Feline Dentistry: Oral Assessment, Treatment, and Preventative Care

FELINE DENTISTRY Oral Assessment, Treatment, and Preventative Care

FELINE DENTISTRY Oral Assessment, Treatment, and Preventative Care Jan Bellows

A John Wiley & Sons, Inc., Publication

Edition first published 2010 © 2010 Jan Bellows Blackwell Publishing was acquired by John Wiley & Sons in February 2007. Blackwell’s publishing program has been merged with Wiley’s global Scientific, Technical, and Medical business to form Wiley-Blackwell.

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Bellows, Jan. Feline dentistry : oral assessment, treatment, and preventative care / Jan Bellows. p. ; cm. Includes bibliographical references and index. ISBN 978-0-8138-1613-5 (hardback : alk. paper) 1. Veterinary dentistry. 2. Cats–Diseases. I. Title. [DNLM: 1. Tooth Diseases–veterinary. 2. Cats. 3. Dental Care–veterinary. 4. Mouth Diseases–veterinary. SF 867 B448f 2010] SF867.B447 2010 636.8′08976–dc22 2009031848 A catalog record for this book is available from the U.S. Library of Congress. Set in 9.5/12 pt Palatino by Toppan Best-set Premedia Limited Printed in Singapore 1

2010

Dedication

This text is dedicated to Dr. Colin E. Harvey Throughout his professional life, Dr. Colin Harvey has taught and mentored others while creating and maintaining the foundation of veterinary dentistry in the United States and around the world. Dr. Harvey graduated from the School of Veterinary Science at the University of Bristol, England, in 1966. He completed an internship and residency in small animal surgery at the University of Pennsylvania, receiving the Diploma of the American College of Veterinary Surgeons in 1972. Dr. Harvey is a diplomate of the American College of Veterinary Surgeons (1972), member of the Organizing Committee and charter diplomate of the American Veterinary Dental College (AVDC, 1988) and the European Veterinary Dental College (1998), and also a charter diplomate of the European College of Veterinary Surgeons (1993). He was section chief of Small Animal Surgery (1974–80) and vice-chair of the Department of Clinical Studies (1996–2002) and was the founding head of the Dentistry and Oral Surgery Service at the University of Pennsylvania (the first dentistry and oral surgery service to be established at a veterinary school in North America). Dr. Harvey has received numerous university, national, and international awards for excellence in teaching, research, and clinical work. He was elected a fellow of the College of Physicians of Philadelphia in 1980. Dr. Harvey has been a board member (1978–83) of

the Comparative Respiratory Society, secretary (1985– 89) of the American Veterinary Dental Society, president (1990–92) and executive secretary (2002–present) of the American Veterinary Dental College, cofounder (1985) of the International Veterinary Ear Nose and Throat Association, charter fellow and secretary-treasurer (1987–89) of the Academy of Veterinary Dentistry, and director (1997–present) of the Veterinary Oral Health Council. Dr. Harvey was editor of the Journal of Veterinary Surgery from 1982 to 1987 and editor of the Journal of Veterinary Dentistry from 1994 to 2000 and has been a reviewer or review board member for numerous other journals. His publications include approximately 70 chapters in textbooks, 130 papers in peer-reviewed journals, and over 100 abstracts and other papers on surgical and dental topics. He has written, edited, or coedited five books on small animal surgery and dentistry. Dr. Harvey’s research interests include veterinary and comparative periodontal disease (including comparative microbiology, standardization of periodontal scoring, and prevention and treatment); the interaction of infectious oral diseases, particularly periodontal disease, with the rest of the body, specifically, distant organ and systemic effects; and the utility and effectiveness of antimicrobial drugs in the management of patients with oral diseases. Feline dentistry has been of special interest to Dr. Harvey. Much of what we know about feline dentistry today is largely due to his and his mentees’ uncompromised research and discovery efforts.

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Contents

Preface, viii Acknowledgments, ix Introduction, x Section I.

Oral Assessment, 3

Chapter 1.

Anatomy, 5

Chapter 2.

Oral Examination, 28

Chapter 3.

Radiology, 39

Chapter 4.

Charting, 84

Chapter 5.

Oral Pathology, 101

Section II.

Treatment, 149

Chapter 6.

Equipment, 151

Chapter 7.

Anesthesia, 169

Chapter 8.

Treatment of Periodontal Disease, 181

Chapter 9.

Treatment of Endodontic Disease, 196

Chapter 10. Treatment of Tooth Resorption, 222 Chapter 11. Treatment of Oropharyngeal Inflammation, 242 Chapter 12. Treatment of Occlusion Disorders, 269 Chapter 13. Oral Trauma Surgery, 280 Chapter 14. Treatment of Oral Swellings/Tumors, 290 Section III. Prevention, 297 Chapter 15. Plaque Control, 299 Index, 305

vii

Preface

Ah, Cats. What would veterinary dentistry be without them! For sure, a lot simpler and less frustrating. Even for procedures so apparently “simple” as a tooth extraction, the cat often has the last word, when we as veterinary dentists hear that quiet but awful ‘snick’ that means that a tooth root has fractured, leaving a root tip somewhere down there. … Since the first-reported mention of oral disease in cats in the 1920s, a lot of progress has been made, but some key knowledge is not yet available. The immunological function of the cat does not seem to obey the same rules as rodents, dogs, and humans; and as a result, immunologically based conditions such as stomatitis continue to frustrate veterinary dentists. Teeth in cats are attacked

viii

by the body’s own tissues for reasons that are still not clear, and our frustrations are heightened by the lack of success of restoring feline teeth undergoing resorption. Squamous cell carcinoma is by far the most common feline oral neoplasm, benign or malignant; and it resists all standard treatments used in management of other malignancies. When we add in that anesthesia is essential for all feline dental procedures (lest our fingers be impaled by the needle-like, plaque-coated canine teeth) and that cats have such a little mouth compared with dogs, it is not surprising that there is some love-hate aspect to the relationship of veterinary dentists to cats. The challenge is one to rise to, and the companionship cats offer makes it all worthwhile. A book dedicated to feline dentistry and related topics is overdue. I am pleased that Dr. Bellows has found the time to pull the material together in a coherent format, so that others may build upon the accumulated experience and knowledge that are described here. Those delicate feline oral structures require all the skill and knowledge that we have and deserve our best efforts to ensure that we are not continuously restarting the steepslope part of the learning curve. Colin E. Harvey

Acknowledgments

The author acknowledges and greatly appreciates the selfless efforts of many in the production of this text. First to my wife Allison who has always supported and encouraged my passion to do the best for my patients and help other veterinarians do their best too. Next my children Wendi, David, and Lauren who have helped in the practice and have been there every step of the journey. Dr. Carlos Rice, currently a dental resident at University of Wisconsin, on a four-month volunteer stint at All Pets Dental in Weston helped catalog thousands of images from our client base to be considered for inclusion in this text. Dr. Rice also reviewed the final text. Dr. Gary Edelson also volunteered to review the text word by word multiple times. His attention to detail is much appreciated. Drs. Gregg DuPont and Alex Reiter reviewed every word and image in this text. They are expert veterinary dentists with decades of teaching and practical experience. Both share a passion for the best in companion animal dental care based on solid peer-reviewed information where available. Their input resulted in the work you have before you.

Additionally, I acknowledge the American Veterinary Dental College (AVDC) in their efforts to “get things right.” I have had the pleasure and honor of being a member and chairman of the college’s nomenclature committee since 2004, during which time the college has improved classifications for tooth resorption stages and types, fractures, periodontal disease, and many anatomical terms. I acknowledge and thank Dr. Paul Pion, the originator of the Veterinary Information Network (VIN). Dr. Pion strives to improve the veterinary community on all levels. Through the give and take on VIN’s message forums, we learn from each other. I also thank Dr. Pion for the use of his talented full-time graphic artist, Tamara Rees, who provided illustrations for the AVDC and this text. Finally, I can’t say enough about the publisher of this text, Wiley-Blackwell. Working with Nancy Simmerman, the Editorial Assistant, has been a pleasure from our initial discussions, in early 2006, throughout the process to the final submission of the manuscript.

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Introduction

Cats are not dogs. Small dogs are plagued primarily with various degrees of periodontal disease (gingivitis and periodontitis). Large dogs more commonly present with gingivitis, fractured teeth, and oral masses. Feline Dentistry: Oral Assessment, Treatment, and Preventative Care was born primarily to give cats their fair due, a book on dentistry dedicated solely to their species. Cats also are affected by periodontal disease and fractured teeth, but their main oral pathologies include tooth resorption, oropharangyeal inflammation, and maxillofacial cancer. Plaque prevention products and techniques covered in this text also differ from those used in dogs. The second goal in writing this text is to introduce to some and reinforce to others the paradigm shift eliminating the terminology “doing a dentistry,” “performing a prophy,” or “Max is in for a dental.” Replacing the old terminology with “oral assessment, treatment, and prevention,” better represents what we do as veterinary dentists. Assessment involves evaluation of the patient before the anesthetic procedure and includes medical and dental history, feeding management, home oral hygiene, and physical and laboratory testing. Once the patient is anesthetized, a tooth-by-tooth examination is conducted to create a treatment plan. Treatment with the goal of eliminating non-functional abnormalities uncovered during assessment is next. The treatment plan often can be accomplished within one anesthetic visit. In some instances, multiple visits or lifelong therapy are indicated. Prevention of periodontal disease is aimed at controlling plaque. Prevention is as important as the assessment and treatment steps. Without prevention, there is

x

little doubt that periodontal disease will either continue or worsen. Plaque control methods must be specifically tailored to the patient and client in order to be effective. Through daily use of the oral assessment, treatment, and prevention process, patients can get the best in veterinary dentistry, which is our ultimate goal. Although a genuine effort has been made to assure that the dosages and information included in this text are correct, errors may occur, and it is recommended that the reader refer to the original reference or the approved labeling information of the product for additional information. Dosages should be confirmed prior to use or dispensing of medications. Jan Bellows, D.V.M. Diplomate, American Veterinary Dental College Fellow, Academy Veterinary Dentistry Diplomate, American Board of Veterinary Practitioners

FELINE DENTISTRY Oral Assessment, Treatment, and Preventative Care

Section I

Oral Assessment

Chapter 1

Anatomy

An understanding and appreciation of feline dental pathology, treatment, and prevention requires a deep awareness of the structure and function of oral tissues that are composed of the teeth and supporting tissues.

Oral Cavity The oral cavity extends from the lips to the pharynx, bounded laterally by the cheeks, dorsally by the palate, and ventrally by the tongue and intermandibular tissues. The oral cavity is divided into the oral cavity proper and the oral vestibule. Within the oral cavity proper are the hard palate, soft palate, tongue, and the floor of the mouth. Caudally, the oral cavity proper ends at the palatoglossal folds. The oral vestibule spans between the lips, cheeks, and dental arches. The labial vestibule is the space between the incisors, canines, and lips. The buccal vestibule is the space between the cheek teeth and the cheeks (figs. 1.1 a–g).

Mucosa Oral mucosa covers the surface of the mouth. The outer layer is composed of variably pigmented nonkeratinized and parakeratinized stratified squamous epithelium. The submucosa is composed of loose connective tissue, salivary glands, blood vessels, muscle fibers, lymphatics, and salivary ducts. The submucosa of the palate is composed of dense collagen.

Muscles The muscles of mastication that close the jaws are the temporal, masseter, and medial and lateral pterygoid muscles, all of which are innervated by the mandibular nerve (the only motor branch of the trigeminal nerve). The digastricus muscle opens the mouth. Its rostral belly is innervated by the mandibular branch of the trigeminal nerve, while its caudal belly is innervated by the facial

nerve. The body (the rostral two-thirds) of the tongue is attached ventrally to the midline of the floor of the mouth by the lingual frenulum.

Tongue The tongue has important functions in grooming, eating, drinking, and vocalization. The tongue is composed of both striated intrinsic and extrinsic muscles. The body of the tongue comprises the rostral two-thirds. The root comprises the caudal one-third and is attached to the hyoid apparatus. The dorsal surface of the tongue is covered by keratinized stratified squamous epithelium that forms papillae. The tongue of a cat is populated by filiform, fungiform, vallate, foliate, and conical papillae. Filiform and fungiform papillae occupy the dorsal surface of the tongue body. Vallate papillae separate the tongue body and root dorsally. Vallate, foliate, and conical papillae occupy the tongue root (figs. 1.2 a, b). Pillars of mucosa and the palatoglossal folds extend to the soft palate at the base of the tongue (fig. 1.3). The ventral tongue surface contains less cornified mucosa. The lingual frenulum connects the tongue to the floor of the mouth within the intermandibular space.

Innervation Sensory input is received from maxillary and mandibular divisions of the trigeminal nerve. The maxillary branch leaves the trigeminal ganglion, then exits the cranial cavity through the foramen rotundum, courses through the alar canal and the pterygopalatine fossa to enter the infraorbital canal. Just before entering the caudal limit of the infraorbital canal, the nerve branches to become the major and minor palatine nerves. These nerves innervate the hard and soft palates and the nasopharynx. The palatine nerves are desensitized with the maxillary nerve block. 5

d

a

e

b

f

c

6

Figure 1.1 a–g Mucosal surfaces of the oral cavity (all images © 2009 Dr. Alexander M. Reiter).

g Figure 1.1 Continued

Figure 1.3

Palatoglossal fold inflammation.

b

a Figure 1.2

a. Tongue and papillae 1. Filiform papillae; 2. Fungiform papillae; 3. Foliate papillae; 4. Vallate papillae. b. Filiform papillae.

7

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Feline Dentistry

The maxillary branch of the trigeminal nerve also gives off the caudal maxillary alveolar nerve, which innervates the maxillary first molar, the buccal gingiva, and mucosa. This area is blocked with the infraorbital nerve block. After giving off the caudal maxillary alveolar nerve, the maxillary nerve enters the infraorbital canal, where it is called the infraorbital nerve. While the infraorbital nerve is traversing the infraorbital canal, it gives off two more branches that exit ventrally from the canal. The middle maxillary alveolar nerve innervates the premolars and associated buccal gingiva. The rostral maxillary alveolar nerve supplies the canines, incisors, and associated buccal gingiva. The remaining fibers of the infraorbital nerve then exit the rostral extent of the infraorbital canal to innervate the lateral and dorsal cutaneous structures of the rostral maxilla and upper lip. The middle maxillary alveolar, rostral maxillary alveolar, and the infraorbital nerves are anesthetized by the rostral infraorbital nerve block. The mandibular division of the trigeminal nerve arises from the trigeminal ganglion, exits the cranium via the foramen ovale, and divides into multiple branches. The divisions include the sensory buccal nerves, lingual nerve, and mandibular (inferior alveolar) nerve. The buccal nerves receive stimuli from the facial musculature, skin and mucosa of the cheek, and buccal gingiva along the caudal mandible. The hypoglossal nerve innervates the tongue, the floor of the mouth, the lingual gingiva, and the mandibular salivary gland. The mandibular nerve enters the mandible on the lingual side, via the mandibular foramen. The nerve then courses rostrally within the mandibular canal to innervate the mandibular teeth to the midline. This nerve can be blocked with the mandibular (inferior alveolar) nerve block. Rostral to the third premolar tooth, the mandibular nerve gives off mental nerve branches. These branches exit through the mental foramina (rostral, middle, and caudal) and innervate the cutaneous areas of the chin and lip, and the rostral buccal gingiva and mucosa. These nerves are blocked with the mental nerve blocks (usually the middle mental nerve is blocked).

Blood Supply and Lymphatic Drainage The external carotid arteries branch off to the maxillary arteries. They further supply the mandibular (inferior alveolar) arteries, which enter the mandibular foramina on the medial sides of the mandibles and then course rostrally in the mandibular canals, where they exit through the mental foramina.

The maxillary arteries also give rise to the major palatine arteries, which anastomose with the infraorbital arteries. The infraorbital arteries exit at the infraorbital foraminae to supply the rostral muzzle. Lymph from the oral cavity drains into the parotid, mandibular, lateral, and medial retropharyngeal, superficial, and deep cervical lymph nodes.

Salivary Glands The major salivary glands in the cat include the parotid, zygomatic, mandibular, and sublingual. Saliva from the parotid gland exits at a papilla in the alveolar mucosa, just caudal to the maxillary fourth premolar. Saliva from the zygomatic gland exits at a papilla in the alveolar mucosa near the maxillary first molar. Saliva from the mandibular and sublingual glands enters the oral cavity through the sublingual caruncles located ventral and rostral to the base of the tongue (figs. 1.4 a, b). Cats have four molar salivary glands. The buccal molar glands empty into the oral cavity through several small ducts. The lingual molar glands are located in the membranous molar pad linguodistal to the mandibular first molar teeth (fig. 1.5).

Periodontium The term periodontium is used to describe tissues that surround and support the teeth, including the gingiva, periodontal ligament, cementum, and alveolar bone.

Gingiva The cat’s oral cavity is lined with keratinized and nonkeratinized stratified squamous epithelium. Gingiva refers to the keratinized oral mucosa that covers the alveolar process and surrounds the cervical portion of the tooth crowns. Unlike the epithelial lining of the digestive tract, the gingiva does not have absorptive capacity but acts as a physiologic permeable barrier that protects underlying structures (fig. 1.6). The gingival epithelium is composed of the following:

•

•

The oral epithelium, also called the outer gingival epithelium, which is keratinized or parakeratinized and covers the oral surface of the attached gingiva and gingival papillae. The sulcular epithelium is a nonkeratinized extension of the oral epithelium into the gingival sulcus. The bottom of the gingival sulcus in a periodontally

Anatomy

9

Figure 1.5 Membranous bulge linguodistal to the mandibular first molar tooth containing a minor salivary gland (lingual molar gland).

a

b Figure 1.4

•

a and b. Sublingual caruncle.

healthy tooth should be slightly coronal to the cementoenamel junction. The junctional epithelium attaches to enamel of the most apical portion of the crown by means of hemidesmosomes and lies at the floor of the sulcus, immediately coronal to or at the cementoenamel junction. The junctional epithelium and gingival connective tissue separate the periodontal ligament from the oral environment. The floor of the gingival sulcus is located on the most coronal junctional epithelial cells.

Marginal gingiva is the most coronal (toward the crown) aspect of the gingiva that is not attached to the

Figure 1.6 Oral mucosa in a patient with gingivitis, periodontitis, and caudal mucositis.

tooth but lies passively against it. When healthy, it appears coral-pink, firm, and with knife-edged margins. Pigment may or may not be normally present. The space between the tooth and the marginal gingiva is the gingival sulcus (or crevice). The normal depth of the sulcus is less than 1 mm in cats. The free gingival margin is the coronal edge of the marginal gingiva. Marginal gingiva is demarcated from

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Feline Dentistry

Figure 1.7 Gingival structures surrounding the left maxillary fourth premolar.

the attached gingiva by the gingival groove, a slight depression on the gingiva corresponding to the normal sulcus depth (fig. 1.7). In the cat, the healthy free gingival margin of premolars and molars lies between 0.5 and 1 mm coronal to the cementoenamel junction, where root cementum meets crown enamel. The attached gingiva is located apical to the marginal gingiva and is normally tightly bound to the periosteum of alveolar bone. Attached gingiva is keratinized to withstand the stress of mastication. The width of the attached gingiva varies in different areas of the mouth. The attached gingiva is widest at the maxillary canines. The firmly attached gingiva is contiguous with loose alveolar mucosa at the mucogingival junction, also referred as the mucogingival line. The mucogingival junction remains stationary throughout life, although the gingiva around it may change in height due to attachment loss (figs. 1.8 a, b). The gingival sulcus is a shallow space between the marginal gingiva and the tooth. The sulcus depth is generally under 1 mm but varies depending on the specific tooth and the size of the cat. In cases of periodontal disease, the abnormal sulcus is termed a pocket, which extends further apically due to destruction of the periodontium (figs. 1.9 a, b).

Periodontal Ligament The periodontal ligament is a dense, fibrous connective tissue that attaches the tooth root to the bony alveolus. The periodontal ligament also acts as a suspensory cushion against occlusal forces and as an epithelial attachment to keep debris from entering deeper tissues. The blood supply to the periodontal ligament originates from the alveolar artery. Arterioles enter the liga-

ment near the apex of the root and from lateral aspects of the alveolar socket and branch into capillaries within the ligament along the long axis of the tooth. Collagen fibers also run through these spaces. The blood vessels are closer to the bone than to the cementum. Venules drain the apex through apertures in the bony wall of the alveolus and into the marrow spaces. Nerve bundles enter the periodontal ligament through numerous foramina in the alveolar bone. They branch and end in small rounded bodies near the cementum. The nerves carry pain, touch, and pressure sensations and form an important part of the feedback mechanism of the masticatory apparatus. The periodontal ligament has great adaptive capacity. It responds to chronic functional overload by widening to relieve the load on the tooth. Vascular communications between the pulp and periodontium form pathways for transmission of inflammation and microorganisms between the tissues.

Cementum Cementum covers the root and provides attachment for the periodontal ligament. Cementum is produced continuously, slightly increasing in thickness throughout life. Acellular cementum is present at the coronal onethird of the root. Cellular cementum is present at the apical two-thirds of the root. It is capable of formation, destruction, and repair. It is avascular but is nourished from vessels within the periodontal ligament. Cementocytes in cellular cementum communicate with each other via canaliculi and with underlying dentin.

Alveolar Bone Alveolar processes house the alveoli, which support the teeth by providing attachment for fibers of the periodontal ligament. An alveolus can be divided into two parts: 1.

2.

Alveolar bone proper, which is a thin layer of bone surrounding the root and allowing attachment to the periodontal ligament. Supporting alveolar bone, which consists of compact, cortical, or cancellous bone on the vestibular and oral aspects of the alveolar process.

The alveolar bone and cortical plates are thickest in the mandible. The shape and structure of the trabeculae of spongy bone reflect the stress-bearing requirements of a particular site. In some areas, alveolar bone is thin with no spongy bone. The alveolar bone proper is also referred to as the cribriform plate and is identified on radiographs as lamina dura (fig. 1.10). The alveolar bone height is an equilibrium between bone formation and bone resorption. When bone

a

b Figure 1.8

a. Gingival structures surrounding the right maxillary cheek teeth. b. Mandibular fourth premolar area.

11

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Feline Dentistry

a Figure 1.9

b a. Periodontal probe with millimeter markings before insertion. b. 3-mm palatal probing depth of the left maxillary canine.

resorption exceeds formation, the alveolar bone height is reduced (figs. 1.11 a, b).

Bones and Joints Cranium The dorsal aspect of the cranium is composed of the paired frontal and parietal bones. The occipital region of the cranium is the caudal aspect of the skull formed by the occipital bone. The temporal region is composed of the lateral walls of the cranium formed by the temporal bones. The rostral wall of the cranium is formed by the ethmoid bone (figs. 1.12 a, b).

Facium

Figure 1.10 Lamina dura (arrows pointing to the white line surrounding the tooth root).

The facial part of the skull, which encloses the nasal and oral cavities, is divided into oral, nasal, and orbital regions. The oral region surrounding the oral cavity is composed of the incisive, maxillary, palatine, and mandibular bones. The region surrounding the nasal cavity is composed of the nasal, maxillary, palatine, and incisive bones. The orbital region is formed by the frontal, lacrimal, palatine,

a Figure 1.11

b a. Alveolus encasing a fractured maxillary canine tooth. b. Decreased alveolar margin height (arrows) secondary to periodontal disease.

Figure 1.12 a. Left lateral aspect of the skull with the zygomatic arch removed; 1. Parietal bone; 2. Squamous temporal bone; 3. Sphenopalatine foramen; 4. Maxilla; 5. Incisive bone; 6. Frontal bone; 7. Lacrimal bone; 8. Optic canal. b. Medial aspect of a sagittal section of the left aspect of the skull: 1. Incisive bone; 2. Maxilloturbinates; 3. Nasal bone; 4. Nasal septum; 5. Palatine bone; 6. Pterygoid bone; 7. Ethmoid bone. c. Dorsal aspect of the skull: 1. Incisive bone; 2. Nasal bone; 3. Maxilla; 4. Frontal bone; 5. Zygomatic process of frontal bone; 6. Zygomatic bone; 7. Parietal bone; 8. Zygomatic process of temporal bone; 9. Lacrimal foramen; 10. Infraorbital foramen. d. Ventral aspect of the skull: 1. Incisive bone; 2. Palatine process of the maxilla; 3. Major palatine foramen; 4. Vomer bone; 5. Pterygoid bone; 6. Frontal bone; 7. Palatine bone; 8. Temporal process of the zygomatic bone; 9. Zygomatic process of the temporal bone; 10. Retroarticular process; 11. Mandibular fossa of the articular surface of the temporomandibular joint. (Images reprinted with permission of Morton Publishing Company.)

a

b 13

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Feline Dentistry

c

d

Figure 1.12 Continued

sphenoid, and zygomatic bones surrounding the orbit (figs. 1.12 c, d).

Maxillary Region The maxillary bones or maxillae form the lateral parts of the face and the part of the hard palate that holds the canine and upper cheek teeth. The maxilla articulates with the incisive bone rostrally, the nasal bone dorsally, the vomer bone medially, and the lacrimal and zygomatic bones caudally (figs. 1.13 a, b). The palatine bone forms the bony part of the hard palate together with the maxillary and incisive bones. The incisive bone located rostrally holds the upper incisors. A pair of openings, the palatine fissures, allows passage of the incisive ducts of the vomeronasal organ. The incisive papilla located just caudal to the maxillary first incisor teeth houses these incisive ducts as they open into the oral cavity (figs. 1.14 a, b). The hard palate separates the oral and nasal cavities. The primary palate is the incisive portion of the palate and associated soft tissues. The secondary palate includes the remaining hard and soft palatal structures. Firmly

attached, heavily keratinized mucosa covers the hard palate. Seven to eight transverse ridges called rugae protrude from the mucosa with rows of papillae between the ridges. The soft palate begins caudal to the maxillary first molar teeth and separates the nasopharynx dorsally and oropharynx ventrally (figs. 1.15 a, b). The infraorbital canal is located apical to the maxillary third and fourth premolars below the orbit. Compared to the dog, the cat’s infraorbital canal is shorter and usually less than five millimeters in diameter.

Mandibles The large bones articulating with the skull that support the lower teeth are the mandibles. Each mandible is composed of a horizontal body and a vertical ramus. The body supports the lower teeth. The ramus has three processes: coronoid, condylar, and angular. The condylar process articulates with the cranium in the temporomandibular joint (figs. 1.16 a–c). The mandibles are connected to each other by a strong fibrocartilaginous joint at the mandibular symphysis. The nerves and vascular supply to the mandibular teeth

Anatomy

15

a

a

b Figure 1.14

a. Palatine fissures. b. Incisive papilla.

Temporomandibular Joint

b Figure 1.13 a. Lateral aspect of right maxilla: 1. Alveolar process; 2. Frontal process; 3. Infraorbital canal; 4. Zygomatic process. b. Medial aspect of the right maxilla: 1. Maxillotubinates; 2. Palatine process.

The head of the condylar process of the mandibular ramus articulates with the base of the zygomatic process of the squamous part of the temporal bone (mandibular fossa) at the temporomandibular joint: a transversely elongated (cigar-shaped), condylar, synovial joint (fig. 1.18). The retroarticular process is a caudoventral extension of the mandibular fossa. The retoarticular process helps prevent caudal luxation of the mandible (fig. 1.19). The insertion of the masseter muscle reaches the ventral and rostral aspect of the joint capsule. There is a thin, cartilaginous intra-articular disc dividing the joint into dorsal and ventral compartments. This disc reduces friction by providing a double synovial film.

Teeth enter the mandibular canal ventrally on the lingual aspect of the angle of the mandible and course rostrally exiting at the caudal, middle, and rostral mental foramina to supply the rostral mandible, chin, lip, buccal gingiva, and mucosa (figs. 1.17 a–c). The tongue and some of the muscles of the hyoid apparatus occupy the intermandibular space.

Dental Formula Normally, there are twenty-six deciduous and thirty permanent teeth in the cat’s oral cavity. Dental formulas (upper number indicates the maxillary teeth, lower number the mandibular teeth) are as follows:

a

b

16

Figure 1.15 a. Sagittal section of dissected head: 1. Choana; 2. Nasopharynx; 3. Epiglottis; 4. Palatine tonsil in tonsilar fossa; 5. Oropharynx; 6. Oral cavity; 7. Hard palate b. Roof of the oral cavity, 1. Hard palate, 2. Palatine rugae, 3. Palatine tonsil, 4. Stick in nasopharynx, 5. Epiglottis (reflected laterally) 6. Palatoglossal arch, 7. Soft palate.

a

b

Figure 1.16 a. Lower jaw. b. Right mandible buccal aspect: 1. Mandibular body; 2. Mandibular ramus; 3. Masseteric fossa; 4. Coronoid process; 5. Condyloid process; 6. Angular process; 7. Middle mental foramen; 8. Caudal mental foramen. c. Right mandible lingual aspect: 1. Mandibular symphysis articular surface; 2. Mandibular foramen.

c

a

b

c

Figure 1.17 a. Mandibular symphysis dorsal view. b. Mandibular symphysis rostral view showing the mental foramina (arrows). c. Mental foramina.

17

Figure 1.18 Temporomandibular joints ventral view: 1. Retroarticular process; 2. Mandibular fossa; 3. Condylar process; 4. Angular process.

Figure 1.19 Lateral aspect of the left temporomandibular joint: 1. Coronoid process; 2. Zygomatic arch; 3. Zygomatic process of the temporal bone; 4. Mandibular ramus; 5. Condylar process; 6. Articular eminence; 7. Tympanic bulla; 8. Mandibular fossa; 9. Retroarticular process; 10. Angular process.

18

Anatomy

• •

The deciduous dental formula for kittens is 2 × (I3/ I3, C1/C1, P3/P2) = 26 teeth. The permanent dental formula for adult cats is 2 × (I3/I3, C1/C1, P3/P2, M1/M1) = 30 teeth.

All of the incisors and canine teeth have one root. The maxillary second premolar, if present, normally has one root; however, studies have shown nearly 40% of the maxillary second premolars have two (sometimes fused) roots. The maxillary third premolar has two roots in most cases (10% of the maxillary third premolars have a small third root), and the maxillary fourth premolars have three roots. The maxillary first molars, if present, usually have two roots. The mandibular cheek teeth in a cat (third and fourth premolars and first molars) have two roots.

Tooth Types Teeth are categorized by location and form. There are four types of teeth in the cat:

Figure 1.20

Maxillary and mandibular incisors.

19

Incisors are small teeth located between the canines. They are used for prehension. Incisors are referred to as right/left, maxillary/mandibular, first, second, and third incisors (fig. 1.20). When using the modified Triadan system, right maxillary incisors are numbered 101, 102, and 103 starting from the first incisor, and left maxillary incisors are numbered 201, 202, and 203. The left mandibular incisors are numbered 301, 302, 303, and the right mandibular incisors are 401, 402, 403 (fig. 1.21). Canines are single-rooted teeth located rostrally in the mouth caudolateral to the incisors. They are used for piercing and biting. Canines are referred to as right/left, maxillary/mandibular canines. The crowns of the maxillary and mandibular canine teeth have vertical grooves (figs. 1.22, 1.23). When using the modified Triadan system, the right and left maxillary canines are numbered 104 and 204, respectively. The root and crown of the maxillary canines help to hold the upper lip outward, so that when the mouth is closed, the coronal tip of the mandibular canine

Figure 1.21 Modified Triadan system incisor tooth numbering.

Figure 1.23

Figure 1.22 Extracted canine tooth.

20

Mandibular canine vertical groove.

Anatomy

slides into the vestibule without traumatizing the upper lip. The left and right mandibular canines are numbered 304 and 404, respectively (in the modified Triadan system, all the canines end in 4 and first molars in 9) (figs. 1.24 a, b; 1.25).

a

Premolars are located caudal to the canines. There are normally three maxillary and two mandibular premolars in the cat. Proper nomenclature of feline premolars is based on the archetypal carnivore model, which has a full dentition of forty-four teeth (six incisors, four canines, sixteen premolars, and twelve molars). The premolar behind the maxillary canine is termed the right or left maxillary second premolar (fig. 1.26). Using the modified Triadan system, the second premolars are referred to as tooth 106 (right) or 206 (left). The second premolar has one or two fused roots. The third premolars (107, 207) have two roots. The fourth premolars (108, 208) have three roots (mesiobuccal, mesiopalatal, and distal)(fig. 1.27). The premolar behind the mandibular canine is termed the left or right mandibular third premolar (307, 407),

b Figure 1.24 Modified Triadan canine tooth numbering: a. Maxillary canines. b. Mandibular canines.

Figure 1.25

21

Figure 1.26

Maxillary premolars.

Figure 1.27

Maxillary fourth premolar.

Normal canine tooth occlusion.

22

Feline Dentistry

followed by the fourth premolar (308, 408), which has two roots (figs. 1.28 a, b). Molars are located caudal to the premolars. There is one set in the maxilla termed right or left maxillary first molar (109, 209) and one set in the mandible termed left or right mandibular first molar (309, 409). The mandibular first molar has one large mesial root and a smaller distal root, which angles caudally (figs. 1.29, 1.30 a–d).

Tooth Composition The exterior surface of the healthy crown is covered with a thin layer of enamel, a hard inorganic substance (96% inorganic) formed by ameloblasts within the tooth bud before eruption. Enamel when damaged is incapable of repair once the tooth has erupted. Dentin located beneath the enamel and cementum composes the majority of the mature tooth mass. Dentin is a specialized connective tissue of mesenchymal origin and is the second hardest tissue in the body after enamel. It is 70% inorganic and 30% organic (water, collagen, and mucopolysaccharide).

Dentin is porous; each square millimeter contains over 40,000 dentinal tubules that communicate between the pulp and the dentin-enamel or dentin-cementum junctions. If there is near-pulp exposure from trauma or resorption, bacteria can travel through the exposed dentinal tubules to the pulp. Near exposure can also transmit painful stimuli (heat, cold, pressure) from the oral environment to the pulp. In cats and other species including the dog, two microscopic features of the dentin known as vasodentin and osteodentin may occasionally exist. Vasodentin is characterized by microscopic vascular inclusions within the outer third of the dentin. It is found to have vascular channels and dentinal tubules coursing through vasodentin randomly. Osteodentin, unlike vasodentin, is most often found in the dentin adjacent to the root canal. Previous studies have demonstrated the presence of these two peculiar microscopic structures in cats with tooth resorption. However, vasodentin and osteodentin have also been found in teeth free of resorption, making a cause-and-effect relationship difficult to confirm. The pulp, located in the center of the tooth, is composed of connective tissue, nerves, lymph and blood vessels, collagen, and odontoblasts, which form dentin throughout the tooth’s life. The pulp cavity consists of a pulp chamber located in the crown and a root canal in

a

b Figure 1.28 a. Teeth of the lower jaw. b. Right mandibular premolars.

Figure 1.29

Dissected left mandibular first molar.

Anatomy

23

b

a

c

d Figure 1.30 a. Modified Triadan system numbering of teeth in the upper jaw. b–d. Modified Triadan system numbering of teeth in the lower jaw.

the root. In a fully mature tooth, an apical delta containing minute openings allowing the passage of vessels and nerves is present at the root apex. Occasionally, there are communication canals present at the furcation of the maxillary fourth premolar and other multirooted teeth (fig. 1.31). During pre-eruptive development and during eruption, the odontoblasts produce primary dentin. Once the

tooth has developed to its final length, the odontoblasts produce secondary dentin, causing the dentinal walls to thicken toward the pulp cavity. This will effectively decrease the width of the pulp cavity as the cat ages. Reparative or tertiary dentin is produced in response to thermal, mechanical, occlusal, or chemical trauma to the odontoblasts. The pulp chamber in cats lies closer to the enamel than in dogs. For this reason, any tooth fracture

24

Feline Dentistry

Figure 1.31 Illustration of sagittal section through the canine tooth.

in the cat should be treated aggressively, since most require endodontic therapy or extraction. Odontoblast processes extend into the dentinal tubules. These processes, together with the fine nerve endings, cause the dentin to be sensitive to temperature and pressure. When traumatized, the pulp reacts to irritants through inflammation. If untreated, severe inflammation spreads up and/or down the pulp, eventually becoming irreversible. Toxic products from damaged tissue and microorganisms in the tissue sustain inflammation. The tooth’s anatomical crown is visible to the naked eye. The root is located in the alveolus encased in the alveolar processes beneath the gingiva. The cribriform plate (lamina dura) lines the alveolus (fig. 1.32).

Tooth Eruption The maxillary teeth generally erupt before their mandibular counterparts. Eruption of the incisors precedes that of the canines, which is later followed by the premolars and molars.

The deciduous tooth eruption is normally complete by two months of age. By seven months, the permanent teeth should be fully erupted (Table 1.1).

Terminology Teeth Incisors are referred to as the (right or left, maxillary or mandibular) first, second, or third incisors numbered from the midline. In the cat, the tooth immediately distal to the maxillary canine is the second premolar; the tooth immediately distal to the mandibular canine is the third premolar.

Surfaces of teeth and directions in the mouth (fig. 1.33) Vestibular is the correct term referring to the surface of the tooth facing the vestibule or lips; buccal and labial are acceptable alternatives.

Anatomy

25

Apical delta Alveolar process Lamina dura Trabecular bone Cortical plate

Periodontal ligament

Cementum

Alveolar mucosa Alveoler crest

Mucogingival line

Gingival margin

Attached gingiva Free gingiva Gingival sulcus

Epithelial attachment

Dentin Pulp

Enamel

Figure 1.32

Canine tooth and surrounding structures.

Table 1.1. Approximate age when teeth erupt (in weeks).

Incisors Canine Premolar Molar

Deciduous

Permanent

3–4 3–4 5–6

11–16 12–20 16–20 20–24

The surface of a mandibular or maxillary tooth facing the tongue is the lingual surface. Palatal can also be used when referring to the lingual surface of maxillary teeth. Mesial and distal are terms applicable to tooth surfaces. The mesial surface of the first incisor is next to the median plane; on other teeth it is directed toward the first incisor. The distal surface is opposite the mesial surface.

Figure 1.33 Directions in the oral cavity.

26

Anatomy

Rostral and caudal are the positional and directional anatomical terms applicable to the head in a sagittal plane in nonhuman vertebrates. Rostral refers to a structure closer to, or a direction toward the most forward structure of the head. Caudal refers to a structure closer to, or a direction toward the tail.

Jaws All mammals have two maxillas (or maxillae) and two mandibles. The adjective maxillary is often used in a wider sense, for example, “maxillary fractures” to include other facial bones, in addition to the maxillary bone proper.

Further Reading American Veterinary Dental College. Veterinary dental nomenclature (available at www.avdc.org). Bishop MA, Malhotra M. An investigation of lymphatic vessels in the feline dental pulp. Am J Anat 1990; 187: 247–253. Crossley DA. Tooth enamel thickness in the mature dentition of domestic dogs and cats: preliminary study. J Vet Dent 1995; 12: 111–113. Floyd MR. The modified Triadan system: nomenclature for veterinary dentistry. J Vet Dent 1991; 8(4): 18–19. Gioso MA, Carvalho VGG. Oral anatomy of the dog and cat in veterinary dentistry practice. Vet Clin North Am Small Anim Pract 2005; 35: 763–780. Gracis M. Radiographic study of the maxillary canine tooth of four mesaticephalic cats. J Vet Dent 1999; 16: 115–128. Gracis M. Orodental anatomy and physiology. In: Tutt C, Deeprose J, Crossley D (eds). BSAVA Manual of Canine and Feline Dentistry, 3rd ed. BSAVA, Gloucester, 2007; 1–21. Harvey CE. Anatomy of the oral cavity in the dog and cat. Veterinary Dentistry, WB Saunders, Philadelphia, 1985; 5–22. Harvey CE, Emily PP. Function, formation, and anatomy of oral structures in carnivores, Small Animal Dentistry, Mosby, St. Louis, 1993; 1–18.

27

Hayashi K, Kiba H. Microhardness of enamel and dentine of cat premolar teeth. Nippon Juigaku Zasshi (Japanese Journal of Veterinary Science), 1989; 51: 1033–1035. Hennet P. Dental anatomy and physiology of small carnivores. In: Crossley DA, Penman S (eds). BSAVA Manual of Small Animal Dentistry, 2nd ed. BSAVA, Cheltenham, 1995; 93–104. Hennet PR, Harvey CE. Apical root canal anatomy of canine teeth in cats. Am J Vet Res 1996; 57: 1545–1548. Holland GR. The dentinal tubule and odontoblast process in the cat. J Anat 1975; 120: 169–177. Hudson LC, Hamilton WP. Atlas of Feline Anatomy for Veterinarians. WB Saunders, Philadelphia, 1993. Nanci A. Ten Cate’s Oral Histology, Development, Structure, and Function, 6th ed. Mosby, St. Louis, 2003. Negro VB, Hernandez SZ, Maresca BM, Lorenzo CE. Furcation canals of the maxillary fourth premolar and the mandibular first molar teeth in cats. J Vet Dent 2004; 21: 10–14. Okuda A, Inoue E, Asari M. The membraneous bulge lingual to the mandibular molar tooth of a cat contains a small salivary gland. J Vet Dent 1996; 13: 61–64. Orsini P, Hennet P. Anatomy of the mouth and teeth of the cat. Vet Clin North Am Small Anim Pract 1992; 22: 1265–1277. Rosenzweig LJ. Anatomy of the Cat. Brown Publishers, Dubuque, 1993. Schaller O. Illustrated Veterinary Anatomical Nomenclature, 2nd ed. Enke Verlag, Stuttgart, 2007. Verstraete FJM. Colour Self-Assessment Review of Veterinary Dentistry. Manson, London, 1997. Verstraete FJM, Terpak CH. Anatomical variations in the dentition of the domestic cat. J Vet Dent 1997; 14: 137–140. Vongsavan N, Matthews B. The vascularity of dental pulp in cats. J Dent Res 1992; 71: 1913–1915. Wiggs RB, Loprise HB. Oral anatomy. In: Veterinary Dentistry: Principles and Practice. Lippincott-Raven, Philadelphia 1997, 55–86. Wilson G. Timing of apical closure of the maxillary canine and mandibular first molar teeth of cats. J Vet Dent 1999; 16: 19–21.

Chapter 2

Oral Examination

Treatment planning is based on the results of clinical examination and diagnostic imaging with direction from patient history and dental habits. The best possible treatment outcome is related to an accurate diagnosis. Using a carefully planned examination, the practitioner can recognize both normal and abnormal conditions. A permanent record should be made of relevant medical and dental history and diagnostic data, as well as treatment recommended, performed, and advised for the future.

Patient History Patient history is an important part of the assessment process. Relevant history should include present and past medical information, vaccination status, amount of time spent indoors and outdoors, and information about other animals in the patient’s environment. Discussion of clinical signs related to oral disease in the cat should include difficulty with prehension; difficulty with chewing and/or swallowing food; pawing at the mouth; periodic pain with vocalization when chewing, opening, or closing the mouth; increased salivation with or without hemorrhage; sneezing; nasal discharge; facial swelling; ocular signs; and decreased self-grooming. The intake discussion should include dialogue with the owner concerning their wishes and perception of type and level of service they are expecting to receive. Additionally, the willingness of the client to provide home care, as well as the acceptance of home care procedures by the patient, should be addressed in order to help construct a treatment plan.

Examination of the Conscious Cat Most cats will allow an initial evaluation of their teeth and oral cavity when approached in a slow and gentle manner. The extent of an examination on a nonsedated cat is dependent upon patient cooperation and expertise 28

of the examiner. Some cats are too fractious or painful to inspect without chemical restraint. After a general physical examination, concentrate on the head and face. Signs of facial asymmetry, differences in palpebral sizes, ocular or nasal discharge, discomfort or swelling, pain on palpation, or discoloration should be noted (figs. 2.1 a–g). While looking in the cat’s eyes, palpate along the mandibles and maxillae. Enlarged unilateral or bilateral mandibular lymph nodes should be noted if present during this examination. Holding the head steady in one hand, the rostral portion of the lips is pulled caudally to examine occlusion; missing, extra, or malpositioned teeth; the presence of periodontal disease or oral masses; and fractured, discolored, or resorbed teeth. The mandibular third premolar, often the first tooth affected by tooth resorption, is difficult to observe unless you move the lower lip ventrally (figs. 2.2a–i and 2.3 a, b). During the conscious patient examination, the mouth is opened and closed to evaluate temporomandibular joint movement. To open a cat’s mouth, place one hand on top of the cat’s head with the thumb and forefinger lightly pressing just behind the lip commisures. Pull the lips caudally to reveal the premolars. Tilt the head backward while applying the forefinger of the opposite hand to the mandibular incisor area, pulling the lower jaw ventrally (fig. 2.4). Pain, crepitus, and decreased ability to open or close the mouth are noted on the medical record. Generally, a scissors bite with the maxillary incisors touching and located slightly rostral to the mandibular incisors is considered normal in domestic short hair cats and a majority of the recognized cat breeds. In brachycephalic breeds (Burmese, Himalayan, and Persian), mandibular mesioclusion, where the maxillary incisors are positioned caudal to their mandibular counterparts, is abnormal but considered “normal occlusion” for the breed. Mandibular distoclusion, where the maxillae extend far in front of the mandibles, is not considered normal in any cat breed (figs. 2.5, 2.6, and 2.7).

d

a

e

b

f

c

Figure 2.1 a. Facial swelling secondary to osteomyelitis. b. Mandibular asymmetry secondary to squamous cell carcinoma. c. Horner’s syndrome and mandibular deformity secondary to trauma. d. Decreased palpebral size of the left eye. e. Mild left-sided facial swelling. f–g. Left mandibular swelling and facial staining secondary to complicated mandibular canine tooth fracture.

g 29

a

d

e

b

f c Figure 2.2 a and b. Tooth resorption at the right maxillary fourth premolar. c. Tooth resorption at the right mandibular canine. d–g. Various appearances of tooth resorption at the mandibular third premolar. h. Possible tooth resorption at the left mandibular first molar. i. Tooth resorption confirmed at surgery.

30

g

h

i Figure 2.2 Continued

31

a

b Figure 2.3

a. Discolored left mandibular canine secondary to tooth resorption. b. Discolored left maxillary second incisor secondary to endodontic disease.

Figure 2.5 Figure 2.4 oral cavity.

32

Proper positioning of the right and left hands to examine the

Normal occlusion.

Oral Examination

33

pressure to elicit a pain response; this could indicate the presence of a possible tooth resorption (fig. 2.10). The mandibular canine tooth crowns are normally located in the diastema between the maxillary third incisor and the maxillary canine teeth. There should not be contact between the mandibular canine and maxillary third incisor or maxillary canine when the mouth is closed. Cheek teeth should not occlude (touch each other) as in humans and dogs (fig. 2.11).

Oral Examination under Anesthesia General anesthesia with intubation is essential to properly immobilize the patient for an in depth tooth-bytooth examination, periodontal probing, and intraoral radiography (fig. 2.12). Figure 2.6

Mandibular distoclusion.

Dental Hand Instruments for Examination Periodontal Probe The periodontal probe is used to measure the depth of the gingival sulcus in millimeters to help evaluate the extent of periodontal support. Probes vary in cross-sectional design (rectangular/ flat, oval, or round), with millimeter markings at the calibrated working end. Because the cat’s gingival sulcus is quite narrow, most periodontal probes used in dogs are not appropriate for cats and can cause damage. The author prefers the Michigan O probe with Williams markings at 1, 2, 3, 5, 7, 8, 9, and 10 millimeters (figs. 2.13 a, b).

Figure 2.7

Mandibular mesioclusion.

Probing Depth The dorsal surface of the tongue is examined for symmetry and ulceration. The sublingual area is also visualized for areas of inflammation, swelling, oral masses, and foreign bodies (figs. 2.8 a–e). Healthy gingiva appears light pink. The gingival margin lies next to the tooth 0.5–1 mm coronal to the attached gingiva. Gingival inflammation clinically presents as erythema and causes “rounding” of the originally knife-edged gingival margin. In cats with advanced periodontal disease, attachment loss clinically appears as periodontal pocket formation or gingival recession with root exposure (fig. 2.9). The teeth are grossly inspected for fracture, obvious resorption, and mobility. If the patient will allow, a Q-tip is applied to the gingival/tooth interface with gentle

The clinical or probing depth is the distance between the base of the pocket and the gingival margin. Inserting the periodontal probe into the gingival sulcus and recording millimeter findings is called probing. With gentle pressure, the probe will stop where the gingiva attaches to the tooth. Every professional oral hygiene procedure conducted under general anesthesia should include probing and charting. Cats normally have probing depths less than 1 mm. Greater depths may indicate periodontal disease requiring further evaluation and treatment (figs. 2.14 a, b, c). Two methods of probing are spot and circumferential. Spot probing is the insertion and withdrawal of the probe at a single area per tooth. Because single areas do not represent the entire tooth, an inaccurate assessment may be obtained. Circumferential probing is insertion of

a

c

d

b Figure 2.8 a. Normal-appearing tongue in a cat with extracted mandibular cheek teeth. b. Sublingual tongue mass secondary to squamous cell carcinoma. c. Inflammatory sublingual tongue mass. d. Thickened asymmetric tongue secondary to squamous cell carcinoma.

34

Oral Examination

35

Figure 2.12 General anesthesia necessary for oral assessment, treatment, and prevention.

Figure 2.9 Inflamed gingiva and alveolar mucosa around the maxillary cheek teeth and mucosa of the caudal oral cavity.

a e Figure 2.10 Q-tip gently placed against gingiva to test for bleeding and sensitivity (note: Q-tips can also be used for plaque removal).

b

Figure 2.13 a. University North Carolina probe (Cislak). b. Williams probe (Cislak).

the probe in the sulcus or pocket in at least four places (two buccal and two lingual/palatal) around the tooth, recording millimeter readings. This method compensates for inaccurate readings when subgingival calculus or isolated areas of vertical bone loss are present (figs. 2.15 a, b, c, d).

Clinical Attachment Level Figure 2.11

Normal canine and premolar occlusion.

The clinical attachment level offers greater diagnostic significance compared to the probing depth. Attachment

a

c

b

Figure 2.14 a. Periodontal probe before insertion on the palatal surface of the maxillary fourth premolar. b. 3-mm periodontal pocket. c. 6-mm maxillary canine palatal pocket.

a

c

b

d

Figure 2.15 a–d. Four probed areas around the mandibular third premolar (mesiobuccal, distobuccal, distolingual/distopalatal, mesiolingual/mesiopalatal).

36

Oral Examination

37

a

a

b

c

d

Figure 2.16 a. Number 17 Orban explorer (Cislak). b. ODU explorer (Cislak). c. Shepherd’s hook explorer (Cislak). d. Combination of periodontal probe and explorer (Miltex).

loss or clinical attachment level is determined by measuring the distance from the cementoenamel junction to the pocket base. Alternatively, this measurement is determined by adding the probing depth to the gingival recession measurement (distance between the cementoenamel junction to the gingival margin). Normally, the gingival margin lies less than 1 mm coronal to the cementoenamel junction. With gingival recession, the gingival margin lies apical to the cementoenamel junction. In these cases, the loss of attachment will be greater than the pocket depth.

Dental Explorer A dental explorer has a sharp point (tip) used to examine the tooth for surface irregularities, calculus, resorption, necrotic cementum, and mobility. The explorer can also be used for examination of pulp exposure. The explorer is not used to remove calculus. Explorer examples useful in feline dental pathology assessment include the number 17 Orban explorer, which has a fine 2-mm tip that extends at a right angle from the shank. The O.D.U. (Old Dominion University) number 11/12 is patterned after the Gracey 11/12 curette. The thin tip is especially useful for examining areas of tooth resorption. A Shepherd’s hook explorer, although thicker, can also be used (figs. 2.16 a, b, c, d). Normally, there is a smooth path when the explorer is inserted and withdrawn from the sulcus or pocket.

b Figure 2.17 a. Compressed air applied to suspected tooth resorption of the right maxillary third premolar. b. Explorer used to help confirm presence of tooth resorption of the left maxillary third premolar.

When there is a ledge of subgingival calculus present, the explorer moves over the tooth surface, encounters the ledge, moves laterally over it, and returns to the tooth surface. When fine deposits of subgingival calculus are present, there will be a gritty sensation as the

38

Feline Dentistry

explorer passes over the fine calculus. In cases of tooth resorption and other structural defects, the probe enters the area of dental hard tissue loss (figs. 2.17a, b).

Further Reading Baxter CJK. Oral and dental diagnostics. In: Tutt C, Deeprose J, Crossley D. BSAVA Manual of Canine and Feline Dentistry, 3rd ed. BSAVA, Gloucester, 2007; 22–40.

Harvey EE, Emily PP. Oral examination and diagnostic techniques, Small Animal Dentistry, Mosby, St. Louis, 1993; 19–41. Holmstrom SE, Frost Fitch P, Eisner ER. Dental records, Veterinary Dental Techniques for the Small Animal Practitioner, 3rd ed. Saunders, Philadelphia, 2004; 1–38. Lobprise HB. Treatment planning based on examination results. Clin Tech Small Anim Pract 2000; 15: 211–220.

Chapter 3

Radiology

Dental radiography plays an integral part in most oral assessments. Dental films are indicated for evaluation of apparent pathology, as a way to monitor progression or resolution of treated disease, and as part of the periodic complete dental evaluation. Intraoral radiography offers the capability of viewing pathology below the gingival margin and inside the tooth. Among many other things, it allows us to visibly evaluate tooth vitality; pre-, intra-, and postoperative endodontic treatment; progression of pulpal pathology and/or periodontal disease; and anatomical orientation and documentation of root structure before extraction. Intraoral radiography is also very useful to determine the cause of chronic nasal discharge and to assess the extent of oral neoplasia and severity of maxillofacial trauma. Examination of intraoral films will also allow postoperative evaluation after extraction to confirm all root fragments were removed. It also provides essential information in evaluating tooth resorption and finally provides a baseline record to compare future radiographic studies.

be anesthetized. After approval of the therapy plan and projected fees, the patient is treated. The following is a typical timeline for one patient (other patients are added to the daily schedule depending on availability of anesthesia units and staff):

•

• •

•

• Incorporating Dental Radiography into General Practice Frequently, patients presenting for “routine teeth cleaning and examination” have significant disease. The decision to extract, perform flap surgery, apply local antibiotics, or only clean and polish is made by visual examination, periodontal probing, and dental radiography. Logistically, when the patient is admitted to the hospital for dental evaluation and care, the pet owner cannot receive an accurate treatment plan until a thorough tooth-by-tooth assessment is conducted. The client is encouraged to return to the office or call at a specific time, or is paged usually two or three hours later to discuss the treatment plan based on clinical examination and radiographic findings while the patient continues to

• •

9:00 a.m.: The patient is examined or left for an examination. The owner is advised to call the office or come back at noon for discussion of dental examination and radiographic findings, while the animal is still anesthetized. 9:30–10:30 a.m.: Preoperative laboratory and electrocardiographic evaluation are performed. An intravenous catheter is placed. 10:30–11:45 a.m.: The patient is anesthetized, teeth are cleaned, the mouth is probed and charted, and oral survey radiographs are exposed by the staff. A treatment plan is formulated by the veterinarian and fees are calculated. 12:00 p.m.: The client calls. The veterinarian discusses examination findings, treatment plan, and fees while the technician is completing the dental cleaning procedure. 12:10 p.m.: When the treatment plan is approved, therapy begins. 2:00 p.m.: Therapy is completed (time depends on procedure). 5:00–6:00 p.m.: The patient is discharged, with a discharge order and picture report discussion with the owner.

