

•

•

Type of dentigerous cyst

•

Either dentition

•

No sex predilection

•

Usually asymptomatic

•

No treatment usually required

•

R/O hemangioma

886

Diseases of blood Physical and chemical injuries Benign and malignant tumors Dental anomalies

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Spicule of bone on occlusal surface of erupting molar

•

•

Incidence 2-3% (25% in CLP)

•

Associations (Pulver): • • • • • •

•

larger maxillary teeth larger affected Es and 6s smaller maxilla small SNA abnormal eruption angle of 6 delayed calcification of some 6s

Self-correction 66% (22% in CLP)

887

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Ectopic #3 and #30 Self-correction

Canine resorption

888

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Fusion of cementum with alveolar bone

•

May occur prior to full eruption

•

Clinically: “submerged” tooth

•

Etiology: unknown

•

Possible extrinsic factors: • trauma; tooth replantation • disturbed local metabolism; localized infection • chemical or thermal irritation

•

Possible intrinsic factors • genetic gap in PDL • aberrant deposition of cementum or bone

889

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Prevalence 1.3-38.5%

•

Most often affected teeth: lower D, lower E, upper D, upper E

•

Multiple teeth as frequent as single

•

Deflected eruption paths

•

Impacted premolars

•

Loss of arch length

•

Supraeruption of opposing teeth (especially maxilla)

890

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Prevalence • 44-97% in 6-year-olds • 33-46% in 9-year-olds • 7-20% in 14-year-olds

•

Racial distribution • higher in African Americans, Mediterranean whites • higher in females at younger ages (?)

• •

• •

Normal development Excessive skeletal growth Pernicious habits Deficiency of tooth material

•

Physical impediment to closure • mesiodens, retained primary teeth • interruption of transseptal fibers

•

• spaced dentition, missing teeth, xs ob and/or oj, others

Artificial • RPE • Milwaukee brace

891

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

•

Usually a combination of orthodontics and bond-o-dontics

892

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

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893

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Constance M. Killian, D.M.D.

Topic Outline Considerations Decision to Use General Anesthesia Planning for General Anesthesia Pre-GA Overall Assessment GA-Specific Assessment Day of Procedure Pre-operative Procedures Intra-operative Procedures Post-operative Management

894

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

General Considerations

Who benefits from GA for dental treatment?

Indicated for the OR?

895

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

General Considerations

How can pediatric dentists interface with hospitals?

General Considerations

GA must be seen as part of a long-term comprehensive treatment plan

896

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

General Considerations

Hospital Dentistry: Communication is critical

Patient Considerations •A patient needing dental treatment presents

at your office as any of the following: • • • •

Pre-cooperative Uncooperative or combative Medically compromised Developmentally delayed

How do you decide if you should take the child to the OR for treatment?

897

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Decision to Use General Anesthesia Extent of treatment needs

Decision to Use General Anesthesia The General Health of the Patient

898

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Decision to Use General Anesthesia • Other options available for treatment • Traditional behavior management techniques • Alternative Restorative Technique (ART)

Decision to Use General Anesthesia •

Will the patient be able to cooperate for the needed treatment without GA?

•

Ask parent about previous experiences

899

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Decision to Use General Anesthesia • What is the patient’s dental history? • Radiographs? • Previous treatment? • Conditions of previous treatment

Decision to Use General Anesthesia • What are the parental expectations? • What are the parental fears? • Communication is essential

900

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Decision to Use General Anesthesia Indications for GA • • • • •

Young age Uncooperative/combative behavior Developmental disability Medical disability Extensive dental disease

Decision to Use General Anesthesia Contraindications to GA • Minimal dental disease • Certain high-risk medical conditions

901

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Decision to Use General Anesthesia Consider the following as they relate to the child: • Indications for GA? • Any contraindications to GA? • Any attempts made to provide treatment

without GA? • Do the benefits of GA for this child’s dental treatment outweigh the risks?

Decision to Use General Anesthesia The Bottom Line

• Recommendation for GA must be justified • Justification for GA must be documented • Provide information for informed consent

902

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

What are the risks of treatment with GA? Physical/Medical risks • Intraoperative incidence of adverse

respiratory events – 22% • 44% of post-operative patients have some symptoms • Post-operative complications studied in 90 children • Pain, agitation, sleepiness, sore throat • Pain at home (more reports in children

>4yo)

What are the risks of treatment with GA? Physical/Medical risks • Risk of serious complication such as brain

damage or death, although rare • Mortality risk in 22,000 GA dental cases was studied – no deaths reported • Undetermined potential risk to developing brain of young child

903

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

What are the risks of treatment with GA? • Behavioral • Fingernail biting • Fear of dark • Needing more parental attention

What are the risks of treatment without GA? • Procedure cannot be completed • Treatment is compromised • Increased risk of injury • Patient may be reluctant to return for future

visits • Increased number of appointments

904

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

What are the risks of no treatment? • A false sense that there is no problem with

not getting the indicated dental treatment • The severity of the disease increases • Decreased quality of life

What are the benefits of GA? • Pain-free delivery of dental care • Dental treatment can be performed under

optimal conditions • Improved behavior of the child at follow-up dental visits • Less cost than multiple sedation visits

905

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

What are the responsibilities associated with GA? Responsibilities of the Pediatric Dentist • Educate regarding etiology of oral disease • Inform parent of need for comprehensive

care • Obtain a thorough pre-op history and assessment • Communicate with medical colleagues about the child • Assist parent in coordinating care

What are the responsibilities associated with GA? • Responsibilities of the Pediatric

Dentist

• Provide pre-op and post-op instructions

regarding the procedure • Stress the need for post-op follow-up care • Provide preventive oral health information • Consider combining procedures under GA

