Myths and misconceptions in veterinary dentistry

1818 VetMedToday:ReferencePoint JAVMA,Vol231,No.12,December15,2007

Periodontal disease is the most common disease identified in dogs and cats.1 Local severity and the

impact on the rest of the body are reasons that all com-panion animal patients should receive an oral examina-tion every time they are at a veterinary facility.2,3

Veterinary dentistry has progressed from the dental or prophylactic procedures of the 20th century, which often involved an injection of a short-acting tranquil-izer or anesthetic and a few minutes spent removing supragingival calculus, to the current comprehensive treatment of periodontal and other dental diseases that require general anesthesia. The days of clean-and-pull or watchful waiting in the case of fractured teeth have been replaced by prevention, recognition, and treat-ment of dental disease and painful oral conditions. As recently as 25 years ago, there were a limited number of veterinary textbooks, continuing education op-portunities for practitioners desiring to improve their dental knowledge and skills, and referral practices for dental care of animals. Currently, veterinary students and practitioners have multiple veterinary dental text-books, journal articles, and quality opportunities for continuing education, and referral to a board-certified veterinary dentist is a realistic option.

Some traditional practices and misconceptions are still being taught and shared. Myths and misconcep-tions in other areas of veterinary practice have been ad-dressed.4-6 The objectives of the information provided here are to clarify new concepts, dispel common mis-conceptions and outdated beliefs, improve awareness of current veterinary dentistry, and aid practicing vet-erinarians in the delivery of a higher quality of dental care.

Myth—Veterinary dentistry involves minor pro-cedures that require no special patient preparation or monitoring during anesthesia.

Reality—Dental patients often become hypother-mic because of the cooling of a patient as a result of continuous use of water in the mouth from power scal-ers and high-speed drills, prolonged procedures, and metal tables. Very small animals (< 5 kg [< 11 lb]) are especially at risk of developing hypothermia because of

Myths and misconceptions in veterinary dentistry

From North Florida Veterinary Dentistry, 2961 Egret Walk Terrace S, Jacksonville, FL 32226 (Hoffman); Animal Dental Center, 2100 W Silver Spring Dr, Milwaukee, WI 53209 (Kressin); and Department of Surgical and Radiological Sciences, School of Veterinary Medicine, University of California, Davis, CA 95616 (Verstraete).

Address correspondence to Dr. Hoffman.

their larger surface area-to-volume ratio, compared with heavier animals.7 Hypothermia defined as mild (36.7o to 37.2oC [98o to 99oF]), moderate (35.6o to 36.7oC [96o to 98oF]), severe (33.3o to 35.6oC [92o to 96oF]), and critical (< 33.3oC) has been correlated with decreases in heart rate, respiratory rate, and blood pressure; CNS depression; alterations in coagulation, cellular and humoral immunity, and wound healing; morbidity; and death.8,9 Bradycardia secondary to hypothermia is unresponsive to anticholinergics.10 Hypothermic ani-mals require more time to recover from anesthesia.11 Simple measures such as continuous monitoring of intraoperative temperature, use of circulating warm water blankets or forced-air warming devices, and IV administration of warm fluids will aid in the preven-tion and correction of hypothermia.

Many patients that undergo dental procedures are old and have other problems, such as mitral valve regurgitation, hepatic disease, or renal disease. Con-sequently, anesthesia of these patients is likely to en-tail greater risk than would anesthesia of younger, healthier patients. The anesthetic protocol should be planned only after careful consideration of results of physical examinations and laboratory tests. Appro-priate IV administration of fluids and monitoring of blood pressure, oxygenation, heart rate and rhythm, and body temperature are especially important in older or compromised patients.4 Measurement of end-tidal carbon dioxide concentrations by the use of capnography can provide clinicians with informa-tion about a patient’s state of perfusion, ventilation, and metabolism as well as indications about equip-ment malfunction.12

Myth—Dental extraction sites should be left open to provide drainage and allow healing by second intention.