Radiograph Unit Although the veterinarian may choose to use a conventional whole-body radiograph unit, acquiring high-quality dental images requires a dedicated dental radiograph unit for a multitude of reasons:

•

Shorter film focal length and automatic collimation result in less scattered radiation and radiation exposure to the patient and staff. 39

40

•

•

Feline Dentistry

Ideal tube positioning is greatly facilitated by tube support, arms of various lengths that allow vertical, horizontal, and rotational movement, resulting in less patient repositioning. Radiographs can be obtained on the dental operatory table rather than moving the patient to a dedicated radiography area (figs. 3.1 and 3.2 a, b, c ).

Most dental units are economically priced between US$3,000 and US$5,000, requiring a small cash outlay, and a long arm can reach two closely located operatory areas. The position indicating device (PID) is an extension placed on the tube head at the collimator attachment. To minimize the amount of radiation exposure, the PID is lead lined. (Note: older units may not be lead lined.) The shape of the PID may be circular or rectangular. Dental lead-lined cones are available in a variety of lengths from 4 to 16 inches. The end of a 4-inch cone may be 8 inches from the radiograph generator. An 8-inch extension (using a 4-inch cone) is referred to as shortcone technique; longer extensions result in a long-cone technique. Exposure adjustments to accommodate different cone lengths employ the inverse square rule. For

example, a 4-inch cone requires one-fourth of the exposure of an 8-inch cone. Generally, short-cone technique, which produces less magnification, is preferable because it uses a quarter of the exposure and is easier to position. The long-cone technique, however, produces films with less divergence and scatter. The arm connects the radiograph tube and the control panel. The control panel contains the timer, kilovoltage (kV), and/or milliamperage (mA) regulators. Most machines have a fixed kV (50–120) and mA (7–15). The only variable parameter is duration of the exposure in fractions of seconds or pulses (figs. 3.3 a, b). The exposure timer regulates the time an exposure lasts. The timer is engaged only while the switch is depressed and automatically stops at the end of the preset exposure. The timer resets after each exposure. Most dental units use 110V, 60Hz AC electricity. A separate dedicated electrical circuit is recommended. The kilovoltage peak (kVp) determines the penetrating power or quality of radiation produced. Kilovoltage affects the contrast (shades of gray). The higher the kVp setting, the higher is the photon energy that strikes an area. To penetrate larger teeth, a higher kilovoltage is required to produce a diagnostic film. When using ultraspeed D film, the kVp setting varies from 40 to 70, depending on the tooth and animal size or on the generator used.

Digital Imaging

Figure 3.1

Ceiling-mounted radiographic generator and monitor.

Digital imaging is a major technical advancement in companion animal dental radiography. Instead of film, an electronic sensor pad is placed against the teeth; the pad senses radiation and transfers the pattern as an image to a computer screen where it can be enhanced, enlarged, e-mailed, printed, or archived. A dental radiographic unit is still needed to expose the sensor. Approximately 1/10 to 1/2 of the nondigital exposure is commonly needed to obtain a diagnostic image; however, some systems need the same amount of radiation as F-speed film. Because of low time exposure settings, older dental radiographic machines may not have fast enough timers to produce digital images. The direct-to-digital sensors used in the patient’s mouth are available in two sizes, similar to film numbers 1 and 2. Phosphor transfer sensors are available in four sizes, similar to film numbers 0, 1, 2, and 4. Parallel and bisecting angle techniques are used to position the sensor and PID properly. The operator selects the tooth or quadrant to be exposed from computer software. In direct systems, images will appear on the screen within a matter of seconds (figs. 3.4 a, b).

a

b

c

Figure 3.2 a. Dental operatory with cabinet mounted radiograph unit. b. Portable handheld radiograph generator (Nomad). c. Wall-mounted radiograph unit (Progeny Vet Vision by Midmark).

41

a

a

b Figure 3.4 a. Wired direct radiography (DR) sensor (EVA AFP Imaging). b. Computed radiography (CR) film plate (Scan X).

b Figure 3.3 a. Control panel Image-Vet 70 plus (AFP Imaging). b. Control panel (Nomad).

42

Radiology

Image quality is equivalent to traditional dental films. The software allows a variety of options for enhancing and manipulating the image for greater diagnostic value. The tools used most often include enlargement, autocontrast, grayscale resolution, spotlight features, inversion of colors, and measurement rulers (figs. 3.5 a–f).

Radiation Safety ALARA Radiation exposure should be “as low as reasonably achievable” (ALARA). This concept endorses exposing the patient (and operator) to the lowest possible amount of radiation necessary to produce a diagnostically acceptable radiograph. Staff of the veterinary facility must be protected against excessive radiation exposure. Radiograph aprons, gloves, and thyroid shields should be worn when exposing films. Personal radiation monitoring devices are required in most states. Veterinarian responsibilities include (1) prescribing only radiographs that are clinically necessary, (2) installing and maintaining the radiographic equipment in a safe working condition, and (3) adequate training, supervision of, and monitoring of personnel who expose radiographs. Two types of radiation apply to operator safety. Primary radiation comes from direct exposure to the radiograph beam. The veterinarian or staff should never hold film or digital sensors in the patient’s mouth with bare or even gloved fingers. To avoid finger exposure, film or sensors can be positioned in the mouth using the endotracheal tube, clay encased in a plastic bag, gauze, or crumpled newspapers, decreasing operator exposure. Secondary (scatter) radiation reflects from areas that have been irradiated by the primary beam. Protective devices must be worn for shielding.

Film Intraoral, nonscreen film can be used in small animal dental radiography. It is inexpensive and flexible and provides diagnostic detail. The author prefers digital imaging using sensors to replace film. Individual dental films are packaged in a light-safe packet made of either Poly-Soft plastic or paper material. The back of the packet has a tab used to open the packet and remove the film for processing. The tabbed side is placed away from the radiation beam. Inside the packet, film is positioned between two sheets of black paper. Lead foil, which protects film from secondary backscatter radiation, is located next to the tab opening (fig. 3.6). Intraoral dental film is packaged with one or two films per packet. The practitioner may use the second film to give to the client or referring veterinarian, or to archive interesting cases.

Film Speed The efficiency with which a film responds to radiograph exposure is known as film sensitivity or speed:

• • •

D speed (Ultraspeed, Kodak) provides high contrast and fine detail. Ultraspeed is the most popular film used for veterinary dentistry. E speed (Ektaspeed, Kodak) requires 25% less exposure time than D speed film, with minimal loss of contrast. F speed (InSight, Kodak) requires 60% less exposure time than D speed film, and 20% less than E speed film.

Kodak film packet backs are color coded to indicate film speed and number of films in the packet.

Film Sizes

•

Personnel Monitoring A film badge service is used to provide radiation monitoring for all members of the office staff functioning near radiation exposure. The dosimeter badge should be worn at all times in the veterinary office. It measures the amount and type of radiation an individual is exposed to in the working environment. The badge should not be worn outside the office. The periodic radiation monitoring report should be evaluated and saved indefinitely.

43

•

•

Small periapical (size 0, Kodak Ultraspeed DF-54) measures ⅞ × 1⅝ inches. Size 0 is used mostly in cats due to the small-sized film. It is appropriate for the parallel technique of the mandibular cheek teeth (P3-M1) (fig. 3.7a). Large periapical (size 2, Kodak Ultraspeed DF-58) measures 1¼ × 1⅝ inches. It is appropriate for the near parallel technique of the maxillary cheek teeth (P2–M1) and bisecting angle of the mandibular incisors and canine teeth (fig. 3.7b). Occlusal (size 4, Kodak Ultraspeed DF-50) film measures 2¼ × 3 inches. Occlusal film is used in extraoral technique and nasal studies. It is appropriate for the maxillary occlusal view (fig. 3.7c).

a

b

c

d Figure 3.5 Rostral mandibles: a. Underexposed film. b. Exposure correction. c. Inverse. d. Enlarged part of image. e. Intraoral radiograph of bilateral tooth resorption at the mandibular canines. f. Software color enhancement (Schick).

44

e

f Figure 3.5 Continued

45

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Feline Dentistry

Figure 3.6

Opened film packet (film light green color).

Digital Format Sensor (Plate) Sizes Direct-to-digital sensors are currently marketed in size 1 and 2 formats (figs. 3.8 a, b, c, d). Phosphor transfer digital plates are available in sizes 1, 2, and 4 (fig. 3.8e).

Film Dot Most dental films are embossed with a raised dot (or dimple) in one of the corners. The dot is used to identify right from left. The side of the film containing the raised (convex) side of the dot indicates the side to be positioned toward the radiation beam (figs. 3.9 a–f).

There are many methods for using the film dot for tooth identification. One method places the raised dot against the cutting edge of the teeth and toward the tube head. Using this system to determine whether a processed film is from the right or left side, the progression of the teeth from molars to incisors is identified, as well as the location of the raised film dot. With this method, the “apple” and “par” rule can be applied. Apple stands for anterior to posterior (rostral to caudal) = left side. Par stands for posterior to anterior (caudal to rostral) = right side.

a

b

c

Figure 3.7 a. Size 0 film. b. Size 2 film. c. Size 4 film.

47

a

d

b

c e Figure 3.8 a. Sizes 1 and 2 digital sensors (EVA, AFP Imaging). b. Schick Technologies 0, 1, and 2 digital sensor sizes. c. Schick Technologies sensor attached to control box. d. Progeny Vet Vision Digital Sensors by Midmark. e. Sizes 2 and 4 digital phosphor plates (Scan X).

48

a

b

e

c f

d

Figure 3.9 a. Scan X digital phosphor plate film position mark “a” circled. b. Film marker “a” indicating left maxilla. c. Digital sensor position marker (arrow) indicating left maxilla. d. Film packet embossed dot (arrows). e. Right mandible film placement with marked film dot. f. Left rostral mandible film placement with marked film dot.

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Feline Dentistry

A lesser used alternative system positions the dot on the right side of the radiographed object. When reading the radiograph, if the dot is in the “air,” it is the right side. If it is in the “bone,” it is the left side. Most digital sensors and phosphor plates are marketed with embedded position indicators.

Tube/Film/Patient Placement

(see Table 3.1)

A radiographic dental survey consists of a minimum of six views:

• • • • • •

Rostral maxilla including the canines Rostral mandible including the canines Right maxillary cheek teeth Left maxillary cheek teeth Right mandibular cheek teeth Left mandibular cheek teeth

the film, creating a nondistorted image. Only the mandibular cheek teeth allow the film to be placed lingually (parallel) in the flexible intermandibular soft tissue parallel to the roots. Parallel technique is not usually feasible for most studies. Instead, the bisecting angle technique is used. Imaginary lines are drawn along the long axis of the tooth/teeth and the plane of the film. The point where these two lines meet creates an angle. Instead of aiming the central beam perpendicular to the film, as in the parallel technique, the central beam is aimed perpendicular to the imaginary line that bisects the angle formed by the plane of the film and the long axis of the tooth.

Positioning for the Maxilla

The film should be placed inside the mouth, as parallel as possible to the long axis of the tooth roots to be radiographed. The nontabbed side faces the tube head. The film can be held in position by the endotracheal tube, wadded-up newspaper, gauze, hair curler devices, lead radiograph gloves (without fingers inside), sponges, clay encased in plastic bags, or by commercial holding devices. Operators must not use their fingers to hold film during exposure. Vertical angulation refers to the up-and-down movement of the PID. Vertical angulation determines how accurately the length of the object being radiographed is reproduced. Horizontal angulation refers to rostral-caudal movements of the tube head. Proper horizontal angulation produces normal interproximal anatomic representation of the teeth without overlapping. Parallel technique places the film parallel to the tooth, and the radiograph beam is positioned perpendicular to

Incisors: Place the film packet or sensor toward the tube head against the incisors and palate. Position the PID perpendicular to an angle that bisects the film and teeth planes (fig. 3.10 a). If present and anatomically normal, both canines should touch the film (figs. 3.10 b, c, d). Canine: Place the film packet facing the tube, between the tongue and maxilla and beneath the canine tooth root. Center the PID over the mesial root of the second maxillary premolar, dorsally or laterally depending on the view needed. Determine the angle between the axis of canine tooth root plane of the canine tooth root and the plane of the film. Position the cone perpendicular to the bisected angle. The lateral oblique view is recommended for close inspection of the periapical region of the canine tooth (figs. 3.11. a, b). Premolars and first molar intraoral technique: Place the film packet as close as possible to the inner surface of the cheek teeth. For the maxillary view of the cheek teeth, the patient is positioned in sternal recumbency with a support placed under the chin, at a height where

Table 3.1. Intraoral Radiographic Overview. View

Position

Technique

Film Size

Exposure Time at 60 kV and 7 mA (in seconds)

Maxillary incisors and canines

Intraoral occlusal

Bisecting angle

2

0.16

Maxillary premolars and molars

Intraoral and/or extraoral

Near parallel

2

0.20

Mandibular incisors and canines

Intraoral occlusal

Bisecting angle

2

0.12

Mandibular premolars and molars

Intraoral

Parallel

0 or 2

0.12

a

b

d

c

Figure 3.10 a. Bisecting angle tooth, sensor, and beam position illustration. b. Patient, sensor, and tube head positions for intraoral films of the maxillary incisors. c. Maxillary incisor teeth touching the digital sensor. d. Rostral maxilla image.

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a

b Figure 3.11 a. Lateral oblique tube head and sensor position. b. Lateral oblique maxillary canine image.

the muzzle is parallel to the tabletop. A size 2 film or sensor is placed into the mouth (film white side toward the palate). Aim the PID at the roots of the premolars at approximately 45 degrees. The maxillary fourth premolar has three roots (mesiobuccal, mesiopalatal, and distal). To avoid overlap of the mesiobuccal and mesiopalatal roots, position the PID caudal oblique (figs. 3.12 a, b).

Due to superimposition of the zygomatic arch over the maxillary cheek teeth, satisfactory views may not be obtained using the standard bisecting angle technique (fig. 3.12c). To avoid the zygomatic arch, use a rostral oblique extaoral bisecting angle projection, aimed at the premolar roots with the PID positioned just ventral to the arch aimed at the palatal surfaces of the teeth. The film is

a

b

c

d

e

Figure 3.12 a. Patient, tube head, and sensor position to expose maxillary cheek teeth. b and c. Maxillary cheek teeth image—note superimposition of the zygomatic arch over the fourth premolar. d and e. Extraoral radiographic patient, tube head, and film and sensor positions. f. Extraoral image without zygoma superimposition.

f

53

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placed extraorally on the table. The cusp tips of the premolars should be near the lower edge of the film, so most of the film is under the maxilla and zygomatic arch (figs. 3.12 d, e, f). The embossed dot is along the lower edge of the film. When extraoral technique is used, right will appear to be left when viewing the film. The raised dot on the film should now be mounted so the indented dimple (concave side) is toward the viewer. This will help to avoid misinterpreting right from left when viewing the mounted intraoral radiograph.

Positioning for the Mandible Place the patient in dorsal or lateral recumbency with support under the neck so the muzzle is parallel to the tabletop.

a

b Figure 3.13 Rostral mandible: a. Tube head and sensor position. b. Image.

Incisors: Position the film packet toward the tube head against the incisors on top of the tongue. Position the PID perpendicular to the bisecting angle (figs. 3.13 a, b). Canine: Place the patient in ventral recumbency. Position the film on top of the tongue. To obtain a lateral view, position the PID approximately 45 degrees toward the canine (fig. 3.14). Premolars and first molar: Place the cat in lateral recumbency, with the film or sensor at the floor of the mouth lingual to the premolars. Place gauze or a hemostat to help depress the film into the floor of the mouth. Aim the PID perpendicular to the tooth roots and film (parallel technique). Occasionally, a slightly caudal oblique position of the PID enables viewing the distal root of the mandibular molar (figs. 3.15 and 3.16 a, b, c, d).

Figure 3.14

Lateral view of the mandibular canine.

Figure 3.15

Parallel technique used when imaging the mandibular premolars.

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a

b

d

c Figure 3.16 a and b. Left mandibular premolars and first molar. a. Patient, tube head, and sensor position. b. Left mandibular premolars and first molar image. c and d. Right mandibular premolars and first molar. c. Patient, tube head, and sensor position. d. Right mandibular premolars and first molar image.

Temporomandibular Joint The temporomandibular joint (TMJ), also called the craniomandibular joint, is a transversely elongated, synovial joint formed by the condylar process of the mandible and the mandibular fossa of the temporal bone. The reticular process is a caudoventral extension of the man-

dibular fossa that partially envelops and prevents caudal luxation of the mandibular condyle. At the rostral margin of the mandibular fossa there is a small, unnamed protuberance. The joint may be affected by congenital defects (most commonly dysplasia), trauma (luxation, fracture), infection (septic arthritis, non-infected degenerative joint

Radiology

57

a

b Figure 3.17

a. Intraoral temporomandibular joint (TMJ) positioning. b. Exposed intraorally obtained temporomandibular joint image.

disease), and neoplasia. Imaging of the TMJ can be difficult. Intraoral or extraoral techniques can be used to view the joint. When using an intraoral technique, a number 2 or number 4 film can be placed in the oropharynx wedged under the endotracheal tube in the area of the TMJ. The PID is placed against the ear canal (figs. 3.17 a, b).

Alternately, an extraoral technique can be used. Standard radiograph views include closed dorsoventral/ ventrodorsal, lateral, lateral oblique, and open-mouth. The dorsoventral (DV) position usually gives the most information concerning the TMJ. The radiograph beam should be centered between the two TMJs with care to assure symmetric positioning of the head. This is

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a

a

b Figure 3.18 a. Dorsoventral positions for exposure of the TMJs. b. Exposed extraoral image with TMJs circled.

b Figure 3.19

often difficult in patients that have suffered head trauma. In those cases, ventrodorsal (VD) views may be easier to obtain. The normal TMJ space is a thin, sharply marginated, radiolucent band of uniform width (figs. 3.18 a, b). Lateral positioning is accomplished with the nose raised 15 to 20 degrees. However, true lateral views of the TMJs are not usually diagnostic due to superimposition, unless the radiograph beam is centered over the third cervical vertebra and the film focal distance is 100 cm. Due to parallax, both TMJs will be visible on one

a. Straight lateral. b. Superimposition of the TMJs.

radiograph with the TMJ closer to the film cassette being more caudal (figs. 3.19 a, b). Lateral oblique is another option that allows the TMJs to be viewed without superimposition. The head is rotated 20 degrees along its median axis, and the TMJ closer to the film cassette is projected clear of the skull ventrally (figs. 3.20 a, b).

Radiology

59

a

b Figure 3.20 a. Extaroral lateral oblique positioning to evaluate left TMJ in a cat skull. b. Lateral oblique image, the left TMJ located ventrally to the opposite TMJ on the radiographic image.

Even with good-quality dorsoventral and lateral oblique views, an accurate diagnosis of TMJ pathology may not be possible based on analog or digital images. In those cases, thin-sliced computed tomography offers superior imaging of the TMJ.

SLOB Rule The “SLOB rule” (same lingual, opposite buccal), also called the “buccal object rule,” is a tube-shift technique that helps identify the relative bucco-lingual location of

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objects in the oral cavity. When two roots of a triplerooted tooth (e.g., the maxillary fourth premolar) are superimposed on the radiograph, it is sometimes difficult to distinguish the individual roots. Defining which root is which is important when pathology associated with advanced periodontal disease or foreign bodies is discovered. To visualize the roots, two radiographs are taken at oblique angles, fixing the vertical position and moving the tube horizontally. Horizontal tube shift will separate the superimposed roots on the film. The root that “moves” in an opposite direction to the horizontal shift of the tube, is labial or buccal. For example, when the tube head is moved rostrally, the mesiopalatal root of the right or left maxillary fourth premolar will be the most rostral root on the radiograph, and the mesiobuccal root will be caudal to the mesiopalatal root. Generally, when a root “moves” in the same direction as the tube head, it is located more lingual or palatal compared to the other root(s). Elimination of movement is essential to image sharpness. During exposure, movement of the film packet, patient’s head, or PID must be avoided.

Film Processing Emulsion film may be developed either manually or automatically. Digital images are processed through the computer. With manual processing, the operator moves the film from the developer, water, and fixer solutions in the practice darkroom or in a chairside darkroom. With the chairside darkroom, a portable light-safe box containing developer, distilled water, and fixer in small containers is placed in the dental operatory. The chairside darkroom is covered with a Plexiglas safety filter, which enables operators to see their hands while handling the film(s). The filter is either amber (when D speed film is exposed) or red (for E or F speed films). Processing time from opening the film packet to initial examination of a rinsed film takes approximately 2 minutes (figs. 3.21 a, b). Developer and fixer jars in the chairside darkroom should be covered when not in use. Depending on the chemical manufacturer, number of films processed, and environmental conditions, the fixer and developer remain usable for 2 days to 2 weeks. To maximize the life of the developer, stock solutions can be stored in a refrigerator. The developer and fixer should be brought to room temperature before use. Manual processing includes the following steps: 1.

After exposure, carry the film into the practice darkroom or chairside darkroom for processing. Slide the

a

b Figure 3.21 a. Chair-side developer unit. b. Individual cups for developer, water, fixer, and water inside the chair-side developer.

film packet tab down to present the film, cardboard, and lead blocker. The film will feel firm to the touch compared to the other film packet contents. 2. Attach a film hanger to the film edge. Touch only the sides of the film with your fingers. Apply a gentle tug to make certain the film is firmly attached to the hanger (fig. 3.22a). 3. Place the film into developer solution for the specified time recommended by the manufacturer (Kodak

Radiology

61

Figure 3.23 Automatic film processor.

4.

a

b Figure 3.22 a. Attached film hanger. b. Film and hanger placed into developer solution.

After removal from the developer, rinse the film in fresh distilled water (wash) for 10 to 15 seconds. Rinsing removes the alkaline developer from the film surface, preventing mixture with the acid fixer. 5. Place the film into fixing solution for at least 2 minutes. Fixer removes the unexposed or underdeveloped silver halide crystals and rehardens the emulsion. 6. Rinse the film for 30 seconds in distilled water. 7. After viewing, place the film back into fixer for 5 minutes, followed by a distilled water rinse for 10 minutes. 8. When rinsing is complete, attach the radiograph to a clip on the drying rack. When using an automatic standard film processor, the dental film can be attached to a larger film with silver photographic tape. This procedure is discouraged because small dental films might become lost in the processor, and/or the tape might harm the processor ’s rollers. An automatic dental film processor with a light-safe feeder can be located in the chairside darkroom or a separate darkroom. Exposed dental film(s) are inserted at one end of the automatic dental processor and exit fully developed, fixed, and dried in 5 to 7 minutes (or in 2 minutes, rapid cycle, for endodontic intraoperative films not fully fixed) (fig. 3.23).

Automatic Processing Rapid Access Chemistry: 15 seconds at 68 degrees). Note: an alternative method starts manual film processing with water immersion to soften the emulsion before placement in the developer (fig. 3.22b).

1. 2.

Remove all wrappers around the film in the darkroom. Insert the film into the film processor.

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Quality Control A good radiograph is useless unless it can be read accurately, and a poor radiograph cannot be read accurately. Daily, a quality assurance film should be exposed to verify that all parts of the dental radiography system are working properly. Use of an aluminum step wedge helps accomplish this goal. The step wedge is composed of graduated pieces of aluminum placed to produce a step effect (figs. 3.24 a, b). To use a step wedge to establish a control radiograph:

1. Lay a dental film tab-side down on a flat surface. 2. Place a step wedge over the film. 3. Use previously described techniques to expose the film. 4. Process the film using new chemicals in a lightsecured area. The processed image should show ten shades of varying densities, from light gray to black. If all ten steps are not apparent, adjust the exposure up or down until all can be distinctly seen. If the lightest steps (from the thickest part of the wedge) are indistinct, the exposure is increased. If the darkest steps (from the thinnest part of the wedge) are indistinct, the exposure is decreased.

a c

b d Figure 3.24 a. Aluminum step wedge placed on film. b. Tube head position to expose quality control film. c. Reference film with clearly identified density shades. d. Reference film processed in exhausted chemicals with blurred density shades.

Radiology

When the correct exposure is determined, this becomes the control film. Thirty reference films are exposed but not processed. Reference films should be stored in a refrigerator. (figs. 3.24 c, d) The control film is placed on the view box. Every day, one of the pre-exposed reference films is developed to confirm that the density (overall darkness of the image) and contrast (number of visible steps of the wedge) remain constant when compared to the baseline film. If they are not identical, the correct processing time and temperature are verified. If more than two steps are lighter than the control film, and other variables have not changed, the developing and fixing solutions should either be replenished or changed. Film quality encompasses many variables, including

• •

• •

Detail: the delineation of minute structure, controlled by kVp and the developing process. Definition: the distinctness and demarcation of the detail that make up the radiographic images, controlled by distance, focal spot size, type of film, and motion. Adequate definition is present when the apical lamina dura, periodontal ligament space, and individual bone trabeculae can be clearly demarcated around a healthy tooth. Density: the degree of whiteness created on the film, controlled predominantly by mAs; settings of 10– 12.5 mAs typically provide adequate detail. Contrast: the relative difference between densities, controlled by kVp (normally between 40 and 75) and processing variables (temperature, humidity, development time, light leaks, and inherent characteristics of film); high-contrast films appear black and white, while low-contrast films demonstrate many shades of gray.

63

Film Fogging Film fogging appears as a gray or dark film and can have several causes:

• • • •

• •

Insufficient fixation time (most common reason). To correct this fault, immerse the film in the fixer for an additional 5 minutes. Exhausted processing chemicals Expired film Light leaks from the film packet or processing area. To evaluate whether the processing area was at fault, place a coin on top of an open unexposed film packet in the dark room for 10 minutes, then process the film; if an outline of the coin shows, there is a light leak in the darkroom. Overdeveloped film Film processed in fixer contaminated with developer solution

No Image

• •

Film immersed in fixer before developer Film unexposed (either due to poor PID positioning, packet placement, or failure to engage the timer)

Light Image

• • • • •

Decreased exposure time Decreased kilovoltage Contaminated or exhausted developing solution Decreased developing time Inappropriate film placement in the mouth

Dark Image

Troubleshooting Foreshortened Image The exposed dental image should be approximately the same size as the patient’s tooth. Foreshortened images, caused by excessive vertical angulation, appear shorter than the patient’s anatomy. To correct a foreshortened image, the vertical angulation is reduced.

• • • • •

Overexposed film Excessive kilovoltage Increased exposure time Overdeveloped film Warm developing solution (ideal temperature is 68 °F)

If the film is black, then it may have been exposed to light before processing.

Partially Visible Image Elongated Image Elongated images, caused by too little vertical angulation, appear longer than the actual tooth. To correct an elongated image, vertical angulation is increased.

• • •

The film was partially immersed in the developer. While in the developer, the film became attached to other films or the side of the container. The film or tube head was incorrectly positioned, creating cone cutoff.

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Feline Dentistry

For labial mounting:

Blurred or Double Images Blurred and double images are caused by movement of the patient, film, or radiograph machine head, or by exposing a film twice. If the movement continued throughout the exposure, the image will be blurred. Movement where the film was in one position for part of the exposure and then maintained in a second position for the remainder of the exposure will display a double image. Tongue movement in lightly sedated patients may move the film during exposure.

•

• • •

Other Complications

• •

• • •

Fingerprints occur from poor handling while processing (wet hands, fingertips). The film should be handled only by the edges. Frosty films occur from insufficient removal of fixer when rinsing manually processed films. The remaining residue dries on the film, leaving a frosty finish. Rinsing a processed film with fresh distilled water for sufficient time easily prevents frosty films. Streaked films might occur when the film is insufficiently developed, fixed, or rinsed. Contaminated processing solutions might be at fault. Crescent-shaped lines occur when the film packet is sharply bent. Low-density tire tracks or geometric patterns on the film occur as the result of directing the radiograph through the lead foil side of the film packet.

• •

All radiographs of the dental survey are placed on a flat view box with the convex side of the dot toward the viewer (any films made using extraoral technique are placed with the convex dot away from the viewer). The radiographs are arranged anatomically; maxillary above, mandibular below. The patient’s right side should be placed on the left side of the box. The maxillary radiographs are positioned with the crowns of the teeth facing the bottom of the view box. The mandibular radiographs are rotated until the coronal portions of the teeth are directed toward the top of the view box. The films are placed into the mount as positioned on the view box. The rostral maxillary and mandibular views are mounted in the upper and lower center mount openings.

Lingual mounting (sitting on the tongue), where films are placed in the mount with raised dots facing away from the viewer, is less commonly utilized. In this method, radiographs are viewed as if the viewer is inside the patient’s mouth looking out; the patient’s left side is on the viewer ’s left side.

Radiograph Interpretation Radiographic Landmarks

Film Storage and Mounting Film mounts are used to organize and store radiographs. Mounts are available in a variety of styles, materials, and sizes of windows (openings) to accommodate the patient’s radiographic survey. All the radiographs in a single series should be in the same mount and labeled with the patient’s name and date of the study. Digitally displaying full-mouth survey films is easy when using templates (fig. 3.25). There are two common methods used to mount films. Both rely on the knowledge of the normal radiographic anatomical landmarks for each region of the mouth, tooth morphology (shape and form), and identification of the embossed corner dot. Labial mounting (nose to nose), wherein the films are placed in the mount with the raised dots facing the viewer, is most commonly used. The radiographs are examined as if the viewer is looking directly at the patient nose to nose; the patient’s left side is on the viewer ’s right side, and the patient’s right side is on the viewer ’s left side.

It is important to be able to look at a film and anatomically identify the area exposed:

•

•

•

•

The maxillary incisor area contains a radiopaque (white) area caudal to the incisors, with two radiolucent (black) ovals representing the palatine fissures (fig. 3.26). The maxillary premolar and molar area contains a radiopaque fine line apical to the roots, representing the nasal surface of the alveolar process—a white line caused by tangential beam to the 45-degree angle of the ventrolateral surface of the maxillary recess (caudally) and nasal cavity (rostrally). The maxillary recess does not extend over the second and third premolars (fig. 3.27). The mandibular incisor area has a linear radiolucent area representing the mandibular symphysis, separating the right and left mandibular bodies (fig. 3.28). The mandibular premolar and molar area has radiolucent areas above and below the body of the mandible (fig. 3.29).

INC CAN-PM-M

CAN M-PM

Figure 3.25

Digitally displayed oral film survey.

CAN-PM-M

INC

CAN PM-M

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Figure 3.28

Mandibular incisors and canines.

Figure 3.26 Maxillary incisors and canines.

Figure 3.27 Maxillary premolars and first molar. Figure 3.29 Mandibular premolars and first molar (affected by Stage 4 periodontal disease).

Mental foramina are normal radiolucent anatomical structures that may be confused with pathology. Cats have three mental foramina:

•

The rostral mental foramen is located ventral to the incisor apices near the symphysis.

•

The middle mental foramen is located ventral to the mesial root of the second premolar in the dog and distal to the root of the canine tooth in the cat. The middle mental foramen may radiographically appear as a periapical lucency suggesting endodon-

Radiology

Figure 3.30

Middle and caudal mental foramina.

Figure 3.31

•

67

tic disease. If in doubt, the tooth can be radiographed in an oblique angle, which will show that the foramen is not connected to the tooth’s apex. The caudal mental foramen is located ventral to the mesial root of the mandibular third premolar (fig. 3.30).

The mandibular canal appears as a lucent tubular structure parallel to the ventral border of the mandible. The mandibular canal may be superimposed on the apices of the mandibular cheek teeth, giving the appearance of periapical disease (fig. 3.31). The alveolar margin (also called alveolar crest) is the cortical border of the alveolar process positioned approximately 0.5–1 mm apical to the cementoenamel junction in the cat. The shape of the alveolar margin varies from pointed to flat. The rostral alveolar margins appear sharply pointed. Normal cheek teeth alveolar margins appear parallel or flat between adjacent cementoenamel junctions (fig. 3.32). The lamina dura is a radiographically visible, thin radiopaque line that represents a layer of compact bone lining the alveolus. The lamina dura is not a structure in its own right but represents the radiographic image of the dense cortical bone that is continuous with the alveolar margin. It appears dense and uniform in the younger

Mandibular canal.

animal, becoming ill-defined in the aged patient or in various disease states. The lamina dura is separated from the root by a radiolucent line, which represents the periodontal ligament space (fig. 3.33). The lamina dura of each tooth should be inspected to see whether it is continuous or breached (indicating pathology). A complete lamina dura generally indicates good periodontal health. In cases of early and established periodontal disease, the coronal lamina dura appears radiographically indistinct, irregular, and fuzzy. Resorption of the alveolar bone with advanced stages of periodontal disease leads to widening of the periodontal ligament space and loss of lamina dura. When viewing the lamina dura and the periodontal ligament space, only the interproximal portions are visible. The buccal and lingual walls of the alveolus do not project a lamina dura since they are perpendicular to the radiograph beam. With disease, the periodontal ligament space may appear with varying thickness, indicating that involvement is not consistent around the entire root. The periodontal ligament space normally appears radiographically as a uniform radiolucent area between the lamina dura and tooth root. It is normally wider in

68

Feline Dentistry

Figure 3.33

•

Figure 3.32 Alveolar margin.

•

• younger animals and narrows with advancing age. The periodontal ligament space also appears wider due to tooth mobility in the presence of periodontal disease.

•

Lamina dura.

Unilocular corticated. The radiolucent space exhibits one space. If they have borders, they are corticated, usually a border of radiopaque rim of bone. Examples: periapical cyst, granuloma, and dentigerous bone cyst. Unilocular noncorticated. There is no presence of the thin radiopaque rim of bone at the periphery. Instead, it appears fuzzy and ill-defined. Examples: osteomyelitis and neoplasia. Focal opacities. Well-defined localized lesions. Examples: condensing osteitis and periapical cemental dysplasia. Irregular or ill-defined opacity. Pattern often observed in malignant conditions as well as osteomyelitis.

Radiographic Terminology

•

•

Radiolucent. That portion of the processed radiograph that is dark or black. Radiolucent structures include resorption, soft tissues, dental pulp, and the periodontal ligament space. Radiopaque. That portion of the processed radiograph that is light or white. Radiopaque structures include enamel, dentin, bone, and mineralization of soft tissues.

Periodontal Disease Periodontal disease can be classified in stages 1 to 4 based on severity of radiographic and clinical signs. In the normal cat without periodontal disease, the alveolar margin resides 0.5–1 mm apical to the cementoenamel junction. The radiograph is used indirectly to determine degree of bone loss. The bone level in periodontal disease often

Radiology

decreases as inflammation extends and bone is resorbed. A significant amount of compact (or cortical) bone is lost before bone loss can be radiographically visualized. Distribution of bone loss is classified as either localized or generalized, depending on the number of areas affected. Localized bone loss occurs in isolated areas. Generalized bone loss involves the majority of the marginal bone. Specific areas of bone loss may be classified as horizontal (perpendicular to the tooth) or vertical (angular along the side of the root). Stage 1, gingivitis, occurs when the gingiva appears inflamed. There is no periodontal support loss or radiographic change. Stage 2, early periodontitis, occurs when attachment loss is less than 25%, as measured from the cementoe-

a

69

namel junction to the apex. Clinically, early periodontitis is typified by pocket formation or gingival recession. Radiographically, stage 2 disease appears as blunting (rounding) of the alveolar margin in addition to bone loss. There may also appear to be a loss of continuity of the lamina dura at the level of the alveolar margin (fig. 3.34a). Stage 3, moderate periodontitis, is diagnosed when 25%–50% of attachment loss occurs. The direction of bone loss may be horizontal or vertical (angular) (figs. 3.34 b, c). Horizontal bone loss radiographically appears as decreased alveolar bone along adjacent teeth. Normally, the alveolar margin bone is located 1 mm apical to the cementoenamel junction. With horizontal bone loss,

b

Figure 3.34 a. Early periodontal disease with less than 25% horizontal bone loss at the mesial root of the right mandibular first molar. b. Radiograph of established periodontitis revealing decreased alveolar bone height of the buccal or lingual alveolus of the mandibular first molar. c. Moderate periodontitis with less than 50% angular (vertical) bone loss at the right mandibular canine. d. Established periodontitis of the distal root of the right mandibular first molar. e. Advanced periodontitis with marked horizontal bone loss.

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Feline Dentistry

d

c

e Figure 3.34 Continued

both the buccal and lingual plates of bone, as well as interdental bone, have been resorbed. Clinically, horizontal bone loss is typified by a suprabony pocket, which occurs when the epithelial attachment is above the bony defect.

Vertical bone loss, resulting from infrabony defects, occurs when the walls of the pocket are within a bony housing. Periodontal disease may cause a vertical defect to extend apically from the alveolar margin. At first, the defect is surrounded by three walls of bone: two mar-

Radiology

ginal (lingual/palatal and facial) and a hemisepta (the bone of the interdental septum that remains on the root of the uninvolved adjacent tooth). As disease progresses, two-, one-, and no-walled (cup) defects may occur. Radiographically, vertical bone defects are generally V-shaped and sharply outlined. Stage 4, advanced periodontal disease, is typified by deep pockets and/or marked gingival recession, tooth mobility, gingival bleeding, and purulent discharge. Attachment loss is greater than 50% of the root length (figs. 3.34 d, e). Furcation exposure results from bone loss at the root junction of multirooted teeth because of advanced periodontal disease. It is sometimes difficult to determine radiographically whether the interradicular space is involved, unless there is a radiolucent area in the region of the furcation. Lack of radiographically detectable furcation involvement is not confirmation of the absence of periodontal destruction. Advanced furcation exposures where both cortical plates are resorbed are easily recognized on radiographs.

•

•

•

71

a

Stage 1 furcation involvement exists when the tip of a probe can just enter the furcation area. Bone partially fills the area where the roots meet. Radiographically, there may be decreased opacity of the bone at the furcation. Stage 2 furcation involvement exists when the probe tip extends horizontally into the area where the roots converge but does not exit on the other side. Radiographically, there will be bone loss at the furcation (fig. 3.35a). Stage 3 furcation exposure lesions exist secondary to advanced periodontal disease. Alveolar bone has resorbed to a point that an explorer probe passes through the defect unobstructed. Radiographically, there will be an area of complete bone loss (fig. 3.35b).

Alveolar Bone Expansion (Chronic Alveolar Osteitis) Alveolar bone expansion clinically appears as bulging alveoli around one or both maxillary and/or mandibular canines. Radiographically, this lesion appears as bone loss around the root and expansile alveolar bone growth (figs. 3.36 a, b, c, d).

Tooth Extrusion Tooth extrusion (also called supereruption) occurs when one or more of the intact canine teeth appear longer than normal. Radiographically, the affected teeth have marked loss of periodontal support (figs. 3.37 a, b).

b Figure 3.35 a. Stage 2 furcation involvement. b. Stage 3 furcation exposure.

a

b

c

d

Figure 3.36 a. Clinical alveolar bone expansion. b. Radiograph image of the bone expansion. c. Bilateral maxillary canine alveolar bone expansion with abnormal extrusion of the left maxillary canine. d. Radiograph of bulging bone surrounding the maxillary canines.

a

Figure 3.37 a. Left mandibular canine tooth extrusion. b. Radiograph confirming advanced periodontal disease.

72

b

Radiology

73

Figure 3.39 Ankylosis and replacement resorption of both mandibular canine tooth roots.

extent of endodontic disease. The pulp is contained within the chamber and canal portions of the tooth. Pulp tissue appears radiolucent radiographically. The radiograph of an endodontically affected tooth is examined for the following: Figure 3.38 Hypercementosis around the mandibular canine apex (image courtesy Dr. Barry Rathfon).

• • •

Hypercementosis Hypercementosis appears as excessive deposition of cementum, usually at the apical third of the root in response to chronic inflammation or abnormal occlusal forces (fig. 3.38).

Ankylosis Ankylosis is the union of cementum with the alveolar bone through destruction of the periodontal ligament. The tooth root becomes fused to the alveolar wall. Radiographically, there will be little or no periodontal ligament space (fig. 3.39).

Endodontic Disease Radiography is essential for evaluation of a tooth affected by endodontic disease. Radiographic images of the teeth and tissues around the root help to define the

•

Apical closure, which is necessary for conventional endodontic therapy Tooth fracture Abnormalities in the root canal, such as obstruction or resorption Periapical pathology, such as widened periodontal ligament space at the tooth’s apex secondary to bone resorption

Periapical disease is a pathologic process surrounding the apex of one or more roots that is due to either inflammation or necrosis of the dental pulp from trauma or infection, or occurs as an extension of periodontal disease. The radiographic appearance of periapical disease consistent with a granulomatous lesion (periapical granuloma) is a widening of the apical periodontal ligament space with circumscribed alveolar bone resorption. In the early stages of abscess formation, bony changes are not radiographically present. A homogeneous radiolucency at the apex or a dark halo in the periapical tissues is typical of an abscess. A sharply outlined circumscribed radiolucent area is commonly caused by a periapical cyst, which usually arises from preexisting granulomas (figs. 3.40 a, b; 3.41 a, b; 3.42 a, b; 3.43 a, b).

a

a

b Figure 3.40 a. Inflammation around the distal root of the right mandibular first molar. b. Radiographic appearance of periapical cyst secondary to root pathology.

b Figure 3.41 a. Enlarged pulp cavity and periapical lucency consistent with pulp necrosis mandibular canine. b. Periapical lucency and ill-defined periapical periodontal ligament of fractured tooth.

74

a

a

b Figure 3.43 a. A markedly enlarged pulp cavity due to pulp exposure soon after the permanent tooth erupted, b. Cut section of tooth after extraction.

b Figure 3.42 a. Complicated fracture of the left maxillary canine. b. Circumscribed apical bone resorption consistent with periapical granuloma.

75

76

Feline Dentistry

Figure 3.44 External root resorption with periapical lucency.

External root resorption may also result from periapical inflammation, orthodontic therapy, or from unknown stimuli. Radiographically, external resorption appears as radiolucent defects on any area of the root surface (fig. 3.44). Internal resorption arises from the pulp. The cause is unknown, but trauma or pulpitis from anachoresis (bacteria gaining access to the injured pulp through vascular channels) are believed to be contributing factors. A dead pulp cannot cause internal resorption (fig. 3.45). Often, it is difficult to determine whether a lesion is due to internal or external resorption. If a normalappearing root canal is visualized radiographically, the lesion is considered external in origin.

Figure 3.45

•

•

Tooth Resorption Tooth resorption is classified as the following:

•

Stage 1 (TR 1): Mild dental hard tissue loss (cementum or cementum and enamel).

•

Internal root resorption.

Stage 2 (TR 2): Moderate dental hard tissue loss (cementum or cementum and enamel with loss of dentin that does not extend to the pulp cavity) (figs. 3.46 a, b, c) Stage 3 (TR 3): Deep dental hard tissue loss (cementum or cementum and enamel with loss of dentin that extends to the pulp cavity); most of the tooth retains its integrity. Internal resorption radiographically appears as focal enlargement of the root canal (figs. 3.47 a, b). Stage 4 (TR 4): Extensive dental hard tissue loss (cementum or cementum and enamel with loss of

b

a

c Figure 3.46 a. Radiograph of Stage 2 tooth resorption lucency in the mid-root area. b. Stage 2 tooth resorption affecting the cementum and dentin. c. Stage 2 tooth resorption approaching the pulp cavity.

77

78

Feline Dentistry

a

b

Figure 3.47 a. Stage 3 tooth resorption radiographic image. b. Extracted third incisor.

•

dentin that extends to the pulp cavity); most of the tooth has lost its integrity. a. Crown and root are equally affected (fig. 3.48a). b. Crown is more severely affected than the root (fig. 3.48b). c. Root is more severely affected than the crown (fig. 3.48c). Stage 5 (TR 5): Remnants of dental hard tissue are visible only as irregular radiopacities, and gingival covering is complete (fig. 3.49).

In addition to the above classification, some investigators believe that three radiographic appearances of tooth resorption should be distinguished in order to create a treatment plan based on clinical and radiographic findings (fig. 3.50): On a radiograph of a tooth with type 1 appearance, a focal or multifocal radiolucency is present in the tooth with otherwise normal radiopacity and normal periodontal ligament space (fig. 3.51).

On a radiograph of a tooth with type 2 appearance, there is narrowing or disappearance of the periodontal ligament space in at least some areas and decreased radiopacity of part of the tooth (fig. 3.51). On a radiograph of a tooth with type 3 appearance, features of both type 1 and type 2 are present in the same tooth. A tooth with this appearance has areas of normal and narrow or lost periodontal ligament space, and there is focal or multifocal radiolucency in the tooth and decreased radiopacity in other areas of the tooth (fig. 3.52).

Neoplastic Disease Neoplasia in the oral cavity may only affect the soft tissues or extend into hard tissue of the skull. Radiographic signs of oral neoplasia in the cat include invasion of the mandible or maxilla with sclerosis, periosteal proliferation, osteolysis and displacement of the locally affected teeth. Occasionally, the teeth will appear to be floating (figs. 3.53 a, b; 3.54 a, b).

a

b

c

Figure 3.48 a. Stage 4a tooth resorption. b. Stage 4b tooth resorption. c. Stage 4c tooth resorption.

Figure 3.49

Stage 5 tooth resorption.

79

Type 1

Type 2 Figure 3.51 Types 1 and 2 tooth resorption.

Type 3

Figure 3.50 Illustrations of radiographic tooth resorption types. Figure 3.52 Type 3 tooth resorption (mesial root type 1, distal root type 2).

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Radiology

81

TMJ Disease

Traumatic Jaw Injury

Luxation of the TMJ is due to trauma or congenital malformation. Usually the mandibular condyle is luxated rostrodorsally, resulting in malocclusion. When there is a fracture of the retroarticular process, a caudal luxation is possible. Ankylosis of the TMJ is a rare condition in the usually young cat that occurs most commonly from previous trauma. Radiographic features include loss of the TMJ space and irregular new bone formation.

Jaw fractures should be evaluated radiographically to help determine a therapy plan. Often the fracture line will include a tooth that should be extracted. Normal breed variations of the mandibular symphysis should not be confused with a fracture that needs therapy (figs. 3.55 a, b).

a

b Figure 3.53

a. Clinical appearance of squamous cell carcinoma affecting the left maxilla. b. Radiographic image of advanced squamous cell carcinoma.

b

a Figure 3.54 a. Lateral oblique radiograph of the left mandible affected by squamous cell carcinoma. b. Lateral radiographic image of squamous cell carcinoma.

a

b

Figure 3.55 a. Normal left temporomandibular joint. b. Fracture of the right temporal bone and condylar process.

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Radiology

Further Reading Bar-Am Y, Pollard RE, Kass PH, Verstraete FJ. The diagnostic yield of conventional radiographs and computed tomography in dogs and cats with maxillofacial trauma. Vet Surg 2008; 37: 294–299. Baxter CJK. Oral and dental diagnostics. In: Tutt C, Deeprose J, Crossley D. BSAVA Manual of Canine and Feline Dentistry, 3rd ed. BSAVA, Gloucester, 2007; 22–40. Bellows J. Radiographic signs and diagnosis of dental disease. Sem Vet Med Surg Small Anim 1993; 8: 138–145. DeForge DH, Colmery BH. An Atlas of Veterinary Dental Radiology. Iowa State University Press, Ames, 2000. DuPont GA, DeBowes LJ. Atlas of Dental Radiography in Dogs and Cats. Saunders-Elsevier, Philadelphia, 2009. Eisner ER. Oral-dental radiographic examination technique. Vet Clin North Am Small Anim Pract 1998; 28: 1063–1087. Gorrel C. Radiographic evaluation. Vet Clin North Am Small Anim Pract 1998; 28: 1089–1110. Harvey CE, Flax BM. Feline oral-dental radiographic examination and interpretation. Vet Clin North Am Small Anim Pract 1992; 22: 1279–1295. Harvey EE, Emily PP. Oral examination and diagnostic techniques. Small Animal Dentistry, Mosby, St. Louis, 1993; 19–41.

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Holmstrom SE, Frost Fitch P, Eisner ER. Dental radiology. Veterinary Dental Techniques for the Small Animal Practitioner, 3rd ed. Saunders, Philadelphia, 2004; 131–174. Lommer MJ, Verstraete FJ. Radiographic patterns of periodontitis in cats: 147 cases (1998–1999). J Am Vet Med Assoc 2001; 218: 230–234. Mulligan TW, Aller MS, Williams CA. Atlas of Canine and Feline Dental Radiography. Veterinary Learning Systems, Trenton, 1998. Niemiec BA. Dental radiographic interpretation. J Vet Dent 2005; 22: 53–59. Niemiec BA, Furman R. Feline dental radiography. J Vet Dent 2004; 21: 252–257. Niemiec BA, Gilbert T, Sabatino D. Equipment and basic geometry of dental radiography. J Vet Dent 2004; 21: 48–52. Niemiec BA, Sabatino D, Gilbert T. Developing dental radiographs. J Vet Dent 2004; 21: 116–121. Schwarz T, Weller R, Dickie AM, Konar M, Sullivan M. Imaging of the canine and feline temporomandibular joint: a review. Vet Radiol Ultrasound 2002; 43: 85–97. Verstraete FJM, Kass PH, Terpak CH. Diagnostic value of fullmouth radiography in cats. Am J Vet Res 1998; 59: 692–695. Verstraete FJM, Kass PH, Terpak CH. Routine use of fullmouth radiographs in the dog and cat. Praktische Tierarzt 2001; 82: 658–667.

Chapter 4

Charting

Dental charting provides a graphic report of the cat’s teeth and mouth. A blank dental chart depicts anatomically correct maxillary and mandibular teeth with space to note abnormalities. Charting provides a place to record examination findings in order to develop an accurate and comprehensive treatment plan, as well as a thorough record of past treatments. To evaluate each tooth individually for charting, complete immobilization (general anesthesia) is necessary. The mouth is generally charted before scaling and can be recharted when a significant amount of calculus has been removed. Chart formats vary from paperless electronic files incorporated in proprietary veterinary software programs to handwritten paper forms (see examples at end of chapter). Whichever system is used, the dental chart should include areas to record the dental history; skull type (brachycephalic, mesaticephalic, dolichocephalic); oral pathology, including the amount and location of plaque and calculus; probing depths; fractured and mobile teeth; oral masses; and radiographic findings. Additionally, therapy provided, therapy recommended but not provided, and the future treatment plan and home care instructions should be noted on the dental chart and medical record.

maxillary quadrant is completed. The right mandibular quadrant (400 series) follows, the endotracheal tube attachment to the anesthetic machine is detached, and the animal’s body and head are rotated for evaluation and charting of the 200 and 300 series. Each tooth is examined completely, including periodontal probing, before the next tooth is viewed. Only abnormalities are noted on the dental chart (figs. 4.1 a, b).

Charting Steps

10.

Four-handed (two person) charting is the fastest and most efficient. One person examines the mouth and the other records information on the chart. The examiner begins by saying “100 series” and “101” (which is the maxillary right first incisor according to the modified Triadan system of tooth identification), noting any abnormalities and then moving distally until the right 84

1.

2.

3. 4.

5. 6. 7. 8. 9.

11.

12.

Examine the occlusion rostrally and caudally before intubation and record any abnormalities. Normally, the teeth of the opposing arches in cats do not touch. After intubation, examine the mouth for missing teeth and circle all visibly missing teeth on the dental chart. The most commonly missing tooth is the mandibular third premolar. Record obviously fractured teeth. Check for tooth mobility using an instrument handle pressed against the tooth. Record abnormal mobility (M1, M2, M3). Record areas of calculus accumulation. Record abnormal probing depths or attachment levels around each tooth. Expose and process dental radiographs. Scale and polish the teeth. Reprobe if a significant amount of calculus was removed. Formulate a treatment plan through tooth-by-tooth evaluation; draw a diagonal line through teeth that need to be extracted. Calculate fees for the treatment plan and contact the owner for approval while the technician is completing the teeth cleaning process. Once the owner approves, perform needed therapy and record all care on the dental chart (figs. 4.2–4.7).

Charting

a Figure 4.1

b a. Two-handed charting. b. Four-handed dentistry.