906

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

What are the responsibilities associated with GA? Responsibilities of the Parent/Guardian • Provide accurate and thorough • • • •

information about child Follow pre-op and post-op instructions Keep follow-up appointment Learn about etiology of oral disease Become a committed partner in the preventive plan

Planning for General Anesthesia The Pre-GA Appointment

Overall Planning/Assessment !Clarify the relationship of the patient and guardian !Verify that the individual has the ability to understand the issues related to treatment and consent

907

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

The Pre-GA Appointment • Review the medical history • Assess overall health • Consult with medical specialists as

indicated • Contributing factors to avoidable mortality and morbidity

The Pre-GA Appointment Examine the patient • Document behavior • Extraoral assessment • Intraoral assessment • Document justification for GA

908

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Mallampati Classification

The Pre-GA Appointment Create a problem list and treatment plan • Treatment plan for long-term success • More aggressive restorative procedures • Sealant success limited in patients with high DMFT • SSCs most successful restorative OR procedure • Patients with developmental disabilities have higher failure rate of SSCs • High % of patients having GA have recurrent oral disease

909

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

The Pre-GA Appointment Create a problem list and treatment plan • Plan for alternatives to original treatment plan • Discuss all of the above with the parent/guardian • Describe the appearance of proposed treatment

Obtain informed consent

Assess health and airway status Overall health status – ASA Classification • • • • • •

P1 (ASA I ) – normal healthy patient P2 (ASA II) – patient with mild systemic disease P3 (ASA III) – patient with severe systemic disease, not incapacitating P4 (ASA IV) – patient with severe systemic disease that is a constant threat to life P5 (ASA V) - moribund P6 (ASA VI)- on support, awaiting organ removal

910

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Assess health and airway status ! Previous history of GA and any

complications ! Known difficult airway ! History of premature birth ! MH-susceptible or 1st degree relative with MH-susceptibility

Assess health and airway status • Physical limitations of the patient • CP • Atlanto-axial instability – Down syndrome • Obesity • Mental Disability – may be difficult to induce anesthesia • Conditions that cause limited opening

911

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Assess health and airway status Possible causes of airway/anesthesia problems

Respiratory problems • Asthma – note last attack, last ER visit, last hospitalization • Reactive Airway Disease • Bronchopulmonary dysplasia • Current/Recent URI/LRI • Obstructive sleep apnea

Assess health and airway status Possible causes of airway/anesthesia problems

Congenital syndromes/conditions • • • • • •

Trisomy-21 Pierre Robin Crouzon Treacher Collins History of repaired cleft palate JRA: decreased cervical mobility

912

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Assess health and airway status Possible causes of airway/anesthesia problems

Cardiac conditions • Congenital heart disease • Document need for SBE prophylaxis

Neurologic conditions • • • •

Seizure disorder V-P shunt present? CP Myopathy

Assess health and airway status • Possible causes of airway/anesthesia

problems • Obesity

• GERD • Obstructive Sleep Apnea

• Oncological disease • History of organ transplantation • Bleeding disorders • History of pseudocholinesterase deficiency

913

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Pre-GA Appointment • Order H&P • Order lab tests as needed • Order any consults as needed

Decision: Hospital Admission vs. Same-Day Procedure •Facility factors •Personnel factors •Patient factors: ASA Classification

State requirements and hospital/facility protocols are the ultimate determinants of admissions requirements

914

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Preoperative Instructions • Individualized to the patient • Information regarding URI • Information regarding infectious disease

exposure • NPO Guidelines

Preoperative Instructions NPO Guidelines • No solids for 6 hours • No formula for 6 hours • No breast milk for 4 hours • No clear fluids for 2 hours 44

915

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Pre-GA Appointment Discussion of Risks of Complications • Don’t be afraid to discuss risks • Common assessment of risk of complications: • 1:3 – sore throat • 1:4 – nausea and vomiting • 1-2:1000 – awareness during anesthesia • 1.4:10,000 – cardiac arrest • 1:20,000 – death • 1:30,000 severe damage to teeth • 1:80,000 brain damage

Pre-GA Appointment Advise parents that procedure may be cancelled at the day of procedure • Fever • NPO violation • Exposure to infectious disease • Wheezing • Cough or runny nose • Recent URI/LRI

916

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Day of Procedure Pre-operative Procedures Meet the family and patient Pre-operative Note • • • • • •

Summarize medical history Describe procedures planned State rationale for GA List/summarize consults obtained Consent obtained Name of surgeon/assistant

Day of Procedure Pre-operative Procedures Pre-operative anxiolytic medication Typically midazolam – 0.25-0.5mg/kg to 10mg max • For combative patients – IM Ketamine 23mg/kg with atropine and midazolam • IV or Mask induction can begin when the patient is sedated •

917

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Intra-operative Procedures Monitors • EKG • BP • Pulse Oximeter • Capnography Device • Precordial Stethoscope • Temperature measuring device • Bispectral Index

Intra-operative Procedures Heating/cooling blankets should be available Neuromuscular blocking agents • Avoid succinylcholine – may cause fatal hyperkalemia • Vecuronium, rocuronium (intermediate-acting) • Mivacurium (short-acting)

918

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Intra-operative Procedures Induction of Anesthesia !By mask !Sevoflurane !Intubation – nasotracheal vs. endotracheal

Intubation

919

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Intra-operative Procedures Induction Complications !Difficult IV access !Compromised airway !Traumatic intubation !Aspiration !Laryngospasm !Malignant Hyperthermia

Malignant Hyperthermia: Overview • Skeletal muscle disorder: hypermetabolic • • • •

state Autosomal dominant inheritance pattern No clinical signs of the condition Triggered by volatile anesthetic gases Testing for susceptibility

920

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Malignant Hyperthermia: Signs • Unexplained increase in CO2 • Unexplained tachycardia • Hypertension • Skin mottling • Muscle rigidity • Hyperthermia • Hyperkalemia-induced arrythmias • Disseminated intravascular coagulation