Reality—Extraction of teeth is a surgical proce-dure. After preoperative radiography, treatment plan-ning, and extraction, the alveolus is debrided carefully with a spoon curette to remove any infected granula-tion tissue, debris, purulent material, or necrotic bone. Rough alveolar bone edges are smoothed.13,14 Ideally, the gingiva should lie flat against the alveolar bone. Sutur-ing the alveolus closed helps to speed healing, prevent infection, and reduce postoperative pain.13 Suturing is mandatory following extraction of multiple mandibu-lar premolars and molars because the gingiva typically falls away from the extraction site, which leaves bone exposed. Exposed bone can cause pain and leads to de-layed wound healing.15 Sufficient gingiva is elevated to

Reference Point

Sharon L. Hoffman, dvm, davdc; Dale J. Kressin, dvm, davdc; Frank J. M. Verstraete, drmedvet, mmedvet, davdc

JAVMA,Vol231,No.12,December15,2007 VetMedToday:ReferencePoint 1819

allow suturing without tension; otherwise, it is likely there would be wound dehiscence. To avoid tension, the flap may be released by further undermining or careful incision of the underlying periosteum. If it is not possible to fully close a gingival flap without ten-sion, then partial closure is preferable to tension; the resulting defect will heal by granulation and epitheliali-zation. Closure or partial closure will also help to keep in place the blood clot that forms in the alveolus fol-lowing tooth extraction, which is important for optimal healing.15

Hemorrhage may be a complication of exodontia. Hemostatic defects may not be apparent until after ex-traction; associated hemorrhage does not stop within a few minutes, and copious bleeding continues and can become a life-threatening situation. Suturing the gin-giva with a hemostatic material in the alveolus can be beneficial.15

When an oronasal fistula is evident before extrac-tion (because of extensive periodontal disease) or after extraction (as a complication), then closure of the fis-tula is required to prevent a constant influx of food and liquid into the nasal cavity.13,16,17

Myth—Swelling or a draining tract located in the facial area below either eye is always an indication for extraction of the maxillary fourth premolar tooth.

Reality—Endodontic disease resulting in periapi-cal inflammation and abscess formation may cause swelling of hard or soft tissues or a draining tract. In dogs, this is most commonly secondary to endodontic disease of the maxillary fourth premolar (carnassial tooth), hence the term carnassial abscess.18 Dental ra-diography with periodontal probing of all teeth on the caudal maxilla is necessary to establish a diagnosis. A similar condition sometimes affects the maxillary first molar or third premolar. A facial (suborbital) swelling or draining tract may also recur when extraction is used as treatment and a root tip is left in place.18 Additional nondental causes of suborbital facial swellings or drain-ing tracts include sialoadenitis,20 bite wound abscess, foreign body abscess (such as gunshot or wood impac-tion), maxillary fracture and bone sequestration, and nasal or maxillary neoplasia.21 Orbital or retro-orbital cellulitis may or may not be related to extension of in-fection from a caudal tooth root. Examination of the caudal portion of the oral cavity and dental radiogra-phy are indicated in patients with decreased retropul-sion of the globe, exophthalmos, ocular discharge, and periocular swelling with or without evidence of pain when opening the mouth. Other differential diagnoses to consider in patients with orbital or retro-orbital cel-lulitis or abscess include extension of a nasal infection (bacterial or fungal), zygomatic sialoadenitis, and for-eign body penetration.22

Radiography is essential in the diagnosis and treat-ment planning for suborbital swellings. Additional helpful diagnostic tests may include periodontal prob-ing, collection of tissue biopsy specimens for histologic examination, or computed tomography.

Extraction of the maxillary fourth premolar tooth may not always be appropriate. Although there are some absolute indications (eg, no other treatment option

exists) for extraction, alternative treatment is recom-mended for strategic teeth (permanent canines and car-nassial teeth) that are periodontally sound. Endodontic treatment and restoration of the crown can allow a tooth to be maintained.23

Myth—Patients that need radiation therapy of the head or neck should always have teeth extracted prior to radiation treatment.

Reality—High-dose radiation therapy of the head and neck causes a hypovascular, hypocellular, and hy-poxic state in the jaws and surrounding soft tissues. This can lead to delayed wound healing and osteoradionecro-sis of bone.24,25 The risk of osteoradionecrosis continues for the remainder of the patient’s life and does not de-crease with time.26

It has long been believed that extraction of teeth in poor condition (those with periodontal disease or car-ies) within the high-dose volume area prior to adminis-tration of high-dose radiation therapy would reduce the risk of osteoradionecrosis. This hypothesis has been ex-tended to patients with teeth in fair to good condition who have a good chance of being cured and a long life expectancy, particularly when the likelihood of main-taining the health of their teeth is in question. Howev-er, findings from a large series of human patients with oropharyngeal cancer who received radiation therapy revealed that extraction prior to radiation treatment does not reduce the risk of osteoradionecrosis, regard-less of the condition of the teeth.25 There was no differ-ence in the rate of osteoradionecrosis between patients with healthy teeth in the radiation-treatment field who had teeth extracted prior to radiation therapy, which indicates no clear benefit to the use of prophylactic ex-tractions.25 In a prospective study24 of 40 patients who received nasopharyngeal radiation therapy, extractions after radiation treatments had a low risk of complica-tions, and results pointed to age of a patient as a factor that may influence wound healing.