Charting Abbreviations The following abbreviations (in alphabetical order) were adapted from the American Veterinary Dental College (AVDC): AB

Abrasion

APG

Apexogenesis

F/AR

Apically repositioned periodontal flap

APX

Apexification

F/CR

Coronally repositioned periodontal flap

AT

Attrition

F/L

Lateral sliding periodontal flap

B

Biopsy

FGG

Free gingival graft

B/E

Biopsy excisional

FRE

Frenoplasty (frenotomy, frenectomy)

B/I

Biopsy incisional

FX

Fracture (tooth or jaw)

F

Flap

BG

Bone graft (includes placement of bone substitute or bone stimulant material)

FX/R

Repair of jaw fracture

C

Canine

FX/R/P

Pin repair of jaw fracture

CBU

Core build-up

FX/R/PL

Plate repair of jaw fracture

CFL

Cleft lip

FX/R/S

Screw repair of jaw fracture

Cleft lip repair

FX/R/WIR

Wire repair of jaw fracture

Cleft palate

FX/R/WIR/C

Cerclage wire repair of jaw fracture

Cleft palate repair

FX/R/WIR/ID

Interdental wire repair of jaw fracture

CR

Crown

FX/R/WIR/OS

Osseous wire repair of jaw fracture

CRA

Crown amputation

CFL/R CFP CFP/R

CR/M

For tooth fracture abbreviations, see under T/FX

G

Granuloma

Crown metal

G/B

Buccal granuloma (cheek-chewing lesion)

CRR

Crown reduction

G/L

Sublingual granuloma (tongue-chewing lesion)

DT

Deciduous (primary) tooth

G/E/L

Eosinophilic granuloma—lip

DTC

Dentigerous cyst

G/E/P

Eosinophilic granuloma—palate

E

Enamel

G/E/T

Eosinophilic granuloma—tongue

E/D FB

Enamel defect Foreign body

GH

Gingival hyperplasia/hypertrophy

85

GR

Gingival recession

OM/PAP

Papillomatosis

GTR

Guided tissue regeneration

OM/SCC

Squamous cell carcinoma

GV

Gingivoplasty (gingivectomy)

IM

Impression and model

IO

Interceptive (extraction) orthodontics

OR

Orthodontic recheck

IO/D

Deciduous (primary) tooth interceptive orthodontics

OST

Osteomyelitis

IO/P

Permanent (secondary) tooth interceptive orthodontics

PC

Pulp capping

IP

ONF

Oronasal fistula ONF/R

Inclined plane

Oronasal fistula repair

PC/D

Direct pulp capping

PC/I

Indirect pulp capping

IP/AC

Acrylic inclined plane

IP/C

Composite inclined plane

PD0

Normal periodontium

IP/M

Metal (i.e., lab-produced) inclined plane

PD1

Gingivitis only

Laceration

PD2

<25% attachment loss

LAC/B

Laceration buccal (cheek)

PD3

25%–50% attachment loss

LAC/L

Laceration lip

PD4

>50% attachment loss

LAC/T

Laceration tongue

PE

Pulp exposure

Malocclusion

PRO

MAL/1

Class I malocclusion (normal jaw relationship, specific teeth are incorrectly positioned)

Periodontal prophylaxis (examination, scaling, polishing, irrigation)

R

Restoration of tooth

MAL/2

Class II malocclusion—mandibular distoclusion (mandible shorter than maxilla)

R/C

Restoration with composite

MAL/3

Class III malocclusion—mandibular mesiocluson (maxilla shorter than mandible)

R/CP

Restoration with compomer

R/I

Restoration with glass ionomer

MAL/LV

Linguoversion mandibular canine tooth

RAD

Radiograph

MAL/RXB

Rostral crossbite

RC

Root canal therapy

MAL/CXB

Caudal crossbite

LAC

MAL

PDI

Periodontal disease index

RC/S

Surgical root canal therapy

MAL/MA

Maxillary-mandibular asymmetry

RD

MN/FX

Mandibular fracture

RPC

Root planing—closed

Maxilla or maxillary

RPO

Root planing—open

MX/FX

Maxillary fracture

RR

Internal root resorption

OA

Orthodontic appliance

RRT

Retained root tip

OAA

Adjust orthodontic appliance

RTR

Retained tooth root

OA/BKT

Bracket orthodontic appliance

S

Surgery

OA/BU

Button orthodontic appliance

S/M

Mandibulectomy

OA/EC

Elastic (power chain) orthodontic appliance

S/P

Palate surgery

OA/WIR

Wire orthodontic appliance

S/X

Maxillectomy

MX

Retained deciduous (primary) tooth

Install orthodontic appliance

SC

Subgingival curettage

OAR

Remove orthodontic appliance

SN

Supernumerary

OC

Orthodontic/genetic consultation

SPL

Splint

OM

Oral mass

SPL/AC

Acrylic splint

OM/AD

Adenocarcinoma

SPL/C

Composite splint

OM/EPA

Acanthomatous ameloblastoma (epulis)

SPL/WIR

Wire-reinforced splint

OAI

86

OM/EPF

Fibromatous epulis

OM/EPO

Ossifying epulis

OM/FS

Fibrosarcoma

ST

Stomatitis ST/CU ST/FFS

SYM

Stomatitis—contact ulcers Stomatitis—feline caudal stomatitis Symphysis

OM/LS

Lymphosarcoma

OM/MM

Malignant melanoma

SYM/S

Symphyseal separation

OM/OS

Osteosarcoma

SYM/WIR

Wire repair of symphyseal separation

T

Tooth

Tooth resorption lesion

Avulsed tooth

TR1

Tooth resorption into enamel only

T/FX

Fractured tooth (see next seven listings for fracture types)

TR2

Tooth resorption into dentin

TR3

Tooth resorption into pulp or root canal

T/FX/EI

Enamel infraction

TR4a

Marked hard tissue resorption of crown and root

T/FX/EF

Enamel fracture

TR4b

T/FX/UCF

Uncomplicated crown fracture

Marked hard tissue resorption of crown more than root

T/FX/CCF

Complicated crown fracture

TR4c

T/FX/UCRF

Uncomplicated crown-root fracture

Marked hard tissue resorption, affecting root more than crown

T/FX/CCRF

Complicated crown-root fracture

TR5

Crown lost, root tips remain

T/FX/RF

Root fracture

TMJ/R

Reduction of TMJ luxation

T/I

Impacted tooth

TRX

Tooth partial resection (e.g., hemisection)

T/LUX

Luxated tooth

VP

Vital pulp therapy

T/NE

Near pulp exposure

X

Simple closed extraction of a tooth

T/NV

Nonvital tooth

XS

Extraction with tooth sectioning, nonsurgical

Pulp exposure

XSS

Surgical (open) extraction of a tooth

T/PE TP

TR

T/A

Treatment plan

87

Date:

Pet’s Name: Breed:

Age:

Sex:

Medical Alert: Presenting Complaint:

Procedure Record

110

108

104

204

208

210

Signs:

Diagnosis:

Treatment:

Clean / Polish / Fluoride:

Routine

Extended

Root Planing /Packing: X-rays: Comments: Antibiotics Dispensed: Pain Medications:

Maxilla Inj:

Right

Dispensed:

Diet:

Left

Mandible

Home Care:

Recheck:

Abbreviation Key AL AT CA CWD ED EP FE FX GH GV/GP LPS M O OP

Attachment Loss Attrition Caries Crowding Enamel Defect Epulis Furcation Exposure Fracture Gingival Hyperplasia Gingivectomy/Plasty Lymphocytic, Plasmacytic, Stomatitis Mobile Tooth Missing Tooth Odontoplasty

OM ONF PE PP RD RE RL ROT RPC RPO RTR X XS XSS

Oral Mass Oronasal Fistula Pulp Exposure Periodontal Pocket Retained Deciduous Root Exposure Resorptive Lesion Rotated Tooth Root Planing, Closed Root Planing, Open Retained Root Extraction Extraction, Sectioned Extraction, Surgical

411

409

404

304

309

311

*Notice: This product license is conditional. Efficacy and/or potency of this product have not been fully demonstrated.

a Figure 4.2

88

Antirobe® and Clavamox® are registered trademarks and Doxirobe™ is a trademark of Pfizer Animal Health. Adapted with permission of Johnathon R. Dodd. DVM. FAVD. Dip. AVDC and Robert B. Wiggs. DVM. FAVD. Dip. AVDC. © 2007 Pfizer Inc

PFE1106008

a. Blank Pfizer feline dental chart. b. Completed chart (courtesy of Dr. Heidi Loprise).

Date:

Pet’s Name: Breed:

Age:

Sex:

Medical Alert: Presenting Complaint:

Procedure Record Signs: 109

108

107 104

204 207

208

209

Diagnosis:

Treatment:

Clean / Polish / Fluoride:

Routine

Extended

Root Planing /Packing: X-rays: Comments: Antibiotics Dispensed: Pain Medications:

Inj: Dispensed:

Maxilla Diet:

Right

Home Care:

Left

Mandible

Recheck:

Abbreviation Key AL AT CA CWD ED EP FE FX GH GV/GP LPS M O OP

Attachment Loss Attrition Caries Crowding Enamel Defect Epulis Furcation Exposure Fracture Gingival Hyperplasia Gingivectomy/Plasty Lymphocytic, Plasmacytic, Stomatitis Mobile Tooth Missing Tooth Odontoplasty

OM ONF PE PP RD RE RL ROT RPC RPO RTR X XS XSS

Oral Mass Oronasal Fistula Pulp Exposure Periodontal Pocket Retained Deciduous Root Exposure Resorptive Lesion Rotated Tooth Root Planing, Closed Root Planing, Open Retained Root Extraction Extraction, Sectioned Extraction, Surgical

409

408 407

404

304

307 308 309

Antirobe® and Clavamox® are registered trademarks of Pfizer Animal Health. Adapted with permission of Johnathon R. Dodd. DVM. FAVD. Dip. AVDC and Robert B. Wiggs. DVM. FAVD. Dip. AVDC. © 2007 Pfizer Inc

b

PFE1106008

Figure 4.2 Continued

89

90 a Figure 4.3

a. Blank peel-off dental chart. b. Abbreviation key. c. Completed dental chart (DentaLabels).

b

c Figure 4.3 Continued

91

92 Figure 4.4 AVImark paperless computer generated and stored dental chart.

Examination Findings 109

Figure 4.5

107

106 104 103 102 101 201 202 203

204 206

207

208

209

103 102 101 201 202 203

ST — Stomatitis ST/CU – Stomatitis – contact ulcers ST/FFS – Stomatitis – feline faucitis-stomatitis SYM — Symphysis SYM/S – Symphyseal separation T — Tooth T/A – Avulsed tooth T/FX – Fractured tooth (see next seven listings for fracture types) T/FX/EI – Enamel infraction T/FX/EF – Enamel fracture 104 204 T/FX/UCF – Uncomplicated crown fracture T/FX/CCF – Complicated crown fracture 106 206 T/FX/UCRF – Uncomplicated crown-root 107 207 fracture T/FX/CCRF – Complicated crown-root fracture 108 208 T/FX/RF – Root fracture T/I – Impacted tooth T/LUX – Luxated tooth 109 209 T/NE – Near pulp exposure T/NV – Non-vital tooth T/PE – Pulp exposure T/V – Vital tooth TMJ — Temporomandibular joint TMJ/D – TMJ dysplaisia TMJ/FX – TMJ fracture TMJ/LUX – TMJ luxation TP — Treatment plan 409 309 TR — Tooth resorption lesion TR1 – TR Stage 1: mild 408 308 dental hard tissue loss (cementum or cementum and enamel). 307 407 TR2 – TR Stage 2: moderate dental hard tissue loss (cementum or cementum and enamel with loss of dentin that does not 304 extend to the pulp cavity). 404 TR3 – TR Stage 3: Deep dental hard tissue loss (cementum or cementum and enamel with loss of dentin that extends to the pulp cavity); most of the tooth retains its integrity. TR4 – TR Stage 4: Extensive dental hard tissue loss (cementum or cementum and enamel with loss of dentin that extends to the pulp cavity); most of the tooth has lost its integrity. TR4a – Crown and root are equally affected. 409 408 407 404 403 402 401 301 302 303 304 307 308 309 TR4b – Crown is more severely affected than the root. TR4c – Root is more RAD — Radiograph PD1 – Gingivitis only OM/EPF – Fibromatous epulis OM/SCC – Squamous cell severely affected than the OM/EPO – Ossifying epulis carcinoma PD2 <25% attachment loss RD — Retained deciduous OM/FS – Fibrosarcoma PD3 25-50% attachment ONF — Oronasal fistula (primary) tooth. Do not use RL. crown. TR5 – TR Stage 5: loss OM/LS – Lymphosarcoma See TR for tooth resorption. OR — Orthodontic recheck remnants of dental hard PD4 >50% attachment loss OM/MM – Malignant RR — Internal root resorption OST — Osteomyelitis tissue are visible only as PE — Pulp exposure melanoma RRT — Retained root tip PDI — Periodontal disease irregular radiopacities, PM1,2,3,4 — Premolar OM/OS – Osteosarcoma index RTR — Retained tooth root and gingival covering is teeth OM/PAP – Papillomatosis complete PD0 – Normal periodontium SN — Supernumerary 403 402 401 301 302 303

AB — Abrasion AT — Attrition C — Canine CA — Caries CFL — Cleft lip CFP — Cleft palate CMO — Cranio-mandibular osteopathy DT — Deciduous (primary) tooth DTC — Dentigerous cyst E – Enamel E/D – Enamel defect E/H – Enamel hypocalcification or hypoplasia FB — Foreign body FX — Fracture (tooth or jaw). For tooth fracture abbreviations, see under T/FX G — Granuloma G/B – Buccal granuloma (cheek chewing lesion) G/L – Sublingual granuloma (tongue chewing lesion) G/E/L – Eosinophilic granuloma – lip G/E/P – Eosinophilic granuloma – palate G/E/T – Eosinophilic granuloma – tongue GH — Gingival hyperplasia/ hypertrophy GR — Gingival recession L1,2,3 — Incisor teeth LAC — Laceration LAC/B – Laceration buccal (cheek) LAC/L – Laceration lip LAC/T – Laceration tongue M1,2,3 — Molar teeth MAL — Malocclusion MAL/1 – Class 1 malocclusion (normal jaw relationship, specific teeth are incorrectly positioned) MAL/2 – Class 2 malocclusion – mandibular distoclusion (mandible shorter than maxilla) MAL/3 – Class 3 malocclusion - mandibular mesiocluson (maxilla shorter than mandible) MAL/1-3/BV – Buccoversion MAL/1-3/CXB – caudal crossbite MAL/1-3/DV – Distoversion MAL/1-3/LABV – Labioversion MAL/1-3/LV – Linguoversion MAL/1-3/MV – Mesioversion MAL/1-3/OB – Open bite MAL/RXB – Rostral crossbite MAL/1-3/XB – Crossbite, see CXB or RXB (do not use “wry bite” or WRY) MN — Mandible or mandibular MN/FX – Mandibular fracture MX — Maxilla or maxillary MX/FX – Maxillary fracture OC — Orthodontic/genetic consultation OM — Oral mass OM/AD – Adenocarcinoma OM/EPA – Acanthomatous ameloblastoma (epulis)

108

Dental charts with American Veterinary Dental College abbreviations.

93

Treatment Provided

94

107

106 104 103 102 101 201 202 203

104

204 206

207

208

209

204

106

206

107

207

108

208

109

209

409

309

408

308 307

407

304

404

409 Figure 4.5 Continued

108

103 102 101 201 202 203

109

403 402 401 301 302 303

APG — Apexogenesis APG — Apexification B — Biopsy B/E – Biopsy excisional B/I – Biopsy incisional BG — Bone graft (includes placement of bone substitute or bone stimulant material) CBU — Core build up CFL/R — Cleft lip repair CFP/R — Cleft palate repair CR — Crown CRA — Crown amputation CR/M – Crown metal CRL — Crown lengthening CR/PFM – Crown porcelain fused to metal CR/P – Crown preparation CRR — Crown reduction CS — Culture/susceptibility F — Flap F/AR – Apically repositioned periodontal flap F/CR – Coronally repositioned periodontal flap F/L – Lateral sliding periodontal flap FGG — Free gingival graft FRE — Frenoplasty (frenotomy, frenectomy) FX/R – Repair of jaw fracture FX/R/P – Pin repair of jaw fracture FX/R/PL – Plate repair of jaw fracture FX/R/S – Screw repair of jaw fracture FX/R/WIR – Wire repair of jaw fracture FX/R/WIR/C – Cerclage wire repair of jaw fracture FX/R/WIR/ID – Interdental wire repair of jaw fracture FX/R/WIR/OS – Osseous wire repair of jaw fracture GTR — Guided tissue regeneration GV — Gingivoplasty (gingivectomy) IM — Impression and model IMP — Implant IO — Interceptive (extraction) orthodontics IO/D – Deciduous (primary) tooth interceptive orthodontics IO/P – Permanent (secondary) tooth interceptive orthodontics IP — Inclined plane IP/AC – Acrylic inclined plane

408

407

404

403 402 401 301 302 303

304

307

308

309

IP/C – Composite inclined plane IP/M – Metal (i.e., lab produced) inclined plane OA — Orthodontic appliance OAA — Adjust orthodontic appliance OA/BKT – Bracket orthodontic appliance OA/BU – Button orthodontic appliance OA/EC – Elastic (power chain) orthodontic appliance OA/WIR – Wire orthodontic appliance OAI — Install orthodontic appliance OAR — Remove orthodontic appliance PC — Pulp capping PC/D – Direct pulp capping PC/I – Indirect pulp capping PRO — Periodontal prophylaxis (examination, scaling, polishing, irrigation) R — Restoration of tooth R/C – Restoration with composite R/CP – Restoration with compomer R/I – Restoration with glass ionomer RC — Root canal therapy RC/S – Surgical root canal therapy RPC — Root planing – closed RPO — Root planing – open S — Surgery S/M – Mandibulectomy S/P – Palate surgery S/X – Maxillectomy SC — Subgingival curettage SPL — Splint SPL/AC – Acrylic splint SPL/C – Composite splint SPL/WIR – Wire reinforced splint SYM/WIR – Wire repair of symphyseal separation TMJ/C — Temporomandibular joint condylectomy TMJ/R — Reduction of TMJ luxation TRX — Tooth partial resection (e.g., hemisection) VP — Vital pulp therapy X — Simple closed extraction of a tooth XS — Extraction with tooth sectioning, non-surgical XSS — Surgical (open) extraction of a tooth

VHUP DENTAL RECORD

Date:

Copyright: Veterinary Hospital of the University of Pennsylvania

R

L

Staff: (circle primary staff) Chief Complaint: Awake

Sedated

MAL/1 MAL/2 MAL/3 MAL/WRY MAL/BN Malocclusion/base narrow mand. canines MAL/ABX, PBX Mal/anterior, posterior crossbite SN Supernumerary tooth DT Deciduous tooth RD Retained deciduous tooth PD0 No perio dx (maybe calculus) PD1 Gingivitis (no bone loss) PD2 Mild periodontitis (< 25% attach loss) PD3 Mod periodontitis (< 50% attach loss) PD4 Severe periodontitis (> 50% attach loss) GH Gingival hyperplasia / enlargement GR Gingival recession ST Stomatitis ST/CU Stomatitis – contact ulcer ST/FFS Stomatitis – Feline faucitis-stomatitis OM Oral mass: OM/EPA OM/EPF OM/EPO OM//MM OM/FS OM/SCC OM/OS OM/AD OM/LS OM/PAP DTC Dentigerous cyst O Missing tooth OTH Other

Anesthetized AT / AB E/D, H CA TR

Attrition/abrasion Enamel/defect, hypoplasia Caries Tooth Resorption (Grade) 1, 2, 3, 4, 5 RR Internal root resorption RTR Retained tooth root RRT Retained root tip T/A, I, LUX Tooth/ avulsed, impacted, luxated T/FX Tooth Fracture ( EI, EF, UCF, CCF, UCRF, CCRF, RF ) T/NV, V Tooth/non-vital, vital G/B, L Granuloma/buccal, sublingual G/E/L, P, T Eosinophilic gran./lip, palate, tongue FB Foreign body OST Osteomyelitis LAC/B, L, T Laceration/buccal, lip, tongue MN/FX MX/FX Jaw fractures SYM/S Symphyseal separation CFP CFL Cleft palate, Cleft lip ONF Oronasal fistula CMO Cranio-Mandibular Osteopathy TMJ/D, FX, LUX TMJ/dysplasia, fracture, luxation

N A - Extraoral/facial

N A – Lymph nodes

N A – Buccal mucosa

N A – Tongue

N A – Palate

N A – Tonsils

N A – Pharynx Tooth

M1

P4

P3

P2

C

I3

I2

I1

I1

I2

I3

C

P2

P3

P4

M1

Triadan

109

108

107

106

104

103

102

101

201

202

203

204

206

207

208

209

Tooth

M1

P4

P3

C

I3

I2

I1

I1

I2

I3

C

P3

P4

M1

Triadan

409

408

407

404

403

402

401

301

302

303

304

307

308

309

Mobility Recession Pocket Furcation Hyperplasia Calculus Plaque Gingivitis

Mobility Recession Pocket Furcation Hyperplasia Calculus

R

L

Plaque Gingivitis

a 95

Figure 4.6

Dental charts (courtesy of Dr. Alex Rieter, University of Pennsylvania).

96

R

R

L

L

RAD Rads (Dental, CDR, CT Scan, Plain Film) Y Photos (Digital, 35 mm) B/I B/E Biopsy – incisional/excisional CS Culture/Susceptibility OC Orthodontic/Genetic Consultation OR Orthodontic Recheck ------------------------------------------------------------------------PRO Periodontal prophylaxis SC Subgingival curettage Bone Curettage RPC Closed root planing RPO Open root planing GV Gingivoplasty Alveoloplasty F/AR Apical repositioning flap F/CR Coronal repositioning flap F/L Lateral sliding periodontal flap CRL Crown lengthening BG Bone graft GTR Guided tissue regeneration FGG Free gingival graft SPL/AC, C, WIR Splint/acrylic, composite, wire reinforced ------------------------------------------------------------------------RC Root canal therapy RC/S Surgical root canal therapy RRX Root resection (crown intact) TRX Tooth partial resection (hemisection) CRR Crown reduction VP Vital pulp therapy PC/D PC/I Direct/indirect pulp capping CRA Crown amputation APX Apexification APG Apexogenesis ------------------------------------------------------------------------R/C, I, A Restoration/composite, GI, amalgam IMP Implant ------------------------------------------------------------------------F Flap X Extr. - closed, no sectioning XS Extr. – closed, w/ sectioning XSS Extr. – open IO/P IO/D Intercept ortho (perm/dec) ONF/R Oronasal fistula repair CFP/R Cleft palate repair CFL/R Cleft lip repair S/P Palate surgery S/M Mandibulectomy S/X Maxillectomy FRE Frenoplasty SYM/WIR Symphyseal separation/wiring FX/R Jaw fracture repair (j. fx. rp.) FX/R/P Pin j. fx. rp. FX/R/PL Plate j. fx. rp. FX/R/S Screw j. fx. rp FX/R/WIR Wire j. fx. rp. FX/R/WIR/C Cerclage wire j. fx. rp. FX/R/WIR/ID Interdental wire j. fx. rp FX/R/WIR/OS Osseous wire j. fx. rp TMJ/C TMJ condylectomy TMJ/R Reduction of TMJ luxation ------------------------------------------------------------------------CBU Core build up CR/P Crown preparation CR/M Crown metal CR/PFM Crown porcelain fused to metal IM Impressions/models IP/AC, C, M Inclined plane/acrylic, composite, metal OAI Ortho appliance – install OAA Ortho appliance – adjust OAR Ortho appliance – remove OA/BKT, BU Ortho app./bracket, button OA/EC, WIR Ortho app./elastic, wire

Nerve Block 0.5% Marcaine Infraorbital Inferior Alveolar Mental Maxillary

RIGHT

LEFT ml ml ml ml

ml ml ml ml

Treatment:

Instructions and medications:

Follow-up:

OTH:

b Figure 4.6 Continued

Copyright: Veterinary Hospital of the University of Pennsylvania

U of MN Dental Record

Feline Dental Record R

L

Date: Staff:

Chief Complaint:

104

204

108

208

AT/AB – attrition/abrasion CU/B, T, PLT – ulcer on cheek/tongue/ palate DTC – dentigerous cyst FX – tooth fracture: EI/EF/UCF/CCF/ UCRF/CCRF/RF GH – gingival hyperplasia/hypertrophy JVG – juvenile gingivitis LAC/B/L/T – laceration cheek/lip/tongue MAL – Mal 1, Mal 2, Mal 3 MAL/WRY – wry bite MN/FX, MX/FX, SYM/S – fractures O – missing tooth

OM – oral mass RC – previous root canal RD – retained deciduous tooth TR1 – lesion into enamel only TR2 – lesion into dentin TR3 – lesion into pulp TR4 (a/b/c) – extensive structural damage TR5 – crown lost TR – Type 1 TR – Type 2

RRT – retained root tip RTR – retained tooth root SN – supernumerary tooth ST – stomatitis (caudal/gingival/buccal) T/A/TLUX – tooth avulsion/luxation PD0 – no perio dx (maybe calculus) PD1 – gingivitis (no bone loss) PD2 – mild periodontitis (<25% attachment loss) PD3 – mod periodontitis (<50% attachment loss) PD4 – severe periodontitis (>50% attachment loss)

Right

408

308

404

304

Tooth M1 Triadan 109 Pocket Buccal Pocket Palatal Recession Furcation (1-3) Mobility (1-3)

P4 108

P3 107

Tooth M1 Triadan 409 Pocket Buccal Pocket Lingual Recession Furcation (1-3) Mobility (1-3)

P4 408

P3 407

History/Comments

VMC #75.2

a 97

Figure 4.7

Dental charts (courtesy of Dr. Gary Goldstein, University of Minnesota).

P2 106

N A – Extraoral/facial N A – Lymph nodes N A – Buccal mucosa N A – Tongue N A – Palate N A – Tonsils N A – Pharynx OTHER:

Left

C 104

I3 103

I2 102

I1 101

I1 201

I2 202

I3 203

C 204

C 404

I3 403

I2 402

I1 401

I1 301

I2 302

I3 303

C 304

P2 206

P3 207

P4 208

M1 209

P3 307

P4 308

M1 309

98

Treatment Plan

R

L Nerve Blocks

104

204

108

208

408

308

404

APX BG BI/BE CFP/R CRA CR/L CR/R F FNA FX/R/WIR/AC GV I/O ONF/R PCD PCI PRO R/C, R/I RC RPC RPO S/M S/P S/X SPL/AC, SPL/COM SYM/WIR VP X XS XSS Other:

apexification bone graft biopsy incisional/excisional cleft palate repair crown amputation crown lengthening (Type 1/Type 2) crown reduction flap fine needle aspirate wire repair jaw fx gingivectomy/gingivoplasty interceptive orthodontics oronasal fistula repair direct pulp capping indirect pulp capping dental prophylaxis restoration com/GI root canal therapy closed root planing open root planing mandibulectomy palate sx maxillectomy splint acrylic/composite symphyseal wiring vital pulpotomy ext closed no sectioning ext closed w sectioning surgical (open) ext

Treatment

Radiographs

Complications

Instructions and Medications

304 Follow-up

This document prepared by the University of Minnesota Veterinary Medical Center. ©Sept 2008 Regents of the University of Minnesota. All rights reserved.

b Figure 4.7

Continued

Figure 4.7 Continued

99

100

Feline Dentistry

Further Reading American Veterinary Dental College (AVDC). Veterinary Dental Nomenclature (available at www.avdc.org). Baxter CJK. Oral and dental diagnostics. In: Tutt C, Deeprose J, Crossley D. BSAVA Manual of Canine and Feline Dentistry, 3rd ed. BSAVA, Gloucester, 2007; 22–40. Floyd MR. The modified Triadan system: nomenclature for veterinary dentistry. J Vet Dent 1991; 8 (4): 18–19. Harvey CE. Shape and size of teeth of dogs and cats: relevance to studies of plaque and calculus accumulation. J Vet Dent 2002; 19: 186–195. Harvey EE, Emily PP. Oral examination and diagnostic techniques. Small Animal Dentistry, Mosby, St. Louis, 1993; 19–41.

Holmstrom SE, Frost Fitch P, Eisner ER. Dental records. Veterinary Dental Techniques for the Small Animal Practitioner, 3rd ed. Saunders, Philadelphia, 2004; 1–38. Mills AW. Oral-dental disease in cats: a feline practitioner ’s perspective. Vet Clin North Am Small Anim Pract 1992; 22: 1297–1307. Schaller O. Illustrated Veterinary Anatomical Nomenclature, 2nd ed. Enke Verlag, Stuttgart, 2007. Tholen MA. The veterinary dental record: key to veterinary dental medicine. Vet Med Small Anim Clin 1983; 78: 1403–1412. Verstraete FJM. Colour Self-Assessment Review of Veterinary Dentistry. Manson, London, 1997.

Chapter 5

Oral Pathology

Variation in Tooth Number and Morphology Abnormalities in the number of teeth in cats can be inherited or result from disturbances during the initial stages of tooth formation. Anodontia, complete absence of all teeth, and oligodontia, decreased number of teeth, are uncommon in cats (fig. 5.1). Supernumerary teeth are more common and may result in crowding and misalignment of teeth, which may predispose to the development of periodontal disease. The mandibular fourth premolars are the most common supernumerary teeth observed in the cat. Supernumerary teeth that result in crowding should be extracted early (figs. 5.2 a–f). Persistence (formerly called retention) of deciduous teeth occurs in cats much less frequently than in dogs. Persistent (retained) deciduous teeth should be extracted as soon as they are diagnosed to make sufficient room for the permanent teeth to erupt into their normal positions. When persistent deciduous teeth are not removed, permanent teeth can deflect lingually (mandibular canine tooth) or rostrally (maxillary canine tooth) (fig. 5.3). Gemination has been observed in the deciduous, as well as in the permanent, dentition. It is an attempt to form two teeth from one enamel organ. This results in a structure with two completely or incompletely separated crowns each with a single pulp chamber and a shared root canal. Occasionally, complete cleavage or twinning occurs resulting in two teeth from one enamel organ. The etiology is unknown, but trauma has been suggested as a possible cause, though a familial tendency has been observed (figs. 5.4 a, b; 5.5 a, b). Fusion is the joining of two tooth germs, resulting in a single large tooth. Fusion may involve the entire length of the tooth or only the roots, depending on the stage of development of the teeth at the time of the union. The root canal can be shared or separate. The etiology is unknown, but trauma and a familial tendency both have been suggested as possible causes. Fusion is also

observed in the deciduous as well as in the permanent dentition. Occasionally, it is difficult to differentiate fusion of supernumerary teeth from gemination.

Periodontal Disease Periodontal disease is the most common oral disease in cats. There are two broad categories of periodontal disease: gingivitis and periodontitis. Gingivitis is the beginning stage of periodontal disease in which inflammation is confined to the gingiva (fig. 5.6a). Periodontitis is the more established form of periodontal disease where there is actual loss of the tooth supporting tissues (figs. 5.6 b, c).

Pathogenesis Within minutes of teeth scaling and polishing, a layer of glycoprotein (acquired pellicle) attaches to the exposed crown surface. Hours later, aerobic and facultative anaerobic bacteria (including Actinomyces and Streptococcus) colonize the glycoprotein layer, forming plaque.

Figure 5.1

Radiograph of a cat skull affected with adontia.

101

a

d

b

e

f c Figure 5.2 a. Supernumerary tooth caudal to the mandibular first molar. b. Radiograph of single-rooted supernumerary tooth caudal to the mandibular first molar. c. Two tooth structures in the maxillary canine position (image courtesy of Dr. Charra Sweeney-Reeves). d. Radiograph of the normal and supernumerary permanent canine (image courtesy of Dr. Charra Sweeney-Reeves). e. Supernumerary mandibular fourth premolars. f. Supernumerary maxillary third premolars.

102

Figure 5.3

b

a Figure 5.4

Bilateral persistent deciduous maxillary canines.

a. Gemination of the left maxillary third premolar. b. Radiograph of the geminated left maxillary fourth premolar.

b

a

Figure 5.5 a and b. Radiographs of geminated right mandibular fourth premolars.

103

104

Feline Dentistry

a

b

c

In some cats, the plaque irritates the gingiva, allowing pathogenic gram-negative bacteria (Porphyromonas, Prevotella, Peptostreptococcus, Fusobacterium) to survive subgingivally. By-products of these bacteria stimulate the host’s immune system to release cytokines and prostaglandins that weaken and destroy the tooth’s supporting tissues. The progression of periodontal disease is dependent on the complex regulatory interaction between bacteria and immune modulators of the host response. Animals that have compromised health often cannot fight periodontal pathogens. Diabetes, hyperthyroidism, hyperadrenocorticism, FIV, and FeLV may predispose cats to periodontal disease. Supragingival and subgingival bacteria form microenvironments of bacterial colonies called biofilms, which are separated from the junctional epithelium by a wall of neutrophils. Gram-positive, nonmotile aerobic cocci (Staphylococcus and Streptococcus spp.) naturally occupy the gingival sulcus in most cats. As plaque accumulates at the gingival margin, subgingival oxygen decreases. Toxins produced by biofilm bacteria stimulate prostaglandin and lysosome release, which can damage the biofilm-neutrophil wall, allowing invasion of the junctional epithelium. Calculus is formed by mineralization of plaque and food debris. Calculus is covered with bacteria, thus

Figure 5.6 a. Gingivitis. b. Periodontal disease at the distal root of the first mandibular molar. c. Advanced periodontal disease at the maxillary third and fourth premolars.

playing a role in maintaining and accelerating periodontal disease by keeping plaque in close contact with the gingival tissues and decreasing the potential for repair and new attachment (fig. 5.7). Appreciating the difference between gingivitis and periodontitis is important. Gingivitis is an inflammatory process affecting the gingiva only. This process does not clinically extend into the alveolar bone, periodontal ligament, or cementum. Periodontitis is inflammation involving the periodontal ligament, alveolar bone, and cementum. Gingivitis can be present without periodontitis. Similarly, periodontal disease can exist without gingivitis in an area of previous periodontitis that has been treated and controlled, relieving inflammation but not attachment loss.

Periodontal Charting After the teeth are cleaned and debris irrigated, periodontal probing is performed. A periodontal probe is the single most important examination instrument used to evaluate periodontal health, and it helps to create a road map to create a dental treatment plan. By gently inserting a calibrated periodontal probe just apical to the free gingival margin and tracing the gingival sulcus

Oral Pathology

Figure 5.7 premolar.

105

Supra and subgingival calculus on extracted maxillary fourth

from mesial to distal buccally and lingually/palatally, a rapid determination of the health of the periodontal tissues can be made (fig. 5.8). Probing depth is the distance from the free gingival margin to the most apical point that the probe reaches when gently inserted into the gingival sulcus. The probe stops where the gingiva attaches to the tooth. Each tooth should be probed completely around the circumference (fig. 5.9). Bleeding on probing is indicative of an inflammatory process in the connective tissue adjacent to the junctional epithelium. If the sulcular lining is intact and healthy, no bleeding will occur. However, if periodontal disease is present, bleeding will usually occur (fig. 5.10). Normal cats should have less than 1 mm sulcular probing depths. Abnormal probing depths are noted on the dental record and discussed with the client, and a treatment plan is mapped out before therapy begins.

Pocketing Defects A periodontal pocket is a pathologically deepened gingival sulcus. The clinical (absolute) pocket depth is the distance from the gingival margin to the base of a pocket, measured in millimeters (figs. 5.11 a, b).

Nonpocketing Defects Gingival recession results in the exposure of the root surface by apical migration of the gingival margin. Periodontal attachment level (PAL) is an accurate measure-

Figure 5.8

Periodontal probe with millimeter markings.

ment of periodontal destruction in cases of gingival recession where little or no pocketing exists. The PAL is measured from the base of the gingival sulcus/periodontal pocket to the cementoenamel junction. The clinical pocket depth plus recession (measured from the cementoenamel junction to the gingival margin) equals the total periodontal attachment loss (fig. 5.12).

Furcation Disease The furcation is a normal anatomical area at the trunk of a multirooted tooth where the roots begin to diverge. Normally, this area is sealed from the oral environment by the periodontium. When the integrity of the periodontium has been lost and junctional epithelium migrates apically, oral microflora can gain access and multiply, resulting in progressive disease. Furcation involvement or exposure occurs secondary to periodontal disease. The slightest radiographic change in the furcation area should be investigated clinically. Intraoral radiographs are helpful in locating furcation involvement. Radiolucency in the furcation suggests furcation exposure.

Figure 5.9

Periodontal probe inserted into a 3-mm periodontal pocket. Figure 5.10 Bleeding on probing between the right maxillary third and fourth premolars.

a

b

Figure 5.11 a. Before probe insertion. b. 2-mm pocket depth at the right maxillary canine tooth palatal defect.

106

Oral Pathology

Figure 5.13

107

Furcation exposure at the right maxillary third premolar.

Figure 5.12 Marked gingival recession at the left maxillary fourth premolar.

Disease affecting the furcation (F) can be classified in stages:

•

•

•

F1 involvement is diagnosed when an explorer can just detect an entrance to the furcation. A portion of alveolar bone and periodontal ligament is intact at the furcation. Generally, there will be less than 1 mm exposure. F2 involvement occurs when an explorer can enter the furcation but does not exit the other side. The undermined furcation is occluded by gingiva or bone on one side. F3 exposure is diagnosed when the periodontium is destroyed to such a degree that the furcation is open and exposed. An explorer can easily pass from side to side (fig. 5.13).

•

•

and up to 0.5 mm. If there is only stage 2 periodontal disease present, nonsurgical therapy and home care is the treatment of choice. If higher stages of periodontal disease are present, extraction should be considered. Stage 2 (M2): Mobility is increased in any direction other than axial over a distance of more than 0.5 mm and up to 1.0 mm. Extraction should be considered unless the client and patient will allow stringent home care after periodontal therapy. Stage 3 (M3): Mobility is increased in any direction other than axial over a distance exceeding 1.0 mm or any axial movement. Treatment of choice is extraction of the affected tooth.

Plaque Index (Silness and Loe) Tooth Mobility (M) Normally there is physiological tooth movement of less than 0.2 mm for incisor teeth and no mobility of others. Teeth may become pathologically mobile in response to increased occlusal forces, trauma, or normal forces exerted on a reduced periodontium. Mobility per se is not diagnostic of periodontal disease, but it reflects a pathologic adaptation to stresses placed on the periodontium.

• •

Stage 0 (M0): Physiologic mobility up to 0.2 mm. Stage 1 (M1): Mobility is increased in any direction other than axial over a distance of more than 0.2 mm

Plaque index (PI) measures the amount of plaque on the tooth surface.

• • • •

PI0: No observable plaque. PI1: A thin film of plaque is detected at the gingival margin by placing a probe or explorer across the tooth surface (fig. 5.14a). PI2: A moderate amount of plaque is detected along the gingival margin. Plaque is visible clinically (fig. 5.14b). PI3: Heavy plaque accumulation is detected at the gingival margin and in the interdental spaces (fig. 5.14c).

108

Feline Dentistry

a

c

b

Figure 5.14 a. PI 1. b. PI 2. c. PI 3.

Calculus Index

•

Calculus index (CI) refers to the amount of calculus on the tooth surface.

• • • •

CI0: No observable calculus. CI1: Scattered calculus covering less than one-third of the buccal tooth surface (fig. 5.15a). CI2: Calculus covering between one- and two-thirds of the buccal tooth surface with minimal subgingival calculus (fig. 5.15b). CI3: Calculus covering greater than two-thirds of the buccal tooth surface and extending subgingivally (fig. 5.15c).

•

•

GI1: Marginal gingivitis. Mild inflammation at the gingival margin only; slight color change at margin; slight edema; no bleeding on gentle probing, and no increase in sulcus depth (fig. 5.16b). GI2: Moderate gingivitis. Increased hyperemia of the marginal gingiva; wider band of inflammation; edema and glazing of marginal gingiva, bleeds on gentle probing; normal sulcus depths (fig. 5.16c). GI3: Advanced gingivitis. Inflammation affecting gingiva from gingival margin to mucogingival junction; marked hyperemia and edema; thickening of gingival margin; ulceration; tendency to spontaneous bleeding. At this stage there will often be periodontitis with attachment loss (fig. 5.16d).

Gingival Index To determine the gingival index (GI), the mouth is irrigated and gently blotted, then a periodontal probe is carefully applied below the gingiva.

•

GI0: Normal, healthy gingiva with sharp gingival margins. Gingiva wrapped tightly around each tooth; gingiva is shrimp-colored and stippled from mucogingival junction to gingival margin; gingival sulcus of normal depth for animal and tooth; no odor; minimal crevicular fluid (fig. 5.16a).

Periodontal Disease Index (PD)

• •

Stage 1 (PD1): Gingivitis only without attachment loss. The height and architecture of the alveolar margin are normal (fig. 5.17a). Stage 2 (PD2): Early periodontitis implies that there is less than 25% of attachment loss. There are early radiologic signs of periodontitis. The loss of attachment of alveolar bone on the root is less than 25% as measured either by clinical attachment level or radiographically as determined by the distance of

Oral Pathology

a

b

c

•

•

109

Figure 5.15 a. CI 1. b. CI 2. c. CI 3.

the alveolar margin from the cementoenamel junction relative to the length of the root. At most, stage 1 furcation involvement exists (fig. 5.17b). Stage 3 (PD3): Moderate periodontitis implies that there is 25%–50% loss of attachment of alveolar bone on the root as measured either by clinical attachment level or radiographically as determined by the distance of the alveolar margin from the cementoenamel junction relative to the length of the root. At most, stage 2 furcation involvement exists (figs. 5.17 c, d). Stage 4 (PD4): Advanced periodontitis implies that there is more than 50% loss of attachment of alveolar bone on the root as measured either by probing depth (figs. 5.17 e, f) or as determined by the distance of the alveolar margin from the cementoenamel junction relative to the length of the root. (figs. 5.17 g, h). Stage 3 furcation involvement will be involved in multirooted teeth. Some teeth are

affected by both pocketing and nonpocketing defects (figs. 5.17 i, j).

Juvenile Hyperplastic Gingivitis Juvenile hyperplastic gingivitis occurs after the permanent teeth have erupted when the cat is between six and eight months old. Although this condition is seen most often in Persian and Abyssinian cats, it can be present in any breed. Clinically, the attached gingiva is markedly inflamed, with overgrowth at times covering the crowns of the premolars and molars creating pseudopockets. Treatment involves cleaning the teeth of affected cats every three to six months and gingivectomy of the hyperplastic gingiva sparing at least 2 mm of attached gingiva. If available, laser ablation of hyperplastic tissue may be helpful. Some of these patients progress to chronic oropharangyeal inflammation; others revert to a

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a

c

b

d

Figure 5.16 a. GI 0. b. GI 1. c. GI 2. d. GI 3.

more normal gingival architecture within months to years of treatment (fig. 5.18).

Juvenile Onset Periodontitis Juvenile onset periodontitis occurs before the kitten is nine months of age. Siamese, Main Coon, and domestic shorthaired cats are predisposed. The most common presenting sign is halitosis at the time of permanent tooth eruption. Physical examination reveals marked generalized inflammation of the marginal gingiva extending to the attached gingiva. Closer examination under general anesthesia will usually reveal marked mandibular incisor mobility, as well as gingival recession, periodontal pocketing, and furcation exposure of the cheek teeth (figs. 5.19 a, b).

Canine Tooth Extrusion (Supereruption) Normally, the alveolar margin should reside within 1 mm apical to the cementoenamel junction. Occasionally, when the maxillary or mandibular canine tooth is affected by advanced periodontal disease, there appears to be greater crown height above the gingiva compared to the contralateral (unaffected) tooth. This condition is called canine tooth extrusion or supereruption. It has been reported that a significant relationship exists between supereruption and tooth resorption. Hypercementosis (cemental hyperplasia) secondary to periapical inflammation may also be involved in the tooth extrusion process. There may even be a common etiology of tooth resorption, alveolar bone expansion, and hypercementosis (fig. 5.20).

d

a

b

e

c Figure 5.17 a. Gingivitis. b. Early periodontal disease, no pocket. c. Moderate periodontal disease (no pocket with calculus in place). d. Moderate periodontal disease, no pocket after calculus removal. e. Advanced periodontal disease before probe insertion into a periodontal pocket at the right maxillary canine. f. 14-mm probing depth. g. Advanced periodontal disease (no pocket). h. Extracted tooth affected with advanced periodontal disease displaying greater than 50% loss of attachment level. i. Advanced periodontal disease exposing greater than 50% of the roots. j. Advanced periodontal disease with pocketing and gingival recession.

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h

f

g

i

j Figure 5.17 Continued

112

a

Figure 5.18

Juvenile hyperplastic gingivitis.

b Figure 5.19 a. Juvenile periodontitis at maxillae. b. Juvenile periodontitis at rostral mandibles.

Figure 5.20

Left mandibular canine tooth extrusion (“supereruption”).

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Alveolar Bone Expansion (Chronic Alveolar Osteitis) Another presentation of stage 3 and 4 periodontal disease in the cat is chronic alveolar osteitis where the alveolar bone around the tooth appears to be bulging. Radiographically, there are areas of expansive buccal alveolar bone (figs. 5.21 a–d).

Fractured Teeth and Endodontic Disease Cats that are hit by cars, fight with other cats or fall from high places may inadvertently traumatize their crowns on one or more teeth (fig. 5.22).

a

In cats, the pulp chamber extends to just under the crown tip compared to mature dogs, which usually have several millimeters of protective dentin under the enamel. When trauma causes pulp exposure, oral bacteria often enter the pulp chamber, infecting the pulp. Infection may then extend to the periodontal ligament, periapical tissues, and alveolar bone. Seldom do cats show obvious signs of endodontic disease. Occasionally, endodontic disease presents as a purulent draining tract either ventral to the orbital rim or under the chin secondary to extension of disease from the pulp periapically. Some cases of chronic rhinitis are secondary to long-standing fractured teeth. Diagnosing endodontic disease is sometimes straightforward with a fine explorer or endodontic file applied to the pulp

b

c

d Figure 5.21 a. Alveolar bone expansion and advanced periodontal disease. b. Radiograph of alveolar bone expansion surrounding the maxillary canines (more advanced on the left maxillary canine). c. Bilateral canine alveolar bone expansion. d. Radiograph of marked bilateral alveolar bone expansion.

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•

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Root fracture. A fracture involving the root (figs. 5.23 j, k).

Tooth Resorption Tooth resorption is a common dental finding clinically affecting between 20% and 75% of mature cats depending on the population researched. One study found histologic evidence of resorption on all teeth in cats that had at least one resorption, leading to the hypothesis that given enough time, all teeth of affected cats will develop tooth resorption. A related study found that in those cats that had at least one resorption, greater than half of nonclinical teeth had histologic evidence of external root resorption. Only 8% of the teeth examined from cats without tooth resorption had similar lesions.

Location

Figure 5.22

Complicated crown fracture.

cavity opening. When the file or explorer enters the pulp cavity, pulp exposure is present. Dental radiographs can help detect gross evidence of pulpal and marked periapical pathology. Radiographs can also be used to evaluate the width of root canal when compared to that of the contralateral tooth (assuming it is vital). A nonvital tooth may have a wider root canal indicating that there was pulp death some time previously that resulted in the cessation of dentin formation. In the cat, the maxillary and mandibular canines are the most common teeth fractured, followed by the incisors.

Fracture Classification

• • • • •

Enamel fracture. A fracture with loss of crown substance confined to the enamel (fig. 5.23a). Uncomplicated crown fracture. A fracture of the crown that does not expose the pulp (figs. 5.23 b, c). Complicated crown fracture. A fracture of the crown that exposes the pulp (figs. 5.23 d, e). Uncomplicated crown-root fracture. A fracture of the crown and root that does not expose the pulp (figs. 5.23 f, g). Complicated crown-root fracture. A fracture of the crown and root that exposes the pulp (figs. 5.23 h, i).

Tooth resorptions are usually clinically apparent at the labial or buccal surface near the cementoenamel junction, occasionally filled in with hyperplasic gingiva. Resorptions can be found on any tooth, although the teeth most commonly affected are the mandibular third premolars, first molars, and the maxillary third and fourth premolars. Many resorptions affecting the canine teeth occur apical to the cementoenamel junction and often are not clinically apparent (figs. 5.24 a–g). Resorption may be confined deep in the alveolus where noninflammatory replacement resorption takes place (tooth substance is resorbed and replaced with bone). Tooth resorption is considered progressive. With coronal progression of the disease into crown dentin, resorption of enamel may take place, exposing the lesion to the oral cavity and bacteria.

Clinical Signs When the resorption progresses along the root surface and erodes through the gingival attachment, the resorption lesion is exposed to oral bacteria, which may result in painful inflammation of surrounding soft tissue. In most cases of tooth resorption, there are no overt clinical signs. However, patients affected with tooth resorption may show hypersalivation, head shaking, sneezing, anorexia, oral bleeding, or may have difficulty with food prehension.

Terminology At one time, these lesions were called cat cavities due to their clinical and radiographic similarity to human caries. This is an incorrect term in that clinically and

c

a

d

b Figure 5.23 a. Enamel fracture illustration. b. Uncomplicated crown fracture illustration. c. Uncomplicated crown fracture. d. Complicated crown fracture illustration. e. Complicated crown fracture. f. Uncomplicated crown-root fracture illustration. g. Uncomplicated crown-root fracture. h. Complicated crown-root fracture illustration. i. Complicated crown-root fracture. j. Root fracture illustration. k. Root fracture.

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e

g

f

h Figure 5.23 Continued

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k

i

j Figure 5.23 Continued

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c

a

d

b Figure 5.24 a–g. Multiple locations and appearances of tooth resorption.

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f

e

g

Figure 5.24 Continued

histologically, tooth resorption is different from human caries (cavity). Caries is caused by cariogenic bacteria (mainly Streptococcus mutans) that ferment highly refined carbohydrates on the tooth surface. Acids are released during this fermentation process, resulting in demineralization of enamel and dentin of the tooth and bacterial infection of the dentin. Tooth resorptions have also been referred to as neck lesions, external odontoclastic resorptions, feline odontoclastic resorption lesions, feline oral resorptions, and cervical line erosions.

Tooth Resorption (TR) Classification

• •

•

Stage 1 (TR 1): Mild dental hard tissue loss (cementum or cementum and enamel) (fig. 5.25a). Stage 2 (TR 2): Moderate dental hard tissue loss (cementum or cementum and enamel with loss of dentin that does not extend to the pulp cavity; figs. 5.25 b–d). Stage 3 (TR 3): Deep dental hard tissue loss (cementum or cementum and enamel with loss of dentin that extends to the pulp cavity); most of the tooth retains its integrity (figs. 5.25 e–g).

•

•

Stage 4 (TR 4): Extensive dental hard tissue loss (cementum or cementum and enamel with loss of dentin that extends to the pulp cavity); most of the tooth has lost its integrity. (a) Crown and root are equally affected (figs. 5.25 h, i); (b) crown is more severely affected than the root (figs. 5.25 j–l); (c) root is more severely affected than the crown (figs. 5.25 m–o). Stage 5 (TR 5): Remnants of dental hard tissue are visible only as irregular radiopacities, and gingival covering is complete (figs. 5.25 p–r).

Some investigators believe that three radiographic appearances of tooth resorption should be distinguished:

•

•

Type 1: There is usually a loss of alveolar bone adjacent to an often well-defined area of tooth resorption; normal periodontal ligament space is maintained at other areas of the tooth. Type 2: There is a loss of the periodontal ligament space and lamina dura due to fusion of the tooth root and alveolar bone (dentoalveolar ankylosis); the resorbing tooth structure may appear less

c

a

d

b Figure 5.25 a. Stage 1 illustration. b. Stage 2 illustration. c. Stage 2 lesion on the maxillary canine. d. Radiograph of stage 2 lesion. e. Stage 3 illustration. f. Stage 3 lesion on a left mandibular molar. g. Radiograph of stage 3 lesion. h. Stage 4a illustration. i. Stage 4a radiograph. j. Stage 4b illustration. k. Stage 4b lesion at the right maxillary canine. l. Stage 4b radiograph. m. Stage 4c illustration. n. Stage 4c lesion at the left mandibular canine. o. Stage 4c radiograph. p. Stage 5 illustration. q. Stage 5 lesion. r. Stage 5 radiograph.

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g

e

f

Figure 5.25 Continued

122

h

i k

l

j Figure 5.25 Continued

123

m

n

124

o

Figure 5.25 Continued

r p

q Figure 5.25 Continued

125

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radiopaque than the unaffected tooth (replacement resorption). Type 3: There are features present of both types 1 and 2.

Examination Findings Examination in the conscious cat often will reveal tooth resorption as an area of missing tooth substance. Any surface of the tooth can be affected. The most common occurrence is on the buccal surface of the maxillary and mandibular premolars. General anesthesia is necessary to conduct a thorough tooth-by-tooth clinical and radiographic examination. In certain cases the overlying gingiva is severely inflamed; in others there is no inflammation to indicate pathology. A dental explorer is used to probe for a defect or indentation at the cementoenamel junction and gingival attachment. All surfaces of every tooth should be explored. Normal anatomical familiarity is important especially of the mandibular first molar where furcation involvement or exposure is often misdiagnosed as tooth resorption.

gingival attachment will expose the resorption to the oral environment. Inflammation of the surrounding tissues then occurs, leading to increased sensitivity. Many noninflammatory lesions do not progress and stay apical to the cementoenamel junction. Resorption lesions that begin near the cementoenamel junction are quickly exposed to the oral environment, where they become contaminated and inflamed early in the process of resorption. Some believe these lesions are caused by plaque accumulation, inflammation, and release of cytokines and lipopolysaccharides that stimulate migration of clastic cells to the area. The tooth resorption then extends down the root, infecting the periodontal ligament and preventing replacement of hard tissue loss with bone- or cementum-like material. Eventually the tooth may become mobile secondary to the loss of attachment and/or fracture from the weakening of tooth substance. Although it is tempting to incriminate plaque and periodontal disease as the etiology of tooth resorption in cats, several studies have not shown a cause-and-effect relationship between tooth resorption and periodontal disease. Periodontal disease may be secondary to the tooth’s rough surface caused by resorption.

Prevalence All cats are susceptible to resorptions. Purebred cats such as Abyssinian, Siamese, Russian Blue, Scottish Fold, and Persian appear to be affected at an earlier age. Any cat with permanent teeth can be affected. Tooth resorption, however, is rarely diagnosed in cats younger than two years of age. Most affected cats develop lesions by four to six years of age. Additionally, tooth resorption has been reported more prevalent in cats that gulp rather than chew their food, only eat table foods, female cats, cats that drink city (compared to well) water, cats that are on a raw liver diet or a low calcium diet, and cats that are exclusively indoors.

Pathenogenesis Tooth resorption occurs secondary to the activity of multinucleated odontoclastic cells, which resorb the dental hard tissues. Resorption typically starts in the cementum anywhere along the root surface and then progresses into dentin apically and/or coronally. The location where the resorption begins usually dictates the outcome. For resorptions that begin on the root surface deep in the alveolus, a progressive noninflammatory process replaces the periodontal ligament and root with bone- or cementum-like tissue. In resorptions that progress toward the crown, loss of dentin and enamel near the

Internal and External Resorption Tooth roots either resorb from the outside toward the inside (external resorption) secondary to disorders of the periodontium or due to endodontic pathology with inflammatory mediators exiting apical foramina or lateral canals to affect the periodontium or resorb from the inside toward the outside (internal resorption) as a result of disorders of the pulp tissues. The lesion affecting cats is typically an external resorption in that it begins on the outside of the tooth root(s). In humans, external root resorption can be further classified as surface, inflammatory, and replacement (noninflammatory). Surface resorption occurs secondary to relatively minor trauma (mastication, orthodontic therapy) to the cementum. Clastic cells will resorb the cementum for a few days as long as osteoclast-activating factors are released at the site of injury. When the resorption stops, cells from the periodontal ligament proliferate and populate the resorbed area, resulting in deposition of reparative tissue. Surface resorption is self-limiting and reversible, but it can eventually progress to become destructive. Tooth resorption that occurs in the cat can be inflammatory but more commonly is characterized by noninflammatory dentoalveolar ankylosis and replacement resorption of unknown etiology. Once the root has fused to the bone, the teeth become part of the alveolar bone

Oral Pathology

remodeling process and eventually resorb, which may take years. This can somewhat be seen as a form of healing, as the bone has accepted the dental hard tissue as part of itself and the tooth becomes involved in the normal skeletal turnover. When the resorptive process is over, osteoblasts form bone in the resorbed area. Thus, the dental hard tissues will gradually be replaced by bone. These lesions are not considered to be painful as long as they remain sealed below the gingival sulcus. Teeth with significant replacement resorption can be treated by means of crown amputation and intentional “root” retention. The resorbing root can be left if there is no evidence of periodontitis, stomatitis, or endodontic/periapical disease. The retained root will continue to be resorbed and replaced by bone until nothing of it is left. This process is asymptomatic (based on what we know from human dentistry). Replacement resorption does not exclude the presence of a viable pulp. The pulp may be normal in most affected teeth. Only in advanced cases will the resorptive process penetrate into the root canal or pulp chamber and gradually fill the pulp cavity with new bone. Inflammatory root (cementum, dentin) resorption is thought to be triggered by a variety of factors, including periodontal inflammation. These painful lesions often begin in the gingival sulcus around the neck (cervical portion) of the tooth. Inflammatory cells in the lesion may recognize osteoclast activating factors of the bare root surface, initiating the resorptive process just apical to the marginal gingiva. Alveolar bone adjacent to an inflammatory root resorption lesion is usually also resorbed. Two subtypes of inflammatory root resorption have been recognized:

• •

Transient resorption is followed by formation of reparative tissue. Progressive resorption is due to continued release of inflammatory mediators. When resorption progresses coronally, enamel is often undermined, breaks off, or is resorbed.