Malignant Hyperthermia: Treatment ! Discontinue triggering agents ! Monitor and treat metabolic acidosis ! Hyperventilate with 100% oxygen ! Sodium dantrolene 2.5mg/kg IV ! Cooling blanket

921

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Intra-operative Procedures Patient Preparation Patient Preparation • • • • •

Padding under pressure points Placement of shoulder roll Eye protection Stabilize head and naso/endotracheal tube Drape head and body

Before Placing Rubber Dam • • • •

Place throat pack Record radiographs Prophylaxis Overall Examination of oral cavity

Standard headrest

Simple towel headrest

922

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Ready to Go

Radiographs in the OR

923

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Be prepared

Intra-operative Procedures Patient Preparation Place Rubber Dam • • • • • • • • •

Perform dental examination Confirm treatment plan Complete operative dentistry Advise anesthesiologist 10 minutes from completion Apply Fluoride varnish Extractions Impressions for any appliances Check mouth and remove throat pack Case Completed

924

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Ongoing Monitoring by Anesthesia

Intra-operative Procedures Complications • Tube problems • IV disconnected • Bleeding • Edema • Arrythmia

925

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Intra-operative Procedures • Extubation • Transport to PACU • Dictate operative report

Post-operative Considerations Nausea/Vomiting • Provide pain relief • Have patient avoid drinking • Antiemetics act independently – use a

single agent • Prophylactic antiemetics preferred over treating nausea/vomiting • Consider propofol IV instead of volatile agents

926

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Post-operative Procedures Pain Management Non-opioid analgesics !Tylenol (Rectal) !IV Ketorolac

Post-operative Orders • Vital signs every 15 minutes until stable • Pain medications • Medications for nausea and vomiting • Ice as needed • Restraint as needed • Disconnect IV when taking oral fluids • Discharge when criteria are met

927

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Post-operative Complications ! Nausea/Vomiting ! Unexpected drowsiness ! Pain requiring medication ! Sore throat ! Hoarseness/croup ! Swelling ! Bleeding ! Fever

Post-operative Visit with Parents • • • • • • • •

Describe patient’s condition and location Speak in lay terms Review discharge criteria Review home care instructions Give contact information for emergencies Verify family contact information Review importance of preventive follow-up Set up follow-up appointment

928

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Post-operative Progress Discharge Criteria ! Vital signs normal ! Able to maintain airway ! Ambulatory ! Awake, alert, appropriate ! Can take fluids orally ! Pain/bleeding controlled ! No vomiting

Post-Anesthesia Recovery Score PARS used in PACU Evaluates patient status based on different organ systems ! Maximum score is 20 ! Score of 18 or higher = ready for discharge !

929

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Follow-up Care

• Low follow-up appointment rate: 54-60% • Future well care: 13-31% • Recare interval based on caries risk

Risk of Repeated Dental GA Risk factors ! 100% involvement of maxillary incisors at initial

GA ! Continued use of bottle at time of GA ! Poor cooperation in dental/medical setting ! Difficult personality as described by parents

930

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Closing Thoughts Dental care delivered under general anesthesia in a hospital setting can be the beginning of a lifetime of oral health. It takes many people, many efforts, a great investment of time and money, and involves significant risk. As child advocates and health providers, we must educate parents and the public of the value and importance of the efforts made on behalf of the child as we welcome them to their dental home.

931

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

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932

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Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Developmental Disabilities

General Considerations ! Physical or mental

disabilities ! Functional limitations ! Need for enhanced services ! Persistent dependency ! Expense: long-term care, medications ! Parent stress higher

Developmental Disabilities

Questions to Ask • Overall family functioning – caretakers • Level of receptive/expressive function • Educational situation • Diet and oral hygiene • Input for behavior management

933

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Build confidence

Engage the child

Promote independence

Provide support and education

934

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Assessing Patient Abilities

935

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

936

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Cerebral Palsy

General Considerations • Disorder of movement and posture • Result of injury to brain motor areas • Motor problems • Static/non-progressive • 300,000 U.S. children affected

Cerebral Palsy

Criteria Posturing/abnormal movements Oropharyngeal problems Strabismus Increased or decreased muscle tone • Evolutional responses • Increased deep tendon reflexes • • • •

937

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Cerebral Palsy

Subtypes of CP Hemiparesis ! Asymmetric CNS damage ! Uneven strength/poor balance ! Progressive scoliosis

Spastic diplegia and quadriplegia Athetoid or ataxic: involuntary movements Hypotonic

Cerebral Palsy

CP Associated Findings • Strabismus • Refractive errors • Hearing loss • 50% Mental retardation • Behavioral problems

938

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Cerebral Palsy

CP Oral Findings • Increased DMFS of permanent teeth • Enamel erosion • Poor gingival health • Malocclusion – High overjet, less crowding • Delayed permanent molar eruption • Tongue thrust • Bruxism • Increased gag reflex

Cerebral Palsy

CP Oral Findings Dysfunctional swallow Drooling: impacts socialization ! Can be treated with botox in

submandibular gland ! Can be treated with transdermal scopolamine ! Can be treated with maxillary appliance

939

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Cerebral Palsy

Dental Management of Patients Infant dental program to start prevention Communication challenges Feeding issues ! May have gastronomy tube ! GERD ! Role of diet and caries ! Caution with sucrose in medications

Cerebral Palsy

Dental Management of Patients Medications ! Baclofen – muscle relaxant ! Botox Consider chlorhexidine to aid in gingival health Treatment needs

940

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Autism Spectrum Disorders ASD

Autism Spectrum Disorders ASD Autism: Neurodevelopmental disorder in which social interaction, language, behavior, and cognitive function are severely impaired