The pretreatment recommendation remains to ex-tract teeth in the proposed high-dose treatment field when they are in poor condition because of existing dental disease. Teeth that are in fair condition, as de-termined by a veterinary dentist, need not be prophy-lactically extracted prior to radiation treatment in an attempt to prevent subsequent osteoradionecrosis.25

During radiation therapy, patients should receive daily dental care by the owners at home and regular professional periodontal debridement (scaling and root planing). A long-term, 3-month interval between professional dental examinations is recommended.26,27 When compliance with daily dental hygiene at home or professional dental care is lacking, which is often the case in companion animals, it may be prudent that teeth affected by dental disease and that will be exposed to radiation be extracted prior to radiation treatment.

Myth—A fractured tooth can always be treated with watchful waiting.

Reality—Veterinarians commonly examine frac-tured teeth in companion animals. A survey19 of oral and dental diseases in 63 anesthetized dogs revealed


that 27% had fractured teeth and 10% had multiple fractured teeth. Signs of pain or discomfort may not be recognized for several reasons. Veterinary patients often do not display signs of pain and discomfort and there-fore may be extremely stoic and silent. Clinical signs of pain and discomfort may only be evident as subtle changes in behavior, and veterinarians and veterinary staff members may not be adequately trained in evalu-ating animal behavior. Physical examinations may not be consistently scheduled for veterinary patients, and oral evaluations are too often inadequate, especially when a patient has pain or discomfort and is protect-ing the oral cavity. A patient with a fractured tooth may initially have severe pain, which subsequently subsides. Later in the disease progression, an affected dog may have pain associated with periapical lesions. Periapi-cal abscesses or draining tracts associated with chronic fractured teeth are often hidden from clear view by the lips and buccal mucosa, whereas periapical granulomas are typically not associated with clinical signs.

Oral radiography is fundamental to the diagnosis of periapical disease. Early intervention for disease pre-vention or disease progression is a superior approach to the watchful waiting paradigm. The American College of Veterinary Anesthesiologists has adopted a position statement that includes the following concept: “Animal pain and suffering are clinically important conditions that adversely affect an animal’s quality of life”.28 Fur-thermore, the American College of Veterinary Anesthe-siologists encourages veterinarians and veterinary staff members to increase their knowledge and skills with regard to pain recognition and management and to ap-ply them to develop effective and safe protocols for the management of pain, which offers clients optimal treat-ment options for their pets.

Veterinarians are encouraged to develop a philoso-phy that promotes prevention and alleviation of pain in animals. A proactive approach to dental care in com-panion animals is an important step. Veterinarians are encouraged to be proactive in recognizing and address-ing dental pain and infection associated with fractured teeth in companion animals. Performing fundamental diagnostic testing (oral radiography and periodontal probing) and determining the correct diagnosis is es-sential, and referral to board-certified specialists is rec-ommended when appropriate dental services cannot be provided by a veterinarian.

Myth—An animal with an abscessed tooth can al-ways be treated with antimicrobials.

Reality—Fractured teeth are subject to bacterial ingress, pulpitis, pulp necrosis, and periapical inflam-mation (abscess, granuloma, or periodontitis).29 Frac-tured enamel or dentin, with or without pulp exposure, does not have the ability to heal or seal over. A tooth does not need to be fractured for there to be periapi-cal inflammation. Acute traumatic injury (blunt trau-ma), chronic trauma (bruxism or concussive chewing forces), or loss of blood supply (luxation) can result in pulpitis, eventual pulp necrosis, and formation of a periapical granuloma or abscess. Discoloration of any tooth is a strong indicator of pulpitis, and pulp necrosis is a likely outcome.30 A periapical abscess may be iden-

tified by facial swellings or draining tracts. Veterinar-ians should examine animals for swellings or draining tracts intraorally and extraorally.