A popular theory to explain tooth resorption in cats stipulates that all cats are affected by surface resorption. In many cases the small resorbed area is “healed” by formation of reparative cementum-like tissue. Those lesions that fail to heal progress to dentin resorption. Additional research has shown that osteoclast numbers and resorptive activity increase in an acidic environment. It is suggested that local pH changes may play a role in the pathogenesis of tooth resorption.

Histology Clastic cells are responsible for mineralized tissue resorption. Bone resorbing cells are usually called osteo-

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clasts; however, when resorbing mineralized dental tissues or mineralized cartilage, they are called odontoclasts or chondroclasts, respectively. Adhesion molecules associated with mineralized tissues—bone sialoprotein and osteopontin, and a cell surface receptor linked with these molecules, alpha v beta 3—are involved in regulating resorption and repair. There are two distinct stages involved in the progression of inflammatory tooth resorption:

•

•

Acute phase—where resorptive lacunae in the dentin are created by odontoclasts. If there is an inflammatory stimulus, increased amounts of blood vessels will populate the tissues covering the excavated dentin. The pulp and adjacent hard tissue is normal in the acute phase. Chronic remodeling (reparative) phase—where cementoblast- or osteoblast-like cells populate the area producing a cementum- or bonelike tissue on top of the excavated dentin. Destruction of the periodontal ligament as well as adjacent alveolar bone occurs. The acute and chronic phases can coexist in a single lesion with both destruction and repair occurring simultaneously.

Etiology There have been numerous studies bringing greater understanding to tooth resorption; however, a specific etiology has not yet been identified for resorption of multiple permanent teeth in domestic cats. One study about prevalence and risk factors associated with tooth resorption found older age and higher magnesium content of the food to be variably associated with tooth resorption. Human bulimic patients have similar-appearing lesions caused by erosion at the cementoenamel junction due to low-pH, caustic stomach contents. It was theorized without confirmation that tooth resorption in cats may be caused by hairball regurgitation. Cat diets may hold the key to unlocking a significant part of the etiologic puzzle. Feral cats have much less prevalence compared with domestic cats. Excessive vitamin D intake from cat diets may be involved. Statistically significant increased concentrations of serum 25-hydroxyvitamin D have been found to be present in cats with tooth resorption compared to cats without. The recommended amount of vitamin D in cat diets is 250 IU/kg dry matter, but 73% of canned foods tested showed in excess of 1,500 IU/kg dry matter, and 31% exceeded the Association of American Feed Control Officials’ maximal allowance of 10,000 IU/kg dry matter. Furthermore, administration of excessive amounts of vitamin D in experimental animals (dogs,

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pigs, rats) resulted in changes to the tooth and periodontal tissues similar to those observed in tooth resorption in cats. Areas explored and found not to be directly associated with tooth resorption include an increased acid content of dry food coating and specific oral pathogenic bacteria (Actinomyces).

Radiographic Findings Intraoral radiographs are a critical diagnostic tool to help the veterinarian classify and treat tooth resorption. Most lesions are localized to the root surfaces within the alveolar bone. Clinically detectable lesions at the cervical portion of the tooth may appear as radiolucent areas near the cementoenamel junction. When one tooth resorption is noted, other resorptions on the same tooth and multiple other teeth are often revealed. There are two commonly used radiographic classification systems applied to feline tooth resorption—stages and types. Radiographic appearance of tooth resorption varies from minute surface radiolucent defects of the tooth at the cementoenamel junction to widespread root replacement resorption that gives the tooth a mottled or moth-eaten look. Treatment planning also involves evaluation of the periodontal ligament space radiographically.

Oropharangyeal Inflammation Widespread oral inflammation of the oral cavity is termed stomatitis, compared to gingivitis or periodontitis with localized support loss (fig. 5.26). Some cases of stomatitis show diffuse inflammation extending past the mucogingival margin (alveolar/labial/buccal mucositis) (figs. 5.27 a, b) or deeper into the bone and bone marrow (osteomyelitis). Some cats are affected by inflammation of the palate (palatitis), lip (cheilitis), and/or tongue (glossitis; fig. 5.28). Finally, some patients present with varying degrees of unilateral or bilateral

a

b

Figure 5.26 Periodontal support loss and inflammation.

Figure 5.27 a. Gingivitis and alveolar mucositis at the maxillary cheek teeth. b. Gingivitis and labial/buccal mucositis at the left mandibular cheek teeth.

Oral Pathology

Figure 5.28 Severe proliferative caudal stomatitis with inflammation extending into the mucosal surfaces of the cheeks, soft palate, and tongue.

caudal stomatitis/mucositis extending to the palatoglossal folds (figs. 5.29 a–e, 5.30). Past references have referred to these conditions as lymphocytic-plasmacytic gingivostomatitis, as well as plasma cell gingivitis, faucitis, and pharyngitis (though the latter two terms are incorrect in that the fauces and pharynx are often not involved in caudal stomatitis). Chronic stomatitis may appear similar but differs from other gingival inflammatory diseases (feline juvenile and adult-onset periodontitis, feline eosinophilic granuloma complex) and other metabolic, nutritional, and neoplastic diseases that may present with a clinical appearance of oral inflammation.

Etiology of Oropharangyeal Inflammation Oral tissues are constantly exposed to pathogens and antigenic proteins. In a healthy mouth, there is a balance between disease, the host, and its immune response. The etiology of oropharangyeal inflammation has not been definitively determined. Dental plaque intolerance is believed to be involved. Either an inadequate or exaggerated host response occurs in the affected cat, which leads to marked gingival and oral mucosal inflammation. A multifactorial etiology is suspected, including genetic predisposition, environmental stress, diet, viral (calici, herpes) and bacterial infection. Only calici virus has shown significant presence in those cats affected by chronic oropharangyeal inflammation (97%) compared with a control group of cats (25%). When specific pathogen-free cats were inoculated with serum from positive feline chronic oropharangyeal inflammation cats, those inoculated developed oral signs of ulceration but did not develop caudal stomatitis.

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In another study of nearly 9,000 cats affected with oral lesions, more than 20% of animals with chronic stomatitis were retrovirus (FeLV and/or FIV) positive. In a study of sixty cats with caudal stomatitis, 7% were positive for FeLV, 8% positive for FIV. None were positive for both FeLV and FIV. Although some cats that have stomatitis are positive for Bartonella spp., a cause-and-effect has not been proven in that there is already a high prevalence rate of antibody-positive cats within the healthy population due to flea exposure. Many cats that have been exposed to the bacteria will have a positive titer, even if not currently infected. Another study found both calici virus and feline herpes virus in 87% of twenty-five cats affected with chronic oral inflammation, while only 21% of cats with periodontal disease were shedding both viruses.

History and Clinical Signs The median age of affected cats is seven years. Patient history often includes dysphagia or anorexia causing weight loss, ptyalism, bruxism (grinding of teeth), and face pawing. There may be resistance to opening the mouth when eating. The cat’s hair coat is often unkempt secondary to poor self-grooming due to oral pain. Halitosis and bleeding within the oral cavity are common. Glossitis, cheilitis, and mandibular lymphadenopathy may also be evident. Widespread inflammation of the palate and pharynx is usually not present. In some cats, inflammation is apparent only around the caudal cheek teeth extending from the gingiva beyond the mucogingival junction into alveolar mucosa. Other cats show marked gingivitis and periodontitis 360 degrees around the incisors, premolars, and/or molars. Caudal stomatitis, incorrectly referred to in the past as faucitis, clinically appears as cobblestone-like ulcerative, proliferative, hyperemic lesions involving the palatoglossal folds and regions lateral to the folds. One study found 15% of the cats only had caudal stomatitis without apparent lesions further rostrally. Mandibular lymphadenopathy is common. Histopathology of the mucosa and submucosa reveals dense infiltrations of plasma cells with lesser numbers of lymphocytes, neutrophils, and macrophages consistent with virtually any inflammation in a cat’s mouth. Unfortunately, the only advantage of histopathology is to rule out neoplasia.

Radiography Intraoral radiographs often reveal moderate to marked periodontal disease, with all stages of tooth

a

d

e b

c

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Figure 5.29 a. Mild caudal oropharangyeal inflammation. b. Marked rightsided caudal stomatitis. c. Mild right-sided vestibular mucositis persisting after extraction of the cheek teeth. d and e. Marked alveolar and vestibular mucositis and periodontal disease.

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resorption, missing teeth, and root fragments (figs. 5.31 a–d).

Occlusion Disorders Many factors determine normal and abnormal occlusion. The mandibular arch is smaller than the maxillary arch at birth. Mandibular growth occurs in a downward and forward direction at a faster rate than maxillary growth. The jaws are divided into upper and lower arches. If the cat has an infection, trauma, or poor nutrition during one of the growth spurts, then the affected part of the jaw might not grow normally, producing a developmental malocclusion. Generally, the teeth are normally arranged to create a self-cleansing mechanism, pushing food away from the tooth/gingiva interface.

• Figure 5.30

Bilateral caudal stomatitis.

The mandibular teeth occlude palatal to the maxillary teeth. The mandibular incisor cusps normally rest on the the palatal side of the maxillary incisors (fig. 5.32a).

a c

b d Figure 5.31 a. Gingivitis periodontitis, and alveolar mucositis, right maxillary cheek teeth b. Radiograph confirming support loss. c. Mandibular mucositis, periodontal disease. d. Mandibular radiograph revealing tooth resorption and periodontal disease.

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c

a

d

Figure 5.32 a. Normal incisor-canine relationship b. Normal third incisor– canine relationship. c. Normal premolar interdigitation. d. Maxillary fourth premolar covering the mandibular first molar.

b

• • •

The mandibular canine crowns lie equidistant between the maxillary third incisors and the maxillary canines (fig. 5.32b). Each mandibular premolar is positioned rostral to the corresponding maxillary premolar (fig. 5.32c). The maxillary fourth premolar covers the mandibular first molar bucally (fig. 5.32d).

When the teeth are crowded, rotated, or malpositioned, the cat is predisposed to early-onset gingivitis,

periodontal disease, damage to the soft tissues, and excessive wear.

Malocclusion Abnormalities of occlusion in cats can be divided into (1) skeletal malocclusion, where the maxillae or mandibles are abnormally positioned, and/or (2) dental malocclusion or malposition, where the maxillae and mandibles

Oral Pathology

Figure 5.34

Figure 5.33 canines.

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Mandibular distoclusion.

Dental malocclusion of the left maxillary and mandibular

are positioned normally but individual teeth are abnormally located (examples: rostromesial inclination of the maxillary canine tooth, lingual displacement of the mandibular canine tooth, crowded mandibular incisors; (fig. 5.33)). Cats are born with mandibular mesioclusion closer to a level bite. This configuration allows the neonatal animal to nurse facilitating suckling as the lips form an O. As the animal grows and the impending transition from the mother ’s milk to solid food occurs, the maxilla goes through a growth spurt, nearly catching up to its relative adult percentage of jaw length. Breeds with medium-length muzzles and those with long, narrow muzzles (certain Siamese) usually do not have spatial problems with accommodating the complete dental numbers. Brachycephalic breeds with short, wide muzzles (Persian, Burmese), on the other hand, occasionally have occlusion-related problems due to the space limitations. To determine whether the likelihood of a malocclusion is genetic in origin, interdigitation of premolars can be studied. In the normal cat, the premolars meet in a saw tooth fashion, wherein the tips of the mandibular premolars point to the spaces between their maxillary interdental counterparts. If the cusp tip of one premolar

points to the tip of another, or if there is an increased space between the cusps of the maxilla and mandible, the malocclusion probably is due to genetic influence. Skeletal malocclusions are generally considered genetic in origin. Dental malocclusions are developmental and can also be genetic.

Skeletal Malocclusion Mandibular distoclusion (Class 2) occurs when there is an abnormal rostral-caudal relationship between the dental arches, in which the mandibular arch occludes caudal to its normal position relative to the maxillary arch (fig. 5.34). Mandibular mesioclusion (Class 3) is present in brachycephalic cats that have short and wide muzzles, or occurs when the mandibles grow longer than the maxillae. The mandibular incisors are positioned rostral to the maxillary incisors. In some cases, this occlusion results in abnormal tooth-to-tooth or tooth-to–soft tissue contact (figs. 5.35 a, b). Maxillary-mandibular asymmetry is a skeletal malocclusion characterized by a loss of the normal symmetry of the maxillary or mandibular arches. This condition includes:

• •

Midline discrepancy, where the midlines of the maxillary and mandibular dental arches do not align with each other (fig. 5.36a) Unilateral mandibular mesioclusion, where one mandible is in mesioclusion and the other is in normal occlusion (fig. 5.36b)

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a

a b Figure 5.36 asymmetry.

b Figure 5.35 a and b. Mandibular mesioclusion.

Dental Malocclusion Distoversion describes a tooth that is in its anatomically correct position in the dental arch but is abnormally angled in a distal direction. Mesioversion describes a tooth that is in its anatomically correct position in the dental arch but is abnormally angled in a mesial direction. This inherited defect may cause secondary maxillary lip lesions due to the abnormal canine tooth position (figs. 5.37 a, b).

a.

Maxillary/mandibular

asymmetry.

b.

Mandibular

Linguoversion describes a tooth that is in its anatomically correct position in the dental arch but is abnormally angled in a lingual direction (fig. 5.38a). Labioversion describes an incisor or canine tooth that is in its anatomically correct position in the dental arch but is abnormally angled in a labial direction (fig. 5.38b). Buccoversion describes a premolar or molar tooth that is in its anatomically correct position in the dental arch but is abnormally angled in a buccal direction. Normally, cats replace their deciduous teeth starting with the first maxillary and mandibular incisors at fourteen weeks. The permanent canines should erupt by six months. Persistent deciduous mandibular canine teeth may fail to exfoliate because the permanent tooth buds were lingually malpositioned. This malposition may result in lingual (base narrow) displacement of the permanent mandibular canine teeth, causing traumatic occlusion with the hard palate. Maxillary fourth premolar impingement results in trauma to the soft tissue (gingiva and alveolar mucosa)

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a

a

b Figure 5.38 a. Linguoversion of the maxillary canines. b. Labioversion of the right mandibular canine.

b Figure 5.37 a. Maxillary canine tooth mesioversion. b. Mandibular canine tooth mesioversion.

surrounding the mandibular first molar buccally. The repeated trauma frequently results in gingival ulceration, proliferation, recession, and exposure of the roots of the mandibular fourth premolar and/or first molar (figs. 5.39 a, b; 5.40 a, b).

Oral Swellings/Tumors Swellings and growths of the oral cavity are relatively common. There are many etiologies of oral masses ranging from cyst, infection, and inflammation to benign and malignant tumors (fig. 5.41).

Osteomyelitis Bone infection and inflammation is often diagnosed as the cause of oral swellings in the cat. These pathologies commonly occur from traumatically induced bone segments that act as sequestra or tooth root fragments. Biopsy and culture are important for treatment planning and to help rule out neoplasia (figs. 5.42 a–e).

Eosinophilic Granuloma Complex This complex can manifest in three ways:

• • •

Eosinophilic (indolent or rodent) ulcer Eosinophilic plaque Eosinophilic granuloma

Only the eosinophilic ulcer and eosinophilic granuloma apply to the oral cavity and adjacent haired areas. Eosinophilic ulcers most commonly affect the upper lip at the philtrum but may occur anywhere in the oral cavity. Ulcers on the upper lip usually have a carvedout, depressed appearance with a yellow-appearing

a

a

b b Figure 5.39 a and b. Right maxillary fourth premolar impingement. Figure 5.40

Figure 5.41

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Pharngyeal mucocele.

a and b. Left maxillary fourth premolar impingement.

c

a

d

b

e

Figure 5.42 a. Marked facial swelling. b. Inflamed gingiva. c. Aspiration of swollen face. d. Inflammatory cytology (neutrophils, macrophages). e. Radiograph revealing root fragments and left maxillary third premolar periodontal disease.

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a

b

c

Figure 5.43 a. Eosinophilic ulcer. b. Eosinophilic granuloma. c. Tongue eosinophilic granuloma.

center. Clinically, the lesions can be mistaken for neoplasia (figs. 5.43 a, b). Even though cats nine months to nine years of age can be affected, there is a higher incidence in middle- to older-aged cats with females predisposed. There may be a genetic component with a predisposition in some inbred lines. The major underlying diseases thought to cause the lip ulcers are flea and/or food allergy, Microsporum canis, and atopic dermatitis; when these underlying conditions are controlled, the lip lesion usually resolves. Diagnosis of lip ulcer is confirmed by deep incisional biopsy. Histopathology reveals hyperplastic, ulcerative, superficial, perivascular dermatitis with eosinophils, neutrophils, mononuclear cells, and fibrosis. Eosinophilic granuloma occurs most commonly in the oral cavity and/or as a linear lesion on the back legs. The etiology is unknown but suspected to be a hypersensitivity reaction. The underlying cause is rarely identified. Oral lesions may occur anywhere in the mouth including the gingiva, hard and/or soft palate, tongue, and oropharynx. Typically, the lesions have a papular to nodular configuration and histologically show granulomas with multifocal areas of collagen. Eosinophils are common in

the biopsies from the face or oral cavity, and there may be a peripheral eosinophilia as well (fig. 5.43c).

Oral Neoplasia Oral tumors in the cat make up approximately 10% of feline neoplasms. Nearly 90% of feline oral tumors are malignant. When presented with an oral swelling, the practitioner needs to use available diagnostic aids, including radiography, fine-needle aspiration for cytology, and biopsy for histopathology to render a diagnosis and treatment plan. Oral tumors may be classified as odontogenic or nonodontogenic, depending on origin, and as inductive or noninductive, based on the interaction of epithelial and mesenchymal tissues.

Benign Neoplasia Peripheral odontogenic fibroma (fibromatous epulis and ossifying epulis) An epulis is a nonspecific clinical descriptive term referring to a benign local growth of the oral mucosa. Histologically, the overlying gingival epithelium is normal to

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Inductive fibroameloblastoma Inductive refers to the relationship between the ameloblastic epithelial cells and the dental pulp–like stroma. Also known as inductive fibroameloblastoma, the feline inductive odontogenic tumor most commonly affects young cats. Osteolytic involvement of the rostral maxilla is usually involved in this rather rare tumor.

Amyloid-producing odontogenic tumor Amyloid-producing odontogenic tumor, previously referred to as calcifying epithelial odontogenic tumor, may be locally invasive in both dogs and cats but has not been reported to metastasize.

Malignant Neoplasia

Figure 5.44

Peripheral odontogenic fibromas.

A ten-year study of 371 neoplasms in the oral cavities of cats found that a majority (89%) were malignant. Squamous cell carcinomas make up a vast majority (61%) of the oral malignant tumors diagnosed, with fibrosarcoma, adenocarcinoma, lymphoma, osteosarcoma, and melanoma occurring less often.

Squamous cell carcinoma

Figure 5.45

Multiple peripheral odontogenic fibromas.

mildly hyperplastic in the sessile forms, but pedunculated epulides often have marked gingival and mucosal hyperplasia with prominent rete ridge formation. A majority of the feline epulides are peripheral odontogenic fibromas. Some have mature osteoid as their major component with only small islands of entrapped periodontal ligamentous stroma within the osteoid (fig. 5.44). The majority of peripheral odontogenic fibromas occur as single oral swellings; however, multiple epulides have been reported. In one study of thirteen cases, the biologic behavior of multiple fibromatous epulides differed from the single lesion in that after local surgical excision, eight of the eleven patients had tumor recurrence (fig. 5.45).

Squamous cell carcinoma (SCC) occurs primarily in the tongue and/or gingiva. A small percentage of cases also involves the palate, pharynx, and one or both tonsils. Metastasis to distant organs is not common. Metastasis, if present, is usually confined to the ipsilateral regional lymph nodes. Oral SCC in the cat displays a significant geographic, environmental, and dietary correlation. Tonsillar SCC are rare in North America but more common in the United Kingdom, while lingual SCC is rare in Australia. One study also found a significant correlation between oral SCC in cats and exposure to secondhand tobacco smoke. Another study found that cats fed canned food were predisposed to oral SCC compared with those fed dry food. The median age of cats with oral SCC is eleven to thirteen years; however, affected cats as young as three months and as old as twenty-one years have been reported. The most common finding is a facial swelling or asymmetry recognized by the cat’s owner or veterinarian during a routine examination (fig. 5.46). Other signs include excessive salivation, anorexia, weight loss, and halitosis. On oral examination, a prominent hard mass will usually be noted on the maxilla or mandible (fig. 5.47). Often the tumor affects the tongue root ventrally near the frenulum, which often appears thickened or ulcerated (figs. 5.48 a, b). If the mass occurs on the gingiva,

a

Figure 5.46 Facial deformity secondary to squamous cell carcinoma.

b Figure 5.48 a. Thickened tongue deformity secondary to squamous cell carcinoma. b. Squamous cell carcinoma tongue mass.

Figure 5.47 Mandibular firm swelling secondary to squamous cell carcinoma.

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Figure 5.51

Figure 5.49 carcinoma.

Radiograph of a right mandible with squamous cell

141

Fibrosarcoma.

Although fine-needle aspiration with cytological evaluation can be used to tentatively evaluate suspected lesions, proper diagnosis of SCC requires an incisional biopsy and histopathological examination. Fine-needle aspiration and cytology is performed if any local lymph nodes are palpable, asymmetric, or enlarged. The typical histologic characteristics of oral SCC include irregular cords of pleomorphic epithelial cells with abundant eosinophilic cytoplasm, prominent intercellular bridges, and keratin pearls (fig. 5.50).

Fibrosarcoma

Figure 5.50 Fine-needle aspiration cytology of squamous cell carcinoma with marked anisocytosis, anisokaryosisa, and prominent nucleoli.

Fibrosarcoma (FSA) is the second most common (although rare) tumor of the feline oral cavity. Oral FSA generally occurs in older cats (average thirteen years); however, cats as young as one year of age and as old as twenty-two years have been reported. There does not appear to be any gender predisposition or any oral cavity site predilection, though the lesions are usually located rostrally on the gingiva. Most cats with oral FSA will present for the same problems as cats with oral SCC; however, cats with oral FSA invariably will have a mass at the primary tumor site. The workup for the oral FSA patient is identical to that discussed above for oral SCC. Procurement of a deep incisional biopsy is recommended to best ensure a correct histopathological diagnosis (fig. 5.51).

Staging of Oral Tumors there may be increased mobility of the adjacent teeth due to loss of support from bone destruction (fig. 5.49). Abnormal laboratory results often show a neutrophilic leukocytosis, anemia, and azotemia. There is also an increased incidence of feline immunodeficiency virus in those cats affected with oral SCC. There is no apparent link to feline leukemia virus. Thoracic radiographs usually do not show evidence of metastasis. Intraoral radiographs commonly reveal marked localized osteolysis with increased hard tissue formation on the affected lower jaw but not on the upper jaw.

In order to compare examination findings and treatment results, oral masses can be staged per the World Health Organization’s TNM system, based on the extent of the tumor, the extent of spread to the lymph nodes, and the presence of metastasis. For staging, the tumor is:

• •

Inspected and palpated for the presence of ulceration or necrosis. Examined for adjacent tooth mobility not related to fracture or periodontal disease.

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• •

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Evaluated for regional lymph node involvement; nodes are checked for size, shape, pain on palpation, and lack of mobility. Radiographed for areas of bone resorption or new bone production; thoracic radiographs are taken for metastatic evaluation (depending on tumor type).

Primary tumor T-1: Tumor less than 2 cm in size T-2: Tumor between 2 and 4 cm in size T-3: Tumor greater than 4 cm in size

Bone invasion (determined radiographically) a: Absent b: Present

Regional lymph nodes N-0: Non-palpable nodes, no metastasis expected N-1: Palpable, ipsilateral, nonfixed, no metastasis suspected N-2: Palpable, contralateral, nonfixed, node metastasis suspected N-3: Fixed nodes, metastasis suspected

Distant metastasis M-0: No distant metastasis M-1: Evidence of metastasis to other than cervical nodes Generally, the ipsilateral mandibular lymph nodes are regarded as the ones to biopsy when striving to determine regional metastasis. Consideration should also be given to examining the parotid and medial and lateral retropharangyeal lymph nodes to more precisely determine regional metastasis. Tissue sampling can be accomplished by fine-needle aspiration, which is also helpful for lymph node sampling. Incisional biopsy is indicated for large lesions and those with a more ominous malignant appearance not conducive to initial total removal. Incisional biopsies can be performed with a scalpel blade, disposable biopsy punch, or a Tru-cut needle. A Michelle trephine or Yamshidi needle can be used to biopsy masses that have bone involvement. Biopsy of an orally visible mass should not be sampled through the skin but rather through an intraoral incision to prevent seeding of the tumor into the surrounding normal external tissues. A pie-shaped or elliptical wedge of soft tissue is removed for incisional biopsy. Incisions on either side of the ellipse should converge in a V shape to join in deeper sublesional tissues. The ellipse length should be

three times the width. Lesions from fixed alveolar or palatal tissue do not require the 3:1 ellipse shape because of the inability to close the surgical defect. Normal tissue is not purposely incised to prevent opening previously unexposed tissue planes. Once the cytologic or histopathologic diagnosis has been rendered, additional surgical excision, chemotherapy, and/or radiation therapy can be performed. Ideally, the surgeon should provide clean surgical margins of at least 1 cm for benign lesions and at least 2 cm for malignant lesions.

Oral Trauma Maxillary and mandibular fractures occur often secondary to facial trauma and rarely from preexisting pathology. Before focusing on the obvious orthopedic problem, the examiner must stabilize the patient. If the cat will allow examination without causing further pain, the oral cavity is initially evaluated for additional pathology. If the cat is uncomfortable, this examination can wait until the cat is anesthetized. Oral examination should include evaluation of range of motion of the temporomandibular joints and palpation for crepitus and areas of discomfort. The traumatized jaws may present in normal occlusion or with displacement toward or away from the side of fracture or dislocation. The hard and soft palates separate the oral and nasal cavities. When the palate has been injured, causing a communication between oral and nasal passages, the nasal cavity may fill with food or fluid during eating and drinking, and aspiration pneumonia may result. Prompt treatment of acquired palate defects is required. Fresh linear midline defects, which often result from falling from a height in cats, can be apposed by simple interrupted sutures and will usually heal readily.

Temporomandibular Joint Dislocation A traumatic rostrodorsal or less commonly caudoventral temporomandibular joint dislocation may be responsible for a cat that acutely presents with a “dropped jaw” or with the jaws in a non-occlusal position. Due to a large retroarticular process that forms a caudal extension of the mandibular fossa, the condylar process usually displaces rostrodorsally (figs. 5.52 a, b). The luxation may be unilateral or bilateral (fig. 5.53). When unilateral, the lower jaw deviates to the side opposite the luxated joint. Diagnosis of luxation alone or luxation with fracture can usually be confirmed with ventrodorsal closed-mouth radiographs.

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a

Figure 5.53 Right-sided temporomandibular joint dislocation computer 3-D reconstruction of CT study.

Open-Mouth Jaw Locking

b Figure 5.52 a. Right-sided rostrodorsal temporomandibular joint dislocation computer 3-D reconstruction of CT study. b. Clinical appearance of rightsided temporomandibular joint dislocation.

Temporomandibular dysplasia can cause joint laxity. This may result in mandibular shift, causing the coronoid process of the mandible to lock on or ventrolateral to the zygomatic arch. The affected cat presents with the mouth wide open and without contact between the maxillary and mandibular teeth. Locking usually occurs opposite to the dysplastic joint. Palpating the zygomatic arch may yield a prominent protrusion contralateral to the affected temporomandibular joint. The open mouth resists closure until either the cat frees the locked coronoid or the veterinarian does so under sedation or anesthesia.

Jaw Fractures Occasionally, the fibrocartilaginous disc in the luxated joint will be torn and folded on itself, preventing the mandibular condyle from settling back in place or reluxating following reduction. If the condyle does not properly reduce back into the fossa, condylectomy may be indicated to allow functional occlusion.

Temporomandibular Joint Ankylosis Temporomandibular joint ankylosis may occur secondary to zygomatic arch and mandibular condyle trauma leading to subsequent loss of effective joint function. Clinically, the cat will be unable to open its mouth normally (figs. 5.54 a, b, c).

Maxillary and mandibular fractures occur most commonly from automobile trauma and falling from heights. Mandibular symphyseal separations are most common, followed by fractures of the mandibular body, mandibular condyle, maxilla, and hard palate.

Mandibular symphysis separation The mandibles are connected to each other by means of a fibrous symphysis (not bone). Separation of the mandibular symphysis is a common condition in cats, typically as a result of falling from a height or other blunt force trauma. Radiographs are exposed and examined to evaluate the symphysis and adjacent structures. Radiographs must be exposed and examined before attempting care (figs. 5.55 a, b).

a

a

b b Figure 5.55 a. Mandibular symphysis separation. b. Radiograph of mandibular symphysis separation.

c Figure 5.54 a. Temporomandibular joint ankylosis (clinical appearance). b. Radiograph with abnormal-appearing temporomandibular joints circled. c. Computed tomography scan confirming ankylosis.

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a

Figure 5.57

b Figure 5.56 a. Midline hard palate defect after motor vehicle trauma. b. Radiograph of traumatic hard palate trauma.

Maxillary fractures Midline maxillary fractures usually result from high-rise or hit-by-car trauma in the cat (figs. 5.56 a,b).

Mandibular fractures Mandibular fractures are the third most common fracture in cats (head of femur and pelvis fractures first and second in a study of 517 cats) (fig. 5.57).

Further Reading Berger M, Schawalder P, Stich H, Lussi A. Feline dental resorptive lesions in captive and wild leopards and lions. J Vet Dent 1996; 13: 13–21. Berger M, Schawalder P, Stich H, Lussi A. “Neck lesion” bei Grosskatzen; Untersuchungen beim Leoparden (Panthera pardus). Kleintierpraxis 1995; 40: 537–549.

Radiograph of mandibular fracture.

Berger M, Stich H, Huster H, Roux P, Schawalder P. Feline dental resorptive lesions in the 13th to 14th centuries. J Vet Dent 2004; 21: 206–213. Berger M, Stich H, Huster H, Roux P, Schawalder P. Feline caries in two cats from a 13th century archeological excavation. J Vet Dent 2006; 23: 13–17. Bertone ER, Snyder LA, Moore AS. Environmental and lifestyle risk factors for oral squamous cell carcinoma in domestic cats. J Vet Int Med 2003; 17: 557–562. Bonello D. Feline inflammatory, infectious and other oral conditions. In: Tutt C, Deeprose J, Crossley D (eds). BSAVA Manual of Canine and Feline Dentistry, 3rd ed. BSAVA, Gloucester, 2007; 126–147. Brown TR. Trismus secondary to squamous cell carcinoma in a cat. J Vet Dent 2003; 20: 218–219. Clarke DE, Cameron A. Relationship between diet, dental calculus and periodontal disease in domestic and feral cats in Australia. Aust Vet J 1998; 76: 690–693. Colgin LM, Schulman FY, Dubielzig RR. Multiple epulides in 13 cats. Vet Pathol 2001; 38: 227–229. Colley PA, Verstraete FJ, Kass PH, Schiffman P. Elemental composition of teeth with and without odontoclastic resorption lesions in cats. Am J Vet Res 2002; 63: 546–550. Cotter SM. Oral pharyngeal neoplasms in the cat. J Am Anim Hosp Assoc 1981; 17: 917–918. DeBruijn ND, Kirpensteijn J, Neyens IJ, Van den Brand JM, van den Ingh TS. A clinicopathlogical study of 52 feline epulides. Vet Pathol 2007; 44: 161–169. DeLaurier A, Allen S, deFlandre C, Horton MA, Price JS. Cytokine expression in feline osteoclastic resorptive lesions. J Comp Pathol 2002; 127: 169–177.

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DeLaurier A, Boyde A, Horton MA, Price JS. Analysis of the surface characteristics and mineralization status of feline teeth using scanning electron microscopy. J Anat 2006; 209: 655–669. DeLaurier A, Boyde A, Horton MA, Price JS. A scanning electron microscopy study of idiopathic external tooth resorption in the cat. J Periodontol 2005; 76: 1106–1112. Diehl K, Rosychuk RA. Feline gingivitis-stomatitis-pharyngitis. Vet Clin North Am Small Anim Pract 1993; 23: 139–153. Dubielzig RR, Adams WM, Brodey RS. Inductive fibroameloblastoma, an unusual dental tumor of young cats. J Am Vet Med Assoc 1979; 174: 720–722. DuPont GA, DeBowes LJ. Comparison of periodontitis and root replacement in cat teeth with resorptive lesions. J Vet Dent 2002; 19: 71–75. Emily P. Feline malocclusion. Vet Clin North Am Small Anim Pract 1992; 22: 1453–1460. Frost P, Williams CA. Feline dental disease. Vet Clin North Am Small Anim Pract 1986; 16: 851–873. Gardner DG. Ameloblastomas in cats: a critical evaluation of the literature and the addition of one example. J Oral Pathol Med 1998; 27: 39–42. Gardner DG. Spontaneous squamous cell carcinomas of the oral region in domestic animals: a review and consideration of their relevance to human research. Oral Dis 1996; 2: 148–154. Gardner DG, Dubielzig RR. Feline inductive odontogenic tumor (inductive fibroameloblastoma): a tumor unique to cats. J Oral Pathol Med 1995; 24: 185–190. Gauthier O, Boudigues S, Pilet P, Aquado E, Heymann D, Daculsi G. Scanning electron microscopic description of cellular activity and mineral changes in feline odontoclastic resorptive lesions. J Vet Dent 2001; 18: 171–176. Gengler W, Dubielzig R, Ramer J. Physical examination and radiographic analysis to detect dental and mandibular bone resorption in cats: a study of 81 cases from necropsy. J Vet Dent 1995; 12: 97–100. Gorrel C, Larsson A. Feline odontoclastic resorptive lesions: unveiling the early lesion. J Small Anim Pract 2002; 43: 422–428. Hale FA. Juvenile veterinary dentistry. Vet Clin North Am Small Anim Pract 2005; 35: 789–817. Harley R, Gruffydd-Jones TJ, Day MJ. Salivary and serum immunoglobulin levels in cats with chronic gingivostomatitis. Vet Rec 2003; 152: 125–129. Harley R, Helps CR, Harbour DA, Gruffydd-Jones TJ, Day MJ. Intra-lesional cytokine mRNA expression in chronic gingivostomatitis in cats. Clin Diag Lab Immunol 1999; 6: 471–478. Harvey CE. Feline dental resorptive lesions. Sem Vet Med Surg Small Anim 1993; 8: 187–196. Harvey CE, Orsini P, McLahan C, Schuster C. Mapping of the radiographic central point of feline dental resorptive lesions. J Vet Dent 2004; 21: 15–21. Harvey CE, Thornsberry C, Miller BR. Subgingival bacteria— comparison of culture results in dogs and cats with gingivitis. J Vet Dent 1995; 12: 147–150. Hayes A, Scase T, Miller J, Murphy S, Sparkes A, Adams V. COX-1 and COX-2 expression in feline oral squamous cell carcinoma. J Comp Pathol 2006; 135: 93–99.

Healey KAE, Dawson S, Burrow R, Cripps P, Gaskell CJ, Hart CA, Pinchbeck GL, Radford AD, Gaskell RM. Prevalence of feline chronic gingivostomatitis in first opinion veterinary practice. J Feline Med Surg 2007; 9 (5): 373–381. Heaton M, Wilkinson J, Gorrel C, Butterwick R. A rapid screening technique for feline odontoclastic resorptive lesions. J Small Anim Pract 2004; 45: 598–601. Herring ES, Smith MM, Robertson JL. Lymph node staging of oral and maxillofacial neoplasms in 31 dogs and cats. J Vet Dent 2002; 19: 122–126. Ingham KE, Gorrel C, Blackburn J, Farnsworth W. Prevalence of odontoclastic resorptive lesions in a population of clinically healthy cats. J Small Anim Pract 2001; 42: 439–443. Klein T. Predisposing factors and gross examination findings in periodontal disease. Clin Tech Small Anim Pract 2000; 15: 189–196. Lewis JR, Okuda A, Pachtinger G, Shofer FS, Pachtinger G, Harvey CE, Reiter AM. Significant association between tooth extrusion and tooth resorption in domestic cats. J Vet Dent 2008; 25: 86–95. Lewis JR, Tsugawa AJ. Gingival hyperplasia and granulation tissue associated with a feline dental resorptive lesion. J Vet Dent 2004; 21: 23–25. Lommer MJ, Verstraete FJ. Concurrent oral shedding of feline calicivirus and feline herpesvirus 1 in cats with chronic gingivostomatitis. Oral Microbiol Immunol 2003; 18: 131– 134. Lommer MJ, Verstraete FJ. Prevalence of odontoclastic resorption lesions and periapical radiographic lucencies in cats: 265 cases (1995–1998). J Am Vet Med Assoc 2000; 217: 1866–1869. Love DN, Johnson JL, Moore LV. Bacteroides species from the oral cavity and oral-associated diseases of cats. Vet Microbiol 1989; 19: 275–281. Love DN, Redwin J, Norris JM. Cloning and expression of the superoxide dismutase gene of the feline strain of Porphyromonas gingivalis: immunological recognition of the protein by cats with periodontal disease. Vet Microbiol 2002; 86: 245–256. Love DN, Vekselstein R, Collings S. The obligate and facultatively anaerobic bacterial flora of the normal feline gingival margin. Vet Microbiol 1990; 22: 267–275. Lund EM, Bohacek LK, Dahlke JL, King VL, Kramek BA, Logan EI. Prevalence and risk factors for odontoclastic resorptive lesions in cats. J Am Vet Med Assoc 1998; 212: 392–395. Luskin IR. Dental-related facial swelling in a cat. J Vet Dent 2001; 18: 132–133. Lyon KF. Gingivostomatitis. Vet Clin North Am Small Anim Pract 2005; 35: 891–911. Mallonee DH, Harvey CE, Venner M, Hammond BF. Bacteriology of periodontal disease in the cat. Arch Oral Biol 1988; 33: 677–683. Marretta SM. Chronic rhinitis and dental disease. Vet Clin North Am Small Anim Pract 1992; 22: 1101–1117. Marretta SM. Feline dental problems: diagnosis and treatment. Feline Practice 1992; 20 (5): 16–20. Meomartino L, Fatone G, Brunetti A, Lamagna F, Potena A. Temporomandibular ankylosis in the cat: a review of seven cases. J Small Anim Pract 1999; 40: 7–10.

Oral Pathology Murphy CJ, Koblik P, Bellhorn RW, Pino M, Hacker D, Burling T. Squamous cell carcinoma causing blindness and ophthalmoplegia in a cat. J Am Vet Med Assoc 1989; 195: 965–968. Muzylak M, Arnett TR, Price JS, Horton MA. The in vitro effect of pH on osteoclasts and bone resorption in the cat: implications for the pathogenesis of FORL. J Cell Physiol 2007; 213: 144–150. Nap RC, Meij BP, Hazewinkel HAW. Fractures of the mandible and maxilla in the dog and cat. Tijdschrift voor Diergeneeskunde 1994; 119: 456–462. Ohba S, Kiba H, Kuwabara M, Yoshida H, Koide F, Takeishi M. Contact microradiographic analysis of feline tooth resorptive lesions. J Vet Med Sci 1993; 55: 329–332. Ohba S, Kiba H, Kuwabara M, Yoshida H, Koide F, Takeishi M. A histopathological study of neck lesions in feline teeth. J Am Anim Hosp Assoc 1993; 29: 216–220. Ohba S, Kuwabara M, Kamata H, Yukawa M, Kiba H. Scanning electron microscopy of root resorption of feline teeth. J Vet Med Sci 2004; 66: 1579–1581. Ohmachi T, Taniyama H, Nakade T, Kaji Y, Furuoka H. Calcifying epithelial odontogenic tumours in small domesticated carnivores: histological, immunohistochemical and electron microscopical studies. J Comp Pathol 1996; 114: 305–314. Okuda A, Harvey CE. Etiopathogenesis of feline dental resorptive lesions. Vet Clin North America Small Anim Pract 1992; 22: 1385–1404. Pedersen NC. Inflammatory oral cavity diseases of the cat. Vet Clin North Am Small Anim Pract 1992; 22: 1323–1345. Pettersson A, Mannerfelt T. Prevalence of dental resorptive lesions in Swedish cats. J Vet Dent 2003; 20: 140–142. Pope ER. Head and facial wounds in dogs and cats. Vet Clin North Am Small Anim Pract 2006; 36: 793–817. Poulet FM, Valentine BA, Summers BA. A survey of epithelial odontogenic tumors and cysts in dogs and cats. Vet Pathol 1992; 29: 369–380. Quimby JM, Elston T, Hawley J, Brewer M, Miller A, Lappin MR. Evaluation of the association of Bartonella species, feline herpesvirus 1, feline calicivirus, feline leukemia virus and feline immunodeficiency virus with chronic feline gingivostomatitis. J Feline Med Surg 2008; 10: 66–72. Reeves NC, Turrel JM, Withrow SJ. Oral squamous cell carcinoma in the cat. J Am Anim Hosp Assoc 1993; 29: 438– 441. Reichart PA, Durr U-M, Triadan H, Vickendey G. Periodontal disease in the domestic cat. A histopathological study. J Periodont Res 1984; 19: 67–75. Reiter AM. Feline odontolysis in the 1920s—the forgotten histopathological studies of feline odontoclastic resorptive lesions. J Vet Dent 1998; 15: 35–41. Reiter AM, Brady CA, Harvey CE. Local and systemic complications in a cat after poorly performed dental extractions. J Vet Dent 2004; 21: 215–221. Reiter AM, Lewis JR, Okuda A. Update on the etiology of tooth resorption in domestic cats. Vet Clin North Am Small Anim Pract 2005; 35: 913–942. Reiter AM, Lyon KF, Nachreiner RF, Shofer FS. Evaluation of calciotropic hormones in cats with odontoclastic resorptive lesions. Am J Vet Res 2005; 66: 1446–1452.

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Reiter AM, Mendoza KA. Feline odontoclastic resorptive lesions: an unsolved enigma in veterinary dentistry. Vet Clin North Am Small Anim Pract 2002; 32: 791–837. Reiter AM, Smith MM. The oral cavity and oropharynx. In: Brockman DJ, Holt DE (eds). BSAVA Manual of Canine and Feline Head, Neck and Thoracic Surgery. BSAVA, Gloucester, 2005; 25–43. Reubel GH, Hoffmann DE, Pedersen NC. Acute and chronic faucitis of domestic cats—A feline calicivirus-induced disease. Vet Clin North Am Small Anim Pract 1992; 22: 1347–1360. Roux P, Berger M, Stoffel M, Stich H, Doherr MG, Bosshard D, Schawalder P. Observations of the periodontal ligament and cementum in cats with dental resorptive lesions. J Vet Dent 2005; 22: 74–85. Sakai H, Mori T, Iida T, Tokuma Y, Maruo K, Masegi T. Immunohistochemical features of proliferative marker and basement membrane components of two feline inductive odontogenic tumours. J Feline Med Surg 2008; 10: 296– 299. Sapierzynski R, Malicka E, Bielecki W, Krawiec M, Osinska B, Sendecka H, Sobczak-Filipiak M. Oral tumors in dogs and cats: retrospective review of 143 cases. Medycyna Weterynaryjna 2007; 63: 1196–1199. Scarlett JM, Saidla J, Hess J. Risk factors for odontoclastic resorptive lesions in cats. J Am Anim Hosp Assoc 1999; 35: 188–192. Schlup D, Stich H. Epidemiologische und morphologische Untersuchungen am Katzengebiß. II. Mitteilung: morphologische Untersuchungen der “neck lesions.” Kleintierpraxis 1982; 27: 179–188. Schneck GW, Osborn JW. Neck lesions in the teeth of cats. Vet Rec 1976; 99: 100. Seawright AA, English PB, Gartner RJW. Hypervitaminosis A in the cat. Adv Vet Sci Comp Med 1970; 14: 1–27. Stebbins KE, Morse CC, Goldschmidt MH. Feline oral neoplasia: a ten-year survey. Vet Pathol 1989; 26: 121– 128. Steinberg S. Histologische Untersuchungen zu Fruehveraenderungen der Felinen Odontoklastischen Resorptiven Laesionen (FORL) an klinisch gesunden Zaehnen [thesis]. Berlin: Free University of Berlin, Faculty of Veterinary Medicine; 2002. Tannehill-Gregg S, Kergosien E, Rosol TJ. Feline head and neck squamous cell carcinoma cell line: Characterization, production of parathyroid hormone-related protein, and regulation by transforming growth factor-beta. In Vitro Cell Develop Biol Anim 2001; 37: 676–683. Trope M. Root resorption of dental origin: classification based on etiology. Pract Periodont Aesthet Dent 1998; 10: 515–522. Trope M, Chivian N. Root resorption. In: Cohen S, Burns RC (eds). Pathways of the Pulp, 6th ed. Mosby-Year Book, St. Louis, 1994; 486–512. Umphlet RC, Johnson AL. Mandibular fractures in the cat: a retrospective study. Vet Surg 1988; 17: 333–337. Van Wessum R, Harvey CE, Hennet P. Feline dental resorptive lesions: prevalence patterns. Vet Clin North Am Small Anim Pract 1992; 22: 1405–1416.

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Verstraete FJ. Anomalous development of the upper third premolar in a dog and a cat. J S Afr Vet Assoc 1985; 56: 131–134. Verstraete FJ, van Aarde RJ, Nieuwoudt BA, Mauer E, Kass PH. The dental pathology of feral cats on Marion Island, part I: congenital, developmental and traumatic abnormalities. J Comp Pathol 1996; 115: 265–282. Verstraete FJ, van Aarde RJ, Nieuwoudt BA, Mauer E, Kass PH. The dental pathology of feral cats on Marion Island, part II: periodontitis, external odontoclastic resorption lesions and mandibular thickening. J Comp Pathol 1996; 115: 283–297.

Verstraete FJM, Terpak CH. Anatomical variations in the dentition of the domestic cat. J Vet Dent 1997; 14: 137–140. White SD, Rosychuck RAW, Janik TA, Denerolle P, Schultheiss P. Plasma cell stomatitis-pharyngitis in cats: 40 cases (1973– 1991). J Am Vet Med Assoc 1992; 200: 1377–1380. Wiggs RB, Lobprise HB. Domestic feline oral and dental disease, Veterinary Dentistry—Principles and Practice, Lippincott-Raven, Philadelphia, 1997; 482–517. Williams CA, Aller MS. Gingivitis/stomatitis in cats. Vet Clin North Am Small Anim Pract 1992; 22: 1361–1383. Zetner K, Steurer I. The influence of dry food on the development of feline neck lesions. J Vet Dent 1992; 9 (2): 4–6.

Section II

Treatment

Chapter 6

Equipment

Acquiring the proper equipment to perform feline dentistry is one of the wisest investments a practitioner can make. There is no other branch of small animal practice wherein a relatively modest financial investment can provide such benefit to the patient, client, and practice (fig. 6.1). Choosing how much equipment, materials, and education to obtain is an individual decision. If feline dentistry is only a small part of the practice, the veterinarian may want to acquire only basic equipment and materials. If advanced dentistry is the goal, additional instruments, materials, and training are needed.

Oral Assessment Instruments and Materials

•

•

Education Tools

• • •

•

•

• • • • •

• • • •

Veterinary Dental Techniques, Holmstrom et al., Saunders, 1999 Veterinary Dentistry: Principles and Practice, Wiggs and Loprise, Lippincott, 1998 Small Animal Dental Equipment, Materials, and Techniques, Bellows, Blackwell, 2004. An Atlas of Veterinary Dental Radiology, DeForge and Colmery, Iowa State University Press, 1999 Atlas of Canine & Feline Dental Radiography; Mulligan, Aller, and Williams; Veterinary Learning Systems; 1998 An Introduction to Veterinary Dentistry; Johnston; an interactive multimedia CD-ROM dental education course comprised of six chapters, including video clips; www.vetschools.ac.uk The Journal of Veterinary Dentistry Veterinary Dentistry, Harvey and Emily, Mosby, 1993 The Practice of Veterinary Dentistry: A Team Effort, Bellows, Iowa State University Press, 1999 Atlas of Dental Radiography in Dogs and Cats, DuPont and DeBowes, Saunders, 2009.

• • • •

Mouth props or gags, which can be placed between the maxillary and mandibular canines or cheek teeth to keep the mouth open during dental procedures (placing spring loaded props between canines is generally not recommended due to potential for iatrogenic damage to the teeth and/or temporomandibular joints (figs. 6.2 a,b). Illuminated dental magnification telescopes (fig. 6.3). Dental mirror (fig. 6.4) Sterile instrument holders (figs. 6.5 a,b) Operator safety equipment (goggles, mask, gloves) (fig. 6.6) Dental radiography (fig. 6.7) 䊊 unit for exposure 䊊 film, digital sensor or CR phosphor plate 䊊 processor—analog (chairside, or automatic) or digital Dental explorer (fig. 6.8) Periodontal probe (fig. 6.9) Charts for dental examination Dental models (figs. 6.10 a,b,c)

Oral Treatment and Prevention Instruments and Materials

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Ultrasonic scaler with multiple tips (figs. 6.11a,b) Polishing equipment—disposable polishing angle, polishing paste (fig. 6.12) Gracey curette feline mini 1/2, 5/6, 9/10, 13/14 (Cislak) Molt periosteal elevator (figs. 6.13 a,b,c) Freer periosteal elevator (fig. 6.14) 151

Figure 6.1 Four-station dental operatory, All Pets Dental, Weston, Florida (Midmark manufacturing case work and dental stations).

a

Figure 6.2 a. Leopold mouth gag (Cislak). b. Proper placement of mouth gag between canines.

b

Figure 6.3

152

Magnification and illumination telescopes (Perioptix).

a

Figure 6.4

Dental mirror.

b

Figure 6.6

Figure 6.5

a. Sterile instrument pouch. b. Sterile extraction pack.

Figure 6.7

Intraoral radiology.

Operator safety equipment.

153

Figure 6.8

Dental explorer (Cislak).

a

b

Figure 6.9

Periodontal probe (Cislak).

c Figure 6.10 Dental teaching models: a. Henry Schein. b. Columbia Dentiform. c. Shipp Laboratories.

154

a

b Figure 6.11

a. Ultrasonic scaler (Midmark). b. Piezoelectric tips.

155

Figure 6.12 Low-speed polishing handpiece with disposable polishing tip.

a

b

c

Figure 6.13 Molt periosteal elevators: a. Peri EX-9 small (Cislak). b Peri EX-9 Large (Cislak). c. Peri EX-7 Large (Cislak). Figure 6.14

156

Freer periostal elevator (Cislak).

Equipment

a

b

c

157

d

e Figure 6.15 a–d. Wing-tipped elevators (EXW1-4 Cislak). e. Short-handle, wing-tipped elevator set (Miltex).

• • • • •

Winged-tipped elevators (figs. 6.15 a,b,c,d,e) Extraction forceps (figs. 6.16a,b) Caries curette (fig. 6.17) Root tip elevator (figs. 6.18 a,b) High-speed/low-speed delivery system (Ultima Dental) (fig. 6.19 a)

• • •

High-speed, low-speed handpiece with contra angle attachment (figs. 6.19 b,c) Assortment of burs: round, inverted, pear, fissure (fig. 6.20) Home care products

a

Figure 6.16 a and b. Extraction forceps (Cislak).

b

a Figure 6.17 Caries curette (Cislak).

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Figure 6.18

b

a and b. Root tip elevators (Cislak).

a

c

b

Figure 6.19 a. High-/low-speed delivery system (Ultima Dental). b. Highspeed handpiece. c. Low-speed handpiece with contra angle and polishing attachment (circled) (Midmark manufacturing whip style).

Figure 6.20 Assorted high-speed burs.

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Endodontic Instruments and Materials

• • • • • • • • • • • • • • • • •

K-files 21 mm long, width sizes 8 to 40 23 gauge and 27 gauge blunted endodontic needles Sodium hypochlorite solution Root canal conditioner, file lubricant Mixing slab and spatula Paper points: 30 mm long, various widths Gutta percha Spreaders: small Pluggers: small Zinc oxide–eugenol or non-eugenol endodontic canal sealer (Sealapex-Kerr) Calcium hydroxide powder and paste College tipped pliers Etching gel Bonding resin and brush Composite restorative Plastic matrix strips Curing light

Orthodontic Instruments and Materials

• • •

Orthodontic buttons Bracket cement Elastics—Masel chain

Power Scaling Professional calculus and plaque removal (scaling) is performed by using hand instruments or scalers powered by electricity, compressed air, or gas while the cat is anesthetized. Powered scalers increase the speed and efficiency of teeth cleaning. There are three types of power-driven scalers: sonic, ultrasonic, and rotary. Because of the potential for iatrogenic damage to the gingiva, dental hard tissues and the pulp, techniques for rotary scaling are not discussed in this text.

Sonic Scaler The sonic (subsonic) scaler is attached to the high-speed outlet of an air-or gas-driven delivery system. Sonic scalers have a wide amplitude (0.5 mm) compared to ultrasonic scalers (0.01–0.05 mm). This wider amplitude may result in greater cementum removal when the scaler is used subgingivally compared to the ultrasonic scaler equipped with a periodontal tip for subgingival use. Additionally, sonic scaler tips vibrate at low frequencies ranging between 3,000–9,000 CPS (ultrasonic 20,000– 50,000 CPS). The lower frequency is best used to

remove plaque and fresh calculus. Most cats requiring scaling present with chronic calculus and plaque accumulation. The sonic scaler unit requires continuous air pressure of 40 psi. A relatively large compressor (>1 hp) is needed for power. If the delivery system is oxygen-, nitrogenor carbon dioxide–driven, use of sonic scalers can consume large volumes of gas, which might not be financially feasible. Daily lubrication is necessary for maintenance.

Ultrasonic Scaler Ultrasonic scalers are classified as magnetostrictive or piezoelectric. Magnetostrictive units use ferromagnetic stacks or ferrite rods to produce tip vibration. Ferromagnetic stacks are strips of laminated nickel attached with solder. When the operator wants to remove plaque and calculus from above the gingiva, the standard P-10 or beavertail insert is selected. When subgingival use is planned, magnetostrictive thin, long subgingival AfterFive (Hu-Friedy) and SLI Slimline (Dentsply Cavitron) inserts can be used safely. When an alternating electrical current is supplied to a wire coil in the magnetostrictive handpiece, a magnetic field is created around the stack or rod transducer, causing the tip to constrict and relax. This vibration energizes the water as it passes over the tip, producing a scouring effect to remove plaque, calculus, and stains. Bubbles are created which implode, affecting bacterial cell walls in the gingival sulcus. The water mist also cools the tip and irrigates debris. A piezoelectric scaler is activated by dimensional changes in crystals housed within the handpiece as electricity is passed over the surface of the crystals. The resultant vibration produces tip movement (fig. 6.21). When choosing an ultrasonic scaler, frequency, tip motion, and potential iatrogenic injury must be considered. Magnetostrictive advocates claim elliptical tip motion is most effective because it generates pathogendestroying cavitation bubbles 360 degrees around the tip. In contrast, the piezo design creates bubbles only at the two ends of the back-and-forth cycle. The sonic scaler does not produce cavitation bubbles.