941

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Autism Spectrum Disorders

Epidemiology and Etiology 10-20 cases of classic autism/10,000 live births 30-50 cases of ASD/10,000 live births Cause is unknown Role of genetics: genetic expression influenced by environment • No ethnic differences • 3% of families have > 1 child with autism • Increased risk with some conditions –Down syndrome: 7-15% –Deaf patients: 15% • • • •

Autism Spectrum Disorders

Early Signs of Autism • • • • • •

No babbling or gesturing by 12 months No words by 16 months No social interaction – smile, eye contact Restricted interests and activities Lack of imagination in play Compulsive behaviors may be evident

942

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Autism Spectrum Disorders

Categories of Autism • Classic autism – most severe • Asperger Syndrome • Pervasive Developmental Disorder, not otherwise specified

Autism Spectrum Disorders

Characteristics of Classic Autism • Impaired social interaction • Impaired verbal and nonverbal communication • Restricted, repetitive patterns of behavior • Poor body awareness/clumsiness ! Slapping, tapping • Conduct problems • Familial pattern • Distorted sensory input

943

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Autism Spectrum Disorders

Asperger Syndrome • Normal curiosity, adaptive behavior and self-help skills during first 3 yrs • Qualitative impairment in social interaction • No delay in language/cognition • More common than classic autism • Lack of demonstrated empathy • Impaired non-verbal contact • Physically clumsy

Autism Spectrum Disorders

Affected Areas of Brain • • • •

Frontotemporal region Synapse dysregulation Amygdala and associated limbic regions Cerebellum

944

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Autism Spectrum Disorders

Deficits in Autism • Ability to recognize and understand mental states of self and others and use this to predict behavior • Executive function • Central coherence

Autism Spectrum Disorders

Effects of Autism on Family • Increased stress • Increase in negative outcomes for

siblings • Loss of employment/income • Lost leisure time • Increased familial conflicts

945

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Autism Spectrum Disorders

Medical Management of ASD Goals • • •

Minimize core features of ASD Minimize family stress Maximize functional independence and quality of life

Autism Spectrum Disorders

Educational Management of ASD • The earlier the better – by 2 years of age • Intensive intervention schedule • 25 hours/week • 12 months/year • Low student/teacher ratio • Family involvement

946

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Autism Spectrum Disorders

Educational Management of ASD • Focus on structure, routine, few distractions • Apply skills to new situations • Educational goals ! Improve social skills ! Improve speech/language ! Increased responsibility & independence ! Improve occupational skills ! Achieve academic goals

Autism Spectrum Disorders

Medical Treatment of ASD Medications – used to treat specific behaviors ! Hyperactivity – methylphenidate (Ritalin, Concerta) –

calm hyperactivity ! Repetitive behaviors – fluoxetine (Prozac) – decreases compulsive behaviors, self-mutilation ! Aggressive behaviors – carbamazepine (Tegretol), risperidone (Risperdal)

947

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Autism Spectrum Disorders

Side Effects of Medications for Autism Methylphenidate (Ritalin, Concerta) - stimulant ! Tachycardia ! Nervousness ! Anorexia ! Insomnia ! Xerostomia

Autism Spectrum Disorders

Side Effects of Medications for Autism Fluoxetine (Prozac) – selective serotonin reuptake inhibitor (antidepressant) ! ! ! ! ! ! ! ! ! ! !

Diarrhea, nausea Somnolence Dizziness Increased bleeding time Potentiates CNS dpressants Erythromycin inhibits metabolism Xerostomia Altered taste Bruxism Stomatitis, glossitis Gingivitis

948

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Autism Spectrum Disorders

Side Effects of Medications for Autism Risperidone (Risperdal) - antipsychotic ! Potentiates CNS depressants ! Xerostomia ! Dysphagia ! Altered taste ! Stomatitis ! Gingivitis ! Tongue edema ! Facial edema

Autism Spectrum Disorders

Side Effects of Medications for Autism Carbamazepine (Tegretol) – anticonvulsant ! Decrease WBC, Increase platelets – longterm use;

! ! ! !

caution with use of aspirin, NSAIDs – risk of increased bleeding Erythromycin inhibits metabolism Xerostomia Stomatitis, glossitis Carbohydrate craving

949

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Autism Spectrum Disorders

Caries, Oral Hygiene, Diet

• Caries rate: similar or less than healthy population • Oral hygiene: difficulty accepting brushing/flossing • Diet: food often used as reward

Autism Spectrum Disorders

Dentistry and Autism • Make initial encounter benign and relaxing • Presence of parents is helpful • TSD useful • Use same treatment room • Keep visits short • Use short, clear commands • Positive and negative verbal reinforcement • Music/DVDs can be used as distractors • Use desensitization – build gradually on interventions

950

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Autism Spectrum Disorders

Dentistry and Autism Protective stabilization may be needed Multiple short visits may be needed Consult with psychiatrist treating patient GA may be needed as adjunctive therapy for treatment • End on a positive note • • • •

Autism Spectrum Disorders

Dentistry and Autism Screening for 5 risk factors can help predict uncooperative behavior Age (<4 or 4-7) Reading (no vs. yes) • Toilet trained (no vs. yes) • Concurrent medical diagnosis (yes vs. no)* • Expressive language used (no vs. yes) Presence of >2 of any of the above risk factors is strongly associated with uncooperative behavior • •

Marshall, Sheller et al, 2007

951

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

952

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

953

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Autism Spectrum Disorders

Oral Findings • Evidence of erosion • Evidence of bruxism • Macrocephaly • Possible bruising/abrasions on

head

954

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Autism Spectrum Disorders

Long-term Considerations for Oral Health • Maximize prevention • Topical fluoride use daily • Decrease cariogenic behaviors – food

choices, frequency

• Increase frequency of recall visits • Caution in allowing patient autonomy in

home care

HIV Infection

955

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

HIV Infection

General Information ! 40,000 new cases yearly in U.S. ! HIV targets cells with CD4 receptor proteins ! Greatly decreased cellular immunity ! Decreased humoral immunity