Frequency Frequency is the number of times the scaler tip vibrates each second. A variety of frequencies are available within the three types of ultrasonic technologies. The higher frequencies (above 40,000 CPS) may provide greater efficiency. Ultrasonic scaling units are also available in manualtuning or auto-tuning models. Some researchers feel that

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compares the tip in use with an original. A loss of one millimeter of the tip equals a 25% loss of efficiency. A two millimeter loss of the tip equals a 50% loss in efficiency and the tip should be replaced. The magnetostrictive types of ultrasonic tips are changed with a pull-out/push-in action. O-rings are used in the handpiece and on the instrument to provide a tight fit and a seal to prevent water leakage. Piezocelectric scalers require a wrench to unscrew one tip and to replace it with another. Magnetostrictive inserts and piezoelectric tips should be cleaned and sterilized after each use. To clean, rinse thoroughly or immerse in an ultrasonic instrumentcleaning unit for 20 minutes. After removal, rinse the inserts with tap water and dry before packaging and sterilizing in a steam autoclave or gas sterilizer. Virtually all brands of magnetostrictive inserts of the same frequencies are interchangeable. Most 30 kHz units will operate only with 30 kHz inserts (a 25 kHz insert will not fit into the handle). Most piezoelectric scalers use tips designed specifically for each brand of scaler, which creates a problem if the manufacturer goes out of business.

Power Scaling Technique Follow these steps for the sonic/ultrasonic technique: 1.

Figure 6.21

Piezoelectric ultrasonic scaler.

better cavitation is achieved at low power settings if the scaler is slightly mistuned. Because auto-tuned scalers perfectly tune to the insert’s frequency, a manually tuned scaler would be preferred.

Tip Activity and Surfaces The activity of piezoelectric scalers is limited to the last 3 mm of the tip. Magnetostrictive metal stack tips are active at the last 4 mm of tip; the magnetostrictive ferrite rod scaler is active a full 12 mm of the tip. The most powerful surfaces of the magnetostrictive stack scaler tip are the underside and the top; the lateral sides are the least active. To prevent trauma to the tooth surface, only the lateral sides should be used against the tooth or within the gingival sulcus. The ferroceramic (ferrite) rod tip is equally active on all sides.

Tip Replacement Tip wear is critical to the efficiency of the scaling procedure. Tip wear can be evaluated using a chart which

Hold the handpiece lightly in a modified pen grasp; i.e., the scaler is held in the dominant hand with the pads of the index finger and thumb opposite to each other on the handle closest to the working end. The thumb and index finger are not touching, thereby creating a tripod effect with the middle finger placed along the shank of the instrument. This tripod effect balances the instrument in the operator ’s hand to provide stability and control by keeping the index finger and thumb separated. 2. The ultrasonic instrument should be grasped lightly, not tightly. It should feel balanced in the hand, with minimal pull from the handpiece cord. The handpiece, not the hands, must be allowed to do the work. The handpiece is balanced on the index or middle finger. A modified pen grasp is not as important in holding the ultrasonic or sonic scaler as it is with hand instruments. To decrease stress on the hand from the pull on the handpiece cord, the cord may be looped over the little finger (fig. 6.22). 3. Use eye, ear, and respiratory protection. 4. Hold the fulcrum or finger rest at a distance further from the tooth than with hand instruments, because the tips do not have cutting edges.

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Figure 6.22

Proper finger position.

Figure 6.23 Adjusted mist for ultrasonic scaling.

5. 6.

7.

8.

9.

10.

Adjust water spray to deliver a steady drip with a small mist halo (fig. 6.23). Apply light pressure to the tip working in a coronal-to-apical direction. The sound waves should do most of the work. Efficiency decreases with increased pressure. Pass the side of the working end over calculus and plaque in short, light vertical strokes. The scaler should not be used on a single tooth for too long to avoid iatrogenic damage. Heavy lateral pressure should be avoided. Keep the lateral surface working end in constant motion. Leaving it in one place too long increases the amount of tooth material removed and can cause thermal damage to the pulp. Never hold the tip perpendicular to the surface of the tooth. This will either etch or groove the surface. Specially designed subgingival periodontal tips may be used subgingivally. To avoid iatrogenic injury, decrease the power with subgingival use. After ultrasonic tooth cleaning is completed, use air from the air/water syringe to gently blow the gingival margin away from the tooth and examine the tooth surface for missed calculus.

High/Low Speed Delivery Systems Compressed air or gas can be used to power handpieces for polishing, tooth sectioning, endodontics, restoration, and oral surgery. The advantages over motorized systems lie in the capability of precise cutting at higher speed, and water cooling to prevent thermal damage to the pulp and surrounding bone. The compressor provides pressurized air for the airwater syringe and handpieces. Compressor size is important. The required capacity of the compressor is related to the number of operatories and handpieces used at the same time in the practice. The compressor must be large enough to maintain pressure of 30–40 psi at a flow rate of 3 cubic feet per minute. When the compressor is too small, it will run almost continuously during use and may overheat. If a sonic scaler or more than one station is used, a minimum of a 1 hp compressor is recommended. Compressors are either air- or oil-cooled. Air-cooling reduces the amount of contaminants (oil) in the line, but can be noisier and usually more expensive than oilcooling. Modified refrigerator oil–cooled compressors (“silent” compressors) are commonly used in smaller

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self-contained delivery systems. Unfortunately, when using an oil-cooled compressor, small particles of oil become mixed with the compressed air, which might contaminate tooth surfaces, interfering with restoration. Compressors for dental delivery systems are attached either to the unit (self-contained) or located remotely in a nearby cabinet, closet, attic or outside the clinic. The advantages of remote compressors include the following:

• • •

Less noise occurs in the operatory. Multiple stations may be attached to one compressor. Less storage is required in the immediate operatory area.

The storage or air tank holds air compressed by the compressor. This stored air is used to power the dental handpieces and air/water syringe. Air tanks come in many sizes. The larger the tank size, the less “work” the compressor needs to do. Pressure inside the air storage tank varies by manufacturer between 80–120 psi. When maintenance pressure is reached, the compressor turns off. When the tank pressure drops below 60 psi, the compressor turns on to refill the tank with compressed air. The assembly delivery system (control panel) contains the air/water supply syringe, tubing for the handpieces, pressure gauge(s), switches for turning water on and off, needle valve to adjust water flow and a switch to change from the high- to low-speed handpiece. The control panel may be part of a cart or mounted on the dental table (figs. 6.24 a,b). The foot pedal starts and stops the system and in some units controls handpiece speed.

Nitrogen-Powered Delivery Systems Some delivery systems use nitrogen to power handpieces. Nitrogen, an inert gas, can provide clean, oil-free power, which may extend the handpiece life. Because power is directly delivered from gas cylinders, compressors and air storage tanks are not necessary. There is no electrical requirement and no compressor noise. Additionally, nitrogen-driven delivery systems require less maintenance than air-driven units. The typical cost of nitrogen is less than US$1.50 per procedure. Nitrogen is not recommended to power air-driven sonic scalers because of the large volume of gas needed (figs. 6.25 a,b). A three-way air/water syringe is part of the delivery system. The syringe produces a stream of air, water or a spray, for rinsing debris from the teeth and drying as needed during dental procedures (fig. 6.26).

a

b Figure 6.24 a. Control panel, air/water syringe, handpieces, and ultrasonic scaler (Midmark). b. Nitair II (CBi).

Dental handpieces are precision-built mechanical devices designed for use with rotary instruments, such as burs, stones, wheels, and discs. Handpieces can be classified according to the revolutions per minute (RPM) or speed at which they operate. Handpieces that run under 100,000 RPM are classified as slow speeds. Models running at 20,000–100,000 RPM are classified as slowspeed type II mid speed. Low speed is a subcategory of slow speed. The handpieces commonly used in veterinary medicine run less than 20,000 RPM and are classified as slow-speed type III low speeds. The (s)low-speed (straight) handpiece commonly used in veterinary dentistry:

• • •

Rotates at 5,000–20,000 RPM Contains forward and reverse controls Operates with high torque

a

b Figure 6.25 a. Nitrogen-powered high-/low-speed delivery system (CBi). b. Portable delivery system.

164

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Figure 6.26 Three-way air/water syringe.

• • •

Generally does not use water (although some are water-equipped) Is used for polishing Is available as one- or multiple-section units

The one-section straight handpiece accepts cutting and polishing burs designated as handpiece (HP). An HP designation means that the cutting or polishing instrument has a long, straight shaft that inserts directly into the straight handpiece and is tightened by rotating the collar clockwise. A prophy head, right-angled handpiece or contra-angle may also attach to the one-section unit. The multiple-section, slow-speed handpiece is composed of a low E (European type) speed motor and a straight nose cone with a reduction gear to drive the prophy head, right-angled handpiece or contra-angle. Many units have a method of quickly connecting and disconnecting the motor and attachments. The contra-angle attaches to the slow-speed straight handpiece to form an extension with an angle greater than 90 degrees at the working end. Angulation provides better access to the posterior teeth. The contraangle’s main use is powering burs for finishing restorations and Gates Glidden drills for pulp chamber and root canal enlargement. The head of the contra-angle attachment contains either a latch or a friction type chuck, into which a dental bur or other rotary instrument is fitted. Latch-type contra-angles hold the end of the cutting instrument by mechanically grasping a small groove on the end of the instrument shaft. Right angle (RA) designates latch-type burs. Friction grip (FG) burs have short, smooth shafts without retention grooves.

The disposable plastic single-use prophy angle is preferred by the author because of reduced crosscontamination, lack of maintenance, ease of operation and low expense. The oscillating disposable prophy angle rotates 45 degrees and reverses. Advantages of the oscillating disposable prophy angle include decreased heat generated on the tooth surface and less lip hair caught in the polishing cup. High-speed handpieces are used when rapid and efficient cutting of the tooth and/or supporting bone is needed. High-speed handpieces are air-powered to 300,000–400,000 RPM. To avoid overheating, an irrigation spray is automatically delivered over the operative field. When choosing the handpiece style, a pediatric head gives the operator improved access in small animals. Some high-speed handpieces have a fiber-optic light built into the head. The light projects a beam from the head of the handpiece directly onto the bur and tooth. High-speed handpieces use friction grip (FG) burs. Attaching a bur to the high-speed handpiece is an easy procedure. The chuck is tightened by thumb control or built-in lever or by using a bur-inserting/-removal tool.

Rotary Cutting Instruments Rotary cutting dental instruments are used to:

•

Section multi-rooted teeth and/or remove part of the buccal alveolus, thus facilitating extraction.

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Feline Dentistry

Perform alveoloplasty to smooth out sharp projections. Provide access points for root canal therapy. Reduce crown height in crown reduction procedures. Remove part of the maxilla or mandible.

Burs are instruments placed into the dental handpiece. Burs consist of two parts: (1) The shaft fits into the handpiece. (2) The head is the cutting end.

Operative Bur Types Carbide steel burs (carbides) are used for cutting and are the most commonly used burs. Diamond points (diamonds) are burs covered with industrial diamond grit used for crown preparation, bone smoothing (alveoloplasty), scarification and shaping teeth (odontoplasty).

Three Types of Bur Shanks Straight handpiece burs have long straight shanks. In dental supply catalogs, they are abbreviated as SH or HP. Latch-type burs have notched shanks and are abbreviated as LA (latch-type angle) or RA (right-angled). Friction grip burs have smooth shanks, which are smaller in diameter than HP burs. They are used in highspeed handpieces. Friction grip burs are identified as FG, FGS (friction grip surgical) or FGSS (friction grip short shank used for tight areas and restorations). Surgical burs have longer (25 mm) shanks used to reach into deep recesses; restorative burs are shorter (20 mm).

Bur Shapes and Sizes Burs come in several sizes, represented by numbers. The lower the number in a series, the smaller the bur head. Round burs are most commonly used to open the pulp chamber in preparation for endodontic treatment, bone smoothing and root atomization. Their sizes range from 0.25–10. Inverted cone burs are wider at the tip with slightly rounded corners for added protection against chipping. Their sizes range from 33.5 to 37L (L indicates long). Inverted cones at one time were used to create undercut restoration sites for filling. Unfortunately, inverted cones may leave unsupported enamel at the restoration site.

Fissure burs have grooved heads and are useful for sectioning teeth and reducing crown height. The sides of straight fissure burs are parallel. The sides of taper fissure burs converge toward the tip. Fissure burs may also contain cross-cuts along the blades (called cross-cut fissure burs), which act like saw teeth to allow additional cutting ability. The size of straight fissure burs ranges from 56–58L, that of cross-cut straight fissure burs from 556–558L and that of taper fissure burs from 699–703. Diamond burs have industrial diamond grit embedded into the working surfaces. Diamonds are used in many places that carbides the tooth to receive are, and especially in restorative dentistry to prepare the tooth to receive prosthodontic crowns, and to help finish composite restorations. Trimming and finishing burs are designed for completing restorations, odontoplasty and alveoloplasty. The more flutes on a finishing bur, the finer will be the finish (a 30-fluted bur, also known as a fine finishing bur, produces a smoother finish than does a 12-fluted bur). Stones are used for polishing and finishing restorations. Stones are mounted on a mandrel (mounting device), which is inserted into the handpiece. Stones are identified by color. White stone burs are commonly used in veterinary dentistry to finish composite restorations or to smooth minor enamel defects. Green stones are used to finish amalgam and smooth enamel. Gray stones, made of carborundum and rubber, are used for polishing fabricated crowns. Finishing discs are used to shape and smooth restorations. They are available in various grades of abrasiveness, from coarse to superfine and are used sequentially from coarse (to shape restorations) to fine grade (to smooth surfaces). The finest-grade disk is used with a paste.

Bur Care Burs are surgical cutting instruments and should be cleaned and sterilized before each use. To remove debris lodged in the bur head, the bur is removed from the handpiece then rinsed, brushed free of debris with a nylon or wire bur brush (or pencil eraser) and soaked in a cold sterile solution for 24 hours.

Equipment Maintenance Dental handpieces are precision instruments and must be maintained properly to ensure optimal operation and maximum life. The veterinarian or technician should check with the manufacturer ’s instructions for specific care.

Equipment

A generic lubrication/sterilization process consists of these steps: 1.

2. 3. 4.

5. 6. 7.

At the end of each procedure, scrub the handpiece with gauze, a sponge, or a brush and cleaning solution to remove debris. Following the manufacturer ’s instructions, rinse the handpiece without immersion. Dry the handpiece with gauze, paper towel, or air from the air/water syringe. For handpieces requiring lubrication, add three drops of lubricant to the smaller of the two large holes (drive air tube) at the connection area. Note: Some handpieces are lubrication-free and will be destroyed if lubricated; check manufacturer ’s instructions. Briefly power the handpiece with the bur inserted to remove excess lubricant. Place the handpiece in an autoclavable envelope. Sterilize the handpiece in the autoclave.

Replacing the High-Speed Turbine The turbine is secured in the high-speed handpiece head by a screwed faceplate. After the faceplate is unscrewed using the manufacturer-supplied tool, the turbine can be easily replaced. To clean and lubricate the low-speed handpiece and attachments, use the following steps: 1. Place the working end of the handpiece into a small bottle of handpiece-cleaning solvent. 2. Power the handpiece backward and forward for one minute. 3. Remove the handpiece from the cleaner and wipe dry. 4. Periodically, disassemble the handpiece, using the special wrench furnished by the manufacturer. 5. Following the manufacturer ’s instructions, place one drop of liquid lubricant on the neck of the head, one drop on each gear of the gear and shaft assembly, and three drops into the back end of the angle. Alternatively, place heavy lubricant (petroleum jelly) on the gears of the handpiece before reassembly.

Compressor Maintenance Oil-cooled compressors are equipped with a dipstick or view port to monitor the oil level. The owner ’s manual should be checked for the recommended replacement oil if needed. Some compressors are “oil free” and do not require oil maintenance.

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Condensation in the air storage tank accumulates with each use. The accumulated fluid should be drained weekly to monthly depending on use and ambient humidity.

Infection Control Disinfection is the process of destroying microbial life by placing instruments in a solution (example: Cidex) for a specified period. Chemical disinfection does not eliminate all viruses and spores. Sterilization kills all microorganisms. The autoclave is a steam chamber for sterilizing instruments. During the sterilization cycle, distilled water flows into the chamber and is heated to create steam. Because the chamber is sealed, pressure increases to approximately 15 pounds per square inch. The increase in pressure causes the heat of the steam to rise to approximately 250 °F. When the instruments are exposed to this high pressure/steam temperature for 15 minutes or more, sterilization occurs. Dental instruments used in the mouth should be sterile. After cleaning, instruments can be placed in an autoclavable see-through sleeve and sterilized. Patient and operator infection control requires the following: An individual set of sterilized instruments should be used on each patient. Human dentists have developed aggressive infection control procedures in response to spreading HIV and hepatitis among patients and staff. Many of these protocols can be adopted in veterinary hospitals for similar reasons. Viral and bacterial particles may become lodged in the paste remaining on the head of the prophy angle and transmitted to the next patient even if the prophy cup is changed. Disposable prophy angles or autoclaved metal angles are recommended for all feline patients to prevent spread of feline leukemia virus and feline immunodeficiency virus. Polishing paste is available in individual cups or in bulk form in a supply container. When using the bulk container, the paste should be applied with a new and clean tongue depressor to avoid contaminating the container. A mask, gloves, and ear and eye protection should be worn when performing dental care. The oral cavity should be rinsed with a 0.12% chlorhexidine solution before oral procedures to reduce the number of bacteria that could enter blood vessels of the patient (bacteremia) or become aerosolized during power scaling. The patient’s head should be angled downward to promote drainage. High-speed delivery system fluid lines can develop a biofilm of potentially harmful viruses and bacteria. Chlorhexidine can be used to flush the fluid lines, thus decreasing the viral and bacterial load.

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Further Reading Deeprose J. Operator safety and health considerations. In: Tutt C, Deeprose J, Crossley D (eds). BSAVA Manual of Canine and Feline Dentistry, 3rd ed. BSAVA, Gloucester, 2007; 56–66. Gorrel C, Penman S. Dental equipment. In: Crossley DA, Penman S (eds). Manual of Small Animal Dentistry, 2nd ed. BSAVA, Cheltenham, 1995; 12–18. Harvey CE, Emily PP. Small animal dental equipment and materials, Small Animal Dentistry, Mosby, St. Louis, 1993; 378–400. Holmstrom SE, Frost Fitch P, Eisner ER. Dental equipment and care, Veterinary Dental Techniques for the Small Animal Practitioner, 3rd ed. Saunders, Philadelphia, 2004; 39–129.

Lipscomb V, Reiter AM. Surgical materials and instrumentation. In: Brockman DJ, Holt DE (eds). BSAVA Manual of Canine and Feline Head, Neck and Thoracic Surgery. BSAVA, Gloucester, 2005; 16–24. Robinson J. Dental instrumentation and equipment. In: Tutt C, Deeprose J, Crossley D (eds). BSAVA Manual of Canine and Feline Dentistry, 3rd ed. BSAVA, Gloucester, 2007; 67–76. Wiggs RB, Lobprise HB. Dental equipment, basic materials and supplies, Veterinary Dentistry—Principles and Practice, Lippincott-Raven, Philadelphia, 1997; 1–54.

Chapter 7

Anesthesia

General anesthesia is necessary for the oral assessment, treatment, and prevention visits. The American Veterinary Dental College (AVDC) created a position statement (below) regarding the need for general anesthesia to provide companion animal dental diagnostics and therapy (fig. 7.1).

Non-Professional Dental Scaling (NPDS) In the United States and Canada, only licensed veterinarians can practice veterinary medicine. Veterinary medicine includes veterinary surgery, medicine, and dentistry. Anyone providing dental services other than a licensed veterinarian, or a supervised and trained veterinary technician, is practicing veterinary medicine without a license and shall be subject to criminal charges. Although the term “Anesthesia-Free Dentistry” has been used in this context, AVDC prefers to use the more accurate term Non-Professional Dental Scaling (NPDS) to describe this combination. This position statement addresses dental scaling procedures performed on pets without anesthesia, often by individuals untrained in veterinary dental techniques. Owners of pets naturally are concerned when anesthesia is required for their pet. However, performing NPDS on an unanesthetized pet is inappropriate for the following reasons: 1.

2.

Dental tartar is firmly adhered to the surface of the teeth. Scaling to remove tartar is accomplished using ultrasonic and sonic power scalers, plus hand instruments that must have a sharp working edge to be used effectively. Even slight head movement by the patient could result in injury to the oral tissues of the patient, and the operator may be bitten when the patient reacts. Professional dental scaling includes scaling the surfaces of the teeth both above and below the gingival margin (gum line), followed by dental polishing. The most critical part of a dental scaling procedure is scaling the tooth surfaces that are within the gingival pocket (the subgin-

3.

4.

gival space between the gum and the root), where periodontal disease is active. Because the patient cooperates, dental scaling of human teeth performed by a professional trained in the procedures can be completed successfully without anesthesia. However, access to the subgingival area of every tooth is impossible in an unanesthetized canine or feline patient. Removal of dental tartar on the visible surfaces of the teeth has little effect on a pet’s health and provides a false sense of accomplishment. The effect is purely cosmetic. Inhalation anesthesia using a cuffed endotracheal tube provides three important advantages—the cooperation of the patient with a procedure it does not understand, elimination of pain resulting from examination and treatment of affected dental tissues during the procedure, and protection of the airway and lungs from accidental aspiration. A complete oral examination, which is an important part of a professional dental scaling procedure, is not possible in an unanesthetized patient. The surfaces of the teeth facing the tongue cannot be examined, and areas of disease and discomfort are likely to be missed.

Safe use of an anesthetic or sedative in a dog or cat requires evaluation of the general health and size of the patient to determine the appropriate drug and dose, and continual monitoring of the patient. Veterinarians are trained in all of these procedures. Prescribing or administering anesthetic or sedative drugs by a non-veterinarian can be very dangerous, and is illegal. Although anesthesia will never be 100% risk-free, modern anesthetic and patient evaluation techniques used in veterinary hospitals minimize the risks, and millions of dental scaling procedures are safely performed each year in veterinary hospitals. To minimize the need for professional dental scaling procedures and to maintain optimal oral health, the AVDC recommends daily dental home care from an early age. This should include brushing or use of other effective techniques to retard accumulation of dental plaque, such as dental diets and chew 169

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a

Figure 7.1 Patient anesthetized, temperature control assist Bair Hugger®, Cardell® monitor, Matrix® anesthetic unit attached to adjustable height hydraulic table (Canis Major, Midmark).

b Figure 7.2 a. ECG evaluation software (DVM Solutions). b. Preanesthesia blood pressure evaluation (DVM Solutions).

materials. This, combined with periodic examination of the patient by a veterinarian and with dental scaling under anesthesia when indicated, will optimize life-long oral health for dogs and cats. For general information on performance of dental procedures on veterinary patients, please read the AVDC Position Statement on Veterinary Dental Healthcare Providers, which is available on the AVDC website (www.AVDC.org). For information on effective oral hygiene products for dogs and cats, visit the Veterinary Oral Health Council website (www. VOHC.org).

Anesthesia protocols vary by patient age, condition, morbidity factors, and length and type of procedure. Local anesthetics are used on all dental surgical cases where tissue is incised (see Table 7.1 at end of chapter).

Preanesthetic Evaluation

Premedication

All anesthetic patients require proper preanesthetic evaluation including a detailed history, physical examination, and laboratory testing. Patients with preexisting medical conditions may need further evaluation to modify the anesthetic protocol (figs. 7.2 a, b). Hyperthyroidism, diabetes mellitus, and chronic renal disease are common feline diseases requiring special anesthetic attention. Generally, unless the patient is in pain, conditions yielding abnormal test values should be corrected before dental care is rendered.

An intravenous catheter is placed and fluids are administered in all patients undergoing anesthesia. Premedication for healthy cats may include hydromorphone 0.1 mg/kg IM or SC or butorphanol 0.2 mg/ kg IM or SC combined with dexmedetomidine 0.0025 to 0.01 mg/kg IM (fig. 7.3). As cats become more debilitated or aged, butorphanol 0.2 mg/kg IM or SC or hydromorphone 0.05–0.2 mg/kg IM or SC with 0.2–0.4 mg/kg midazolam IM can be considered.

Anesthesia Protocols

Anesthesia

171

must be considered when anesthetizing older or ill patients.

Etomidate

Figure 7.3

Preanesthetic medication.

For fractious cats presenting without feline hypertrophic cardiomyopathy, a combined dose of medetomidine HCl 0.01–0.02 mg/kg, plus buprenorphine 0.01–0.02 mg/kg, ketamine HCl 1–3 mg/kg, and butorphanol tartarate 0.1 mg/kg are mixed in one syringe and administered IM; for fractious cats with feline hypertrophic cardiomyopathy, low-volume medetomidine (0.005 mg/kg) plus butorphanol tartarate 0.1–0.2 mg/kg plus or minus midazolam HCl 0.2 mg/kg may be administered. All patients should be individually assessed and a patient-specific anesthetic premedication protocol developed, as the above are simply examples of typical premedication protocols.

Etomidate (0.5–1.5 mg/kg IV) is the induction drug of choice for patients that have cardiovascular disease or arrhythmias (except A-V dissociation) because cardiac output and blood flow to the kidneys are maintained. However, there have been reports of hemolysis in cats after etomidate injection. A premedicant (e.g., butorphanol IV, SC, IM; diazepam; or midazolam IV) should be administered prior to etomidate administration.

Pain Control Anesthesia protocols linked to pain control (in addition to local anesthesia) include the following:

•

•

Expected mild to moderate pain–-buprenorphine 0.01–0.03 IM, IV sublingually mg/kg plus midazolam 0.2 mg/kg, plus 0.0005–0.075 mg/kg dexmedetomidine (0.0025–0.005 μg/kg). Expected moderate- to high-level pain–-hydromorphone 0.1 mg/kg plus midazolam 0.2 mg/kg, plus dexmedetomidine 0.0005–0.075 mg/kg (0.5–7.5 μg/ kg).

Induction There are many feline anesthesia protocols for the healthy young to middle-aged cat.

Chamber or Mask Induction Chamber or mask induction should be avoided due to catecholamine release during the excitement phase from the struggle against restraint or as a reaction to the pungent odor of the inhalant anesthetic agent.

Propofol Propofol (2,6-diisoproylphenol) (3–4 mg/kg IV; 3 mg/kg if opioid is given as a premedicant), with half of the dose given as a slow bolus over 40–60 seconds the rest to effect, is a nonbarbiturate hypnotic. Slightly higher doses are required for cats than dogs, and recoveries are longer in cats than dogs when the infusion lasts more than 30 minutes due to decrease in glucuronide conjugation. Propofol provides no analgesia in the cat. Propofol is a direct myocardial depressant resulting in both venous and arterial relaxation, thus creating hypotension. This hypotension is well recognized clinically and

Intubation All cats placed under anesthesia for oral assessment and treatment must be intubated and the airway secured with an inflatable cuff. Topical lidocaine may be applied to the laryngeal mucosa to facilitate passage of the endotracheal tube. The endotracheal tube should be secured before the cuff is inflated. The cuff should be inflated to a light seal. Overinflation of the endotracheal cuff must be avoided. Subcutaneous emphysema and pneumothorax have occurred during or after anesthesia in cats anesthetized for dental care. It is critical that anytime the head is moved from side to side during assessment or dental treatment, the endotracheal tube be disconnected from the anesthesia machine and reconnected after the new position is reached (figs. 7.4 a, b).

Maintenance Anesthesia is generally maintained with isoflurane or sevoflurane and oxygen. Little isoflurane or sevoflurane

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a a

b Figure 7.5 a. Hot Dog® patient warmer. b. Bair Hugger® used below the patient.

to support body temperature. It is much easier to prevent hypothermia than to treat it (figs. 7.5 a, b). b Figure 7.4 a. Lateral thoracic radiograph before anesthesia. b. Pneumothorax, pneumomediastinum, and pneumoabdomen secondary to endotracheal tube–induced tracheal tear.

is metabolized. The insolubility of the inhalants allows for a rapid induction and recovery. Patient body temperature control is necessary. Long anesthetic procedures coupled with the frequent use of water and the ambient room temperature may create hypothermia. In a risk determination study of 138 anesthetized cats, 71 (51%) had rectal body temperatures ≤35 °C (95 °F); the lowest recorded temperature was 28.8 °C (83.8 °F). Prolonged anesthesia dramatically increased the risk of hypothermia. In addition to the increased infection rate seen in hypothermic patients, there is increased risk of fatal ventricular arrhythmias in patients with body temperatures <33 °C. Bair Huggers®, Therma-drapes®, warm water circulating blankets, lowflow anesthesia, a heat and moisture exchanger, plastic wrap, leg wraps, radiant heating (Hot Dog ® patient warming system), and warmed fluids may all be used

Preparation of the Anesthetized Dental Patient The use of gauze sponges placed in the pharyngeal area to absorb debris is controversial. Danger lies in gauze entering the esophagus and either being vomited after the surgical procedure is completed or ingestion leading to gastrointestinal obstruction. In the author ’s opinion, packing the pharyngeal area with gauze is not necessary because the seal provided by the endotracheal cuff is sufficient to prevent iatrogenic injury secondary to aspiration of surgical debris.

Monitoring Often, dental assessment results in a treatment plan that requires multiple hours of anesthesia. Constant monitoring of the cat’s physiological status is critical to a consistent positive outcome. Monitoring is accomplished through clinical appearance as well as electrical monitoring systems. During anesthesia the cat should have minimal jaw tone and

Anesthesia

173

Mannitol is particularly useful in well-hydrated geriatric cats with chronic renal failure (with normal cardiac function) to ensure diuresis. The dose of mannitol is 0.25–0.5 g/kg IV over 15–20 minutes. Anesthesia may be induced with a combination of propofol and diazepam. Ketamine and barbiturates should be avoided. Maintenance with isoflurane is standard. Hypotension should be closely monitored and if present adjusted with crystalloid administration.

Hyperthyroidism

Figure 7.6 Wireless monitor with esophageal probe.

Figure 7.7

Monitor display (DVM Solutions).

palpebral reflex. The pulse should be palpable and the perfusion time should be two seconds or shorter. Breathing during anesthesia should be even and regular. Electronic monitoring includes electrocardiogram, blood pressure, pulse oximetry, and end tidal CO2. Apnea, temperature monitoring, and respiratory rate are additionally helpful in assessing the cat’s response to anesthesia (figs. 7.6, 7.7).

Medical Conditions Requiring Tailored Protocols Renal Disease Some cats with kidney disease may be dehydrated due to their inability to concentrate urine. The dehydration should be corrected before anesthesia if possible.

Chronic unregulated hyperthyroidism can result in cats that present thin, azotemic, with hypertrophic cardiomyopathy, and with multiple oral issues, including tooth resorption, oropharangyeal inflammation, and periodontal disease. If possible, patients should be euthyroid before anesthesia. Patients with enlarged hearts on thoracic radiographs should have echocardiograms performed before anesthesia. Anesthesia protocol in the controlled hyperthyroid cat should be tailored to prevent catecholamine release, avoid arrhythmias, and promote normal blood pressure. Premedication with an opioid is advised due to its calming effect and minimal cardiovascular compromise. Midazolam, etomidate, and diazepam are considered safe to use for induction. Ketamine should be avoided. Barbiturates may also increase heart rate and should not be used. Propofol, a generally accepted premedication in the healthy patient, can also impair myocardial function in the ischemic myocardium and should be used with caution. Patient monitoring during anesthesia is critical, especially with regard to blood pressure measurement and ECG. Hypotension can usually be managed with proper intravenous fluid administration without overload. Patients with hypertrophic cardiomyopathy have decreased compliance and ventricular volume. Dopamine administration may be useful to increase blood pressure to ensure adequate renal perfusion. Cardiac tachyarrhythmias may be managed with propanolol.

Diabetes Mellitus Diabetes mellitus requires special consideration in the feline dental patient. Anesthesia should be scheduled in the morning to avoid normal diurnal fluctuations of blood glucose levels. The client should be instructed to give the patient only half the normal amount of insulin the day of surgery. Unless the cat has secondary organ compromise, generally there are no specific medications to avoid for induction or anesthetic maintenance. Diabetes can lead to neutrophil dysfunction and impaired wound

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healing. Intravenous antibiotics (ampicillin) can be administered at induction and six hours later if surgery is performed. Blood glucose levels should be monitored at least every thirty minutes. Adjustment with either intravenous glucose or insulin should be administered to maintain blood glucose concentrations between 100 and 200 mg/dL. Periodic blood glucose monitoring after recovery is also recommended until the patient is stable.

Benefits of Local and Regional Anesthesia

• • • • •

Local/Regional Anesthesia Pain management must be instituted when approaching the feline surgical patient. General anesthesia is not sufficient to control dental pain. Local and regional anesthesia not only help decrease pain before, during, and after surgery, but also result in less inhaled general anesthesia due to decreased hyperventilation.

Regional Analgesia A similarity exists in the way dogs, cats, and humans feel dental pain. Regional anesthetics are agents that when injected decrease or halt nerve conduction in a limited area of the body. Regional anesthesia occurs after depositing an appropriate agent in close proximity to a nerve innervating the area intended for dental treatment. Following the injection, anesthetic molecules move by diffusion into the nerve, blocking its normal action. Local anesthetics work by inhibiting the influx of sodium ions into the nerve axon, preventing the development of the action potential necessary for sensory propagation along the axon. The loss of sensation can be complete when properly administered. The trigeminal nerve is responsible for the sensory innervation of the oral cavity. The maxillary teeth, as well as maxillary soft and hard tissues, are innervated by the maxillary nerve, which branches into the infraorbital nerve. The mandibular nerve branches into the lingual nerve, which innervates the tongue and the inferior alveolar nerve, which branches into the mental nerves. To obtain complete anesthesia following an injection, the nerve must be permeated by a sufficient concentration of the anesthetic base to inhibit conduction in all fibers. Induction is the length of time from the deposition of the anesthetic solution to complete and effective conduction blockage. The action of a local anesthetic continues until the concentration is carried away by the bloodstream. Duration is the length of time from induction until the reversal process is complete.

Decreased pain during and after surgical procedures Decreased risk of vagally mediated reflex bradycardia Lower inhalant anesthetic requirement; decreased minimum alveolar anesthetic concentration needed to provide analgesia Less immediate postoperative analgesic medication needed Improved level of anesthesia, thus decreasing the variation of anesthetic depth when painful stimulation occurs

Indications for Local and Regional Anesthesia

• • • • • • •

Surgical and nonsurgical extractions Root canal therapy Mandibulectomy, maxillectomy Jaw fracture repair Vital pulp therapy Periodontal procedures including flaps, gingivectomy, and oronasal fistula repair Oral mass incision or excision

Contraindications for Local and Regional Anesthesia

• •

Local anesthetic agents may not be effective when injected into a region of increased acidity (e.g., area of infection). Epinephrine-potentiated local anesthetics should not be used in cardiac patients.

Duration The action of a local anesthetic will continue until the concentration is carried away by the vascular system to other tissues. Local anesthetics are metabolized primarily in the liver and excreted through the kidneys. Anesthetic duration is related to the amount of medication bound to proteins in the nerve membrane. The greater the binding affinity to nerve proteins, the longer the duration of action. For example, the increased protein binding of bupivacaine compared with mepivacaine causes a two- to fourfold increase in the bupivacaine’s duration. A similar relationship exists between lidocaine and its longer-acting analogue etidocaine. Local anesthetics that have the greatest potency usually exhibit the longest duration of action. Local anesthetics are vasodilators. Vasoconstrictors (epinephrine) incorporated into the local anesthetic solution enhance the duration and effectiveness of anes-

Anesthesia

thesia, decrease systemic toxicity by lowering the blood concentrations of the anesthetic, and decrease local bleeding at the injection site.

Local and Regional Anesthesia Equipment Disposable 1-cc tuberculin syringes equipped with a 0.75- or 1.5-inch, 27-gauge needle are most commonly used, although human dental local anesthetic administration syringes that allow one-hand aspiration can also be used in cats.

Dosage A combination of 0.5% bupivacaine hydrochloride with epinephrine (Marcaine®, 1 mg/kg) and lidocaine 2% (1 mg/kg) in a 4:1 ratio is commonly used in veterinary dentistry. Mixing 0.8 mL of bupivacaine with 0.2 mL of lidocaine in the same tuberculin syringe accomplishes the 4 : 1 ratio. The recommended volume for regional anesthesia is 0.1–0.3 mL per injection site. Maximum patient dosage of this mixture would be 0.1 mL/kg, or approximately 0.25 mL/jaw quadrant in case all quadrants need anesthesia in a 5-kg cat.

Injection Precautions Injection into a blood vessel can alter cardiac function. To be careful that the solution is not being injected into a vessel, the operator needs to aspirate before injecting.

Nerve Blocks Desensitization of the teeth occurs mainly through the pulp. Regional anesthesia is obtained by injecting the anesthetic solution in the proximity of the nerve trunk.

Infraorbital nerve block Branches of the infraorbital nerve supply sensory innervation to the maxillary dental arcade. The caudal maxillary alveolar nerve, which branches off the infraorbital nerve before it enters the infraorbital canal, innervates the caudal maxillary teeth. Within the infraorbital canal, the middle maxillary alveolar nerve branches to supply the middle maxillary teeth. The rostral maxillary alveolar nerve branches off the infraorbital nerve just before its exit from the infraorbital canal. This branch supplies innervation to the maxillary canine teeth and incisors. The infraorbital artery and vein travel with the infraorbital nerve within the canal and should be avoided when injecting the local anesthetic agent. Regional anesthesia placed deep in the infraorbital foramen desensitizes the maxillary premolar, canine, and incisor teeth on the same side of the injection.

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The infraorbital foramen lies as a depression in the alveolar mucosa apical to the distal root of the maxillary third premolar. The distal extent of the infraorbital canal can be estimated by palpating the caudal ventral margin of the bony orbit. Advance the needle rostrocaudal (horizontal) to the entrance of the foramen. Before injection, aspirate the syringe in several directions to make sure the tip is not located intravascular. To desensitize caudal to the maxillary fourth premolar on the same side of the injection, advance the 0.63-inch needle through the infraorbital foramen and several millimeters into the infraorbital canal. 50% more anesthetic (not to exceed 2 mg/kg) is slowly injected for 30–60 seconds. After injection, digital pressure is applied over the foramen for 1 minute to force the agent to diffuse caudally into the infraorbital canal (figs. 7.8 a, b, c). This block will not likely anesthetize the maxillary molar located 3–4 mm caudal to the injection site.

Maxillary nerve block The maxillary nerve block desensitizes the palatal soft tissues, dentition, lip, and bone on the injection side of the maxilla. The middle and caudal maxillary alveolar nerves enter the maxilla on the ventral floor of the orbit and innervate the molar and premolar teeth. To adequately block these nerves, the anesthetic agent needs to be introduced in the rostroventral aspect of the orbit into the pterygopalatine fossa, with an approach from the ventral orbital rim. The injected area is rich in neurovascular structures supplying the eye. For this reason the infraorbital block is preferred. With the cat’s mouth open, palpate the zygomatic arch where it meets the maxilla between the fourth premolar and molar. Direct the needle next to the bone and advance dorsally along the caudal aspect of the notch to a level just beyond the root tips. Aspirate the needle and slowly inject the anesthetic agent (fig. 7.9).

Middle mental nerve block The middle mental nerve block anesthetizes the lingual and buccal soft tissues of the mandibular incisors and canine on the side injected, as well as the third premolar when the needle contents are deposited inside the foramen. If the anesthetic agent is deposited outside of the foramen, only the buccal soft tissues from the canine forward to the midline will receive analgesia. Locate the middle mental foramen in the center of the space between the mandibular canine and third premolar, then half the distance between dorsal and ventral borders of the mandible under the lip frenulum. Insert the needle through the foramen aspirate and inject (figs. 7.10 a, b).

Infraorbital Foramen

Mental Block

a

b Figure 7.8 a–c. Infraorbital nerve block.

Figure 7.9

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Middle Mental Foramen

c

Anesthesia

a Figure 7.10

177

b a. and b. Middle mental nerve block.

Mandibular nerve block The mandibular branch of the trigeminal nerve exits the foramen ovale, dividing into the anterior and posterior branches. The posterior divides into the lingual and mandibular nerves. The mandibular nerve reenters the mandibular foramen on the medial surface just rostral to the angle of the mandible to occupy the mandibular canal. The mandibular nerve can be anesthetized by intraoral or extraoral techniques. The mandibular nerve is located 0.5–1 cm from the ventral border of the mandible. The mandibular nerve block will desensitize the mandibular body, the lower portion of the mandibular ramus, all mandibular teeth on the same side, the floor of the mouth, the rostral two thirds of the tongue, the gingiva on the lingual and labial/buccal surfaces of the mandible, and the mucosa and skin of the lower lip and chin. When using the intraoral approach, infiltrate the mandibular nerve where it enters the mouth at the angle of the jaw. Gently “walk” the needle along the medial border of the mandible just caudal to the last molar. Then advance the needle toward the angular process to an area half the dorsoventral width of the mandible. Aspirate the syringe, then deliver the anesthetic agent at the location of the mandibular foramen. When using the author-preferred transcutaneous (extraoral) approach, clip and prepare a small area of skin ventromedial to the angle of the mandible just rostral to the angular process. Insert the needle at a point ventral to the lateral canthus. Direct the tip medially along the border of the mandible. Aspirate the syringe, then slowly inject the anesthetic agent (figs. 7.11 a, b, c).

Systemic Analgesia During dental procedures, cats experience pain similar to that of humans, and they need to have their pain controlled. In pain management, the choice of medication varies depending on the anticipated level of discomfort. The opioid family of medication is recommended for controlling dental pain in cats. When oral surgery is planned, use of an opioid in premedication, as well as intraoperatively, will provide pain control while waiting for the regional nerve block to take effect. Butorphanol has a duration of effect for pain control of 1–2 hours, oxymorphone 1.5–3 hours, and morphine 2–4 hours. Morphine is unpredictable in its onset of effect and duration of action. This may be due in part to the cat’s low capacity for hepatic glucuronidation. Postoperatively, the author prefers oral buprenorphine, which provides 8–10 hours of analgesia.

Constant Rate Infusion (CRI) CRI is being used more widely to provide analgesia both intraoperatively and perioperatively. CRI avoids the peaks and troughs in the plasma levels when the medications are given as repeated injections. The aim of the infusion is to maintain the plasma level of the drug within the therapeutic range. In order to perform a CRI, an opioid is selected and the dose calculated for a specific period of time. The total dose is then drawn up into a syringe and administered over time using a syringe pump; or it is added to a volume of fluids, and then the fluids are administered at a specific rate for the desired period of time.

a

b

c

Figure 7.11 a. Extraoral approach to mandibular nerve block. b. and c. Transcutaneous approach to the mandibular nerve block.

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179

Table 7.1. Analgesic and anesthetic medications.

Figure 7.12

Medication

Dosage

Bupivacaine

1–2 mg/kg regional block

Buprenorphine

0.005–0.03 mg/kg q 6–8 h SC, IM, IV, sublingual q 6–12 h

Butorphanol

0.2–0.4 mg/kg SC, IM, IV q 2–4 h 0.5–1 mg/kg orally q 6–8 h

Carprofen

1–4 mg/kg SC, preoperatively, then 2 mg/kg orally limit two days

Codeine

0.5–2.0 mg/kg orally q 6–12 h

Fentanyl

25 μg/kg/h transdermal patch Loading dose 1–2 μg/kg IV, then CRI 1–4 μg/kg/h IV

Gabapentin

3 mg/kg orally q 24 h

Hydromorphone

0.02–0.05 mg/kg SC, IM, IV q 2–6 h

Ketamine

Loading dose 0.2–0.5 mg/kg IV, then CRI 10–20 μg/kg/ min IV during surgery, then 2 μg/kg/min after surgery for up to 18 hours (60 mg ketamine in 1000 mL of Lactated Ringers Solution given at 2 mL/kg/h)

Ketoprofen

1–2 mg/kg IM or SC once, then 0.5–1 mg/kg PO, SC q 24 h for a maximum of 5 days

Lidocaine

Maximum 2 mL total dose (0.25–0.5 mg/kg slow IV)

Medetomidine

1.0 μg/kg with equal volume of butorphanol IV (producing heavy sedation and not recommended if planning on proceeding to general anesthesia) Before surgery with atropine + opiate: 5–10 μg/kg IM After surgery used alone: 4–8 μg/kg IM After surgery with opiate: 2–4 μg/kg IM (After surgery, opiate is given at one-half the dose used in premedication; e.g., butorphanol at 0.2–0.4 mg/kg in premedication is used at 0.1–0.2 mg/kg after surgery)

Meloxicam

0.3 mg/kg SC once 0.2 mg/kg orally q 24 h × 1 day, 0.1 mg/kg PO q 24 h × 2 days (extra-label)

Morphine

0.05–0.2 mg/kg SC, IM q 4–6 h 0.02–0.1 mg/kg IV q 1–4 h Postoperatively, CRI 0.1–0.3 mg/kg/h (morphine is delivered in 3–4 mL/kg/h fluids)

Oxymorphone

0.05–0.1 mg/kg SC, IV, q 1–3 h

Piroxicam

0.3 mg/kg PO q 24–72 h for a maximum of 7 days

Tramadol

4 mg/kg orally q 12 h

Fentanyl transdermal patch.

Techniques for setting up a CRI involve the use of a syringe pump or a fluid pump, and the drug to be used is administered slowly at the bottle concentration or diluted in maintenance fluids. During surgery, it is recommended that the drug be administered separately from the maintenance fluids since fluid boluses are commonly used under anesthesia to treat hypotension and blood loss. A CRI commonly used is a combination of butorphanol and ketamine that can be infused continuously (e.g., 12 mg butorphanol and 60 mg ketamine in one liter of lactated Ringer ’s solution given at 1–2 mL/kg/hr). The CRI can be continued after surgery is completed in order to ease recovery.

Transdermal Pain Patch Fentanyl delivered transdermally through an adhesive patch will also help to control pain. A 25 μg/h patch is recommended for small to medium sized cats. The patch should be placed in a location where the patient or small children cannot access it, and covered with a bandage. The patch can be applied the evening before surgery to ensure serum levels are appropriate preoperatively. Time from application of a patch to onset of analgesia is approximately 6–8 hours, with maximum effect at 12 hours. The patch may stay applied for up to 4 days. Butorphanol should not be used while waiting for onset of analgesia from the fentanyl patch, as it is a competitive antagonist and will decrease the patch’s effectiveness. In addition, warming devices may accelerate fentanyl’s absorption (fig. 7.12).

Postoperative Analgesia Buprenorphine is an effective opioid for pain control in the cat. The small volume, ease of administration, and lack of undesirable side effects make it suitable for home administration. The buccal or transmucosal route results in an onset of action in 20–30 minutes and a duration of 8–12 hours.

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Further Reading American College of Veterinary Anesthesiologists. Suggestions for monitoring anesthetized veterinary patients (available at www.acva.org/professional/position/monitor.htm). Beckman BW. Pathophysiology and management of surgical and chronic oral pain in dogs and cats. J Vet Dent 2006; 23: 50–60. Hale FA, Anthony JMG. Prevention of hypothermia in cats during routine oral hygiene procedures. Can Vet J 1997; 38: 297–299. Hardie EM, Spodnick GJ, Gilson SD, Benson JA, Hawkins EC. Tracheal rupture in cats: 16 cases (1983–1998). J Am Vet Med Assoc 1999; 214: 508–512. Holmstrom SE, Frost Fitch P, Eisner ER (eds). Regional and local anesthesia. Veterinary Dental Techniques for the Small Animal Practitioner, 3rd ed. Saunders, Philadelphia, 2004; 625–636. Joubert K, Tutt C. Anaesthesia and analgesia. In: Tutt C, Deeprose J, Crossley D (eds). BSAVA Manual of Canine and Feline Dentistry, 3rd ed. BSAVA, Gloucester, 2007; 41–55. Mazzafero E, Wagner AE. Hypotension during anesthesia in dogs and cats: recognition, causes, and treatment. Comp Cont Ed Pract Vet 2001; 23: 728–737.

Mitchell SL, McCarthy R, Rudloff E, Pernell RT. Tracheal rupture associated with intubation in cats: 20 cases (1996– 1998). J Am Vet Med Assoc 2000; 216: 1592–1595. Reuss-Lamky H. Administering dental nerve blocks. J Am Anim Hosp Assoc 2007; 43: 298–305. Richey M. Anesthesia and pain management in dental and oral procedures. In: Holmstrom SE, Frost Fitch P, Eisner ER (eds). Veterinary Dental Techniques for the Small Animal Practitioner, 3rd ed. Saunders, Philadelphia, 2004; 601–624. Robertson SA, Lascelles BDX, Taylor PM, Sear JW. PK-PD modeling of buprenorphine in cats: intravenous and oral transmucosal administration. J Vet Pharmacol Therap 2005; 28: 453–460. Rochette J. Regional anesthesia and analgesia for oral and dental procedures. Vet Clin North Am Small Anim Pract 2005; 35: 1041–1058. Silva MLA, Santana MI, Araujo LV, Elston F. Topography and anesthetic blockage of mandibular nerve in cats. Rev Port Cienc Vet 2006; 101: 187–192. Woodward TM. Pain management and regional anesthesia for the dental patient. Top Comp Anim Med 2008; 23: 106–114. Zetner K, Rausch WD, Weissensteiner J, Kruzik P, Steurer I. Pain relief after dental treatment in cats. Praktische Tierarzt 1996; 77: 678–682.

Chapter 8

Treatment of Periodontal Disease

Goals of periodontal therapy include removing irritants and debris from the tooth surfaces and periodontal pockets, and minimizing pocket depth and attachment loss while maintaining at least two millimeters of attached gingiva. Periodontal therapy ranges from removing plaque and calculus in cases of gingivitis, to mucogingival surgery, to extracting affected teeth. Periodontal therapy decisions should be made by evaluating clinical and radiographic examination results together with client input concerning expectation, finances, and ability to provide essential after care. Stage of disease at the time of the oral assessment dictates the recommended therapy (table 8.1). Gingivitis is confined to gingival soft tissue inflammatory changes. Periodontitis is diagnosed when there is loss of tooth support from the peridontium.

•

•

•

Stage 1 disease is characterized by gingival inflammation without loss of periodontal support. Radiographs are developed and examined to give more information about additional pathology present. Gingivitis is treated with plaque and calculus removal, polishing, and irrigation of the crown and the gingival sulcus. Once the irritating plaque and calculus are removed, the gingiva returns to normal as long as home care is instituted. Stage 2 early periodontitis is present when there is less than 25% loss of periodontal support. Stage 2 disease is treated as above, plus removal of plaque and calculus from the exposed root surface (subgingival scaling root planing) and gingival curettage. Stage 3 established periodontitis exists when 25% to 50% of the periodontal support is lost. The prognosis is better when there are nonpocket defects compared to pocket defects, which readily accumulate oral debris after the oral assessment, treatment, and prevention (Oral ATP) visit. Efforts of plaque and calculus removal versus extraction must be weighed against the ability to provide daily home care.

•

Stage 4 advanced periodontitis occurs where there is greater than 50% loss of periodontal support. Extraction is generally the treatment of choice.

Plaque and Calculus Removal Plaque and calculus can be removed by hand using fine curettes or with the help of ultrasonic scalers equipped with periodontal tips. Ultrasonic sound waves are composed of alternate compressions and rarefactions. During the low-pressure rarefaction cycle, microscopic bubbles are formed. Through the high-pressure compression cycle, the bubbles collapse or implode. These implosions produce

Table 8.1.

Summary of periodontal therapy.

Stage

Disease

Description

Therapy

Stage 1

Gingivitis

Inflammation without periodontal support loss

Supragingival scaling, irrigation, and polishing

Stage 2

Early periodontitis

Inflammation, swelling, gingival bleeding upon probing, with up to 25% periodontal support loss

Supragingival and subgingival scaling, irrigation, and polishing

Stage 3

Established periodontitis

Inflammation, edema, gingival bleeding upon probing, pustular discharge, moderate bone loss, between 25% and 50% periodontal support loss

Supragingival and subgingival scaling, irrigation, and polishing; extraction of affected teeth if owner cannot provide home care

Stage 4

Advanced periodontitis

Inflammation, edema, gingival bleeding upon probing, pustular discharge, tooth mobility, marked (>50%) periodontal support loss

Extraction of affected teeth

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Figure 8.2 Adjusted ultrasonic spray. Figure 8.1 Anesthetized cat for oral ATP visit.

shock waves (cavitation) that disrupt the bacterial cell wall and lead to bacterial cell death. Additionally, acoustic streaming occurs when a continuous torrent of water produces tremendous pressure within the confined space of the periodontal pocket, resulting in a decreased number of bacteria. Gram-negative, motile rods in particular are sensitive to acoustic streaming because of their thin cell walls.

Operator and Patient Protection To protect from bacterial aerosols and other effects of ultrasonic scaling, the operator should wear a surgical mask, ear protection, gloves, glasses, and/or a face shield, surgical cap, and smock. The anesthetized patient should have artificial tears ophthalmic preparation applied to the corneal surfaces to protect from drying and irritation. When in lateral recumbency, the cat’s head should be cushioned to protect the eye closer to the table surface from abrasion and to raise it off the table to prevent water contamination. The upper eye should be draped to protect it from fomites and from prolonged exposure to the procedure light (fig. 8.1). The mouth is rinsed with 0.12% chlorhexidine gluconate or acetate before the scaling begins.

Supragingival (Above the Gum Line) Scaling 1.

Hold the ultrasonic handpiece lightly at a distance further from the tooth than with hand instruments.

Figure 8.3

Proper position of ultrasonic scaler against crown surface.

2. Adjust water spray to deliver a steady drip with a small mist halo (fig. 8.2). 3. Apply the side of the scaler lightly to the crown in a coronal-to-apical direction. The sound waves should do most of the work. Efficiency decreases with increased pressure. 4. Keep the lateral surface working end in constant motion. Leaving it in one place too long increases the amount of potential heat or mechanical damage to the tooth or gingiva. To prevent enamel damage, never hold the tip perpendicular to the surface of the tooth (fig. 8.3).

Treatment of Periodontal Disease

183

Subgingival (Below the Gum Line) Scaling Calculus, coated with bacteria, left on the root surface contributes to the progression of periodontal disease. If subgingival calculus removal is not performed, the teeth have not been adequately cleaned. Subgingival root cleaning can be accomplished with curettes or special ultrasonic, thin, periodontal tips manufactured specifically for root surface use. When there is enough space between the marginal gingiva and root, a fine curette can be inserted with the face of the blade flush against the tooth. When the instrument reaches the bottom of the pocket, the working angulation of the instrument–-usually anywhere between 45 and 90 degrees–-is established. The instrument is then pushed against the tooth and pulled coronally. This process is repeated until all subgingival calculus is removed (fig. 8.4). To avoid iatrogenic injury when using the ultrasonic scaler with periodontal tips for removal of plaque and calculus, decrease the power and increase the amount of water irrigation. After ultrasonic tooth cleaning is completed, use air from the air/water syringe to gently blow the gingival margin away from the tooth, and examine the tooth surface for missed plaque and calculus. Water from the air/water syringe is used to lavage unattached debris from the sulcus or pocket after cleaning.