HIV Infection

Pediatric HIV Sources • Perinatal transmission • Blood products • IV drug abuse • Unprotected sexual

activity

956

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

HIV Infection

Pediatric AIDS • Lymphadenopathy • Hepatosplenomegaly • Nephropathy • Chronic eczema • Oral candidiasis • Weight loss • Failure to thrive • Diarrhea • Encephalopathy

HIV Infection

HIV Management • Antiretroviral therapy • Taken daily • Physician monitoring every 1-2 weeks until stable • Physician monitoring every 2-3 months when stable – CD4 counts, viral loads – CBC, BUN/Cr, electrolytes, UA

957

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

HIV Infection

HIV Management - CD4 counts What is CD4 and how is it affected by HIV? • Cluster of differentiation 4 (CD4): glycoprotein expressed on surface of T-4 helper lymphocytes, monocytes, and macrophages • Normal CD4 = >1000 • HIV infection causes decrease in number of T-cells with CD4 receptors • Decreased CD4 count indicates an increase in HIV disease status

HIV Infection

HIV Management - Viral load testing ! Quantitative plasma HIV RNA level –Lower limit 50 copies/mL ! Level undetectable – patient is still infectious

958

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

HIV Infection

Medications for HIV Nucleoside RT inhibitors (“nukes”) • Interrupt early stage of virus copying

itself • Prevent RNA to DNA conversion • Target newly infected cells • Zidovudine, Didanosine, Stavudine

HIV Infection

Medications for HIV Non-nucleoside RT inhibitors (“non-nukes”) • • • • •

Interrupt early stage of virus copying itself Bind to viral RT Disrupt RNA to DNA conversion Target newly infected cells Nevirapine, Delavirdin

959

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

HIV Infection

Medications for HIV Side effects of RT inhibitor medications • Decreased RBC, WBC • Pancreatic inflammation

HIV Infection

Medications for HIV Protease inhibitors • Block protease needed for viral formation and growth • Targets new and older infected cells • Saquinavir, Ritonavir, Kaletra • Side effects • Nausea, diarrhea, GI symptoms • May interfere with other drugs

960

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

HIV Infection

Medications for HIV Fusion inhibitors • Blocks virus’s ability to enter and infect

human immune cells • Used in combination with other HIV treatment • Reduces level of HIV in blood • Fuzeon (T20)

HIV Infection

Medications for HIV HAART – Highly Active Anti-Retroviral Therapy ! Helps addresses HIV resistance ! Involves use of 3 or more different drugs ! Reduces amount of circulating virus to nearly

undetectable levels ! Does not affect oral soft tissue disease in HIV-infected children

961

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

HIV Infection

Dental Considerations • Determine stage of disease • Current lab parameters – Hematologic – HIVD status • Type of ongoing care • Medications and side effects/drug interactions • Potential sites of infection • Considered ASA III

HIV Infection

HIV to AIDS Conversion Average survival after diagnosis is increasing Challenges still exist • Treatment-resistant viral strains • Late HIV testing • Inadequate access to treatment • Poor treatment compliance

962

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

HIV Infection

HIV Oral Lesions Significance of Oral Lesions in pediatric HIV ! Oral lesions common ! Associated with decreased immunity ! May signal advancing disease ! CD4 depletion common when oral lesions present ! Poor cell-mediated immunity ! Humoral dysregulation ! Phagocytic cell defects ! Symptomatic patients have more oral lesions

Herpes Simplex

Aphthous ulcer

Hairy leukoplakia

963

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Pseudomembranous Candidiasis Angular chelitis

Linear gingival erythema

Parotid enlargement

964

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

HIV Infection

The Management of HIV Oral Lesions Candidiasis (pseudomembraneous, erythematous) • Treatment with antifungal agents – –

Topical: Nystatin, Clotrimazole 2x daily for 14 days Systemic: Fluconazole, systemic given for 5-7 days

Angular cheilitis • Antifungal + topical steroid

Herpes simplex • Systemic antiviral - Acyclovir

HIV Infection

The Management of HIV Oral Lesions Linear gingival erythema • Chlorhexidine

Parotid enlargement • Anti-inflammatory, analgesics, antibiotics, steroids • Saliva replacements, fluoride rinses

Recurrent minor aphthae • Topical steroids

965

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

HIV Infection

Dental Management/Considerations • • • • • •

Consult with patient’s physician Universal precautions Drug interactions Susceptibility to infection Thrombocytopenia – increased bleeding Delayed exfoliation of primary teeth

HIV Infection

Dental Management/Considerations • More caries than unaffected household peers • Caries increases as CD4 counts decrease • Prevention is critical – Regular recalls – Chlorhexidine daily – Fluoride supplementation as indicated

966

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

HIV Infection

Dental Management/Considerations Rapid HIV testing in dental office • OraQuick Advanced test • Results in 20 minutes • Pre and Post-test counseling

needs to be done

Pediatric Malignancy

967

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Pediatric Malignancy

General Considerations • Affects 1 in 7,000 children each year • ALL most common (24%) • CNS Tumors (22%) • 5 year survival > 75%

Pediatric Malignancy

Pediatric vs. Adult Cancer What makes pediatric cancer different? • • • • • • • •

Rare No risk factors to modify No effective screening Early detection does not influence outcome 70% will be long-term survivors Chemotherapy used for almost all patients Intensive therapy – usually in hospital Late effects of therapy noted

968

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Pediatric Malignancy

Absolute Neutrophil Count: ANC • Indicates ability to fight infections • ANC = WBC x (% seg + % bands) • Neutropenia if ANC < 1,000

Pediatric Malignancy

Dental Issues • • • • • •

Immune system compromise Potential for oral infection Risk of bleeding Cranial or facial radiation Timing of chemotherapy Indwelling catheters