Tooth Polishing Polishing smoothes minor enamel defects and removes some of the plaque missed during previous steps. Regardless of how careful scaling and curettage are performed, minor defects (microetches) of the tooth surface occur. Polishing teeth decreases the surface area of enamel and cementum microetches, retarding plaque reestablishment. Tooth polishing can be accomplished by applying polishing paste on the prophylaxis cup attached to a slowspeed handpiece. Cross-contamination can be avoided between different cats by using disposable polishing angles and individual paste cups. When polishing, light pressure is applied to each tooth until the cup edge flares. Care must be taken not to hold the cup on one spot for more than a few seconds to prevent overheating and subsequent damage to the pulp. Cementum and dentin are softer than enamel. When exposed from gingival recession, they should be polished for a few seconds only to avoid further wear.

Figure 8.4 Thin curette (NVO Cislak).

Air polishing uses sodium bicarbonate to “sandblast” the tooth surface smooth in addition to or as a replacement for conventional polishing. The small size of cat teeth generally precludes air polishing due to potential iatrogenic damage to the gingiva.

Fluoride Application Potential fluoride advantages in veterinary dentistry include reduction in tooth sensitivity from exposed dentinal tubules, decreased plaque accumulation, increased enamel resistance to acid demineralization, and a clientpleasing cherrylike aroma after application (FluraFom Virbac Products). Fluoride can be applied while the cat is anesthetized, after the teeth are cleaned and polished and before the plaque barrier gel OraVet® is applied. Both the gel and foam have a pH of 3.0, which may cause gastric irritation and nausea if swallowed; it is therefore administered in the clinic while the patient is still intubated and has a barrier in the oropharynx. Fluoride is deposited in the gingival sulcus with a cotton-tipped applicator, a soft toothbrush, or a foam

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a

b

Figure 8.5

Fluoride.

applicator and is allowed to remain in contact with the tooth surface for three minutes. When using fluoride foam, approximately one-half inch of the foam is rubbed over the teeth. After three minutes, the foam is removed with suction or with a dry gauze sponge. Irrigation is not used after fluoride application (fig. 8.5).

Barrier GEL c

OraVet® (Merial) can be applied to the crown and root to provide a barrier against plaque attachment. The waxy gel is applied with an applicator device on dried teeth at the gingiva/tooth interface before the cat is awakened from anesthesia (figs. 8.6 a, b, c). The at-home product should be applied weekly to help prevent plaque accumulation. In a double-blind study on OraVet®, those cats treated with the professional application during the oral assess-

Figure 8.6 a. OraVet® professional application kit. b. Applying OraVet® to the tooth surface during anesthesia. c. Applying OraVet® supra- and subgingivally with a polishing cup.

ment, treatment, and prevention visit, followed by weekly application, showed significant decrease in the amount of plaque accumulation compared with controls during the fifty-six-day evaluation period.

Treatment of Periodontal Disease

Antibiotics Bacterial load in the mouth and bacteremia can be significantly decreased when the oral cavity is rinsed with 0.12% chlorhexidine gluconate after general anesthesia is induced and before tooth cleaning or oral surgery. Antibiotics are not indicated in most patients with periodontal disease. The goal of periodontal therapy is to remove the cause of inflammation–-plaque, calculus, or periodontal pockets. Treating the infection with antibiotics but without mechanical debridement will at best result in a temporary improvement and at worst cause the development of resistant pathogens. In stage 3 and 4 periodontal disease, antibiotic use is controversial but may be indicated. Choosing the appropriate antibiotic can be challenging. One in-vitro study found either amoxicillin-clavulanic acid or cefadroxil most effective against gram positive and negative aerobic bacteria in cats with gingivitis. For anaerobic bacteria, amoxicillin-clavulanic acid or clindamycin were most effective. Pulse therapy is the use of periodic (i.e., first five days of every month) oral antibiotic administration to help control the bacterial load. However, this is only rarely recommended as an adjunct in cases where periodontal pocket disease has been treated and the client can provide daily home care. Pulse therapy is not indicated in cases where periodontal disease exists, anesthesia is not performed due to client or practitioner concerns, or as a substitute for home care.

Bone Grafting Bone grafts are used to preserve or restore the alveolar height in deep, narrow, three-walled infrabony pockets, such as defects on the palatal side of canine teeth, that do not extend into the nasal cavity. The goals of bone grafting are to restore normal bony architecture, rebuild the periodontal ligament and soft tissue, and prevent further periodontal pocket formation. Many materials have been used for cat bone grafts, including autogenous bone, alloplasts, and synthetic bioactive ceramic such as Bioglass® (Consil®, Consil Putty Nutramax Laboratories), which develops a direct bond to tissue and becomes osteoconductive when implanted into an osseous defect. The ceramic is surrounded by and incorporated into the new bone within weeks.

2.

3.

4.

5.

1.

If chlorhexidine is used as an irrigant during surgery, rinse it off thoroughly with lactated Ringer ’s solu-

tion. Chlorhexidine can devitalize periodontal ligament cells and interfere with attachment. Create an access flap with interdental and sulcular incisions. Plane the root smooth with a curette and remove excess granulation tissue. Add four to six drops of the patient’s blood, sterile water, or saline to 0.5 mL of the graft material in a dappen dish. Mix the liquid and granules (e.g., Consil®) in the dappen dish with a spatula for ten seconds to achieve the consistency of firm wet sand and apply it into the defect area. Alternatively, carry the granules to the defect and mix with the patient’s blood. In two to three minutes, a chemical change occurs within the granules that initiates the process of bone regeneration. Consil Putty® can also be applied into the defect. Suture the access flap without tension.

Postoperative care includes pain control and antimicrobial medication. The cat is fed a soft diet for several days. Gentle brushing can begin one week after surgery. The surgical site is reexamined every two weeks until clinical healing is confirmed. The area is radiographed in four months.

Technique for the Palatal Periodontal Pocket Palatal pocket therapy is indicated in cases where there is >25% attachment loss on the palatal aspect of one or both maxillary canine teeth and the periodontal probe does not yet enter the nasal cavity (figs. 8.7 a, b). When deep pockets are diagnosed, pocket therapy should be performed or the tooth extracted and the defect closed. If untreated, the pocket might progress until it penetrates the nasal cavity, creating an oronasal fistula. 1.

2. 3.

4.

General Technique

185

5.

Make 2–4 mm mesial and distal incisions to the bone at 20-degree angles palatally from the affected tooth (figs. 8.7 c, d). Use a Molt or Freer periosteal elevator to gently raise a full-thickness flap (figs. 8.7 e, f). Use a thin curette to clean accessible granulation tissue, calculus, and plaque between the root and alveolus (figs. 8.7 g, h). Carry bone-grafting particles into the cleaned defect (fig. 8.7 i). Oppose the flap snugly against the tooth with 4-0 absorbable suture on an atraumatic needle (fig. 8.7j).

a

b

c

Figure 8.7 a. Maxillary canine teeth palatal bleeding after dental scaling. b. 7-mm palatal periodontal pocket. c. Palatal incision. d. Buccal incision. e. and f. Freer elevator used to move palatal tissue caudally exposing subgingival calculus. g. Curette used to remove plaque and calculus. h. Prepared palatal defect. i. Consil® application into the defect. j. Sutured palatal defect.

186

f

d

g

e Figure 8.7 Continued

187

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Feline Dentistry

i h

j Figure 8.7 Continued

Alveolar Bone Expansion Maxillary and/or mandibular canine teeth affected by chronic alveolar osteitis clinically present with unilateral or bilateral thickening (bulging) of the buccal alveolar bone (fig. 8.8a). Oral probing and radiographic examination usually reveal stages 2 to 4 periodontal disease (fig. 8.8b). Teeth

affected with stage 4 disease should be surgically extracted after the bulging alveolus is exposed. The bulge is flattened via alveoloplasty before flap closure (fig. 8.8 c–q). In cases where the maxillary canine tooth has been extracted, the mandibular canine tooth crown may now interfere with the lip, requiring extraction or crown reduction and restoration (fig. 8.9; see chap. 9, pp. 209 for technique).

a

d

b

e

c

Figure 8.8 a. Bilateral maxillary canine alveolar osteitis. b. Left maxillary canine 12-mm probing depth. c. Incision caudal to the affected left maxillary canine. d. Molt elevator used to separate attached gingiva from underlying periosteum. e. Molt elevator used rostrally. f. Reflected attached gingiva. g. Alveolar bone expansion site exposed. h. Removal of the coronal alveolus to aid extraction. i–k. Wing-tipped elevator used to create mobility. l. Delivery of tooth from the alveolus. m and n. After additional alveoloplasty, the periosteum is partially excised to free up gingiva for tension-free closure. o. Before suturing, gingiva is opposed over defect. p. First suture at most coronal point. q. Defect sutured.

189

h

f

g Figure 8.8 Continued

190

i

j

l

m

k Figure 8.8 Continued

191

n p

o

Figure 8.8 Continued

192

q

Treatment of Periodontal Disease

Figure 8.9

193

Mandibular canine lip impingement secondary to extraction of the ipsalateral maxillary canine tooth.

Multiple Tooth Extractions for Advanced Periodontal Disease Often the best approach to care for the cat with advanced periodontal disease is multiple extractions. In most cases the surgical area heals without incident and the cat rapidly returns to normal function (figs. 8.10 a–f).

Gingival Enlargement Benign proliferation of the gingiva is termed gingival hyperplasia. Gingival hyperplasia, rare in the cat, results in increased pocket depths, caused by augmented gingival height, not attachment loss. The resultant “pseudo pocket” can accumulate plaque and, if untreated, may progress to attachment loss. Gingival hyperplasia is treated by gingivectomy and strict home care to help prevent recurrence. At least two millimeters of attached gingiva should remain after gingivectomy.

a e

b

c f

d

194

Figure 8.10 a. Stages 3 and 4 periodontal disease and tooth resorption. b. Flap exposure. c. Partial removal of the coronal buccal alveolus and sectioning of the teeth before extraction. d. Extraction of the mandibular third premolar. e. Separation of the gingiva from the lingual side of the mandible to allow smoothing of the sharp alveoli (alveoloplasty). f. Alveoloplasty.

Treatment of Periodontal Disease

Further Reading Beebe DE, Gengler WR. Osseous surgery to augment treatment of chronic periodontitis of canine teeth in a cat. J Vet Dent. 2007; 24: 30–38. Harvey CE. Management of periodontal disease: understanding the options. Vet Clin North Am Small Anim Pract 2005; 31: 819–836. Harvey CE, Emily PP. Periodontal disease. Small Animal Dentistry. Mosby-Year Book, St. Louis, 1993; 89–144. Harvey CE, Thornsberry C, Miller BR, Shofer FS. Antimicrobial susceptibility of subgingival bacterial flora in cats with gingivitis. J Vet Dent 1995; 12: 157–160.

195

Holmstrom SE, Frost Fitch P, Eisner ER. Dental prophylaxis and periodontal disease stages, Veterinary Dental Techniques for the Small Animal Practitioner, 3rd ed. Saunders, Philadelphia, 2004; 175–232. Holmstrom SE, Frost Fitch P, Eisner ER. Periodontal therapy and surgery, Veterinary Dental Techniques for the Small Animal Practitioner, 3rd ed. Saunders, Philadelphia, 2004; 233–290. Norris JM, Love DN. In vitro antimicrobial susceptibilities of three Porphyromonas spp and in vivo responses in the oral cavity of cats to selected antimicrobial agents. Aust Vet J 2000; 78: 533–537.

Chapter 9

Treatment of Endodontic Disease

Endodontic treatment or extraction is required when the pulp is exposed by trauma. When exposed to the oral environment, pulpal contents undergo irreversible degenerative inflammation resulting in necrosis. There are many clinical presentations for a tooth affected with endodontic pathology. The crown may or may not be fractured. If fractured, the pulp may or may not be visible. Pulpitis may result if there is no obvious fracture–-it may only be visible clinically as a discolored tooth. In advanced cases, fistulous tracts apical to the mucogingival junction can be observed. A majority of cats presented with fractured teeth do not show any signs of discomfort, even though animals experience pain similar to humans. Cats frequently do not show overt signs of pain because they would be regarded as weak. When the pulp necroses, the pain decreases unless periapical lesions form. The mere fact that a cat does not appear to be in pain does not eliminate the need to treat the fractured tooth. Secondary signs related to fractured teeth include:

• • • • • • • • • • •

Chewing on one side Dropping food from the mouth when eating Excessive drooling Grinding of teeth Pawing at the mouth Facial edema Fistulous tract below the eye or under the mandible Regional lymph node enlargement Shying away when the face is petted Refusing to eat hard food Refusing to chew on hard treats or toys

When presented with a tooth that is fractured and has pulp exposure (complicated tooth fracture), the practitioner has two choices: 1. 2.

196

Extract the tooth. Perform endodontic therapy, which usually allows the tooth to be saved and returned to function. Endodontic therapy is less invasive than open extraction.

Specific endodontic therapy depends on the severity of damage to the tooth structure, periapical and periodontal pathology, the functional significance of the tooth, equipment available, and the confidence and ability of the veterinarian to perform endodontic therapy (or refer the case).

Severity of Damage to the Tooth Structure In cats, the pulp lies closer to the enamel compared with dogs. Some fractures are limited to enamel and require little or no therapy; others involve dentin and might not require endodontic care; still others expose enamel, dentin, and pulp, and require endodontic care or extraction. Due to the proximity of the pulp chamber to the coronal enamel, even moderate dentin involvement without obvious pulp exposure should be treated. The ultimate goal of endodontic care is to return the tooth to function if possible, and if not possible, to extract the tooth to prevent further pain. When pathology secondary to pulp necrosis and/or concomitant disease renders the tooth nonfunctional, extraction is the treatment of choice (figs. 9.1a, b, c; 9.2 a–e).

Degree of Periapical and Periodontal Changes Tooth support is critical to long-term success of endodontic treatment. If marked periodontal disease is present before therapy, success will be unlikely unless epic measures are taken and strict home care is provided (figs. 9.3 a, b, c).

Functional Significance of the Tooth Although endodontic care can be performed on any tooth, in the cat, the canines and maxillary fourth premolars generally are the only teeth where endodontic

a

c

b

Figure 9.1 a. Complicated crown fracture of the right maxillary canine. b. Radiograph revealing periapical lucency. c. Root canal therapy four months postoperatively showing partial resolution of periapical lucency (prognosis guarded).

197

a

c

b

d Figure 9.2 a. Complicated crown fracture of the left maxillary canine in a four-year-old cat. b. Radiograph revealing an enlarged pulp cavity and an open apex indicating fracture occurred when the cat was between six and nine months old, halting tooth maturation. c. Extracted tooth cut along its long axis. d. Complicated crown fracture. e. External and possible internal tooth resorption present in addition to the fracture.

198

e

Figure 9.2 Continued

a

c

b

Figure 9.3 a. Crown-root fracture, mandibular fourth premolar. b. Radiograph revealing enlarged root canal and periodontal disease of the fractured crownroot segment. c. Postextraction radiograph.

199

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Feline Dentistry

therapy would be considered due to the surgical discomfort that accompanies extraction.

Owner’s Expectation and Desires Before commencing endodontic therapy, the owner must be made aware of the prognosis, fees involved, and follow-up care required.

is so beneficial in the healing response in other body areas creates swelling leading to pulpal death and necrosis due to the nonelastic and hard surroundings of the pulp cavity (fig. 9.4). Pulpitis is uncommonly associated with tooth resorption in the cat, for which extraction is the treatment of choice. Root canal therapy can be performed on a discolored tooth without radiographic signs of resorption, with a guarded prognosis. If there are radiographic signs of resorption, root canal therapy will not halt the progression of resorption.

Clinician’s Availability and Skill If the client refuses advanced endodontic therapy, the veterinarian is unable to perform endodontics, or referral is not available, extraction may be the only option for care of the fractured tooth with pulpal exposure.

Endodontic Care Based on Presentation Pulpitis Occasionally, teeth can be traumatized by blunt trauma, hyperthermia from ultrasonic scaling, and/or overly aggressive polishing. The resulting inflammation may be sufficient to cause vascular damage, hemorrhage, and pulpal swelling. The pulp is contained within a solid unyielding chamber with limited blood supply and no collateral support; thus, the inflammatory process that

Figure 9.4

Discolored tooth consistent with pulpal hemorrhage.

Uncomplicated Tooth Fractures Uncomplicated fractures are classified into enamel, crown, and crown/root fractures. An enamel fracture occurs when there is loss of crown substance confined to the enamel (fig. 9.5). The dentin or pulp is not exposed. Intraoral radiographs should be exposed and examined as a baseline and to check for additional root fracture. The tooth should be radiographed six and twelve months later for evidence of periapical pathology. Treatment of enamel fractures entails smoothing and contouring the surface with a white stone or fine

Figure 9.5

Enamel fracture illustration.

Treatment of Endodontic Disease

diamond bur on a water-cooled, high-speed handpiece to remove sharp edges, which could cause trauma to the lips and tongue. Light-cured dentin bonding resin material can be placed at the fracture site according to the manufacturer ’s instructions to protect against dentin exposure. An uncomplicated crown fracture (figs. 9.6 a, b) occurs when a fracture of the crown does not expose the pulp but extends into the dentin. Bacteria have an indirect pathway to the pulp through the dentinal tubules. If the injury is recent and a pink spot (pulpal blush) is evident on the fracture site, a near-pulp exposure is present. If untreated, the pulp may become necrotic, eventually appearing as a dark spot through the thin dentin. In cats, the pulp chamber extends to just under the crown tip compared with that of mature dogs, which usually have

a

201

several millimeters of protective dentin under the enamel. For this reason even fractures that do not show gross pulp exposure are considered contaminated, necessitating root canal therapy or extraction. The patient’s age also affects the treatment plan. When intraoral radiographs do not reveal periapical pathology and the patient is less than nine months old, a dentinal bonding agent can be applied to the injured site and covered with composite. If the cat is between nine months and six years old, root canal therapy can be performed with generally favorable results. Alternatively, indirect pulp capping using a bonding agent and restorative agent is performed. When indirect pulp capping procedures are used, follow-up radiographs should be taken at six-month intervals after treatment for several years to examine the pulp chamber for internal resorption and pathology of periapical structures. When intraoral radiographs do not reveal periapical pathology and the patient is older than six years, a wait-and-see approach can be initiated. Those that are older than six years with fractures that just enter the dentin usually have sufficient dentin between the fracture and pulp, alleviating the need for root canal therapy. When periapical pathology exists with a radiographically closed apex, and if the patient is older than nine months, root canal therapy and crown restoration are the treatments of choice, usually resulting in a saved, nonpainful tooth. When periapical pathology radiographically exists and there is an open apex (fracture occurred before the patient was nine months old), either tooth extraction, an apexification procedure, or surgical endodontic care is performed. In uncomplicated crown-root fractures, the fracture involves enamel, cementum, and dentin, extending from the crown subgingivally into the root without exposing the pulp (fig. 9.7). Treatment is similar to the uncomplicated crown fracture; however, additional treatment may be necessary to treat the subgingival area void of cementum and dentin due to the fracture extension. The goal of therapy in this area is to remove significant periodontal pocketing either through gingivectomy (providing that at least 2 mm of attached gingiva remain) or an apically positioned flap.

Complicated Tooth Fractures b Figure 9.6 a. Uncomplicated crown fracture illustration. b. Complicated and uncomplicated canine fractures.

Complicated crown fractures have pulp exposure (fig. 9.8a). The pulp usually appears as a red (vital pulp often a recent injury) or black/brown spot (usually an older injury) on the fracture site. When pulp exposure exists,

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a Figure 9.7

Uncomplicated crown-root fracture illustration.

endodontic therapy should be performed (vital pulp therapy, standard root canal therapy, or surgical root canal therapy) or the tooth extracted (figs. 9.8 b–l). In complicated crown fractures, there is direct communication between the oral bacterial environment and the pulp. The bacterial exposure frequently leads to irreversible pulpitis, pulp necrosis, apical granuloma formation, periapical abscessation, and pain. The process may occur within a month or may be prolonged, smoldering for years (figs. 9.8 m–q). A complicated crown-root fracture occurs when the crown and root are fractured and there is pulp exposure. Treatment for complicated crown-root fractures is the same as for complicated crown fractures, with additional attention to the developing periodontal pocket at the subgingival fracture site (fig. 9.9).

b Figure 9.8 a. Complicated crown fracture illustration. b. Chronic hyperplastic pulpitis (pulp protruding through the fracture site) of the right maxillary fourth premolar treated with tooth extraction. c. Vertical releasing incision. d. Sulcular incision. e. Application of molt elevator. f. Molt elevator used to separate attached gingiva from underlying alveolar bone. g. Removal of the buccal coronal alveolus. h. Sectioning of the maxillary fourth premolar. i. Sectioned tooth. j. Wing-tipped elevator utilized to deliver the sectioned crown-root segments. k. Tooth fully extracted (note smooth apices). l. Removing the sharp alveolar margins with a high-speed, water-cooled round bur before suturing. m. Rostral mandibular swelling. n. Pustular discharge from the ventral mandible. o. Left mandibular complicated crown fracture. p. Radiograph revealing marked internal and external resorption. q. Extracted canine.

c f

g d

e

h Figure 9.8 Continued

203

l

i

m

j

n

k Figure 9.8 Continued

204

o

Figure 9.9

Complicated crown-root fracture illustration.

p

q Figure 9.8 Continued

205

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Feline Dentistry

Figure 9.10 Root fracture illustration.

Root fractures are classified by the anatomic location of the fracture (coronal, middle, or apical third) and usually have pulp exposure. Coronal root fractures often present with a mobile crown (fig. 9.10). Treatment usually consists of tooth extraction and removal of the fractured coronal and apical root fragments.

Figure 9.11 Radiograph of a complicated right maxillary canine tooth fracture in seven-month-old cat.

exposure and closed root apices can be treated with standard root canal therapy.

Age of the Patient Age of the patient is also important when choosing endodontic therapy options. Canine teeth of patients younger than nine to twelve months of age may have open root apices (fig. 9.11). Mandibular molar teeth generally have closed apices by seven months of age. Standard root canal therapy is not performed on cat teeth with open root apices because appropriate sealing of the apex cannot be assured. Treatment options for teeth with open root apices include (1) vital pulp therapy (partial coronal pulpectomy, direct pulp capping, and restoration) to promote apexogenesis in a tooth with vital pulp or (2) an apexification procedure if the pulp is dead. Teeth with pulp

Age of the Fracture Age of the fracture influences endodontic treatment. Shortly after pulp exposure, inflammation occurs less than 2 mm from the exposure site. In acute fractures, the pulp appears pink or red at the fracture surface. The pulp of a long-standing fracture will appear brown or black. Vital pulp tissue can be found several millimeters deeper within the pulp, which might respond to vital pulp procedures (i.e., vital pulp therapy). In the mature animal that has an acutely or chronically fractured tooth with a closed apex, standard root canal therapy results in a more predictable outcome compared to vital pulp therapy.

Treatment of Endodontic Disease

207

a

b

c

Figure 9.12 a. Paper points. b. Gutta percha points. c. Tooth obturated with gutta percha.

Materials for Endodontic Therapy Paper Points Paper (absorbent) points are rolled sterile papers used to absorb irrigation solutions in the prepared root canal. Paper points are long, narrow, and tapered to fit into the root canal (fig. 9.12a).

Gutta Percha Points Gutta percha points are slender, tapered, and pointed to fit to the contours of the root canal when compressed. Gutta percha is a combination of zinc oxide (66%), gutta percha rubber (23%), and radiopaque barium sulfate (11%). Gutta percha advantages include being an inert material, radiopaque, nonirritating, and removable for retreatment if root canal therapy fails (figs. 9.12 b, c).

Mineral Tri-Oxide Aggregate (MTA) MTA is composed of a calcium and silicate. It is supplied as a powder, which when hydrated sets in two to four hours. When set, MTA is biologically compatible with adjacent tissues and can be used in vital pulp therapy (direct pulp capping), surgical endodontics, root perforations, and one-step apexification procedures. Calcium hydroxide can also be used in a similar fashion as MTA and has many uses for feline endodontic care. Calcium hydroxide offers the following features:

•

Can be used (1) during the apexification procedure to stimulate hard tissue closure of an open apex in a nonvital tooth and (2) in apexogenesis to stimulate dentinal bridge formation under a direct pulp capping and hard tissue closure of an open apex in a vital tooth.

Sodium Hypochlorite (Bleach) Zinc Oxide–Eugenol Zinc oxide–eugenol (ZOE) is a cement that acts as a sealer between the gutta percha and root dentin. Endodontic sealing cement is also available without eugenol.

Sodium hypochlorite (common household bleach) acts as a solvent for necrotic tissue, a lubricant, and disinfectant for irrigation of the root canal. Depending on the practitioner ’s preference, sodium hypochlorite may be

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diluted with one to two parts distilled water or be used without dilution as it comes from the bottle. To apply sodium hypochlorite, a sterile 1-cc disposable plastic syringe with a blunt 20–23 gauge endodontic needle is used. The needle may be bent at an angle to facilitate access to the canal. Care should be taken not to apply excessive pressure on the syringe contents. Damage to the periapical structures may occur if sodium hypochlorite solution is pushed out of the apex into the periapical tissues.

Ethylenediaminetetracetic Acid (EDTA) EDTA is available in a liquid and a gel. The gel is used as a file lubricant, a dentin softening agent, and an effervescent that helps lift debris from the root canal. It can be introduced by dipping the files into the gel. The liquid is used to remove the smear layer from the root canal wall after filing and is introduced using endodontic flushing needles on a syringe.

Instruments for Endodontic Therapy The goal of standard root canal therapy is to remove toxins, microbes, and necrotic debris by thoroughly debriding the root canal(s) and then sealing the space to prevent further infection. Burs, files, broaches, spreaders, and pluggers are used to accomplish this goal. It is essential that endodontic instruments and accessories be sterile before placement into the root canal. A sterilized endodontic pack is prepared with the necessary instruments.

Endodontic Files Endodontic files are used to enlarge, debride, shape, and smooth the root canal. Kerr (K) files and Hedstrom (H) files are most commonly used. K files cut or shave the root canal walls during rotation. They are applied in a push-pull or clockwise quarter rotation push-rotate fashion to pull dentin debris coronally. The file is extended to its root canal apex before withdrawal. Files come in various lengths and sizes. K files are stronger and more flexible than H files and less prone to breakage. File length chosen depends on the root canal length from tooth access to its apex. Files can be purchased in groups of five in one size or assorted sizes. H files are sharper than K files. They cut efficiently and quickly, and they are used when significant removal of dentin is desired, such as enlarging the access in the coronal third of the tooth. H files are not intended for use in the apical third. They cut on the up (pull) stroke

Figure 9.13

Endodontic files.

(K files cut on both clockwise and counterclockwise rotations and on insertion and withdrawal). To prevent a corkscrew apical penetration, H files should not be rotated (fig. 9.13). Nickel titanium (NiTi) files have become the preferred file of choice for many human and veterinary dentists. These instruments are used by hand or in a powered handpiece at speeds ranging from 150 to 2000 rpm. NiTi files, available in H or K varieties, are more flexible than files made from stainless steel. The International Standards Organization (ISO) sets standardization from one manufacturer to another regarding lengths and widths of flutes, taper, relationship between successive sizes, and coloration. Most files are purchased with color-coded handles, which correlate with various widths. ISO width sizes are numbered 8 to 140 (0.8–1.4 mm at the tip). File handle color correlates to the diameter at the working end (e.g., all #10 file handles are purple, #15 are white, #20 are yellow, and so on). Standard ISO file widths typically increase in 0.05-mm increments (15, 20, 25, etc.). It would be rare to need to use a file greater than size 50 in the cat.

Treatment of Endodontic Disease

Files are also measured by lengths. Human dental files are sized 21, 25, and 30 mm, sufficient for working on feline companion animal patients. With repeated use, endodontic files fatigue and eventually separate (break). As instruments are prepared for sterilization, they should be individually checked for signs of wear, weakness, or fracture. Some practitioners color code the files with endodontic stops relating to the number of times each file is used. The safest practice is to use new files with each patient. To mitigate the expense of using fresh files for each case, a sterile endodontic surgical pack fee can be charged to the client. Should the instrument separate within the root canal, retrieval is attempted. In some cases, apical surgery or extraction of the tooth becomes necessary.

209

a

Endodontic Stops Endodontic stops are small, round pieces of rubber or plastic that act as visual stopping point references to assist the veterinarian in preparing the canal. The stops are placed toward the file handle and the file is placed into the root canal to make a confirming radiograph before root canal therapy is initiated. The stop is readjusted when the file is at the internal end of the apex, as confirmed by a working-length radiograph. All succeeding files are fitted with endodontic stops at the working length. Some of the newly designed instruments, such as LightSpeed, have length-measuring rings, eliminating the need to set and reset stops during treatment.

Spreaders and Pluggers Spreaders and pluggers are available in multiple diameters and lengths, used to compact and adapt gutta percha to the prepared root canal. The smooth-pointed spreader is a hand-operated, tapered metal instrument that compacts gutta percha laterally into the root canal space, forcing sealant into apical and nonapical ramifications and dentinal tubules, and creates room for insertion of additional gutta percha. The blunt-tipped plugger compacts gutta percha vertically toward the apex (figs. 9.14 a, b). For feline teeth, which are short, human pluggers and spreaders can be used.

College Pliers College pliers, also called cotton pliers or endodontic locking pliers, enable the operator to pick up and hold paper or gutta percha points in place for insertion into the prepared root canal. Pliers can also be used for holding cotton pledgets for cleaning tooth surfaces.

b Figure 9.14

a. Spreader. b. Plugger (Cislak).

They are available in both locking and nonlocking styles, with plain or serrated tips (fig. 9.15).

Spatulas Spatulas are instruments used to mix dental materials. Cement spatulas are thin and nonflexible (fig. 9.16).

Irrigation Needles Irrigation needles (available in 23, 25, 27 guage sizes) are used to flush fluids into the canal in order to remove dentinal shavings and debris that accumulate during instrumentation. Irrigation needles have a slotted tip or a lateral opening for fluid to exit around the needle and not through the apex, preventing apical damage from overzealous irrigation.

Vital Pulp Therapy Vital pulp therapy involves partial pulpectomy, direct pulp capping, and restoration.

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• • • • •

Paper points Retrograde amalgam carrier Chlorhexidine solution (0.12%) Calcium hydroxide powder or MTA Restorative material

Technique Vital pulp therapy has limited use in the cat. It can be used for treatment of acutely (treatment within hours of injury) fractured teeth and surgical crown reduction for orthodontic care. 1. 2. 3. 4.

5. Figure 9.15 College-tipped pliers (Cislak).

6.

7. 8.

9.

10. 11.

Figure 9.16 Spatula with zinc oxide–eugenol cement.

Instruments and Materials

• • •

701, #1 and #2 round carbide burs Sterile saline Cotton dressing forceps

12.

Administer parenteral pain medication preoperatively. Obtain an intraoral dental radiograph to determine root maturity and to evaluate dental pathology. Clean and polish the teeth ultrasonically. Infuse a local anesthetic with epinephrine around the tooth or perform a nerve block to desensitize the pulp. Disinfect the oral cavity with 0.12% chlorhexidine gluconate antiseptic solution. A sterile punctured glove may be placed over the crown. Access directly through the exposed pulp with a #1 or #2 sterile round bur in a sterile high-speed handpiece under sterile saline irrigation (figs. 9.17 a, b, c, d). Remove 3 mm of coronal pulp tissue, using a round or diamond bur (fig. 9.17e). To control pulpal bleeding, irrigate the pulp chamber with cold sterile saline initially; follow by applying sterile paper points to absorb hemorrhage. Bleeding that is not controlled within five minutes might be indicative of an inflamed pulp that might not be treatable by vital pulp therapy. Gently apply 2 mm of calcium hydroxide (CaOH) powder with a retrograde amalgam carrier on top of the exposed vital pulp. MTA can also be used instead of CaOH. Slightly undercut the access area to prepare for placement of the final restoration (figs. 9.17 f, g, h). Restore the tooth with a light-cured composite resin; the final restoration layer should be at least 2 mm thick (fig. 9.17i). Obtain a final radiograph. Send the patient home with pain control and prophylactic antibiotic medication.

The tooth is examined and radiographed at six months postoperatively and every year or two opportunity arises during future oral hygiene procedures. In the immature tooth, a radiographic visible dentinal bridge often forms below the restoration. The presence of a

a

c

b

d

Figure 9.17 a. and b. Mandibular canine tooth before crown reduction to prevent upper lip impingement after maxillary canine extraction. c. Cross-cut fissure bur used to reduce the crown height. d. Crown height reduced. e. Inverted cone bur used to remove 3–5 mm of the coronal pulp. f. Retrograde amalgam plugger used to administer calcium hydroxide over the excised pulp. g. Inverted cone bur used to prepare the tooth for restoration. h. Appearance of calcium hydroxide before restoration. i. Restored tooth.

211

e

g

h

f

Figure 9.17 Continued

212

i

Treatment of Endodontic Disease

dentinal bridge does not guarantee success. On sequential radiographs, the root canal of a vital tooth should appear narrower because of continued dentin production. Apexogenesis (root development and apical closure) is the desired outcome when vital pulp tissue is exposed in a young cat (<9 months of age). Vital pulp therapy is performed to allow continued growth of the root and apical closure (figs. 9.18 a–j). In the mature tooth, radiographic success of vital pulp therapy is evident when periapical structures present without pathology.

Standard Root Canal Therapy Standard root canal therapy entails removing the entire pulp (total pulpectomy), shaping and disinfecting the pulp cavity, sealing the apex and ramifications, and restoring the access and fracture sites. Indications for standard root canal therapy include pulpitis from trauma and pulp exposure from fracture, attrition, or abrasion. Contraindications include concurrent advanced periodontal disease requiring extraction, open apices, and tooth resorption.

Minimum Set of Radiographs At least five radiographs are needed for standard root canal therapy: 1.

2.

3. 4.

5.

The initial radiograph is exposed and examined before therapy to identify peculiarities of the tooth to be treated, anatomy of the pulp chamber, and root angulation. Most cat canine tooth root canals are slightly curved. Sharply curved canals present a challenge to the veterinary dentist, particularly if flexible NiTi files are not used. An intraoperative film is exposed with a “first” file in the root canal to establish working length (file reaches the internal end of the apex). The final instrumentation film is exposed when the “last” file reaches the internal end of the apex. The completion film is exposed when the root canal is obturated and the fracture and access sites are restored. Follow-up radiographs are taken 4–6 months postprocedure the first year, followed by periodic rechecks dictated by the case (fig. 9.19).

Instruments and Materials

• • • •

#1 and #2 round or pear-shaped burs for access Gates Glidden burs (size 2) Files 10–80 diameter, 21 mm long RC Prep

• • • • • •

213

Sodium hypochlorite or 0.12% chlorhexidine (causes less apical inflammation due to leakage) Sterile saline Absorbent paper points Gutta percha points Root canal sealer AH-26 or zinc oxide eugenol Finger spreaders and pluggers

Accessing the Root Canal Local anesthetic is injected before the standard root canal therapy commences. Cat canine teeth are usually entered from the fracture site, compared to dog’s canine teeth, which are entered through an access site coronal to the gingival margin (fig. 9.20a).

Preparing the Root Canal Cleaning and shaping procedures are designed to remove deleterious debris from the root canal system while producing a smooth funnel shape for ease of complete filling. This process is called debridement or instrumentation. The thoroughness of debridement facilitates successful dimensional sealing during the obturation (filling) phase. 1.

H and K files are used to shape and clean the root canals. The pretreatment radiograph can be used to estimate the file length needed to reach the apex. Endodontic stops applied to prevent placing the instrument too far into the root canal through the apex into the periapical tissues. The working length is established when the tip of the file rests on the apical floor of the canal (fig. 9.20b). 2. The first file used should just barely engage the root canal walls when it is carried to the working length. H files should be inserted and partially removed without rotation. The H file works on the pull stroke. Use H files to flare the coronal third of the root canal. Use K files to prepare the middle and apical thirds of the root canal, particularly in short (<31 mm long) canals. Turn K files clockwise 90 degrees, remove 1–2 mm, and reinsert multiple times. Apply chelating agents (e.g., RC Prep) on the first two or three files introduced into the root canal to soften dentin for easier debridement and file lubrication. 3. Take a radiograph to verify that the file is within the tooth’s apical terminus. If the file tip has not reached the apex, continue filing. The workinglength distance may vary from 0.1 to 2.0 mm from the radiographic apex due to differences in patient age, size of tooth, and root canal anatomy (fig. 9.20c).

a

c

b

d

Figure 9.18 a. Acutely fractured left maxillary canine twelve hours before presentation—note inflamed pulp. b. Radiograph confirming fracture limited to the crown. c. Round bur used for partial pulpectomy. d. After 3–5 mm of coronal pulp removed. e and f. Calcium hydroxide applied to the pulpectomy site using a retrograde amalgam filler. g. Bonding agent applied. h. Composite resin applied. i. White stone used to finish the restoration. j. Postoperative intraoral radiograph.

214

e

g

f

h

Figure 9.18 Continued

215

i Figure 9.18 Continued

216

j

Treatment of Endodontic Disease

Figure 9.19

4.

5.

217

Follow-up radiograph six months after conventional root canal therapy.

After the working length is established, slide an endodontic stop to the tooth level and apply at the same distance to all successive files. Instrumentation of a file is complete when it can be inserted to full working length and withdrawn without resistance. Introduce progressively larger files, enlarging the root canal until a size is found that does not easily reach the working length. Then with apical pressure, cut the dentin until the apex is reached. This file is termed the master or final apical file. a. With the step-back method, the veterinarian uses smaller diameter files nearest the apex progressing to larger sizes further away from the apex. Alternatively, the crown-down method may be employed where the veterinarian works from the crown of the tooth, shaping the root canal as he or she moves toward the apex. The first instruments are H files, which create the coronal flaring; H or K files are used in the mid-

b.

c.

root region, followed by smaller K files toward the apex (figs. 9.20 d, e). Between files, irrigate the root canal with 5.25% sodium hypochlorite full strength or diluted 50% with sterile saline, or with 0.12% chorhexidine to remove dentinal debris, dissolve soft tissue, disinfect, and provide a bleaching effect. Introduce the irrigation solution by using a slotended endodontic needle to prevent periapical extrusion of dentin debris and bleach. Bleach is employed when the apex is closed. Irrigate the root canal with sterile saline between the last three file sizes to remove the irrigation solution. EDTA solution is also used to remove the smear layer. As the procedure progresses, reinsert the last file that reached the apex to the full apical extent to recapitulate the root canal and remove dentinal debris that might have accumulated near the apex.

a

c

b

d

e

Figure 9.20 a. Radiograph confirming complicated crown fracture. b. Tooth approached through the fracture site. c. Radiograph of working-length file in root canal. d and e. Increasing file sizes for root canal cleaning. f. Paper point placed in prepared canal. g. Zinc oxide–eugenol sealer applied to endodontic file. h. Gutta percha point placed after sealer introduction. i. Completed root canal therapy.

218

f

h

g

i

Figure 9.20 Continued

219

220

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Feline Dentistry

When file flutes reveal clean dentinal shavings, irrigate the root canal with saline and dry by repeatedly placing sterile paper points into the opening of the tooth to the apex (fig. 9.20f). When the points are removed dry, the tooth is ready to be filled and sealed. Blood present on the paper points indicates either apical perforation or inadequate pulp removal. If bleeding persists, take radiographs to confirm that the apex has not been perforated. If the apex is intact, use additional filing to remove all the pulpal contents and stop the bleeding.

5. 6.

7. 8.

Obturating the Root Canal Obturation is the three-dimensional filling and sealing of the entire root canal, preventing leakage and establishing an environment that allows periapical healing. After the tooth has been successfully prepared (cleaned and shaped) and disinfected, the root canal and pulp chamber are obturated with permanent filling material. Healing of the periapical tissues occurs when the conditions favorable for growth of bacteria are eliminated by debridement, disinfection, and obturation of the root canal.

9.

10. 1. Place a gutta percha master cone (same size as the master file) into the root canal to the apex and obtain a radiograph. Position the cone to a depth that feels snug. Good apical fit is evidenced by receiving a tug-back when the point is at the floor of the root canal. Mark the master cone with cotton pliers at the line where it is flush with the access opening of the tooth, and remove for application of root canal sealer cement. 2. Use root canal cement to seal the apex, dentinal tubules, and accessory canals and to fill irregularities in the root canal. Zinc oxide eugenol is a commonly used sealer; however, the trend is to use calcium hydroxide–based sealers with little to no eugenol (Sealapex-Kerr) or an intermediate (glass ionomer, calcium hydroxide) filler if composite restoration is planned. 3. To merge zinc oxide and eugenol, mix a dime-sized amount of zinc oxide powder and several drops of eugenol liquid to a creamy consistency with a #5 spatula on a glass slab for approximately one minute. Incorporate small amounts of powder into the liquid and wipe over a large area of the mixing pad. Mixing is finished when a half-inch string of the cement can be drawn between slab and spatula (fig. 9.20g). 4. An endodontic file is loaded with sealer and rotated counterclockwise in the root canal, releasing the cement toward the apex and dentin walls. Alterna-

tively, gutta percha points can be dipped in sealer before insertion into the root canal, carrying the sealer to the apex. Gutta percha is placed into the prepared and sealed canal using college-tipped pliers (fig. 9.20h). Use a plugger to vertically compact the gutta percha apically. The plugger should be slightly smaller than the root canal width. Use a spreader to laterally compact the master cone and sealer against the root canal walls. Cut multiple accessory cones to 3- to 5-mm lengths. The apical third of the root canal is filled by placing these accessory gutta percha points in the space made by the root canal spreader alongside the master cone. The accessory cones are vertically and laterally condensed until the operator cannot compress the spreader within 5 mm of the internal end of the apex. Take a radiograph to confirm a dense apical fill. If absent, spend more time compacting the gutta percha toward the apex. If present, back-fill the coronal portion of the root canal and compact, using cut gutta percha, spreaders, and pluggers (fig. 9.20i). Remove excess gutta percha and cement extending from the fracture and access site with an inverted cone or pear-shaped bur on a high-speed, airdriven handpiece, a heated spreader, or iris scissors.

Restoring Fracture and Access Sites Following radiographic confirmation of a complete root canal fill, the access is restored with glass ionomer cement and/or light-cured composite. If endodontic sealer contains eugenol (which interferes with polymerization of composite), then glass ionomer must be applied between obturation material and composite. Follow the manufacturer ’s directions when applying the restorative material to the fracture site.

Follow-up Follow-up radiographs are recommended at six months and periodically when the animal is placed under anesthesia for other procedures.

Further Reading Beckman BW. Engine driven rotary instrumentation for endodontic therapy in a cat. J Vet Dent 2004; 21: 88–92. Clarke DE. Endodontics of dogs and cats: an alternative to extraction. Aust Vet J 1995; 72: 383–389.

Treatment of Endodontic Disease Eisner ER. 353 sequential canine and feline endodontic cases: a retrospective study in an urban veterinary practice. J Am Anim Hosp Assoc 1992; 28: 533–538. Girard N, Southerden P, Hennet P. Root canal treatment in dogs and cats. J Vet Dent 2006; 23: 148–160. Holmstrom SE. Feline endodontics. Vet Clin North Am Small Anim Pract 1992; 22: 1433–1451.

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Holmstrom SE, Fitch PF, Eisner ER. Endodontics. In: Veterinary Dental Techniques for the Small Animal Practitioner, 3rd ed. Saunders, Philadelphia, 2004; 339–414. Lemmons M, Carmichael DT. Dental fracture treatment options in dogs and cats. Vet Med 2008; 103: 363–371. Niemiec BA. Fundamentals of endodontics. Vet Clin North Am Small Anim Pract 2005; 35: 837–868.

Chapter 10

Treatment of Tooth Resorption

Classification of Tooth Resorption (see chap. 5 for additional resorption coverage) The following classification is based on the assumption that tooth resorption is a progressive condition.

• • •

•

•

Stage 1: Mild dental hard tissue loss (cementum or cementum and enamel) (fig. 10.1a). Stage 2: Moderate dental hard tissue loss (cementum or cementum and enamel with loss of dentin that does not extend to the pulp cavity; fig. 10.1b). Stage 3: Deep dental hard tissue loss (cementum or cementum and enamel with loss of dentin that extends to the pulp cavity); most of the tooth retains its integrity (fig. 10.1c). Stage 4: Extensive dental hard tissue loss (cementum or cementum and enamel with loss of dentin that extends to the pulp cavity); most of the tooth has lost its integrity. Sublevels of stage 4 are (a) crown and root are equally affected (fig. 10.1d), (b) crown is more severely affected than the root (fig. 10.1e), and (c) root is more severely affected than the crown (fig. 10.1f). Stage 5: Remnants of dental hard tissue are visible only as irregular radiopacities, and gingival covering is complete (fig. 10.1g).

Tooth resorption is also classified as types 1 to 3 based on the radiographic appearance of the tooth and the periodontal ligament space (fig. 10.2).

•

•

• 222

On a radiograph of a tooth with type 1 appearance, a focal or multifocal radiolucency is present in the tooth with otherwise normal radiopacity and normal periodontal ligament space. On a radiograph of a tooth with type 2 appearance, there is narrowing or disappearance of the periodontal ligament space in at least some areas and decreased radiopacity. On a radiograph of a tooth with type 3 appearance, features of both type 1 and type 2 are present in the

same tooth. A tooth with this appearance has areas of normal and narrow or lost periodontal ligament space, and there are focal or multifocal areas of decreased radiopacity surrounded by normal radiopacity in some areas, and a generalized decreased radiopacity in other areas of the tooth.

Therapy Options Noninflammatory resorptions limited to the root surface that have not progressed to the pulp should not be painful to the cat. Once dentin destruction has progressed to pulpal exposure or enamel cavitation that is open to the oral cavity, then discomfort and/or pain are likely. The main goal of treatment is to relieve the cat of present pain and future discomfort. A treatment plan is developed for each tooth affected by resorption. The veterinarian has options based on clinical and radiographic findings, including careful monitoring, tooth extraction, crown amputation with intentional root retention and gingival closure, or referral to a facility that can evaluate and provide appropriate therapy. Presurgical radiographs are important to evaluate root anatomy and pathology. If the veterinarian is not able to radiograph the patient’s teeth, the case should be referred for proper pre- and postoperative evaluation and treatment.

Restoration Preserving a tooth affected with pathology and returning it to painless function is our ultimate goal. Unfortunately, tooth resorption is considered to be progressive regardless of therapy. Results of restoration using a variety of restorative materials and techniques have shown that the long-term likelihood of retaining an intact tooth is very poor. Likewise, applying topical medicaments, laser energy, and

a

c

b

d

Figure 10.1 a. Stage 1 tooth resorption. b. Stage 2 tooth resorption. c. Stage 3 tooth resorption. d. Stage 4a tooth resorption. e. Stage 4b tooth resorption. f. Stage 4c tooth resorption. g. Stage 5 tooth resorption.

223

e

f

224

g

Figure 10.1

Continued

Treatment of Tooth Resorption

225

cautery to surface lesions has not resulted in halting the progress of resorption, nor are these methods effective in treating the pain from tooth resorption.

Type 1

Monitoring without Surgery Some teeth have asymptomatic replacement root resorption isolated to the root without exposure to the oral environment. In these teeth, resorption is considered progressive; careful monitoring of such teeth both clinically and radiographically at least every six months can be chosen as an alternative to immediate extraction. If on follow-up examination the lesions become exposed to the oral environment, extraction is indicated.

Crown/Root Atomization

Type 2

Crown and/or root atomization is not recommended as a therapy option in the care of tooth resorption. Root atomization is a procedure performed using a round bur loaded on a water-cooled, high-speed handpiece to blindly eliminate a root fragment. This procedure is wrought with potential iatrogenic negative outcomes, including perforation into the nasal cavity or mandibular or infraorbital canal, sublingual soft tissue trauma, and subcutaneous emphysema.

Tooth Extraction

Type 3

The current recommendation is to fully extract those teeth that have normal radiographic appearance of the root and periodontal ligament space in addition to tooth resorption. These lesions typically start at the cementoenamel junction and can extend in all directions. Extracting these teeth helps prevent a future nidus for continued inflammation. Additional indications for complete tooth extraction include cats that have caudal stomatitis, are positive for FeLV and FIV and have viral associated oral inflammation or in some patients that have chronic oral inflammatory disease.

Instruments and Materials

• • Figure 10.2

Resorption types based on radiographic appearance.

• • • • •

Disposable #15 scalpel blade and #3 handle Periosteal (Freer and Molt #2) elevators to reflect and retract periosteum from the surface of the bone Curved Iris scissors (11 cm) Winged elevators (1–5 mm) Castroviejo needle holder to allow controlled suturing of delicate flaps Miller surgical bone curette #10 (Cislak EX2) Bishop-Harmon tissue forceps

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#6 India sharpening stone (autoclavable for use during surgical procedures) Monocryl 5-0 suture with RB-1 taper needle

Considerations Treatment planning after clinical and radiographic examination is critical for a successful outcome. The surgeon must be aware of the extent of tooth resorption as well as adjacent structures before surgery begins. Important points to evaluate include the amount of resorption present, location of lesions on the tooth, and the radiographic appearance of replacement resorption if present. The canines, the incisors, and often the maxillary second premolars are single rooted. The maxillary first molars, though anatomically double or triple rooted, can be treated as single rooted due to root fusion. The maxillary fourth premolar has three roots, and all remaining premolars have two roots. The oral cavity is prepared after intubation and patient stabilization under anesthesia by rinsing with 0.12% chlorhexidine gluconate, scaling, and polishing the visible teeth, followed by rinsing again. The chlorhexidine gluconate helps to reduce the bacterial load to the patient and operator. Full oral survey intraoral radiographs are exposed and examined to evaluate crown and root morphology. Local nerve block anesthesia is provided before any incisions are made.

Periodontal (Gingival) Flap Periodontal flaps expose the alveolar bone and underlying root surface, preserve attached gingiva, and allow suturing in a fashion that reduces the periodontal pocket and promotes reattachment of soft tissue to the root surface. The base through which the attachment and circulation is maintained is called the pedicle. Flap design should allow maximum utilization and retention of keratinized gingival tissue and have ample length to fully evaluate the root surface not covered with bone. Tissue tags should be removed to allow rapid healing and prevent formation of undesired granulation tissue. Flap closure sutures should be placed tension free from movable to nonmovable tissue when possible. Surgical knots should not lie on the incision line. Tooth extraction requires the removal of several millimeters of the coronal buccal alveolar bone underlying the attached gingiva. This is accomplished through periodontal flap exposure. There are numerous types of flaps. The full-thickness flap is used to gain visibility and access for osseous surgery, root planing, and pocket

elimination. A full-thickness flap, which includes the periosteum, can be elevated by blunt dissection using a periosteal elevator in a rocking motion until the periosteum is lifted from the underlying bone. Envelope flaps, preferred by the author, are conservative full-thickness elevations coronal or apical to the mucogingival line, used to expose gingival pockets through intrasulcular incisions. The horizontal incision is made along the alveolar margin at least one tooth distal and mesial to the site of operation. In the unmodified envelope flap, there are no vertical releasing incisions. After the root surface is cleaned and irrigated, sutures are placed to close the flap. A triangular flap includes one vertical releasing incision. The papilla is included in the mesial extent of the incision when the vertical incision is on the mesial side of the flap, or in the distal extent when the vertical incision is on the distal side of the flap to make repositioning and suturing easier. A pedicle flap is created with two vertical releasing incisions. The partial- or split-thickness flap leaves the periosteum at the donor site, avoids larger blood vessels, and allows suture placement in the periosteum. Partialthickness flaps are indicated when thin bony plates are present, in areas of dehiscence or fenestration where bone must be protected, and in areas where bone loss is permanent.

Extraction Technique 1.

Incise mesially and distally (if necessary) 1–2 mm coronal to the mucogingival junction. One mesial releasing incision is preferred so as not to interrupt the distal blood supply. Placing the incision totally in attached gingiva helps preserve the blood supply during and after surgery and takes advantage of the rapid epithelial migration encountered in this area during wound healing. 2. The blade tip is angled toward the root, incising 360 degrees into the pocket or sulcus (figs. 10.3 a, b, c). 3. A freshly sharpened periosteal elevator (Molt or Freer) is used to expose the alveolar bone by freeing the attached gingiva and alveolar mucosa past the mucogingival junction (figs. 10.3 d, e). 4. A #1 or #2 carbide round bur on a high-speed, water-cooled handpiece is used to remove the coronal one-half to three-fourths of the buccal alveolar plate from the tooth root. Occasionally, radiographs reveal a bulbous root apex, which requires additional widening of the overlying alveolus (fig. 10.3f). 5. Multirooted teeth are sectioned into single-rooted crown-root segments using a cross-cut fissure or

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Figure 10.3 Extraction of the right mandibular third premolar: a. Caudal vertical releasing incision. b. Sulcular incision. c. Rostral incision. d. Molt periosteal elevator used to raise a gingival flap. e. Attached gingiva reflected. f. Removing the coronal alveolus. g. Sectioned two-rooted tooth. h. Wing-tipped elevator placed between the crown-root segments. i. Wing-tipped elevator placed on the outside of the distal crown-root segment. j. Alveoloplasty. k. Suture placement. l. Gingival flap sutured without tension.

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Figure 10.3 Continued

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small #1 round bur. The sectioning begins at the furcation and is carried coronally until the tooth is split into single-rooted segments (fig. 10.3g). When extracting mandibular teeth, be aware that the mandibular canal lies immediately beneath the cheek tooth apices. Marked hemorrhage and damage to the mandibular nerve may occur when the mandibular canal is entered. Excessive hemorrhage can usually be controlled by digital pressure and closure of the gingival defect. 6. A winged elevator is used to stretch the periodontal ligament and gently elevate the tooth root from the alveolus. The blade is introduced between the root and the alveolus, and each movement of rotation is maintained for at least ten seconds (fig. 10.3 h, i). The tooth or segments can usually be delivered from the alveolus with the operator ’s fingers or through gentle torsion with extraction forceps. If the root fractures during the extraction proce-

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dure, a trench can be created around the root fragment with a 701L cross-cut taper fissure bur to provide a purchase area for a dental elevator or root tip pick. 7. After extraction, the remaining rough edges of alveolar bone are contoured and smoothed with a round bur placed in a high-speed water-cooled handpiece (fig. 10.3j). 8. A radiograph is exposed and examined to confirm extraction. 9. A bone curette is used to clean out alveolar socket debris. 10. The gingiva is sutured without tension where the extraction is greater than 1 mm in circumference (figs. 10.3 k, l). Maxillary fourth premolars affected with tooth resorption are extracted in a similar fashion (figs. 10.4 a–j).

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Figure 10.4 a. Right maxillary third and fourth premolars affected by tooth resorption. b. Appearance after elevation of attached gingiva. c. Gingiva reflected past the mucogingival junction. d. Coronal alveolus removed. e. Sectioning the fourth premolar. f. Sectioning the two-rooted third premolar. g. Delivery of the mesiobuccal and mesiopalatal roots of the fourth premolar. h. Alveoloplasty. i. Suture placement. j. Sutured gingival flap without tension.

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i Figure 10.4 Continued

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Treatment of Tooth Resorption

Crown Amputation with Intentional Partial Root Retention Root resorption is considered a progressive disease. It is believed that bone- and cementum-like tissue replaces the periodontal ligament, dentin, and pulp in many cases of tooth resorption (root replacement resorption). In these cases, crown amputation with intentional partial root retention followed by gingival closure is the treatment of choice because the root is already resorbing and not painful. Case selection is based on radiographic appearance of the root, which will have decreased radiopacity (mottled or moth-eaten with no or little periodontal ligament space surrounding it; figs. 10.5 a–e). Contraindications for crown amputation with intentional partial root retention include periodontal disease as evidenced by horizontal or vertical bone loss, endodontic disease, stomatitis, and positive retroviral status (figs. 10.6 a–m). Procedure for intentional crown amputation and gingival closure (figs. 10.7 a, b): 1.

An envelope flap (preferred) or a mucoperiosteal flap is created both labially and buccally by vertically incising several millimeters interproximally mesial and distal to the affected tooth. 2. A fine periosteal elevator is used to expose the cementoenamel junction and alveolar margin (fig. 10.7c). 3. The crown and 1–2 mm of the coronal root apical to the alveolar margin are removed using a #2 sterile or cross-cut fissure bur on a high-speed water-irrigated handpiece (fig. 10.7d).

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4.

Sharp alveolar margin projections are removed with a round bur. 5. The resulting defect is sutured with 5-0 absorbable suture (figs. 10.7 e, f) 6. The operative area is radiographed to document the postoperative result.

Extraction of Teeth Based on Patient History Occasionally, patient history reveals partial anorexia, face rubbing, face scratching, or periodic pain-related vocalization. Often, the signs will resolve once teeth affected with apparent stage 2 tooth resorption are extracted (figs. 10.8 a–o).

Dealing with Root Fragments When a tooth fractures during the extraction process, the root fragment can usually be retrieved after removal of more alveolar bone and elevation with a small root tip pick elevator. Avoid displacement of root fragment(s) into the mandibular or infraorbital canal, nasal cavity, or maxillary sinus. In cases of oropharangyeal inflammation, it is essential that no root fragment remains. If a root fragment is left in place, the owner should be informed and provision made for radiographic followup (figs. 10.9 a, b, c).

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Figure 10.5 a–e. Teeth affected with type 2 tooth resorption (dentoalveolar ankylosis and root replacement resorption) that may be treated with crown reduction and gingival suturing.

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Figure 10.6 Teeth that should be extracted entirely (crown and roots): a and b. Endodontic disease in addition to tooth resorption. c and d. Teeth with type 1 radiographic appearance at least on one root (normal-appearing periodontal ligament and root opacity. e–g. Teeth with type 3 lesions. h and i. Clinicalappearing endodontic abscess coupled with radiographic evidence of type 2 tooth resorption. j. Exposed resorbed area of canine root. k and l. Marked clinical resorption with type 3 tooth radiographic appearance. m. Surgical exposure.

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Figure 10.7 a and b. Type 2 tooth resorption. c. Flap exposure. d. Crown reduction. e. Sutures placed. f. Surgical site ten days postsurgery.

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b d Figure 10.8 a. Intraoral radiograph of the mandibular canines and incisors in a cat with persistent episodes of vocalized pain and scratching at the mouth. Canine radiographs consistent with stage 2 tooth resorptions. All signs of pain resolved within three weeks of maxillary and mandibular canine extraction. b. Initial incision rostral to the left mandibular canine. c. Sulcular incision. d. Incision caudal to canine to create a gingival flap. e–h. Molt elevator used to separate attached gingiva from the periosteum and alveolus. i and j. Removal of the coronal buccal alveolus. k–m. Luxator used to create tooth mobility. n. Delivery of the mandibular canine from the alveolus. o. Alveoloplasty before closure.

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Continued

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Treatment of Tooth Resorption

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Postoperative Recommendations The diet should be softened for at least one week after surgery. This can be accomplished by instructing the client to prewet the animal’s food for about twenty minutes before feeding. A 0.12% chlorhexidine solution can be sent home with the owner to apply twice daily for a week as an oral rinse.

Further Reading Blazejewski S, Lewis JR, Reiter AM. Mucoperiosteal flap for extraction of multiple teeth in the maxillary quadrant of the cat. J Vet Dent 2006; 23: 200–205. DeBowes LJ. Simple and surgical exodontia. Vet Clin North Am Small Anim Pract 2005; 35: 963–984. Dupont G. Crown amputation with intentional root retention for advanced feline resorptive lesions: a clinical study. J Vet Dent 1995; 12: 9–13. DuPont GA. Crown amputation with intentional root retention for dental resorptive lesions in cats. J Vet Dent 2002; 19: 107–110.

Figure 10.9 a. Multiple inflamed areas on the mandibular gingiva. b. Radiograph of mandibular premolar and molar root fragments. c. Gingival flap exposing retained root fragments before extraction.

DuPont GA. Radiographic evaluation and treatment of feline dental resorptive lesions. Vet Clin North Am Small Anim Pract 2005; 35: 943–962. Gunew M, Marshall R, Lui M, Astley C. Fatal venous air embolism in a cat undergoing dental extractions. J Small Anim Pract 2008; 49: 601–604. Lyon KF. Feline dental disease: treatment of subgingival resorption lesions. J Vet Dent 1990; 7 (1): 13–14. Lyon KF. Subgingival odontoclastic resorptive lesion, classification, treatment, and results in 58 cats. Vet Clin North Am Small Anim Pract 1992; 22: 1417–1432. Reiter AM. Dental surgical procedures. In: Tutt C, Deeprose J, Crossley D (eds). BSAVA Manual of Canine and Feline Dentistry. BSAVA, Gloucester, 2007; 178–195. Smith MM. Extraction of teeth in the mandibular quadrant of the cat. J Vet Dent 2008; 25: 69–74. Smith MM, Smith EM, La Croix N, Mould J. Orbital penetration associated with tooth extraction. J Vet Dent 2003; 20: 8–17. Zetner K, Steurer I. Long-term results of restoration of feline resorptive lesions with micro-glass-composite. J Vet Dent 1995; 12: 15–17.

Chapter 11

Treatment of Oropharyngeal Inflammation

Therapy for feline stomatitis can be frustrating. Plaque control using diligent homecare does not usually lead to long-term success. In resistant cases, the practitioner is left with medical, surgical, or a combination therapy to help control the disease. The practitioner must understand that stomatitis often is a combination of many conditions, including gingivitis, periodontitis, palatitis, glossitis, chelitis, and caudal stomatitis, as well as inflammation of the alveolar and vestibular mucosa.

Antimicrobials The inflammed gingiva is also commonly infected. Approved antimicrobials for use in dental infections can be prescribed to decrease the bacterial load but should not be regarded as a preferred form of monotherapy.

• • •

Medical Therapy It is thought that chronic stomatitis has a multifactoral etiology. Currently, there is no medical protocol that yields consistent long-term positive results. Treating solely with anti-inflammatory medication is, unfortunately, covering up the problem without treating the underlying issue (hypersensitivity to plaque). Corticosteroids, gold salts, coenzyme Q-10, metronidazole, megestrol acetate, meloxicam, antibiotics, bovine lactoferrin, azithromycin, alpha-interferon, interferon omega, and omega-3 fatty acid supplements have been used to treat the disease, with mixed long-term results.

Corticosteroids Repeated repositol corticosteroid injections usually provide clinical improvement initially, but eventually they decrease the body’s ability to resist the inflammatory process and predispose cats to diabetes mellitus. Prednisone (2 mg/kg orally) initially daily, followed by every other day may be helpful to control inflammation but should not be regarded as a preferred form of therapy. Intralesional triamcinolone, although temporarily effective in controlling inflammation, is not considered a viable long-term therapy. 242

Clindamycin 5–10 mg/kg PO BID for 10–30 days Amoxicillin/clavulanate potassium 10–20 mg/kg PO BID for 7–10 days. Metronidazole at 11–22 mg/kg PO in divided dose twice daily for 7–10 days. In addition to its antibacterial activity, metronidazole has some antiinflammatory action, which may be beneficial in treating this disease.

Non-Steroidal Anti-Inflammatory and Immune-Modulating Drugs

• •

•

Solganol, Gold Salts (Shering): 1 mg/kg IM every week until improvement (up to 4 months), then every 20 days. Piroxicam: 0.3 mg/kg PO q 72 h, or compounded into a liquid and administered at 1 mg/cat orally every 72 hours; side effects of piroxicam include gastrointestinal ulceration. Azathioprine: A 50-mg tablet is crushed into 15 mL of liquid vitamin syrup; give 0.3 mg/kg (0.33 mL/8 lb) PO every 48 hours. Azathioprine can cause fatal toxicity in cats.

Interferon Interferon (Virbagen [FelFN], Virbac) has antiviral and antiproliferative effects. Use of interferon in cases of refractory chronic oropharangyeal inflammation may decrease the calicivirus load. Clinically in a small number of cases, there appeared to be a slight reduction in the targeted mucosal inflammation, but according to the clients, when questioned, there had been marked

Treatment of Oropharyngeal Inflammation

improvement in attitude and disposition. An unpublished study of chronically calici virus–affected cats that continued to have significant oral inflammation more than two months after full mouth extraction showed similar results using interferon compared to oral prednisone. Interferon is a glycoprotein that is likely to be destroyed by the gastrointestinal system. Oral administration results in transmucosal absorption. This way, interferon acts at a lower dosage using another pathway than it acts when given systemically. There are various interferon protocols for the management of refractory feline oropharangyeal inflammation after the initial assessment and surgical care. Monitoring the cat’s weight is an objective way to monitor therapy.

• •

•

20–40 IU orally daily or 1 IU submucosal injection into the caudal oral cavity every 2 weeks. The preferred method is 5 IU via submucosal administration at the junction between healthy gingiva and diseased tissues immediately postoperatively while the cat is still anesthetized. This is accomplished by using a 10-MU vial, half the volume drawn into an insulin syringe mixed with 1–2 mL of saline or sterile water to provide a reasonable volume for use. The contents are administered in fractions of 0.1–0.2 mL over the inflammed areas. The remaining 5 MU from the vial is injected into a 100-mL saline bag for oral use by fractionating the 100 mL mixture into 10-mL syringes that are frozen for future oral use. Oral dosage is 1 mL/day until all the units are used. Frozen shelf life is 1 year; refrigerated, 3 weeks. 1 MU/kg FelFN SC every other day for five treatments; after the fifth dose 10,000 IU in 2 mL of isotonic saline given orally once daily for 2 months, then every other day for the 3rd month. This method appears to be less effective than the submucosal and oral routes.

Other Medical Options (None expected to cure caudal stomatitis)

• • •

•

Chlorambucil 2 mg/kg orally every 2–3 days or 20 mg/kg every other week. Bovine lactoferrin 40 mg/kg applied to the oral mucosa. Megestrol acetate 1 mg/kg every 1–4 days, or 2.5 mg PO every 24 hrs for 10 days followed by every other day for 10 days, then as needed. Megestrol acetate consistently decreases inflammation but predisposes the patient to weight gain, polydipsia, polyuria, and diabetes mellitus. Levamisole 25 mg orally every other day for 1 week.

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Doxycycline (Vibramycin; 10 mg/mL) Pfizer, 5 mg/ kg orally BID, if effective reduce to 2 mg/kg BID, if still works decrease to 0.2 mg/kg BID. Doxycycline can also be administered in subantimicrobial doses of 5 mg/cat/day (Periostat), usually 9 to 12 months after initiating or until favorable results. Doxycycline has inhibitory effects on the secretion of matrix metalloproteinases (which destroy collagen and other matrix components) by gingival PMNs. Use of submicrobial doses of doxycycline may result in a decrease of gingival collagen destruction. Eicosanoids are compounds derived from C20 fatty acids (eicosanoic acids), including prostaglandins, leukotrienes, thromboxanes, and hydroxyeicosatetraenoic acids. Lysine 250 mg/cat PO BID (Enisyl-F dosing syringe with 250 mg/mL, Vetoquinol) Cyclosporine alters the immunological response from blocking T-helper cells. This is a specific and reversible inhibition in which immunocompetent lymphocytes and T-lymphocytes are preferentially inhibited. The T-helper cell is the main target, but T-suppresser cells may also be suppressed. Lymphokine production and release is inhibited, including interleukin-2 or T-cell growth factor (TCGF). Side effects include hepatic dysfunction, impaired renal function, and anemia. Oral absorption during chronic cyclosporine use is erratic. The doses of cyclosporine vary, and it is essential that these patients have blood levels evaluated to avoid toxicity (high levels). Cyclosporine serum levels taken at 4 to 6 weeks after initiation should be greater than 300 ng/mL in order to result in clinical improvement. The risk increases with increasing dose and duration of cyclosporine therapy. Cyclosporine takes time to be beneficial, with some benefit seen by 4 weeks and the maximum benefit by 8 weeks. The absorption rates will also vary with the form of this medication. Sandimmune® and Neoral® are not bioequivalent and cannot be used interchangeably. In liver transplant patients treated with Neoral, peak levels were 40% to 106% greater than those treated with Sandimmune. Sandimmune (ScheringPlough) has an expected absorption rate on oral administration of about 30% and Neoral (Novartis) about 60%. The higher absorption rates are related to the microemulsion form of the cyclosporine with generics having the lowest absorption. Recommended dosage is 2 mg/kg PO BID (Neoral and Atopica), up to 7.5–15 mg/kg PO BID (Sandimmune). Adjunct therapy with corticosteroids is recommended in some patients. Cyclosporin should only be administered to indoor cats (outdoor cats are at higher risk of infection [especially toxoplas-

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mosis] and immunosuppression, as well as impaired ability to fight infection adequately).

FIV-Positive Cats with Chronic Stomatitis Cats affected with feline immunodeficiency virus (FIV) can develop stomatitis secondary to immune dysfunction. Medical therapy with corticosteroids should be avoided. Total mouth extraction is the treatment of choice. In those cases with poor response after total mouth extraction, zidovudine (AZT) at 5–10 mg/kg orally or subcutaneously every 12 hours may yield promising results. AZT blocks the viral reverse transcriptase enzyme, which effectively inhibits FIV replication, reduces the plasma viral load, and improves the patient’s clinical status.

Specific Therapy for Mild Stomatitis Initial care for mild cases of non-caudal stomatitis includes teeth cleaning with ultrasonic and hand instruments above and below the gingival margin, followed by a tooth-by-tooth clinical examination and full-mouth intraoral radiography. All abnormalities are charted, including probing depths. Those teeth affected with greater than stage 1 periodontal disease should be extracted. Home plaque control includes daily application of OraVet® plaque barrier gel and antimicrobial mouth rinses containing chlorhexidine gluconate (Oral Hygiene Rinse-Virbac, Fort Worth, TX) to help decrease the oral bacterial load. Daily rubbing with a Q-tip applicator dipped in water-packed tuna juice (for taste) to the free gingival margin to remove plaque may also be helpful. A hypoallergenic diet (Hills® z/d, Waltham-Royal Canin® HP23) and feeding from ceramic or glass dishes (not plastic ones) may also be beneficial.

Surgical Management of Refractory Caudal Stomatitis When caudal stomatitis or marked vestibular mucositis is present and there is no visible inflammation surrounding the canines and incisors, and when radiographic changes are absent on those teeth, extraction of all teeth and root fragments caudal to the canine teeth is the treatment of choice. If the gingiva surrounding the canines or incisors are inflammed or abnormal on radiographs, they also should be extracted. If available, carbon dioxide laser rastering of inflammed and proliferative tissue in the caudal oral

cavity is performed after extractions to remove surface area for plaque to accumulate. Antibiotics approved to treat dental infections are administered for two weeks postoperatively. Pain relief and anti-inflammatory medication are also dispensed for the short-term. The prescribing of azithromycin as the antibiotic of choice for the treatment of feline oropharangyeal inflammation even in Bartonella-positive cats is controversial and not substantiated by scientific studies. Supragingival and subgingival plaque appears to be one of the multifactoral initiating sources of oropharyngeal inflammation. The only treatment thus far shown to have long-term positive results without the need for further medication in a majority of affected cats is tooth extraction. Removing teeth decreases the plaque burden. The decision whether all teeth are extracted or only the premolars and molars is based on examination findings. If marked inflammation, periodontal pockets or tooth resorption are noted around the canines and/or incisors, the affected teeth are also extracted. To evaluate response to extraction in cases of chronic caudal stomatitis, a retrospective study of dental extractions in sixty calicivirus-positive cats was conducted. In that study 50% of the cases resolved without the need for further treatment, 37% significantly improved requiring less medication to control the stomatitis than before the extractions, 13% improved but required similar amounts of continuing anti-inflammatory treatment, and 7% did not improve from medical or surgical care. For those patients with anorexia prior to presentation that present in poor condition, nutritional support via pharyngostomy or gastrostomy tube is indicated preand/or postoperatively until eating returns to normal (figs. 11.1 a–h). Pain management in surgical patients is accomplished with pre-anesthetic opioid administration (buprenorphine), intraoperative local anesthetics (bupivacaine), and postoperative opioids given orally for five to seven days. Presurgical radiographs are important to evaluate root anatomy and pathology. Teeth with tooth resorption lesions are often undergoing root replacement resorption, making luxation and elevation difficult. Pulverizing or atomizing the root within the alveolus with a water-cooled high-speed handpiece and dental bur may result in removing excess supporting bone, removing too little tooth, or causing trauma to adjacent anatomy, and should be avoided. Postoperative examination is performed two weeks after surgery. If any teeth are left, application of a plaque preventative is recommended, and the client is shown how to control plaque daily with Q-tips, OraVet®, and 0.12% chorhexidine gluconate irrigation.

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h Figure 11.1 a. 14 French red rubber feeding tube premeasured to the eighth intercostal space. b. Curved carmault tip placed in the cranial esophagus with downward pressure on the handle. c. Incision made over the tip. d. Placement of the tube tip in the hemostat jaws. e. Tube pulled out of the mouth before redirected down the esophagus. f. Caudal section of tube placed in the esophagus exiting from the skin (note previously marked area). g. Modified Chinese fingertrap friction suture used to secure feeding tube. h. Bandaged patient.

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In cases where oropharangyeal inflammation persists for months despite extractions and laser rastering caudal to the canines, extraction of all remaining teeth and root fragments is indicated. If lesions persist and the patient has been affected for months to years, the condition is termed refractory oro-

pharangyeal inflammation. Removing multiple teeth and root fragments together with periodic laser thermoablation and medication (prednisone every 2–3 days) may be helpful in these cases (figs. 11.2 a–y, 11.3 a–d, 11.4 a–l, 11.5 a–k, 11.6 a–o).

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c Figure 11.2 a. Right maxillary alveolar mucositis and periodontal disease. b. Radiograph of right cheek teeth. c. Left maxillary alveolar mucositis. d. Radiograph of the left maxillary cheek teeth showing radiolucency between the furcation. e. Caudal vestibular stomatitis. f. Right mandibular alveolar mucositis. g. Radiograph of the right mandibular cheek teeth showing tooth resorption and stage 4 periodontal disease. h. Left mandibular cheek teeth. i. Radiograph of the left mandibular cheek teeth showing tooth resorption and stage 4 periodontal disease. j. Right maxillary canine and cheek teeth extracted. k. Radiograph confirming extraction at the right maxilla. l. Left maxilla radiograph confirming extractions. m. Left mandibular canine and cheek teeth extractions. n and o. Radiographs of the right and left mandibles after extractions. p. Preoperative rostral maxilla. q. Preoperative rostral maxilla radiograph. r. Radiograph of postoperative rostral maxilla after extractions. s. Preoperative rostral mandible radiograph. t. Postoperative surgical image of mandible. u. Postoperative radiograph of the rostral mandible. v. Persistent caudal mucositis three months after surgery. w. Surface CO2 laser ablation of the inflammed tissues. x. Four months postoperatively. y. Eight months postoperatively, inflammation resolved.

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Figure 11.3 a. Unilateral caudal stomatitis. b. Increased plaque accumulation due to a supernumerary right mandibular fourth premolar. c. Preoperative radiograph. d. Resolution after extraction of the right mandibular cheek teeth.

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Figure 11.4 a. Gingivitis, periodontitis, and mild alveolar mucositis around the maxillary cheek teeth. b. Gingivitis, periodontitis, and alveolar mucositis of the mandibular cheek teeth. c. Close-up of the right maxillary cheek teeth. d. Close-up of the right mandibular cheek teeth. e and f. Immediate postoperative views after extraction of the teeth caudal to the maxillary and mandibular canines. g–l. Six months postoperatively, resolution of inflammation.

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Figure 11.5 a–d. Gingivitis, periodontitis, and alveolar mucositis before surgery. e. Radiograph of the maxilla confirming extraction. f. Radiograph of the rostral maxilla confirming extractions. g and h. Radiographs of the mandibles confirming extractions. i–k. Six months after all teeth were extracted; full resolution of previous oral disease.

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Figure 11.6 a. Right maxillary fourth premolar and mandibular molar alveolar mucositis and periodontal disease. b. Radiograph of right mandibular first molar distal root bone loss (arrows). c. Left maxillary fourth premolar and mandibular first molar alveolar mucositis and periodontal disease. d. Radiograph of the left mandibular first molar distal root bone loss (arrows). e. Right maxillary fourth premolar extracted. f. Postoperative radiograph of right maxilla. g. Left maxillary fourth premolar extracted. h. Postoperative radiograph of left maxilla. i. Left mandibular first molar extracted. j. Postoperative radiograph of left mandible. k. Right mandibular first molar extracted. l. Postoperative radiograph of right mandible. m–o. Three months postoperatively, resolution of inflammation.

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Treatment of Oropharyngeal Inflammation

Preoperative Laboratory Evaluation Laboratory evaluation should include CBC, serum profile, coagulation profile, thyroid tests, urinalysis, and tests for feline leukemia (FeLV) and FIV. A majority of the cases will have elevated globulin levels and are negative for FeLV as well as FIV. The purpose of the workup is not to reach a diagnosis per se but rather to identify possible underlying causes and to provide information to ensure the safest possible anesthetic episode.

Technique for Multiple Tooth Extraction 1.

Perform maxillary and/or mandibular nerve blocks to provide regional anesthesia. 2. Incise the sulcular gingival attachment 360 degrees with a #15 scalpel blade around all teeth to be extracted (figs. 11.7 a–h). 3. To aid excision of the canine and cheek teeth, make a vertical releasing incision into alveolar mucosa beyond the mucogingival junction mesial to the canine tooth. 4. Elevate the flap bucally and lingually, using a freshly sharpened Molt periosteal elevator. This full-thickness mucoperiosteal flap will free the attached gingiva and several millimeters of alveolar mucosa from the underlying bone (figs. 11.7 i–m).

5.

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Use a round carbide bur loaded on a high-speed, water-cooled handpiece to remove at least half of the buccal alveolus, exposing the root surface. Alternatively, sterile saline is irrigated (instead of water from the drill) on the surgical site by an assistant. Removal of a 2- to 4-mm–long slot between the tooth and periodontal ligament as a “purchase” place for wing-tipped elevator blade helps the extraction process (figs. 11.7 n, o). 6. Section multirooted teeth into single-rooted crownroot segments with a #1 or #2 round or a taper fissure bur. Sectioning should begin at the furcation and extend toward the coronal aspect of the tooth (figs. 11.7 p, q). 7. Gently stretch the periodontal ligament and elevate single-rooted segments using a #1 or #2 wingtipped elevator between the roots. The mesiopalatal root of the maxillary fourth premolar is best approached after extraction of the mesiobuccal and distal roots by exposure of overlying septal bone. 8. Narrow-beaked extraction forceps are used to deliver the teeth from the oral cavity once sufficiently mobile. 9. The alveolar sockets should be debrided with a spoon curette to remove vestiges of the periodontal ligament and cementum. 10. Use a large diamond-coated round bur to perform an alveoloplasty after extraction to remove diseased bone and sharp bone fragments and to smooth the alveolar margin.

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d Figure 11.7 a–d. Gingivitis, periodontitis, and alveolar mucositis around the maxillary and mandibular cheek teeth. e. Red marker used to identify teeth to be extracted. f–h. Sulcular incisions. i and j. Molt elevator used to detach gingiva from the teeth and alveolar bone. k–m. Exposure of the mandibular and maxillary alveolar processes past the mucogingival junction. n and o. Removal of the coronal buccal alveolus. p. Sectioning the left mandibular fourth premolar. q. Sectioning the left maxillary fourth premolar. r. Extracted maxillary premolars and molars. s. Extracted mandibular premolars and molars. t. Deep and wide suture placement. u. Sutured maxillae. v. Sutured mandibles. w. Resolving stomatitis one month after surgery.

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Figure 11.7

Continued

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Figure 11.7 Continued

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14. 15.

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Expose and examine intraoral films of all extraction sites. Close the gingiva over the extraction sites without tension. If tension exists, dehiscence often occurs. To create a larger flap to suture without tension, lightly incise in a distomedial direction over the connective tissue of the inside of the flap. Suture using 4-0 or 5-0 absorbable material with reverse cutting or round tapered needles (figs. 11.7 r–v). Postoperative films are exposed and examined. Postoperatively, administer an antibiotic approved for dental disease and pain control medication for one week. Soft food is recommended for one month (fig. 11.7w).

See figures 11.8 a through l for examples of full-mouth extractions, and figures 11.9 a through e for extraction of teeth caudal to the canines.

Root Fragment Removal A fully extracted tooth should have a smooth round apex. When this is not observed, often a root fragment remains in the alveolar socket. Every effort should be made to retrieve from the alveolus any remaining root fragments created during the extraction procedure. If these fragments are not removed, a nidus of chronic infection may develop. A fine elevator or root-tip pick is used to retrieve the root fragment. If this approach does not allow extraction, the buccal alveolar plate covering the fragment is removed, exposing the underlying root. A slot between the tooth and periodontal ligament is created to place the blade of the wing-tipped elevator, which is used to elevate and extract the root fragment. 1. 2. 3. 4.

Intraoral radiographs are exposed and examined, revealing the root fragment and adjacent anatomy. A mucoperiosteal flap is created. A root-tip elevator is advanced around the root remnant to create mobility and delivery. If the root-tip elevator is not effective in delivering the root remnant, removal of additional buccal alveolar bone should expose the root tip for easier visualization and delivery (figs. 11.10 a, b, c).

Postoperative Recommendations The diet should be softened for at least one week after surgery. This can be accomplished by instructing the client to soak the animal’s food for about twenty minutes before feeding. A 0.12% chlorhexidine solution can be

sent home with the owner to apply twice daily for a week as an oral rinse.

Laser Adjunctive Therapy Carbon dioxide and diode laser ablation may be helpful as an adjunct therapy modality in cases of stomatitis where proliferative caudal stomatitis is present and multiple extractions have been performed. Laser therapy can be performed at the time of initial extraction surgery and as part of follow-up therapy. Clinically, laser therapy appears to increase patient comfort as evidenced by a prompt return to eating (fig. 11.11a). Laser therapy removes part of the proliferating tissue and bacteria, thus decreasing the antigen load. After laser ablation, a portion of the inflammatory mass is replaced with fibrous, less-reactive scar tissue. Laser treatment does not cure oropharangyeal inflammation and should not be recommended as monotherapy for this condition. Often, monthly retreatment is necessary for the three months after extractions, followed by semiannual reevaluation and possible laser application (figs. 11.11 b, c, d). The operator and all assistants in the immediate area of the laser should wear protective eye wear. Warning signs should be posted on all entrances to the operatory area when the laser is being used. An anti-inflammatory dose of dexamethasone sodium phosphate is administered (0.125–0.5 mg/kg IV) before laser ablation to minimize oropharyngeal swelling. The patient is placed in sternal recumbency with the maxillae supported between two adjustable intravenous fluid poles with tape or held open by an assistant. After insuring adequate seal of the endotracheal cuff, a moistened gauze is wrapped around the endotracheal tube in the pharynx to prevent the laser from contacting it. A smoke evacuator is placed near the patient’s mouth. Four-quadrant regional anesthesia with long-acting 0.5% bupivicaine is administered. The CO2 laser is set to 6 watts in continuous mode delivered to a 0.8-mm ceramic tip used in focused (cutting) noncontact mode to thermoablate visible proliferative tissue of the caudal oral cavity. After gross removal of proliferative tissue, the wave-guide can be changed to accommodate a scanning handpiece capable of efficient ablation of remaining visible proliferative tissue. The scanning handpiece is used at a setting of 6 watts in continuous mode. The tissue at the base of the excised portions is ablated layer by layer. This will usually create a char layer. Removal of char is recommended with saline-soaked cottontipped applicators. This process is repeated multiple times until all visible proliferative tissue is removed. The remaining tissue shows a decreased tendency to

a

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Figure 11.8 a and b. Right caudal vestibular mucositis and periodontal disease. c. Maxillary incisor fractures. d. Left maxillary fourth premolar alveolar mucositis and periodontal disease. e and f. Left caudal vestibular mucositis. g–i. Delivery of left maxillary cheek teeth during the full-mouth extraction procedure. j–l. Resolved oropharyngeal inflammation after full-mouth extraction.

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Figure 11.8 Continued

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Figure 11.9 a. Caudal vestibular gingivitis and mucositis. b. Right caudal vestibular stomatitis. c. Right mandibular gingivitis and mucositis. d and e. Resolution after extraction of the teeth caudal to the canines.

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b Figure 11.10 a. Maxillary incisor inflammation. b. Radiograph showing retained tooth roots (arrows). c. Radiograph after incisor root fragment extraction.

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c Figure 11.11 a. Diode laser. b. Diode laser tip applied to inflammed gingiva. c. CO2 laser ablating inflammed tissue. d. CO2 laser used to remove inflammed caudal stomatitis tissue.

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b

a

Figure 11.12 a. Gingivitis and caudal stomatitis. b. Laser ablation of the inflammed tissue after full-mouth extractions. c. Resolution of inflammation.

spontaneous bleed when touched with a gauze sponge. The treated surfaces are sprayed with 2 mg of lidocaine before extubation (figs. 11.12 a, b, c). Postoperative pain medication (buprenorphine, hydromorphone, fentanyl patches), oral steroids (administered twice daily for one week followed by every other day for two weeks), and dental-specific antimicrobials are dispensed when the laser patient is released.

Further Reading Addie DD, Radford A, Yam PS, Taylor DJ. Cessation of feline calicivirus shedding coincident with resolution of chronic gingivostomatitis in a cat. J Small Anim Pract 2003; 44: 172–176. Bellei E, Dalla F, Masetti L, Pisoni L, Joechler M. Surgical therapy in chronic feline gingivostomatitis (FCGS). Vet Res Commun 2008; 32: 231–234. Hennet P. Chronic gingivo-stomatitis in cats: long-term followup of 30 cases treated by dental extractions. J Vet Dent 1997; 14: 15–21. Kobayashi S, Sato R, Aoki T, Omoe K, Inanami O, Hankanga C, Yamada Y, Tomizawa N, Yasuda J, Sasaki J. Effect of bovine lactoferrin on functions of activated feline peripheral

c

blood mononuclear cells during chronic feline immunodeficiency virus infection. J Vet Med Sci 2008; 70: 429–435. Lewis JR, Tsugawa AJ, Reiter AM. Use of CO2 laser as an adjunctive treatment for caudal stomatitis in a cat. J Vet Dent 2007; 24: 240–249. Lyon KF. Gingivostomatitis. Vet Clin North Am Small Anim Pract 2005; 35: 891–911. Niza MMRE, Mestrinho LA, Vilela CL. Feline chronic gingivostomatitis: a clinical challenge. Rev Port Cienc Vet 2004; 99 (551): 127–135. Sato R, Inanami O, Tanaka Y, Takase M, Naito Y. Oral administration of bovine lactoferrin for treatment of intractable stomatitis in feline immunodeficiency virus (FIV)-positive and FIV-negative cats. Am J Vet Res 1996; 57: 1443–1446. Southerden P, Gorrel C. Treatment of a case of refractory feline chronic oropharangyeal inflammation with feline recombinant interferon omega. J Small Anim Pract 2007; 48: 104–106. Williams CA, Aller MS. Gingivitis/stomatitis in cats. Vet Clin North Am Small Anim Pract 1992; 22: 1361–1383. Zetner K. Evaluation of the effects of an intraoral administration of recombinant feline omega-interferon (Virbagen OmegaReg.) on feline oropharangyeal inflammation and the general condition of cats suffering from chronic inflammation of mouth and pharynx. Praktische Tierarzt 2008; 89: 630–634.

Chapter 12

Treatment of Occlusion Disorders

The goal of treatment for cats affected by malocclusion disorders is to return the patient to a functional condition. This may involve orthodontic tooth movement, extraction, or crown reduction and restoration.

Ethics of Performing Veterinary Orthodontics The shape and size of the head and the number and position of teeth are genetically controlled. Occasionally, owners of show cats seek orthodontic care to correct abnormal tooth position. Organized cat show associations do not allow a cat that has had orthodontic care to compete in the show ring. Cats that have pain or periodontal disease secondary to occlusal abnormalities deserve treatment to alleviate lesions and make the mouth comfortable. Orthodontic care in show cats that have been neutered or nonshow cats can be performed with a clear conscience.

2.

3. 4. 5.

Extrusion is the easiest to accomplish, followed by tipping. Intrusion is the most difficult.

Force Force must be applied at least six hours each day for proper orthodontic tooth movement to occur. Orthodontic appliances result in different types of forces:

•

Principles of Orthodontic Tooth Movement Teeth are anchored to the alveolar bone by the periodontal ligament fibers. Orthodontic tooth movement results from light, persistent pressure that stimulates bone remodeling. This movement involves at least three variables: magnitude, direction, and duration of force. Tooth movement for orthodontic care is considered an advanced dental procedure that should not be undertaken without appreciation of the science, treatment options, and sequelae. There are five basic tooth movements in orthodontics: 1.

Tipping involves a single force applied to the crown, which causes the tooth to rotate around its center of

resistance. The crown moves in one direction and the root apex in the opposite direction. Bodily movement (translation) occurs when two forces are applied simultaneously to the crown of a tooth, causing the crown and apex to move in the same direction. Rotation (torsion) moves the tooth around its long axis. Extrusion moves the tooth out of the alveolus. Intrusion moves the tooth inward into the alveolus.

•

Intermittent force: This can be applied with rest periods characterized by an abrupt decline of force to zero every time the load is released. An inclined plane used to treat lingually displaced canine teeth would be an example of an intermittent force appliance. Continuous force: This produces effective tooth movement when light forces are used. Orthodontic buttons and elastics applied to an anchor and target tooth would be an example of continuous force orthodontic movement.

Pressure Pressure of the tooth against bone, caused by orthodontic devices designed to push or pull teeth, results in blood vessel compression. This blood flow compression leads to cell death within hours. Through biological 269

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feedback, the body increases osteoclastic activity on the side of increased pressure and increases osteoblastic activity on the side of decreased pressure. The result is a shift in the position of the alveolar socket in the direction of applied force. With sustained light force, movement usually begins in two weeks. Excessive force might cause interference with the periodontal ligament and alveolar bone blood supply, which can lead to pulp and bone necrosis. Damage to the periodontal structures may produce tooth mobility and eventual exfoliation.

2. 3. 4.

5.

Orthodontic Buttons and Elastics Tooth movement with elastics and buttons involve socalled anchor and target teeth. The anchor tooth or teeth must have a greater root surface area, which provides higher resistance to movement compared with that of the target tooth. Ideally, the anchor tooth remains stable, allowing target tooth movement. Healthy anchor teeth and periodontal support are critical to successful target tooth movement. Commonly, the maxillary third and fourth premolars are used together as anchors to move rostrally deviated canines caudally. Orthodontic buttons are cemented on the teeth to provide attachment for elastics, wires, or springs. Elastic chains are used as a source of force for many appliances.

Additional Instruments and Materials

• • • • • • • •

Right-angled handpiece Rubber polishing cup Fine pumice Cotton pliers Bracket cement—CB Metabond (Parkel, Farmingdale, N.Y.) Metal brackets, Ormesh curved lingual pad with button (Ormco Corp.) Elastic Masel chain, flattened elastic with an arrangement of holes to allow attachment to buttons or brackets Bracket placement tweezers

Technique for Button Placement and Force Activation 1.

Polish the tooth surfaces free of plaque and debris using a rubber cup on a prophy angle and slurry of pumice/water. Fluoride paste should not be

6.

7. 8. 9. 10.

used because the fluoride might prevent the etching process of the enamel. Thoroughly rinse the teeth for at least thirty seconds. Dry the teeth with oil-free compressed air. Apply etching solution or gel according to the manufacturer ’s instructions on the enamel surface where the button is to be affixed. After etching, rinse and air-dry the tooth surface. Use of hot air from a hair blower is not recommended because of potential damage to the tooth and surrounding tissue. After etching, the tooth surface should appear dull and chalky. If not, repeat the etching process. With a small absorbent square cotton pellet attached to cotton pliers, or a brush, mix the sealant and accelerator; paint the mixture on the etched surfaces of one or more teeth. Choose the location for button placement to provide a straight line between the anchor and target. Mix the adhesive and hardener with a brush to a putty consistency. Select metal orthodontic buttons with bracket forceps or college-tipped pliers. Apply the adhesive/hardener mixture to the base of the button (hold with bracket placement pliers). Position the button on the tooth and press into the adhesive. Remove excess bonding material with a hand scaler.

Elastics may be placed on the buttons approximately fifteen minutes after cementation. To place elastics, apply light force to the elastic power chain. If the bracket does not come off the tooth, pull the chain to test the bond. If the bracket is dislodged, it can be reapplied using the adhesive/hardener mixture. Check the cat weekly to monitor progress and replace elastics. Tooth movement is not expected in the first two weeks because it takes that long to recruit osteoclasts and osteoblasts. Movement in the first two weeks would be secondary to bone necrosis, not remodeling, indicating excessive force and eventual failure. The goal is slow movement over two to four months. At the recheck appointment, possible anchor tooth movement should also be checked and, if present, elastics removed or additional anchor teeth added (figs. 12.1 a–e).

Extraction of Malpositioned Teeth The advantages of extraction compared to orthodontic movement include less total treatment time and fewer anesthetic procedures to accomplish the therapy goal of relieving discomfort. The disadvantage of extraction is loss of a permanent tooth.

Treatment of Occlusion Disorders

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c Figure 12.1 a. Mandibular maxillary asymmetry. b. Orthodontic buttons and elastics used to move the left and right maxillary canines caudally. c–e. Functional occlusion after three months of orthodontic treatment.

Crown Reduction with Vital Pulp Therapy When a malpositioned tooth impinges on the opposing gingiva or interferes with other teeth, crown reduction with vital pulp therapy and restoration may return the

cat’s mouth to normal function. The procedure is often quicker than canine tooth extraction and still maintains the function of the tooth. The disadvantage lies in the possibility of composite shrinkage causing the restoration to fail and allowing oral bacteria to enter the pulp, which ultimately leads to pulp necrosis (figs. 12.2 a–e).

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Figure 12.2 a and b. Mandibular mesioclusion exposing rostral lower jaw. c. Diamond disk used to reduce the crowns of the mandibular canines (Author comment: crosscut fissure bur is effective and safer). d. Reduced and restored mandibular canines. e. Rostral mandible covered normally.

Specific Occlusion Disorders Persistent Deciduous Teeth Normally, cats’ deciduous (primary) tooth roots are resorbed as the permanent (secondary) teeth erupt. The mechanism that causes physiological resorption of the deciduous tooth roots is not fully understood, nor is the mechanism that leads to failure of the roots to resorb. When resorption fails, the permanent teeth occupy the same alveolus as the deciduous teeth. Double sets of teeth may overcrowd the dental arch, moving the per-

e

manent teeth to abnormal locations, which causes malocclusion. Double sets of roots may also prevent the normal development of the alveolus and periodontal support around the permanent tooth, resulting in early tooth loss. A persistent deciduous tooth should be extracted as soon as the permanent tooth starts to erupt in the same alveolar socket. If extraction is performed early, the abnormally positioned permanent tooth usually moves to its normal location. When a wait-and-see approach is taken to see whether the persistent deciduous tooth is exfoliated on its own

Treatment of Occlusion Disorders

accord, the permanent tooth occasionally becomes permanently malpositioned, requiring orthodontic movement, crown reduction, or extraction.

Supernumerary (Extra) Teeth

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buds, genetic influence (especially Persian cats), or skeletal abnormalities. Treatment for canine mesioversion includes:

•

Orthodontic movement with elastics. The best time for this treatment is between 9 and 18 months. Tooth movement to a functional position takes two to six months. Extraction Crown reduction with vital pulp therapy and restoration (figs. 12.3 a–o)

Supernumerary teeth can cause periodontal disease from crowding and displacement of normal teeth. Following intraoral radiographs, supernumerary teeth should be extracted if crowding or gingival impingement exists.

• •

Missing Teeth

Mandibular Canine Linguoversion

Missing teeth (hypodontia) usually occurs in the premolar area, but any tooth in the mouth may be absent. The clinically absent tooth may be present below the gingival margin. Dental radiographs are indicated to determine whether the tooth is not present, nonerupted, or missing its crown with the fractured root positioned subgingivally. Where teeth or root fragments are located subgingivally, extraction is indicated if gingival inflammation, sinus tracts, or signs of endodontic/periapical disease are present.

Lingually displaced mandibular canines may traumatize the hard palate. Treatment options include mandibular canine extraction, crown reduction with vital pulp therapy and restoration, orthodontic movement with buttons and elastics, or fabrication of an acrylic inclined plane on the maxilla to move the mandibular canines buccally.

Mesioversion of Canine Teeth Mesioversion (rostral displacement, lance, or spear teeth) of the maxillary or mandibular canine teeth occurs when the affected teeth are angled in a mesial direction. This may be caused by malpositioned permanent tooth

Maxillary Fourth Premolar/Mandibular First Molar Interference Treatment options for the impinging tooth (the maxillary fourth premolar) include odontoplasty to decrease the sharp penetrating edge, crown reduction with vital pulp therapy and restoration, or extraction. Extraction of the mandibular teeth affected by gingival recession may also be performed (figs. 12.4 a–q, 12.5 a–c).

b a Figure 12.3 a. Left and right mandibular canines impinging on the upper lips. b–e. Mesiolinguoversion of the maxillary canines. f. Orthodontic buttons and elastics applied to move the right maxillary canine caudally. g. Right and left maxillary orthodontic buttons and elastics applied. h and i. After two months right and left maxillary canines moved to functional positions. j. Mandibular canines impinging on the upper lips. k. Mandibular canine crown reduction and application of calcium hydroxide during vital pulp therapy. l–m. Crown-reduced canines in functional occlusion before final restoration finishing. n and o. Patient’s canines no longer protruding.

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Figure 12.3 Continued

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Figure 12.4 a. Right maxillary fourth premolar impinging on the buccal gingiva and alveolar mucosa of the right mandibular first molar. b–d. Gingival recession and inflammation at the right mandibular first molar secondary to the impinging right maxillary fourth premolar. e–h. Crown height reduction. i and j. Inverted cone bur used to remove 2 mm of the coronal pulp. k. Calcium hydroxide applied over the exposed pulp. l. Bonding agent applied to the area. m. Light curing acrylic resin composite. n. Polymerized composite. o and p. White stone bur used to finish the restoration. q. Area healed on 3-month follow-up exam.

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Further Reading Emily P. Feline malocclusion. Vet Clin North Am Small Anim Pract 1992; 22: 1453–1460. Gioso MA, Carvalho VG, Carvalho PE. Construction of dental study models. J Vet Dent 2004; 21: 122–126. Hale FA. Juvenile veterinary dentistry. Vet Clin North Am Small Anim Pract 2005; 35: 789–817. Lobprise HB, Wiggs RB, Peak RM. Dental diseases of puppies and kittens. Vet Clin North Am Small Anim Pract 1999; 29: 871–893.

Figure 12.5 a. Left maxillary fourth premolar penetrating gingival buccal to the left mandibular molar. b. Marked proliferative inflammation of the gingiva and alveolar mucosa of the left mandibular first molar secondary to impingement by the left maxillary fourth premolar. c. Inflammation resolved after extraction of the maxillary fourth premolar and the mandibular first molar.

Sarkiala-Kessel E. Malocclusion in a cat. J Vet Dent 2001; 18: 76–77. Surgeon TW. Surgical exposure and orthodontic extrusion of an impacted canine tooth in a cat: a case report. J Vet Dent 2000; 17: 81–85. Van de Wetering A. Orthodontic correction of a base narrow mandibular canine tooth in a cat. J Vet Dent 2007; 24: 22–28. Wissdorf H, Hermanns W. Permanent milk canine teeth in the upper jaw of a domestic cat. Kleintierpraxis 1974; 19 (1): 14–16.

Chapter 13

Oral Trauma Surgery

Knowledge of surgical anatomy, pathology, and operative principles is essential to positive outcomes.

Treatment Considerations Functional occlusion is more important than cosmetics. Intact teeth in the fracture line should not be extracted if they do not interfere with fracture reduction. Vital teeth that have been malpositioned by the fracture are extracted or repositioned and splinted into functional position. Esophagostomy tube placement may be necessary. Bone plates are not commonly used in mandibular or maxillary fracture repair. Interdental fixation with wire, acrylic splints, or orthodontic buttons and elastics are preferred methods for repair.

mandibular condyle from settling back in place or reluxating following reduction. If the condyle does not properly reduce back into the fossa, condylectomy may be indicated to allow functional occlusion. Fractures of the condylar process are not repairable by fixation of the fragments. If the jaw can be closed, treat the cat conservatively with a loose tape muzzle unless it becomes clear that the range of motion of the jaw is reduced and the patient is unwilling to eat by itself. If there is an additional rostral mandible fracture, rigid fixation may be indicated (figs. 13.2 a–o).

Temporomandibular Joint Ankylosis Treatment of temporomandibular joint ankylosis involves excision arthroplasty of the temporomandibular joint, condylectomy, or caudal mandibulectomy to allow functional range of motion of the lower jaw.

Temporomandibular Joint Dislocation Open-Mouth Jaw Locking Treatment of a temporomandibular joint dislocation involves placing the cat under general anesthesia, inserting a fulcrum (a pencil or tubular device) across the region of the maxillary and mandibular carnassial teeth on the side of the luxation, and closing the jaws, which inserts the mandibular condyle into the mandibular fossa. The condyle must first pass over the articular eminence before it can properly be reduced into the mandibular fossa. This is best accomplished by gently pulling the mandible of the luxated side rostrally to disengage the condyle from the dorsal surface of the articular eminence. The mouth is then closed on the fulcrum and the mandible is pushed caudally to properly reduce the condyle within the fossa. No postreduction fixation is necessary unless there are additional maxillary or mandibular fractures requiring stabilization (figs. 13.1 a–h). Occasionally, the fibrocartilaginous disc in the luxated joint will be torn and folded on itself, preventing the 280

Acute treatment involves opening the lower jaw further to release the coronoid process from the ventrolateral aspect of the zygomatic arch, then closing the mouth. A tape muzzle may provide temporary stabilization. Definitive surgical treatment, partial zygomectomy (by removing the part of the zygomatic arch that catches the coronoid process), usually results in resolution of the open-mouth jaw locking. If intraoperatively this does not resolve the locking, then several millimeters of the dorsal aspect of the coronoid process are also resected (partial coronoidectomy). The coronoid process can be palpated when it is deviated laterally in an abnormal position which also allows for a lateral surgical approach. A periosteal elevator is used to peel away temporal muscle from the dorsal aspect of the coronoid process exposing the underlying periosteum. Then 3–5 mm of the dorsal aspect of the coronoid process are removed with a rongeur.

a d

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f

c Figure 13.1 a. Lower jaw deviated to the left secondary to a right temporomandibular joint (TMJ) luxation. b. Right (red) TMJ rostrodorsal luxation dorsoventral image. c. Syringe placed between the right maxillary fourth premolar and mandibular first molar teeth to act as a fulcrum. d. Mandible pulled forward and downward by gently closing the lower jaw. e. Luxation corrected. f. Functional occlusion reestablished. g. Reexam two months postoperatively (after extraction of the left maxillary and mandibular canines and root canal therapy on the right maxillary canine). h. Patient appearance after treatment.

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h g Figure 13.1 Continued

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Figure 13.2 a. Cat presented with maxillofacial deformity and asymmetry. b. Deviated rostral lower jaw. c. Rostral mandibular fracture. d. Radiograph confirming fracture involving incisors and mandibular symphysis. e and f. Radiographs of caudal mandibular fracture. g. Fine pumice used to clean teeth before etching. h. Etchant applied before bonding. i. Light-cured acrylic resin applied to maxillary and mandibular canines. j. Gold instrument used to place bonding material between the tooth surfaces. k. Light curing. l. White stone used to shape cured acrylic. m. Canines bonded in functional occlusion with sufficient space to move tongue and to breathe comfortably (esophagostomy tube placed). n. Acrylic has been removed; functional occlusion achieved after one month of acrylic holding canines together. o. Clinical appearance (note persistent left-sided Horner’s syndrome).

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Figure 13.2 Continued

Maxillary/Mandibular Fractures The endotracheal tube often serves as an impediment to properly evaluating occlusion and repairing maxillary and mandibular fractures. To remove the endotracheal tube from the rostral oral cavity, the trachea can be intubated through a tracheotomy site or preferentially from

o

within the oropharynx via a pharyngostomy incision between the ramus of the mandible and the epihyoid bone.

Mandibular Symphysis Separation In most cases, the mandibles can be apposed and stabilized for fibrous attachment to occur by means of self-

Oral Trauma Surgery

cured temporization material (3M™ ESPE™ Protemp 3™ Garant™; figs. 13.3 a–h). Alternatively, the mandibular symphysis can be stabilized with cerclage wiring. 1. Two centimeters of the rostral lower jaw are prepared for surgery. 2. An 18-gauge needle is passed through the skin ventral to the canine teeth up and around one side of the mandible to exit just behind the canine tooth. 3. Orthopedic wire (22 gauge) is inserted through the needle and grasped with a needle holder when the needle is withdrawn. 4. The needle is reinserted at the other side in similar fashion as described above. 5. The intraoral end of the wire is inserted into the sharp end of the needle, and the needle is removed. 6. Both wire ends are twisted sufficiently to approximate the mandibles and compress the separation site (fig. 13.4). Care should be taken not to compromise the blood supply to the area through excessive compression. Clinical union of the symphyseal separation usually occurs within six weeks.

Mandibular Fractures Fractures in the mandibular incisor area can usually be fixed in correct alignment by applying an acrylic splint from canine tooth to canine tooth, incorporating all of the incisor teeth on that jaw. Dental composite may also be applied between the maxillary and mandibular canines to stabilize mandibular fractures. Mandibular body fractures are more common than fractures in the incisor region. Depending on the extent of displacement there are multiple therapy options:

• • • •

Interdental wiring with intraoral resin oversplint. Application of a muzzle for fractures with minimal displacement. Temporary bonding of the maxillary and mandibular canines in normal occlusion until the fracture site has healed into a functional position. Segmental mandibulectomy for fractures deemed not repairable.

Maxillary Fractures Midline maxillary fractures result from trauma in the cat. Suturing the palatal defect is usually curative. Unstable fractures of the maxilla can usually be held in reduction with a splint extending across the palate from the canine tooth on one side to the canine tooth on the other side (figs. 13.5 a–f).

a

Figure 13.3 a. Mandibular symphysis separation. b. Radiograph of rostral lower jaw. c. Teeth cleaned with fine pumice. d and e. Partial application of temporization material. f. Trimmed and polished splint. g. Postoperative radiograph. h. Immediate appearance after splint removal six weeks postinjury.

285

b

c

d

e

f

g Figure 13.3 Continued

286

h

Figure 13.4

Ends of cerclage wire exiting ventrally to repair mandibular symphysis separation.

a

b Figure 13.5 a. Traumatic midline hard palate defect. b. Maxillary radiograph revealing extent of fracture. c. Temporization material applied to the maxillary canines for stabilization. d. Material notched with high speed bur to allow for clearance of the opposing mandibular canines. e. Maxillary and mandibular temporization material applied with room for functional occlusion. f. Maxillary fracture healing two weeks after splint application.

287

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c

d

e

Figure 13.5 Continued

Further Reading Anderson MA, Orsini PG, Harvey CE. Temporomandibular ankylosis: treatment by unilateral condylectomy in two dogs and two cats. J Vet Dent 1996; 13: 23–25. Barbudo GR, Selmi AL, Canola JC. Oral and maxillofacial reconstruction in a cat using wire and acrylic. J Vet Dent 2000; 17: 168–172. Beam RC, Kunz DA, Cook CR, Carson RL, Briscoe P, Cook JL. Use of three-dimensional computed tomography for diagnosis and treatment planning for open-mouth jaw locking in a cat. J Am Vet Med Assoc 2007; 230: 59–63. Bennett JW, Kapatkin AS, Marretta SM. Dental composite for the fixation of mandibular fractures and luxations in 11 cats and 6 dogs. Vet Surg 1994; 23: 190–194. Bilgili H, Kurum B. Treatment of fractures of the mandible and maxilla by mini titanium plate fixation systems in dogs and cats. Aust Vet J 2003; 81: 671–673.

f

Boudrieau RJ, Kudisch M. Miniplate fixation for repair of mandibular and maxillary fractures in 15 dogs and 3 cats. Vet Surg 1996; 25: 277–291. Chambers J. Principles of management of mandibular fractures in the dog and cat. J Vet Orthop 1981; 2: 26–36. Eisner ER. Bilateral mandibular condylectomy in a cat. J Vet Dent 1995; 12: 23–26. Kapatkin AS, Matthiesen DT. Feline high rise syndrome. Comp Cont Ed Pract Vet 1991; 13: 1389–1398. Legendre L. Maxillofacial fracture repairs. Vet Clin North Am Small Anim Pract 2005; 35: 985–1008. Legendre L. Use of maxillary and mandibular splints for restoration of normal occlusion following jaw trauma in a cat: a case report. J Vet Dent 1998; 15: 179–181. Legendre LFJ. Management and long term effects of electrocution in a cat’s mouth. J Vet Dent 1993; 10 (3): 6–8. Lobprise HB, Wiggs RB. Modified surgical treatment of intermittent open-mouth mandibular locking in a cat. J Vet Dent 1992; 9 (1): 8–12.