969

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Pediatric Malignancy

Dental Objectives • Arrest dental disease • Restore oral health • Prevent or manage complications from

medical therapy • Educate patient and caregiver

Pediatric Malignancy

New Diagnosis of Malignancy New Diagnosis of Malignancy: Dental Consult • • • • • • • • • •

Nature of disease Time of diagnosis Modalities of treatment received to date Complications/relapses Hospitalizations Infections Current hematologic status Medications, allergies Review of systems Confirm presence/absence of central line

970

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Pediatric Malignancy

New Diagnosis of Malignancy Dental Protocol • • • •

Examination Radiographs as possible Prioritized treatment plan Complete all care prior to start of cancer therapy

Pediatric Malignancy

Example: Medical Treatment Plan of ALL • Remission induction (28 days) • CNS preventive therapy: irradiation and/or intrathecal chemotherapy • Consolidation/intensification: minimize development of drug resistance • Maintenance: chemotherapy 2.5-3 years

971

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Pediatric Malignancy

Prevention of Oral Disease • • • • • •

Brush teeth and tongue 2-3x/day with soft brush Consider chlorhexidine – helps perio condition Non-cariogenic diet Topical fluorides Stretching exercises (if radiation planned) Frequent recall appointments

Pediatric Malignancy

Dental Treatment Prior to Cancer Therapy • ANC > 1,000 – no need for antibiotic prophylaxis unless infection present • ANC < 1,000 defer elective care • Platelets > 75,000 no additional support except aggressive local measures • Platelets 40,000-75,000 consider platelet transfusion prior to and 24 hrs. after dental care • Platelets < 40,000, defer care

972

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Pediatric Malignancy

Dental Treatment Prior to Cancer Therapy • Restorative and surgical treatment – under

GA • Pulp therapy for primary teeth • Endo considerations for permanent teeth – Complete 1 week prior to start of cancer treatment OR – Extract and start antibiotics – Asymptomatic endo needs can be deferred

Pediatric Malignancy

Dental Treatment Prior to Cancer Therapy Let patient tolerance and oral hygiene be your guide… • • • • •

Remove fixed orthodontic appliances Band/loop or lingual arch Removable appliances Operculectomy for risky partially erupted molars Exfoliating primary teeth - leave or extract

973

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Pediatric Malignancy

Oral Complications • Chemotherapy affects oral mucosa • Salivary effects of chemotherapy/radiation

to head and neck – Reduced flow – Thickened • Immunosuppression – Overgrowth of opportunistic organisms

Pediatric Malignancy

Oral Conditions w/ Cancer Therapy • Candidiasis – Nystatin rinse and swallow qid – Mycostatin pastilles qid – Clotrimazole troches – Fluconazole 5 mg/kg

974

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Pediatric Malignancy

Oral Conditions w/ Cancer Therapy • Xerostomia – Stimulate flow with xylitol gum – Replace secretions with ice water, ice chips, carboxymethylcellulose solution – Humidify sleeping area – Avoid caffeine – Lip lubricants

Pediatric Malignancy

Oral Conditions w/ Cancer Therapy • Apthous ulcerations – Triamcinolone in orabase (topical steroid) • Herpetic ulcers – Benadryl + Kaopectate elixir – Viscous xylocaine 2% – Acyclovir • Traumatic ulcers – Triamcinolone in orabase

975

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Herpes Simplex Aphthous ulceration

Pediatric Malignancy

Oral Conditions w/ Cancer Therapy Stomatitis • Identify cause to determine best

therapy • PO or IV fluids • Systemic analgesics • Topical anesthetics

976

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Pediatric Malignancy

Oral Conditions w/ Cancer Therapy Bleeding • Low platelets • Poor liver function • Decreased vascular integrity • Poor oral hygiene • Intraoral bleed may precede intracranial

bleeding – call for medical consult

Pediatric Malignancy

Graft Versus Host Disease (GVHD)

Post-Bone Marrow Transplantation • Usually occurs in first 100 days • Diagnosis of acute oral GVHD

Presence of systemic disease – Exclusion of other sources for lesions – Erythema – tongue, floor of mouth, gingival, labial mucosa – Lesions appear, worsen, or persist beyond day 21 – Prevention of systemic GVHD decreases oral lesions –

977

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Pediatric Malignancy

Long-term Systemic Effects • • • • • • • •

CNS, psychosocial Endocrine Reproductive Secondary neoplasms Cardiac dysfunction Hepatic dysfunction Cataracts Dental

Pediatric Malignancy

Long-term Dental Effects Severity affected by: • Age of patient at time • Stage of tooth development at time • Type and dose of antineoplastic agent • Radiation causes most damage

978

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Pediatric Malignancy

Long Term Dental Effects • Salivary secretions decreased • Increased caries risk • Dental malformations • Risk of ORN questionable

Panograph Age 15

Panograph Age 8

979

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Pediatric Malignancy

Long Term Dental Effects Craniofacial effects

• Malocclusion • Ectopic eruption • Facial deformities, skeletal hypoplasia • Trismus

980

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Pediatric Malignancy

Long Term Dental Effects Orthodontic treatment considerations Light forces ! Shorten treatment time ! Choose simplest method for treatment ! Consider no treatment for mandible ! Use appliances to minimize root resorption !

Solid Organ Transplantation

981

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Solid Organ Transplantation

Demographics 1996-2005: Pediatric organ transplant recipients increased by 23% •
Forms of Solid Organ Transplantation • • • • •

Renal Hepatic Cardiac Pulmonary Pancreatic

982

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Solid Organ Transplantation Common Features • • • •

Patient is on waiting list Management of patient in debilitated state Transplantation requires match of blood type, HLA factors Lifelong immunosuppression therapy

Solid Organ Transplantation What is the oral-systemic relationship? • • • •

Certain inflammatory cytokines (IL-1#,IL-6) are elevated in inflamed gingiva IL-6 can identify individuals at risk for organ rejection Higher serum IL-6 in individuals with chronic periodontitis compared to those without Serious implications for transplant

983

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Solid Organ Transplantation Pre-Transplant Dental Considerations • Medical consult • Conduct thorough periodontal/dental exam • Record radiographs as possible • Develop treatment plan • Meticulous home care instruction • Treatment carried out • Chlorhexidine rinse pre-op • SBE prophylaxis as indicated • Post-op antibiotics as needed

Solid Organ Transplantation Post-Transplant Dental Considerations • • • • • • •

Medical consult Reinforce oral hygiene program for patient Monitor and treat opportunistic infections – Candida Caution with antibiotics – nephrotoxicity Treat xerostomia Increased risk for caries – post renal transplant Increased risk of “de novo” dysplasias & malignancies • Epithelial dysplasia • Non-Hodgkins lymphoma • Squamous cell & Basal cell carcinomas

984

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Organ Transplantation

Immunosuppression Medications Medications Post Organ Transplant Name

Mechanism

Side Effects

Cyclosporine Neoral Sandimmune

Inhibits production and release of interleukin II

Gingival hypertrophy Hypertension Nephrotoxicity Tremor

Tacrolimus Prograf

Suppress T-cell humoral immunity

Hypertension Anemia Pruritus Nephrotoxicity

Azathioprine AZA Imuran

Antagonizes purine metabolism

Thrombocytopenia Leukopenia Anemia

Steroids Prednisone Solu-medrol

Decreases inflammation Decreases lymphatic system activity

Insomnia Nervousness Increased appetite

Organ Transplantation

Immunosuppression Medications Immunosuppression medications • Cyclosporine – use has decreased • Tacrolimus (Prograf) • Azathioprine (AZA) • Steroids • Calcium channel blockers (Nifedipine)

985

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Organ Transplantation

Immunosuppression Medications Cyclosporine-induced Gingival Overgrowth

Organ Transplantation

Immunosuppression Medications: Gingival Overgrowth • Cyclosporine: 30%

" Gingival effects may reverse if medication is stopped or dose is reduced • Tacrolimus (Prograf) – less gingival overgrowth than

Cyclosporine • Nifedipine: 15% (potentiates effects of Cyclosporine)

" Gingival enlargement can be controlled w/meticulous oral care

986

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Organ Transplantation

Immunosuppression Medications Pathophysiology of gingival overgrowth with Cyclosporine and Nifedipine • Cyclosporine increases fibroblast production of collagen and protein • Nifedipine – inhibits apoptosis of cells, and inhibits macrophage-induced death of fibroblasts (potentiates cyclosporin)

Other Conditions – See Manual Pediatric Kidney Disease Pediatric Liver Disease Hearing Loss Visual Impairment Obstructive Sleep Apnea Muscular Dystrophies Spina Bifida Patients with Gastric Feeding Tube Eating Disorders Pediatric Depressive Disorders Adolescent Pregnancy

987

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Special Needs Patients: A case

!

I would first want to find out about her overall health. I would review the medical history with her parent before proceeding with any dental examination

You are told that her medical history is significant for 22q11.2 deletion syndrome. She has developmental delay, history of cardiac surgery to repair Tetrology of Fallot, cleft palate repair, and immunological problems (all part of 22q11.2 deletion syndrome). What is your next step?

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• I would want to consult with her physician. Particularly

I’m concerned about the need for SBE prophylaxis, since she has had surgery to repair Tetrology of Fallot. • Other concerns would be her immune status, her ability to cooperate for any dental treatment (since she has some developmental delay), and her growth and development in terms of orthodontics. • I would also want to find out if she is under the care of a cleft palate team. • My first step would be to call/write her physician.

Her physican advises that she does need antibiotic prophylaxis, and otherwise should be seen as a well-child. She does see a cleft team annually, and has been evaluated by the orthodontist on the team. What is your next step? • I would want to go over her past dental history, and find out if she has had any restorative dental care, and how that went. • Then I would want to do a clinical examination, and consider ordering radiographs. (I would check first with the orthodontist to see if they had recorded any.)

989

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Discuss your findings. What other diagnostic records would you need to provide comprehensive care for this patient? • Looking at the patient, she’s in the late mixed dentition, I can see enamel hypoplasia affecting her permanent teeth, and she looks to be crowded. Tooth #7 is erupting in crossbite. She also has a very prominent maxillary labial frenum, and you can see the scar from her cleft palate surgery. • Based on her age and dental development, I would recommend a panoramic radiograph, bitewings to detect for caries, and possibly study models to assess the crowding. • Based on the right lateral being small, it may eventually need some restorative treatment.

990

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Assume that there is no caries. What is your diagnosis for this patient? • 22q11.2 deletion syndrome, with need for antibiotic prophylaxis for dental treatment, repaired cleft palate • Slightly advanced dental development • I can’t tell her molar/canine Angle classification from the photos, but she has a crowded malocclusion, with deep bite, midline deviation, and crossbite of #7. • Enamel hypoplasia affecting a number of permanent teeth • Atypical anatomy #7

Discuss your overall management of this patient. • Based on her medical condition, she would be considered high caries risk. So I would work on a strong preventive plan, use of topical and systemic fluoride, oral hygiene (with parental supervision), more frequent recare exams, and dietary discussion. • I would discuss with her mom that she will be needing orthodontic care and I’d consult with her orthodontist.

991

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How would you manage the orthodontic care of this patient? • I would work with the orthodontist on the cleft palate team, and recommend some interceptive procedures as the patient can tolerate them. • She would initially be indicated for space analysis. If she were not able to tolerate any active interceptive therapy, perhaps placement of a mandibular lingual arch to preserve E space would be a good choice. • I would advise the parents that it will be a team effort, especially keeping up with the preventive treatment during orthodontics.