Oral Trauma Surgery Masztis PS. Repair of labial avulsion in a cat. J Vet Dent 1993; 10 (1): 14–15. Okumura M, Kadosawa T, Fujinaga T. Surgical correction of temporomandibular joint ankylosis in two cats. Aust Vet J 1999; 77: 24–27. Piemattei DL, Flo GL. Fractures and luxations of the mandible and maxilla. In: Handbook of Small Animal Orthopedics and Fracture Repair. Saunders, Philadelphia, 1997; 659–675. Reiter AM. Symphysiotomy, symphysiectomy and intermandibular arthrodesis in a cat with open-mouth jaw locking:

289

case report and literature review. J Vet Dent 2004; 21: 147–158. Wallace Bennet J, Kapatkin AS, Marretta SM. Dental composite for the fixation of mandibular fractures and luxations in 11 cats and 6 dogs. Vet Surg 1994; 23: 190–194. Zetner K. Treatment of jaw fractures in small animals with parapulpar pin composite bridges. Vet Clin North Am Small Anim Pract 1992; 22: 1461–1467.

Chapter 14

Treatment of Oral Swellings/Tumors

Inflammatory Lesions Abscesses and osteomyelitis can result in oral swelling. Removing the cause of inflammation is usually curative (figs. 14.1 a–d, 14.2). Cysts are rare in the oral cavity but do occur. Aspiration for diagnostics and marsupialization if possible are therapeutic options (figs. 14.3 a, b). Tongue eosinophilic granulomas, if large, can be treated by surgical debulking, laser ablation, and medical therapy (figs. 14.4 a–d).

Benign Tumors Unlike canine peripheral odontogenic fibromas, feline odontogenic fibromas appear to recur frequently after surgical excision. Wide margins are indicated to prevent reoccurrence.

Malignant Tumors Squamous Cell Carcinoma Squamous cell carcinoma (SCC) accounts for nearly 75% of malignancies involving the cat’s oral cavity. SCC is an invasive malignant neoplasm. Usually by the time a clinical diagnosis is made, there is no form of therapy that renders a predictably favorable prognosis. Greater than 90% of affected and treated cats will either be euthanized or die from secondary local effects from the tumor within one year of diagnosis. Without therapy, most cats will be euthanized within a month of diagnosis due to local effects of the tumor. Intraoral radiographs are helpful to evaluate the extent of the tumor within hard tissue. Computed tomography (CT) examination will usually provide greater information concerning the extent of tumor invasion. Deep incisional biopsy and histopathologic examination are necessary to definitively diagnose SCC. 290

Fine-needle aspiration of regional lymph nodes may be diagnostic for metastasis. Treatment options include surgery, radiation therapy, and chemotherapy.

Fibrosarcoma Fibrosarcoma (FSA) is the second most common tumor of the feline oral cavity. Approximately 10% to 20% of feline oral tumors are FSA compared to nearly 75% for SCC. A deep incisional biopsy is recommended to obtain a correct histopathological diagnosis. Similar to SCC, oral FSA is an invasive malignancy necessitating wide surgical excision. Inadequate surgical margins generally result in recurrence. Even aggressive surgery and histopathologically determined “clean” margins may result in recurrence in 20% to 30% of cases. As a primary mode of therapy, the use of radiation therapy in cats with oral FSA is generally discouraged. However, the use of radiation may be beneficial in cases with incomplete surgical resection, or if the radiation is being used palliatively (3–6 large doses). Chemotherapy is generally not effective in oral FSA due to relative chemoresistance of soft-tissue sarcomas. Chemotherapy is occasionally used in cats with large oral FSA in an attempt to downstage the tumor for later surgical resection or in cats with high-grade FSA that have a greater chance for metastasis. Surgical prognosis is better for oral feline FSA compared with SCC, with survival times of those cases treated with combined immunotherapy, chemotherapy, and cryosurgery varying between 382 days (mandible) and 1,205 days (hard palate) compared to 49 and 59 days for SCC.

Mandibulectomy and Maxillectomy Surgery as a sole treatment for SCC is generally unrewarding with the median survival rate between six and nine months. Generally, those cats that survive one year

c

a

d

b Figure 14.1 a and b. Left side of face swollen. c. Intraoral radiographs revealing periodontal disease and root fragments. d. Two months after surgical removal of the teeth and root fragments.

Figure 14.2 Marked inflammation and exuberant tissue secondary to underlying osteomyelitis from mandibular first molar root fragment local reaction.

291

a b Figure 14.3 a. Soft swelling in the area of the right tonsil. b. Aspiration fluid consistent with pharyngeal mucocele.

a

b

Figure 14.4 a. Eosinophilic granuloma affecting a cat’s tongue. b. Surgical debulking. c and d. CO2 laser used to partially ablate the underlying tissue.

292

Treatment of Oral Swellings/Tumors

293

d

c

after surgery were also alive at year two, indicating a favorable prognosis in those cats that survive one year. Surrounding the tumor is a pseudocapsule composed of normal and neoplastic cells and a reactive zone composed of inflammatory cells. The optimum goal is to render the patient tumor free. When this goal is not possible because of the extent of disease, palliative surgery can be performed to achieve temporary local control. Maxillectomy and mandibulectomy are considered advanced oral surgical procedures. Before surgery, the cat is treated with appropriate antibiotics and pain relief medication. When anesthetized, the oral mucosa is irrigated with 0.12% chlorhexidine. Regional nerve blocks are also performed. After surgery, the patient is maintained on a soft gruel diet or fed through a pharyngostomy tube until normal prehension and swallowing are restored. Antibiotic and pain relief medication are administered for two weeks postoperatively. Cats with small lesions involving the rostral mandible may be able to undergo an aggressive rostral mandibu-

Figure 14.4 Continued

lectomy with good to excellent results. The surgical goal should be tumor removal with at least 1 cm clinically and radiographically clean margins. Mandibulectomies are classified according to the part excised: unilateral or bilateral; rostral, central, or caudal mandibulectomy; and three-quarter or total mandibulectomy. After the soft tissue attachments are incised to the bone, osteotomies are performed. For a rostral mandibulectomy, the first osteotomy is at the mandibular symphysis followed by a second at the predetermined area between the premolar teeth. A curved mosquito hemostat can be used to locate the mandibular alveolar artery for ligation. If the artery retracts into the mandibular canal, the canal can be packed with bone wax or hemostatic sponges (Vetspon, Novartis) to control hemorrhage. After tumor removal, the lip mucosa is sutured to the sublingual and contralateral mandibular mucosa without tension. When the chin has been included in the resection, skin is sutured to the mucosa of the floor of the mouth rostrally to reconstruct a lip margin.

294

Feline Dentistry

Total unilateral mandibulectomy may lead to a drift of the remaining mandible toward the mandibulectomy side, although this rarely produces a functional problem other than the remaining mandibular canine tooth traumatizing the hard palate. Crown reduction and vital pulp therapy with restoration or extraction should be considered to prevent palate trauma. The infraorbital artery is located apical to the distal root of the maxillary third premolar. The major palatine artery emerges from the hard palate at the level of the maxillary fourth premolar, midway between the midline and dental arcade. These vessels should be ligated if the tumor removal requires their transection. A large area of maxillary resection often exposes the nasal cavity, which needs to be covered with a full-thickness mucoperiosteal flap.

Radiation Therapy Radiation therapy as a sole treatment modality for SCC has median survival times of less than three months. One radiation therapy protocol involves megavoltage radiation in 8 Gray (Gy) fractions delivered on days 0, 7, and 21 for a total dose of 24 Gy. Treatment fields include the tumor, 1-cm margins, and tumor-draining lymph nodes. Slightly better results are obtained using an accelerated protocol (14 fractions of 3.5 Gy in 9 days). Radiotherapy complications include mucositis, serosanguinous oral discharge, pain, and dysphagia. Coarse fractionation radiotherapy does not result in palliation in cats with inoperable oral SCC.

include CBC, blood profile, urinalysis, and blood pressure measurement. Cats that are prescribed NSAIDs for chronic use also need to be periodically monitored, and this is considered an extra-label use. Recently, a human medication used in the treatment of head and neck tumors, zoledronate, a potent aminobisphosphonate, has shown promise in the treatment of oral SCC. Zoledronate displays antineoplastic effects, including impaired neoplastic neovascularization, decreased tumor angiogenesis, and decreased malignant osteolysis. In vitro and in vivo efficacy has been demonstrated in cats.

Combined Radiotherapy and Chemotherapy Mitoxantrone is a chemotherapeutic agent related to doxorubicin. Eleven cats affected with oral SCC were treated with mitoxantrone and radiation therapy (44– 65 Gy, 10–15 fractions over a three-week period). Eight of the eleven cats went into clinical remission for 28 to 485 days, but survival rates were not available.

Combined Surgery and Radiotherapy Eleven-month, disease-free, interval median results were obtained in a small study of seven cats affected with oral SCC. Tumors >4 cm in diameter were treated with mandibulectomy and full-course radiation (five orthovoltage, one cobalt, one combined). The overall median survival time was fourteen months.

Chemotherapy Epidermal Growth Factor Receptor Though relatively few reports exist on the sole use of chemotherapy (doxorubicin, mitoxantrone, and/or carboplatin) for feline oral SCC, it is generally felt to be minimally beneficial. Research is ongoing to determine if inhibition of cyclooxygenase-2 (COX-2) can play a role in the treatment of oral SCC to enhance the anticancer effects of chemotherapy and radiation therapy. Initial research showed that COX-2 was present in only 9% of feline oral SCC. The absence of COX-2 expression suggests that COX-2 inhibitors will likely have a low potential as a cancer agent for oral SCC therapy. NSAIDs such as piroxicam have been given at 0.3 mg/ kg PO once daily to help decrease inflammation. Meloxicam is dosed at 0.1 mg/kg once daily. Administration of NSAIDs should be reserved for normotensive adult cats without history of bleeding disorders or renal, hepatic, or gastrointestinal disease. Screening blood tests should

New methods in humans with head and neck cancer are aimed at blocking epidermal growth factor receptor (EGFR), which is overexpressed in patients with oral SCC. Squamous cells proliferate in response to the binding of polypeptide growth factors with transmembrane receptors. Blocking of the EGFR is currently being investigated as therapy for human head and neck SCC. It has been demonstrated that EGFR is overexpressed in feline SCC similar to humans. It is hoped that research aimed at human treatment will benefit cats also.

Further Reading Beatty JA, Charles JA, Malik R, France MP, Hunt GB. Feline inductive odontogenic tumour in a Burmese cat. Aust Vet J 2000; 78: 452–455.

Treatment of Oral Swellings/Tumors Bradley RL, Mac Ewen EG, Loar AS. Mandibular resection for removal of oral tumors in 30 dogs and 6 cats. J Am Vet Med Assoc 1984; 184: 460–463. Bregazzi VS, LaRue SM, Powers BE, Fettman MJ, Ogilvie GK, Withrow SJ. Response of feline oral squamous cell carcinoma to palliative radiation therapy. Vet Radiol Ultrasound 2001; 42: 77–79. DiBernardi L, Dore M, Davis JA, Owens JG, Mohammed SI, Guptill CF, Knapp DW. Study of feline oral squamous cell carcinoma: potential target for cyclooxygenase inhibitor treatment. Prostaglandins Leukotrienes & Essential Fatty Acids 2007; 76: 245–250. Farrelly J, Denman DL, Hohenhaus AE, Patnaik AK, Bergman PJ. Hypofractionated radiation therapy of oral melanoma in five cats. Vet Radiol Ultrasound 2004; 45: 91–93. Fidel JL, Sellon RK, Houston RK, Wheeler BA. A nine-day accelerated radiation protocol for feline squamous cell carcinoma. Vet Radiol Ultrasound 2007; 48: 482–485. Hahn KA. Vincristine sulfate as single-agent chemotherapy in a dog and a cat with malignant neoplasms. J Am Vet Med Assoc 1990; 197: 504–506. Harvey CE. Oral surgery. Radical resection of maxillary and mandibular lesions. Vet Clin North Am Small Anim Pract 1986; 16: 983–993. Hayes AM, Adams VJ, Scasey TJ, Murphy S. Survival of 54 cats with oral squamous cell carcinoma in United Kingdom general practice. J Small Anim Pract 2007; 48: 394–399. Hutson CA, Willauer CC, Walder EJ, Stone JL, Klein MK. Treatment of mandibular squamous cell carcinoma in cats by use

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of mandibulectomy and radiotherapy: seven cases (1987– 1989). J Am Vet Med Assoc 1992; 201: 777–781. Jones PD, de Lorimier L-P, Kitchell BE, Losonsky JM. Gemcitabine as a radiosensitizer for nonresectable feline oral squamous cell carcinoma. J Am Anim Hosp Assoc 2003; 39: 463–467. Lascelles BDX, Henderson RA, Seguin B, Liptak JM, Withrow SJ. Bilateral rostral maxillectomy and nasal planectomy for large rostral maxillofacial neoplasms in six dogs and one cat. J Am Anim Hosp Assoc 2004; 40: 137–146. Lester S, Pratschke K. Central hemimaxillectomy and reconstruction using a superficial temporal artery axial pattern flap in a domestic short hair cat. J Feline Med Surg 2003; 5: 241–244. Moore AS, Wood CA, Engler SJ, Bengtson AE. Radiation therapy for long-term control of odontogenic tumours and epulis in three cats. J Feline Med Surg 2000; 2: 57–60. Northrup NC, Selting KA, Rassnick KM, Kristal O, O’Brien MG, Dank G, Dhaliwal RS, Jagannatha S, Cornell KK, Gieger TL. Outcomes of cats with oral tumors treated with mandibulectomy: 42 cases. J Am Anim Hosp Assoc 2006; 42: 350–360. Verstraete FJ. Mandibulectomy and maxillectomy. Vet Clin North Am Small Anim Pract 2005; 35: 1009–1039. Wypij JM, Fan TM, Fredrickson RL, Barger AM, de Lorimier LP, Charney SC. In vivo and in vitro efficacy of zoledronate for treating oral squamous cell carcinoma in cats. J Vet Int Med 2008; 22: 158–163.

Section III

Prevention

Chapter 15

Plaque Control

One of the biggest challenges in veterinary dentistry is how to prevent periodontal disease (gingivitis and periodontitis) through daily plaque control after the oral assessment, treatment, and prevention (ATP) visit. Prevention is not a substitute for periodic (at least yearly) professional examination under general anesthesia to evaluate and treat areas above and under the gingival margin and to search for tooth resorption, which affects more than half of the mature domestic cat population worldwide. Before periodontal treatment is initiated, a discussion with the pet owner concerning commitment and ability to provide aftercare should be conducted. There is little reason to perform intermediate or advanced dental procedures if the pet owner will not or cannot brush the pet’s teeth. If there is minimal commitment for home care, it may be better for the veterinarian to extract a tooth affected with stage 3 or 4 periodontal disease. Follow-up progress visits are essential to monitor periodontal healing. The time between oral examinations should be based on the degree of disease and the client’s ability to provide home oral hygiene. Progress visits are initially scheduled weekly until the owner is comfortable with the home care process. Thereafter, advanced periodontal cases should be rechecked every other week to once monthly. Pets that have been treated for stage 1 or 2 disease and whose teeth are brushed once or twice daily could be rechecked every six months. The reminder interval for recheck can be linked by computer to the degree of periodontal disease (i.e., if the patient is treated for grade 3 periodontal disease, a monthly progress reminder can be automatically generated).

Home Care and Follow-Up There are numerous products available to help reduce plaque and calculus. The Veterinary Oral Health Council reviews independent efficacy studies and approves products that significantly decrease plaque and/or calculus. Table 15.1 shows diets that have been awarded the Veterinary Oral Health Council seal for use in cats.

Toothbrushing The gold standard in human dentistry to prevent plaque is toothbrushing at least twice daily. Human baby softbristled toothbrushes or small animal mini toothbrushes can be used. Most cats will permit toothbrushing when approached gradually as kittens. The client should begin by massaging the side of the cat’s muzzle in a rostral to caudal direction. Most cats will tolerate this because it simulates their natural behavior when they rub against a person or object and mark their saliva on the property. This is followed by using a washcloth or gauze sponge to gently rub the teeth and gingiva. Once the cat is comfortable with fingers rubbing inside the mouth, a toothbrush or Q-tip is substituted. Tuna juice can be applied to the end of the brush or Q-tip to gain acceptance (figs. 15.1 a–d). C.E.T.® paste and Oral Hygiene Gel, Maxiguard® Oral Cleansing Gel, Dermapet’s Dentacetic Gel™, and Oxygene® paste can be used as dentifrices to help control plaque and maintain good oral hygiene. It is the mechanical removal of plaque from brushing that is most important (fig. 15.1e).

Oral Rinses/Gels Chlorhexidine is the most effective chemical agent for prevention and reduction of plaque accumulation.

Table 15.1.

Products awarded the Veterinary Oral Health Council seal.

Product

Type of Product

Claim

Company

Friskies® Feline Dental Diet

Diet

Plaque and Tartar

Friskies Petcare Co.

New and Improved Prescription Diet® Feline t/d

Diet

Plaque and Tartar

Hill’s Pet Nutrition Inc.

Purina Veterinary Diets® DH Dental Health™ brand Feline Formula

Diet

Plaque and Tartar

Nestle Purina PetCare

299

d a

b

e

c

300

Figure 15.1 a. Mini-toothbrush (Virbac). b. Correct angle for toothbrushing. c. Cat toothbrush (Virbac). d. Using a Q-tip to remove plaque. e. Cat toothbrush and dentifrice.

Plaque Control

301

by decreasing plaque through their antimicrobial effect (figs. 15.3; 15.4 a, b, c). Sodium hexametaphosphate inhibits mineralization of plaque by binding salivary calcium, thus inhibiting calculus formation on tooth surfaces. Unlike chlorhexidine, sodium hexametaphosphate has no known effect on the microbial population of the oral cavity. It is available as coatings on various cat foods, treats, chews, and oral hygiene wipes.

Plaque Barrier Gel

Figure 15.2

C.E.T. oral rinse.

Plaque barrier gel (OraVet® Merial) is an inert polymer positioned to help prevent plaque. When applied after an oral assessment, treatment and prevention visit, OraVet is designed to create a barrier on the entire tooth surface against plaque formation by interferring with pellicle fomations between the tooth surface and the gum line. This action decreases the attachment of plaque to the tooth surface at the gingival margin, preventing bacterial colonization beneath the gum line. One double-blind study of thirty-one client-owned cats showed that OraVet® significantly (p < 0.05) reduced plaque compared to negative controls (figs. 15.5 a, b).

Drinking Water Additives Containing Xylitol Xylitol has been shown to have antibacterial effects and also decreases plaque formation (figs. 15.6 a, b).

Diet

Figure 15.3

OraZn (Addison Biological Laboratory, Inc.).

Chlorhexidine is effective against most oral bacteria, fungi, and many viruses. Compared to using antibiotics, chronic chlorhexidine use will not result in development of bacterial resistance. By decreasing or eliminating the pathogen load, chlorhexidine may have a place in stomatitis care. To be effective, chlorhexidine should stay in contact with the gingiva for at least two minutes. Humans swish chlorhexidine solution in their mouths for this period of time (fig. 15.2). Zinc and zinc ascorbate can be used as oral antiseptics to slow the development and progression of gingivitis

Dry food would appear better to help control plaque compared to moist or semimoist foods. Hills diets t/d® and Science Diet® Oral Care for cats, all Eukanuba® diets except kitten foods, and Friskies® Feline Dental Diet are 20% or more effective in controlling plaque than control diets. Hills and Friskies diets have obtained the Veterinary Oral Health Council seal of acceptance (figs. 15.7 a, b, c).

Treats C.E.T. Chews for Cats® contain oxidizing properties, which are believed to decrease plaque. Feline Greenies® has been shown in studies to decrease plaque and gingivitis (figs. 15.8; 15.9 a, b).

Oral Exercise Items softer than the teeth, such as the Feline Kong® and small rubber toys, promote gingival health.

c

b a Figure 15.4 a. Maxi/Guard Oral Cleansing Gel (with attached vitamin C). b. Adding vitamin C to the gel. c. Application of gel with finger to the side of the cat’s mouth.

b a Figure 15.5 a. OraVet® homecare product. b. OraVet® applied with applicator to dried teeth.

a b 302

Figure 15.6

a. AquaDent. b. BreathaLyser.

Plaque Control

303

c a

b

Figure 15.7 a. Hill’s Prescription Diet t/d Feline®. b. Hill’s Science Diet® Oral Care Feline. c. Friskies® Dental Diet.

b

Figure 15.8

CET Oral Hygiene Chews for Cats®.

a Figure 15.9

Scheduling the Next Oral ATP Examination Once the teeth are clean, the patient’s oral health is reevaluated and a long-term oral health program is developed or updated. Choosing the appropriate time for recall should be tailored to each individual patient. If surgery was performed, the first recheck should be days after surgery to follow the healing process. After the operative area has clinically healed, the client’s efforts at plaque control should be carefully monitored.

a and b. Feline Greenies®.

In some cases, this is performed monthly; in other cases, recall every six months is sufficient. A recall system is essential to a successful prophylactic program, because the client is unlikely to schedule periodic appointments without first being reminded. Cats with basically healthy teeth and gingiva will benefit from annual professional dental care. Cats with early periodontal disease should have at least semiannual professional evaluations. Pets with advanced periodontal disease benefit from professional clinical evaluation monthly to prevent the condition from progressing.

304

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Further Reading Aller S. Dental home care and preventive strategies. Sem Vet Med Surg Small Anim 1993; 8: 204–212. Boyce EN. Feline experimental models for control of periodontal disease. Vet Clin North Am Small Anim Pract 1992; 22: 1309–1321. Clarke DE. Clinical and microbiological effects of oral zinc ascorbate gel in cats. J Vet Dent 2001; 18: 177–183. Clarke DE. Drinking water additive decreases plaque and calculus accumulation in cats. J Vet Dent 2006; 23: 79–82. DuPont GA. Prevention of periodontal disease. Vet Clin North Am Small Anim Pract 1998; 28: 1129–1145. Gawor JP, Reiter AM, Jodkowska K, Kurski G, Wojtacki MP, Kurek A. Influence of diet on oral health in cats and dogs. J Nutr 2006; 136: 2021S–2023S. Gorrel C. Home care: products and techniques. Clin Tech Small Anim Pract 2000; 15: 226–231. Gorrel C, Inskeep G, Inskeep T. Benefits of a ‘dental hygiene chew’ on the periodontal health of cats. J Vet Dent 1998; 15: 135–138. Ingham K, Gorrel C, Bierer B. Effect of a dental chew on dental substrates and gingivitis in cats. J Vet Dent 2002; 19: 201–204. Ingham KE, Gorrel C, Blackburn JM, Fransworth W. The effect of tooth brushing on periodontal disease in cats. J Nutr 2002; 132: 1740S–1741S. Logan EI. Oral cleansing by dietary means: feline methodology and study results. Proc Comp Anim Oral Health Conf 1996; 31–34.

Logan EI. Dietary influences on periodontal health in dogs and cats. Vet Clin North Am Small Anim Pract 2006; 36: 1385–1401. Richardson RL. Effect of administering antibiotics, removing the major salivary glands, and toothbrushing on dental calculi formation in the cat. Arch Oral Biol 1965; 10: 245–253. Robinson JGA. Chlorhexidine gluconate: the solution for dental problems. J Vet Dent 1995; 12: 29–31. Roudebush P, Logan E, Hale FA. Evidence-based veterinary dentistry: a systemic review of homecare for prevention of periodontal disease in dogs and cats. J Vet Dent 2005; 22: 6–15. Studer E, Stapley RB. The role of dry foods in maintaining healthy teeth and gums in the cat. Vet Med Small Anim Clin 1973; 68: 1124–1126. Theyse LFH, Vrieling HE, Dijkshoorn NA. A comparative study of 4 dental home care regimens in client owned cats. Proc Hill’s Europ Symp Oral Care, Amsterdam, 2003; 60–63. Veterinary Oral Health Council (VOHC). Products awarded the VOHC seal (available at http://vohc.org/accepted_ products.htm). Vrieling HE, Theyse LFH, van Winkelhoff AJ, Dijkshoorn NA, Logan E, Picavet P. Effectiveness of feeding large kibbles with mechanical cleaning properties in cats with gingivitis. Tijdschrift voor Diergeneeskunde 2005; 130 (5): 136–140. Watson AD. Diet and periodontal disease in dogs and cats. Aust Vet J 1994; 71: 313–318.

Index

Abscesses extraction and, 234 radiology and, 73, 74, 75 treatment of, 290 Acoustic streaming, 181 Acquired pellicle, 101, 104 Aggregate. See Mineral tri-oxide aggregate Air-bone rule, 50 Air-cooled compressors, 162–163 Air polishing, 183 ALARA, 43. See also Radiation safety Allergies, lip ulcers and, 138 Alpha V beta 3 receptors, 127 Alveolar bone, 10–12, 127 Alveolar bone expansion overview of, 114 radiology and, 71–73 treatment of, 188, 189–193 Alveolar margin (crest), 67, 68 Alveolar nerve, 8, 174 Alveolar process, 24 Alveoli, 10, 13, 115 Alveoloplasty, 166, 194, 240, 257 Ameloblasts, 22 American Veterinary Dental College (AVDC), 169– 170 Amoxicillin, 185, 242 Ampicillin, 174 Amyloid-producing odontogenic tumors, 138 Analgesia, 171, 177–179 Anesthesia evaluation before, 170 induction of, 171 intubation and, 171 laser therapy and, 262 local/regional, 174–177 maintenance of, 171–172 medical conditions requiring special protocols for, 173–174 monitoring during, 172–173 overview of, 169–170

pain control and, 171 patient preparation and, 172 protocols for, 170 root canal therapy and, 213 tooth resorption and, 126 Anesthesia-free dentistry, 169–170 Ankylosis radiology and, 73 of temporomandibular joint, 143, 144, 280 Anodontia, 101 Antibiotics diabetes mellitus and, 174 periodontal disease and, 185 stomatitis and, 242, 244 Apexogenesis, 213 Apical closure, 73 Apple-par rule, 46 AquaDent, 302 Arteries, 8. See also Specific arteries Artificial tears, 182 As low as reasonably achievable. See ALARA Atopic dermatitis, 138 ATP. See Oral assessment, treatment, and prevention visits Attached gingiva, defined, 10, 11 Autoclaves, 167 AVDC. See American Veterinary Dental College AVImark paperless charts, 92 Azathioprine, 242 Azithromycin, 244 AZT. See Zidovudine Bacteria caries and, 120 equipment and, 167 plaque and, 101, 104 ultrasonic scaling and, 181 Barbiturates, 173 Barrier gel, 184, 185 Biofilms, 104, 167 Bioglass, 185 305

306

Index

Biopsies, 142 Bisecting angle technique, 50, 51, 52 Bitewing film, 46, 47 Bleach (sodium hypochlorite), 207–208, 217 Bleeding, periodontal probing and, 105, 107 Blood pressure, anesthesia and, 170 Blood supply, anatomy of, 8 Blurred images, 64 Bodily movement (translation), 269 Body temperature. See Temperature control Bone curettes, 160 Bone grafting, 185–188 Bone invasion, 142 Bone loss, 68–71 Bones, 12–15. See also Specific bones Books, 151 Brachycephalic breeds, 28, 133 Breathalyser, 302 Buccal, defined, 24, 26 Buccal object rule, 59–60 Buccoversion, overview of, 134 Bupivacaine, 174, 175, 179, 262 Buprenorphine, 171, 179 Burs, 161, 165–166 Butorphanol, 170–171, 177–179 Buttons, 270, 271 Calcifying epithelial odontogenic tumors, 138 Calcium hydroxide, 207, 210, 212, 215, 220 Calciviruses, 244 Calculus, 104, 108, 181, 188 Calculus index (CI), 108 Canine teeth anatomy of, 19–21 extrusion of, 110, 113 malocclusion and, 134, 135, 273–274 radiography of, 50, 54, 55 terminology of, 24–26 Canine tooth extrusion, 113 Carbides, 166 Carbon dioxide laser ablation, 244, 262, 267, 268 Carboplatin, 294 Carotid artery, anatomy of, 8 Carprofen, 179 Cat cavities. See Resorption Catecholamines, 171 Caudal, defined, 26, 27 Cavitation, 181 Cefadroxil, 185 Cementum anatomy of, 10 radiography and, 73 tooth anatomy and, 22 tooth resorption and, 76, 77

Cervical line erosions. See Resorption C.E.T. Oral Hygiene Chews, 303 C.E.T. paste/rinse, 299, 301 Chamber induction, 171 Charting abbreviations for, 84–87 overview of, 84, 88–99 of periodontal disease, 104–105 Cheilitis, 128 Chemotherapy, 290, 294 Chlorambucil, 243 Chlorhexidine bone grafting and, 185 infection control and, 167 plaque control and, 299 root canal therapy and, 220 scaling and, 181 stomatitis and, 244 Chondroclasts, 127 Chronic alveolar osteitis overview of, 114 radiology and, 71–73 treatment of, 188, 189–193 CI. See Calculus index Cidex, 167 Circumferential probing, defined, 33, 37 Clavulanic acid, 185, 242 Clindamycin, 185, 242 Clinical pocket depth, defined, 105 Codeine, 179 College pliers, 209, 210 Complicated crown fractures, defined, 115, 116–117 Complicated crown-root fractures, defined, 115, 117–118 Compressors, 162–163, 167 Computed tomography (CT) scans, 290 Condylar process fractures, 280 Consil Putty, 185, 186 Constant rate infusion (CRI), 177–178 Contra-angle, 165 Contrast, defined, 63 Control films, 63 Corticated, defined, 68 Corticosteroids, 242 Cotton pliers, 209 COX-2 inhibitors, 294 Craniomandibular joint. See Temporomandibular joint Cranium, anatomy of, 12, 13 CRI. See Constant rate infusion Cribriform plate anatomy of, 12 radiography and, 67, 68 tooth anatomy and, 24

Index

Crown, 24, 76, 232 Crown-down method, 220 Crown fractures classification of, 115 illustrations of, 116–117, 201, 202, 206 treatment of, 218 Crown reduction, malocclusion and, 271–272, 275 CT scans. See Computed tomography scans Cuffed endotracheal tubes, 169 Curettes, 160, 182–183 Cyclooxygenase-2 (COX-2) inhibitors, 294 Cyclosporine, 243–244 Cysts, 290 Cytokines, 104 Cytology, squamous cell carcinomas and, 139, 141 Debridement (instrumentation), 213, 220, 257 Definition, 63 Density, defined, 63 Dental artery, 10 Dental explorers, 37–38, 154 Dental formulas, 15, 19 Dental malocclusion, 134–135 Dental mirrors, 153 Dentin tooth anatomy and, 22 tooth resorption and, 76, 77 types of, 23 vital pulp therapy and, 210 Dentinal bridges, 210 Dentinal tubules, 24 Dermapet’s Dentacetig Gel, 299 Detail, defined, 63 Developer tanks, 60–61 Dexamethasone, 262 Dexmedetomidine, 170, 171 Diabetes mellitus, anesthesia and, 173–174 Diamond burs, 166 Diamonds, 166 Diazepam, 173 Diet recommendations for, 300, 301, 303 squamous cell carcinomas and, 139 stomatitis and, 244 tooth resorption and, 127–128 Digital imaging, 40–42, 47 Direct-to-digital sensors, 40 Disinfection, 167 Distal, defined, 25, 26 Distoversion, overview of, 134 Dosimeter badges, 43 Double images, 64 Doxorubicin, 294 Doxycycline, 243

307

Drinking water, 301 Dropped jaw, 142 D speed film, 43 ECG (electrocardiography), 170 EDTA (ethylemediaminetetracetic acid), 208 Education tools, 151, 155 EGFR. See Epidermal growth factor receptor Eicosanoids, 243 Elastics, 270, 271 Elevators endodontic disease and, 203 overview of, 156–158, 160 periodontal disease and, 185, 187 tooth resorption and, 238 Elongated images, 63 Enamel, 22, 76 Enamel fractures, 115, 116, 200–201 Endodontic disease damage to tooth structure and, 196, 197, 198–199 degree of changes and, 196, 198–199 equipment for, 160 instruments for therapy, 208–209, 210 materials for therapy, 206–208 pathology of, 114–115 physical examinations and, 32 pulpitis and, 200, 203 radiology and, 72–76 root canal therapy and, 197, 200, 213, 217–221 tooth fractures and, 197–199, 200–206 treatment overview for, 196 vital pulp therapy and, 209–213, 214–216 Endodontic files. See Files Endodontic stops. See Stops Endotracheal tubes, 169, 171 Eosinophilic granuloma complex, 135, 138, 290, 292–293 Epidermal growth factor receptor (EGFR), 294 Epinephrine, 174–175 Epulides, 138, 139. See also Peripheral odontogenic fibroma Equipment for assessment, 151 burs, 166 education tools, 151 endodontic disease therapy and, 202, 206–209, 210 high/low speed delivery systems, 162–163 infection control and, 153, 167 maintenance of, 166–167 nitrogen-powered delivery systems, 163–165 radiology and, 39–40 rotary cutting instruments, 165–166 for treatment and prevention, 151–162 Eruption, tooth, 24, 25

308

Index

Esophagostomy, 280 E speed film, 43 Etching, 270 Ethics, orthodontic movement and, 269 Ethmoid bone, 12 Ethomidate, 171 Ethylenediaminetetracetic acid (EDTA), 208 Etidocaine, 174 Eugenol. See Zinc oxide-eugenol Examinations, 28, 33–38 Exposure timers, 40 External odontoclastic resorption. See Resorption Extraction forceps, 159 Extractions crown amputation and, 231 malocclusion and, 270 periodontal disease and, 193, 194 postoperative care and, 241 root fragments and, 231 stomatitis and, 257, 262 technique for, 226, 231 tooth resorption and, 225–234 Extrusion, 71, 73, 269 Eyes, 28, 29 Face, 28, 29 Facial, defined, 26 Facium, 12–14 FelFN, 242–243 Feline hypertrophic cardiomyopathy, 171 Feline immunodeficiency virus (FIV), 139, 244 Feline odontoclastic resorption. See Resorption Feline oral resorption. See Resorption Fentanyl, 179 Fibroameloblastoma, 138 Fibromatous epulis, 138, 139 Fibrosarcoma (FSA), 141, 290 Files, 208–209 Filiform papillae, 7 Film, overview of, 43–50 Film badges, 43 Film dots, 46, 49, 50, 54 Film size, 46, 47 Film speed, 43 Fingerprints, 64 Finishing burs, 166 Finishing discs, 166 Fissure burs, 166 FIV. See Feline immunodeficiency virus Fixer tanks, 60–61 Fleas, lip ulcers and, 138 Fluoride, 183–184, 270 FluraFom Virbac Products, 183, 184 Focal opacities, defined, 68

Fogging of film, 63 Folate papillae, 7 Food. See Diet Food allergy, lip ulcers and, 138 Force, orthodontic movement and, 269 Forceps, 159 Foreshortened images, 63 Four-handed charting, 84, 85 Four-station dental operatory, 152 Fractures (jaw), 82, 83, 143–145, 282–288 Fractures (tooth) abscesses and, 75 classification of, 115 endodontic disease and, 196, 197–199, 200–202, 203–207 extractions and, 263–264 facial swelling, tooth staining and, 29 pathology of, 114–115 treatment of, 282–284 Freer periosteal elevators, 160, 185, 187 Frequency, scalers and, 160 Friction grip burs, 165 Frosty films, 64 FSA. See Fibrosarcoma F speed film, 43 Fungiform papillae, 7 Furcation, overview of, 105 Furcation bone loss, 71 Furcation disease, 105–107 Fusion, 101 Gabapentin, 179 Gates Glidden drills, 165 Gauze sponges, 172 Gemination, 101, 103 GI. See Gingival index Gingiva anatomy of, 8–10, 11 hyperplasia of, 193 physical examinations and, 33 squamous cell carcinomas and, 139 Gingival hyperplasia, 193 Gingival index (GI), 108 Gingival sulcus, defined, 9, 10 Gingivectomy, 193 Gingivitis. See also Juvenile hyperplastic gingivitis advanced periodontitis and, 111 charting and, 91 extractions and, 252–254, 258–261, 265 laser therapy and, 268 overview of, 101, 104 periodontitis vs., 104 treatment of, 181, 182 Glass ionomer filler, 220

Index

Glossitis, 128 Glycoproteins, plaque and, 101, 104 Gold Salts, 242 Grafting, 185–188 Granulomas, 74 Greenies, 303 Gutta percha points, 206, 207, 219, 220 Halitosis, 110 Handpieces, 163–165, 167 Hard palate overview of, 5, 6, 14 trauma to, 145, 287–288 Head, 28, 29 Hedstrom (H) files, 208, 213, 217 Hemisepta, 71 Hemorrhages, pulpal, 200 H files. See Hedstrom files High/low-speed delivery systems, 161, 162–163, 167 Histories, 28 Horizontal angulation, 50 Horizontal bone loss, 69–70 Horner’s syndrome, 29, 284 Hydromorphone, 170, 179 Hypercementosis, 73, 110 Hyperplasia, 193 Hyperthermia, 200 Hyperthyroidism, anesthesia and, 173 Hypodontia, 273 Hypoglossal nerve, anatomy of, 8 Hypotension, 171 Hypothermia, 172 Illumination telescopes, 152 Immune system, 104, 138. See also Inflammation Impingement, 138, 193, 273, 276–279 Incisive papilla, 15 Incisor teeth anatomy of, 19, 20 radiography of, 50, 51, 54 terminology of, 24–26 Inductive fibroameloblastoma, 138 Infections, equipment care and, 167 Inflammation lesions and, 290 oropharyngeal, 128–131 pulp and, 24 pulpitis and, 200 stomatitis and, 242 tooth resorption and, 126–127 Infraorbital arteries, 8 Infraorbital canal, 14 Infraorbital foramen, 175 Infraorbital nerve, anatomy of, 8

Infraorbital nerve block, 175, 177 Infusion, 177–178 Innervation, anatomy of, 5, 8 Instrumentation. See Debridement Interferon, 242–243 Interleukin-2, 243 Intermandibular space, 15 International Standards Organization (ISO), 208 Interpretation, radiography and, 64–68 Intrusion, 269 Intubation, 171 Inverted cone burs, 166 Irrigation needles, 209, 217 ISO. See International Standards Organization Isoflurane, 171–172 Jaw anatomy of, 27 fractures of, 81, 143–145, 282–288 locking of, 142–143, 280 luxation of, 142 traumatic injuries to, 81 Joints. See Temporomandibular joint Junctional epithelium, defined, 9 Juvenile hyperplastic gingivitis, 109–110, 113 Juvenile onset periodontitis, 110, 113 Kerr (K) files, 208, 213, 217 Ketamine, 171, 173, 177–179 Ketoprofen, 179 K files. See Kerr files Kidney disease, 173 Kilovoltage peak (kVp), defined, 40 kVp. See Kilovoltage peak Labial, defined, 24, 26 Labial mounting, 64 Labial vestibule, 5, 6 Labioversion, overview of, 134, 135 Laboratory panels, preoperative, 257 Lactoferrin, 243 Lamina dura anatomy of, 12 radiography and, 67, 68 tooth anatomy and, 24 Landmarks, radiography and, 64–68 Laser therapy, 262, 267, 268 Leopold mouth gags, 152 Levamisole, 243 Lidocaine, 174, 179 Ligament. See Periodontal ligament Lingual, defined, 25, 26 Lingual mounting, 64 Lingual nerve, anatomy of, 8

309

310

Index

Linguoversion, 134, 135, 273–274 Lips impingement of, 193, 211 inflammation of, 128 ulcers of, 135–138 Local anesthesia, 174–177, 213 Luxation, jaw, 142, 280, 281 Lymphatic drainage, 8, 28, 141–142 Lymphokines, 243 Lysine, 243 Lysosome, 104 M. See Mobility Magnetostrictive scalers, 160, 161 Magnification telescopes, 152 Maintenance, equipment and, 166–167 Malocclusions, 132–135. See also Occlusion Mandibles anatomy of, 14–15, 17 arteries of, 8 fractures of, 143, 145, 282, 285–288 jaws and, 27 malocclusion and, 133–134 radiography and, 64, 66 radiography of, 54 squamous cell carcinomas and, 140, 141 Mandibular canal, radiography and, 67 Mandibular glands, 8 Mandibular mesioclusion, 28, 133 Mandibular nerve, 8, 174 Mandibular nerve block, 8, 177, 178 Mandibular symphysis separation, 143, 144, 282, 284– 285, 287 Mandibulectomy, 290, 293–294 Mannitol, 173 Marginal gingiva, defined, 9–10 Mask induction, 171 Masseter muscle, 15 Maxiguard Oral Cleansing Gel, 299 Maxi/Guard Oral Cleansing Gel, 302 Maxillary, defined, 27 Maxillary bones anatomy of, 14, 15 arteries of, 8 fractures of, 143, 284–288 jaws and, 27 radiography and, 64, 66 radiography of, 50–54 Maxillary-mandibular asymmetry, 133–134 Maxillary nerve, anesthesia and, 174 Maxillary nerve block, 5, 175, 177 Maxillectomy, 290, 293–294 Medetomidine, 171, 179 Megestrol, 243

Meloxicam, 179 Mental foramina, radiography and, 66–67 Mental nerve blocks, 8, 175, 177, 178 Mepivacaine, 174 Mesial, defined, 25, 26 Mesioversion, 134, 135, 273 Metastasis, oral tumor staging and, 142 Metronidazole, 242 Michigan O probes, 35 Microsporum canus, 138 Midazolam, 170, 171 Middle mental nerve block, 175, 177, 178 Mineral tri-oxide aggregate (MTA), 207, 210 Mirrors, 153 Mitoxantrone, 294 Mobility (M), 107 Models, 155 Molar teeth anatomy of, 22 radiography of, 50–52, 54, 56 terminology of, 24–26 Molt periosteal elevators, 156, 203, 238 Monitoring, 43, 172–173 Morphine, 177, 179 Mouth gags, 151, 152 MTA. See Mineral tri-oxide aggregate Mucoceles, 138, 292 Mucogingival junction, 10, 11 Mucosa, anatomy of, 5, 6 Mucositis extractions and, 252–261, 263–265 overview of, 128–129, 130, 131 radiotherapy and, 294 stomatitis and, 244 treatment of, 247, 248 Muscles, anatomy of, 5, 17 Neck lesions. See Resorption Needles, 209, 217 Neoplasias. See also Squamous cell carcinomas benign, 138, 290 malignant, 139, 290 overview of, 138–142 radiology and, 78 staging of, 141–142 Neoral, 243 Nerve blocks, 175–177, 178 Nerves, anatomy of, 5, 8 Neutrophils, 104 Nickel titanium (NiTi) files, 208 NiTi files. See Nickel titanium files Nitrogen-powered delivery systems, 163–165 Nonodontogenic tumors, 138 Nonpocketing defects, 105, 111–113

Index

Non-professional dental scaling (NPDS), 169–170 NSAIDs, 294

Oxygene paste, 299 Oxymorphone, 177, 179

Obturation, 219, 220 Occlusal film, 43–46 Occlusion abnormal, 28, 33 brachycephalic breeds and, 28 charting and, 84 crown reduction, vital pulp therapy and, 271–272 disorders of, 131–135 extraction and, 270 impingement and, 273, 276–279 linguoversion of canine teeth and, 134, 135, 273– 274 mesioversion of canine teeth and, 134, 135, 272, 273 missing teeth and, 273 normal, 28, 32, 35 orthodontic movement and, 269–270, 271 persistent deciduous teeth and, 272–273 supernumerary teeth and, 101, 102, 273 Odontoblasts, 22, 23, 24 Odontoclasts, 126, 127 Odontogenic tumors, 138 Odontoplasty, 166 ODU explorers, 37, 38 Oil-cooled compressors, 167 Opacities, defined, 68 Open-mouth jaw locking, 143 Open root apices, 202 Opioids, 177, 179 Oral assessment, treatment, and prevention (ATP) visits, 181, 299, 301 Oral cavity. See also Specific elements anatomy of, 5, 6, 16 inflammation of, 128–131 swelling and tumors of, 135–142 Oral epithelium, defined, 8 Oral Hygiene Gel, 299 Oral rinses/gels, 299 Oral tumors. See Neoplasias Oral vestibule, overview of, 5, 6 OraVet, 183, 185, 244, 301, 302 OraZn, 301 Orban explorers, 37, 38 Oronasal fistulas, 185 Oropharynx, 128–131. See also Stomatitis Orthodontic tooth movement, 269–270, 271 Ossifying epulis, 138, 139 Osteoblasts, 127, 270 Osteoclasts, 127, 270 Osteodentin, 22 Osteomyelitis, 29, 135, 290, 291 Osteopontin, 127

Pain control, 171, 177–179 Pain patches, transdermal, 179 PAL. See Periodontal attachment level Palatal, defined, 25 Palatal pocket therapy, 185–188 Palate. See also Hard palate; Soft palate arteries of, 8 bone of, 14 fissures of, 14 inflammation of, 128 nerves of, 5 Palatitis, 128 Paper points, 207, 219 Papillae, 5, 7, 15 Parallel technique, 50, 55 Parotid glands, anatomy of, 8 Patient histories, 28 Peel-off dental charts, 90–91 Periapical cysts, 76 Periapical disease, overview of, 73–76 Periapical film, 43 Periapical lucencies, 76 Periodontal attachment level (PAL), defined, 105 Periodontal disease. See also Gingivitis; Periodontitis alveolar bone expansion and, 114, 188, 189 antibiotics and, 185 barrier gel and, 184, 185 bone grafting and, 185–188 calculus index and, 108, 109 canine tooth extrusion, 110, 113 charting of, 104–105 extractions and, 193, 194, 255–257 fluoride application and, 183–184 furcation disease, 105, 107 gingival enlargement and, 193 gingival index and, 108, 110 juvenile hyperplastic gingivitis, 109–110, 113 juvenile onset periodontitis, 110, 113 nonpocketing defects, 105, 111–113 overview of, 101 pathogenesis of, 101–104 patient, operator safety and, 182 periodontal disease index and, 108–109 plaque, calculus removal and, 181, 188 plaque index and, 107–108 pocketing defects, 105, 111–113 polishing and, 183 radiology and, 68–71 scaling and, 182–183 staging of, 181, 182, 194

311

312

Index

Periodontal disease (cont’d) therapy overview, 181, 182 tooth mobility and, 107 Periodontal disease index (PDI), 108–109 Periodontal ligament, 10, 73 Periodontal ligament space, 67–68 Periodontal probes charting and, 104–105 gingival index and, 108 overview of, 33, 35–37, 154 use of, 107 Periodontal tips, 182–183 Periodontitis extractions and, 252–254, 258–261 gingivitis vs., 104 juvenile onset, 110, 113 overview of, 101 radiography and, 69–71 treatment of, 181, 182 Periodontium cementum, 10, 22, 72, 73, 76, 77 gingival sulcus, 9, 10 overview of, 8–12 periodontal ligament space, 67–68 Periosteal elevators, 156, 157, 185 Peripheral odontogenic fibroma, 138, 139 Persistence, 101, 103 Persistent deciduous teeth, 272–273 Personal protective equipment (PPE), 181, 262 Pfizer feline dental charts, 88–89 Pharynx, 5, 6, 138 Phosphor transfer sensors, 40 Physical examination, 32 PI. See Plaque index PID. See Position indicating devices Piezoelectric scalers, 155, 160 Piroxicam, 179, 242 Plaque. See also Scaling control of, 299–303 glycoproteins and, 101, 104 oropharyngeal inflammation and, 244 periodontal disease and, 181, 188 staging of, 107–108 Plaque barrier gel, 301 Plaque index (PI), 107–108 Pliers, 209, 210 Pluggers, 209, 212 Pneumoabdomen, 171, 172 Pneumomediastinum, 171, 172 Pneumothorax, 171, 172 Pocketing defects, 105, 111–113 Polishing, 156, 183 Position indicating devices (PID), 40, 50 Positioning, radiography and, 50–60

Position statement on anesthesia, 169–170 Power scaling, 160 Prednisone, 242, 246 Premolar teeth anatomy of, 21–22 extraction of, 227–228, 231 impingement of, 138 radiography of, 50–52, 54, 55, 56 terminology of, 24–26 Pressure, orthodontic movement and, 269–270 Primary palate, 14 Primary radiation, overview of, 43 Probes charting and, 104–105 gingival index and, 108 overview of, 33, 35–37, 154 use of, 107 Probing depth, defined, 105 Processing of films, 60–61 Propofol, 171 Proportions, 173 Prostaglandins, 104 Pulp. See also Endodontic disease complicated tooth fractures and, 201–202, 206 internal root resorption and, 76 necrosis of, 196 tooth anatomy and, 22 Pulpal blush, 201 Pulp capping, 201, 207. See also Vital pulp therapy Pulp cavity, 22–23, 76, 77 Pulp chamber, 22–24, 114 Pulpectomy. See Root canal therapy; Vital pulp therapy Pulpitis, 200, 203 Pulse therapy, 185 Q-tips, 33, 35 Quality control, radiography and, 62–63 Radiation safety, 43–50 Radiation therapy, 290, 294 Radiology alveolar bone expansion and, 71–73 ankylosis and, 73 digital imaging and, 40–42 endodontic disease and, 73–76 equipment for, 39–40 film and, 60–64 hypercementosis and, 73 neoplastic disease and, 78 oral inflammation and, 129–131 overview of, 39 periodontal disease and, 68–71 quality control and, 62–63 radiograph interpretation and, 64–68

Index

root canal therapy and, 213–218 safety and, 43–50 stomatitis and, 244 terminology of, 68 TMJ disease and, 81 tooth extrusion and, 71, 73 tooth resorption and, 73, 75–80, 81, 120–126, 128 traumatic jaw injury and, 81 trouble-shooting and, 63–64 tube/film/patient placement and, 50–60 Radiolucent areas, 64, 68 Radiopaque, defined, 68 Regional anesthesia, 174–177 Renal disease, anesthesia and, 173 Resorption classification of, 120–126, 222, 223–225 crown/root atomization and, 225 etiology of, 127–128 extraction and, 225–231 histology of, 127 internal and external, 126–127 monitoring of, 225 overview of, 115, 119–120 pathogenesis of, 126 periodontal disease and, 194 physical examinations and, 30–32, 38 prevalence of, 126 pulpitis and, 200, 205 radiography of, 128 radiology and, 73, 75–80, 81 restoration and, 222, 225 therapy options for, 222 Retention. See Persistence Retroarticular process, 15 Root canal, 22–23, 76 Root canal therapy, 197, 200, 213, 217–220 Root fractures defined, 115, 118 endodontic disease and, 202, 206 Roots extractions and, 231, 241, 262, 266 furcation bone loss and, 71 numbers of, 19 persistent deciduous teeth and, 272–273 scaling and, 182–183 SLOB rule and, 59–60 Root tip elevators, 160 Rostral, defined, 26, 27 Rotary cutting instruments, 165–166 Rotation (torsion), 269 Round burs, 166 Safety. See also Personal protective equipment equipment for, 154, 167

laser therapy and, 262 periodontal disease treatment and, 181–183 radiology and, 43–50 Salivary glands, 8, 9. See also Specific salivary glands Sandimmune, 243 Scaling above gingiva, 182 below gingiva, 183 non-professional dental scaling and, 169–170 overview of, 160–162 periodontal disease and, 182–183 technique for, 161–162 ultrasonic, 155, 160, 181–183 Scatter radiation, 43 SCC. See Squamous cell carcinomas Sealapex-Kerr, 220 Secondary palate, 14 Secondary (scatter) radiation, 43 Sensory buccal nerves, 8 Sevoflurane, 171–172 Shanks, 166 Shepherd’s hook explorers, 37, 38 Sialoprotein, 127 Skeletal malocclusion, 133–134 SLOB rule, 59–60 Sodium bicarbonate, 183 Sodium hexametaphosphate, 301 Sodium hypochlorite (bleach), 207–208, 217 Soft palate, 5, 6, 14 Software, radiography and, 40, 44–45 Solganal, 242 Sonic scaler, 160 Spatulas, 209, 210 Speed, handpieces and, 163–165 Spot probing, defined, 33 Spreaders, 209 Squamous cell carcinomas (SCC) overview of, 139–141 physical examinations and, 29, 34 treatment of, 290, 293–294 Staging of oral tumors, 141–142 of periodontal disease, 181, 182, 194 of tooth resorption, 222, 223–225 Step-back method, 217 Step wedges, 62 Sterile packs, 153 Sterilization, 167 Stomatitis FIV and, 244 laboratory evaluation and, 257 laser therapy and, 262, 268 medical therapy for, 242–244 multiple tooth extraction and, 257, 262

313

314

Index

Stomatitis (cont’d) overview of, 128–129, 130, 131, 242 root fragments and, 262 surgical management of, 244–246 Stones, 166 Stops, 209 Storage, radiographs and, 64 Streaked films, 64 Streaming, 181 Sublingual glands, anatomy of, 8 Sulcular epithelium, defined, 8–9 Supereruption. See Extrusion Supernumerary teeth, 101, 102, 273 Systemic analgesia, 177–179 T cell growth factor (TCGF), 243 TCGF. See T cell growth factor Teaching models, 155 Teeth. See also Specific teeth composition of, 22–24 dental formulas for, 15, 19 eruption of, 24, 25 functional significance of, 196, 200 malocclusions of teeth, 134–135 terminology of, 24–27 types of, 19–22 variations in number and morphology of, 101 Telescopes, 152 Temperature control, 170, 172 Temporomandibular joint anatomy of, 15, 18 ankylosis of, 143, 144, 280 dislocation of, 280, 281 radiology and, 56–59, 81 T-helper cells, 243 Thin curettes, 185 Tipping, 269 TMJ disease, 81 Tongue anatomy of, 5, 7 eosinophilic granulomas and, 290, 292–293 inflammation of, 128 physical examinations and, 33, 34 squamous cell carcinomas and, 139, 140 Tonsils, 139 Toothbrushing, 299, 300 Tooth extrusion. See Extrusion Tooth fractures. See Fractures Tooth mobility. See Mobility

Tooth resorption. See Resorption Tooth resorption (TR) classification, 120 Torsion. See Rotation Tramadol, 179 Transdermal pain patches, 179 Translation. See Bodily movement Trauma, 142–145, 280–288 TR classification. See Tooth resorption classification Triadan system (modified), 19–23, 84 Triamcinolone, 242 Trigeminal nerve, 5, 8, 174 Trimming burs, 166 Tumors. See Neoplasias Turbines, 167 Two-handed charting, 84, 85 Ultrasonic scalers, 155, 160, 181–183 Uncomplicated crown fractures, defined, 115, 116 Uncomplicated crown-root fractures, defined, 115, 117 Unilocular corticated, defined, 68 Unilocular noncorticated, defined, 68 University of Minnesota dental charts, 97–99 University of Pennsylvania dental charts, 95–96 Vallate papillae, 7 Vasoconstrictors, 174–175 Vasodentin, tooth anatomy and, 22 Vasodilators, 174 Vertical angulation, 50, 63 Vertical bone loss, 68, 70–71 Vestibular, defined, 24 VHUP dental charts, 95–96 Virbac, 242–243 Viruses, 129, 244 Vital pulp therapy, 209–213, 214–216, 271–272, 275 William’s probes, 35 Wing-tipped elevators, 158 Xylitol, 301 Zidovudine (AZT), 244 Zinc, 301 Zinc oxide-eugenol (ZOE), 207, 210, 219, 220 ZOE. See Zinc oxide-eugenol Zoledronate, 294 Zygomatic arch, radiography and, 52 Zygomatic glands, anatomy of, 8