How would you manage the preventive care for this patient? • I would find out if she has any exposure to systemic fluoride, and would make use of topical and systemic fluoride, oral hygiene (with parental supervision), more frequent recare exams, and have a dietary discussion to reinforce healthy snack and eating habits. • She is high caries risk, and in order to maintain her oral health, it will be critical to focus on preventive efforts.

992

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The patient’s mother is concerned about the appearance of her front teeth and asks what can be done for them – her family dentist recommended porcelain veneers. How do you respond? • I would tell the mother that the child is not indicated for veneers at this point because the teeth are not yet fully erupted, there would be too much loss of healthy tooth structure, and she can have a great result with some composite resin bonding on these teeth. • Additionally, they may wish to wait until after we know if she will have orthodontic appliances placed on these teeth. Perhaps it would be best to wait until after ortho to restore these teeth.

During her examination she gets upset and refuses to open her mouth and becomes resistant and physically difficult to manage. Her mother insists you finish the examination. How do you manage the child’s behavior? • First, I would see if it may be best to reschedule for another time. If that wasn’t possible, I’d use communicative behavior management – voice control, distraction (I assume tell-show-do wasn’t working). • If that were unsuccessful, and she absolutely had to have the examination, I would consider protective stabilization. I would show it to her mom, discuss it’s use, and obtain her consent before using it. If the child was still hysterical, I would immediately cease the procedure and recommend we try another day.

993

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994

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Constance M. Killian, D.M.D.

Outline Child Development and Behavior Management of Behavior

995

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Child Development and Behavior

Behavior Basics • Most children develop in the normal range • Behavior has meaning • Development is a series of gains and plateaus • Temperament • Interventions must be built on strengths, not deficits

Child Development and Behavior

Temperament Temperament is the “hard-wiring”

996

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Child Development and Behavior

Temperament Temperament descriptions • Easy • Difficult • Slow to warm up • Mix

Child Development and Behavior

Temperament Temperament can be a predictor of behavioral concerns and problems

997

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Child Development and Behavior

Temperament Development is also influenced by temperament

Child Development and Behavior

Temperament Temperament helps characterize child’s individuality

“Goodness of fit” • match of temperament between parent and child • helps predict adaptability • “fit” of temperament to a given situation

998

Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.

Child Development and Behavior

Temperament Resiliency • Positive demeanor and attitude leads to success • Better predictor than biomedical or sociological

variables

Child Development and Behavior

Attachment Attachment: the emotional bond felt by humans toward special people in their lives • • • •

Occurs during latter part of first year of life Attachment figure is a central to social development Once secure base is established, child is confident in exploring Lack of attachment may relate to behavior difficulties

999

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Child Development and Behavior

Attachment Levels of attachment • •

Secure attachment Insecure attachment

Child Development and Behavior

Temperament-Attachment Relationship • Differences in behavior related to differences in temperament • Children with disruptive behavior usually display attachment disorders and….. vice versa

1000

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Child Development and Behavior

Theories of Child Development Maturational Theory: Hall & Gesell • Development is internally-driven • Basis for the developmental milestones

and age norms • Very little depends on parenting • Development depends on maturation

Child Development and Behavior

Theories of Child Development Psychosexual Theory: (Freud) • Emotional life influences behavior and development • Emotions, dreams, feelings, frustrations matter • Interactions between parent and child influence

personality, resiliency, behavior, and adjustment • Children have an active mental life before speech • Emotional past can help assess current behavior

1001

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Child Development and Behavior

Theories of Child Development Behaviorism Theory: (Pavlov, Watson, Skinner) • Environment-source of behavioral change • Patterns of reinforcement • Conditioning • Stimulus-response • Reward and punishment

Child Development and Behavior

Theories of Child Development Social Learning Theory: outgrowth of behaviorism

• Social context provides feedback on behavior • Integration of internal processes and environment • Development is a series of upward spirals • Social experiences provide feedback for future

development

1002

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1003

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Child Development and Behavior

Application of Behavioral Techniques • Link between behavior and consequence • Consistency • Timing • Rewards better than punishment

Child Development and Behavior

Application of Behavioral Techniques Piagetian Principles: Jean Piaget • Children think differently than adults • Cognitive development proceeds in distinct

stages – based on age • Children learn through interaction with environment • Child is an active learner not a passive responder

1004

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Child Development and Behavior

Piagetian Stages of Cognitive Development Piagetian Stages of Cognitive Development Stage

Age (years)

Way of Understanding

Sensorimotor

birth - 2

Direct sensations

Preoperational

2-6

Own perceptions

Concrete operations

6 - 11

Reason using stable rule system

Formal operations

> 12

Abstract thought, can reason about ideas

Child Development and Behavior

Language Development What is the role of language in dentistry? • Interaction with child • Communicative behavior guidance • Detection problems in language development

1005

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Child Development and Behavior

Language Development How does language develop? • Sound recognition • Comprehension = understanding • Production of sounds/words • Accelerates rapidly during second year of life • Early Language Milestone Scale

Child Development and Behavior

Language Development What is the connection between language and cognitive development? • Language delay related to verbal-based

learning disabilities • Atypical language development related to global developmental delay

1006

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Child Development and Behavior

Language Development Language/Speech Delay • More subtle than motor development delay • Epidemiology • Causes – – – – – – –

Mental retardation – >50% Hearing loss Maturation delay Bilingualism Psychosocial deprivation Autism Cerebral Palsy

1007

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Child Development and Behavior

Behavioral Theory and Dentistry • Behavior in the dental setting is related to overall behavior • Understanding the theories of behavior helps us to understand • Child/parent interaction • Child temperament and attachment issues • Behavioral disorders

Chil