A common practice for veterinarians is to treat an animal with an abscessed tooth by administration of an-timicrobials. It is important to understand that antimi-crobials alone are ineffective in treating most periapical abscesses. The typical outcome associated with antimicrobial treatment is variable degrees of clinical im-provement (none to substantial) during treatment with immediate recurrence of clinical signs after the cessa-tion of antimicrobial administration. The variability in effectiveness of antimicrobial treatment may be related to the antimicrobial (spectrum of activity, dose, or route of administration), patient (age, immune status, apical blood supply, or drugs concurrently administered), or cause of the abscess (chemical, thermal, or infectious agent). When an abscess caused by bacteria is treated by administration with an antimicrobial that has an ide-al spectrum of activity, the number of organisms within the infected pulp may be excessive (or overwhelm the host defense) or the blood supply may be inadequate for effective treatment. For these reasons, antimicrobial treatment alone will rarely be an effective treatment for animals with endodontic disease. Teeth associated with a periapical lesion must be treated by endodontic treat-ment or extraction. Antimicrobials may be beneficial as an adjuvant treatment. Antimicrobials should never be considered a monotherapy for treatment of animals with oral infections and should not be used as preven-tive management of oral conditions.31

Myth—Accumulation of supragingival calculus on teeth is an indicator of the severity of periodontitis.

Reality—Periodontal disease encompasses inflam-mation, infection, and subsequent destruction of the periodontium (gingiva, cementum, periodontal liga-ment, and alveolar bone). Gingivitis is gingival inflam-mation without loss of connective tissue attachment (periodontal pockets).32 Periodontitis involves gingivi-tis and destruction of the periodontium. This destruc-tion may or may not result in gingival recession, but it often results in subgingival attachment loss; periodon-tal pockets; and, eventually, tooth loss.

Supragingival calculus may not always indicate the severity of periodontitis. There can be minimal supragin-gival calculus and gingival recession in animals with ad-vanced periodontitis.33 Periodontal probing to determine attachment loss and intraoral radiography can be used to indicate the severity of periodontitis.33,34 An associa-tion between attachment loss and body weight has been reported.35 Attachment loss decreased significantly with increasing body weight, with the most evident decrease detected when comparing very small (< 7.3 kg [< 16.1 lb]), small (7.3 to 13.6 kg [16.1 to 29.9 lb]), and me-dium-sized (14.0 to 27.3 kg [30.8 to 60.1 lb]) dogs. The process of attachment loss is hastened by the higher ratio of tooth size to jaw size in small dogs.35

Myth—Periodontal disease can be treated by scal-ing teeth to remove supragingival calculus.

Reality—This myth involves 2 misconceptions. The first misconception is that calculus causes peri-


odontal disease. The primary cause of gingivitis and periodontitis is accumulation of dental plaque on tooth surfaces. Contrary to common belief, calculus is only a secondary etiologic factor. Supragingival calculus, per se, does not exert an irritant effect on gingival tissues. In fact, there may be a normal attachment between the periodontal connective tissue and calculus if the cal-culus surface has been disinfected with chlorhexidine. Sterile calculus encapsulated in connective tissue does not cause severe inflammation or abscesses. It has been clearly established that the rough surface of calculus alone does not initiate gingivitis. The main importance of calculus in periodontal disease appears to be its role as a plaque-retentive surface. Accumulation of plaque on tooth surfaces induces an inflammatory response, and removal of plaque leads to resolution of the clini-cal signs of inflammation.36,37 A layer of plaque always covers calculus.23 The continual assault of supragingi-val plaque on the local immune system causes gingivi-tis, and in susceptible animals, gingivitis can progress to periodontitis as subgingival plaque acts in combi-nation with the host’s immune system to destroy the periodontium.38

The second misconception is that periodontal dis-ease can be corrected by treating teeth by use of a su-pragingival process. Periodontitis that has progressed to subgingival attachment loss and pocket formation requires treatment other than scaling of the crowns of teeth. Periodontal treatment includes supragingival and subgingival scaling, root planing with curettes, or peri-odontal débridement with an ultrasonic scaler designed for that purpose; polishing; subgingival lavage; and, sometimes, periodontal surgery.23 It may also include subgingival application of doxycycline in a biodegrad-able system.39

Myth—Dental radiography is not necessary prior to extraction of severely mobile teeth.

Reality—Severe tooth mobility in veterinary den-tistry is described as mobility increased in any direc-tion other than axial over a distance exceeding 1.0 mm or any axial movement.40 There are multiple causes of tooth mobility including periodontal disease, trauma, and neoplasia. The extent of periodontal disease; a frac-ture of the alveolus, root, mandible, or maxilla; and neoplasia are not always evident on oral examination alone. Preoperative radiographs are mandatory to as-sess the pathologic changes and identify morphologic abnormalities (eg, curved or fracture roots, root resorp-tion, or fractures) prior to exodontia.23 Preoperative dental radiographs of mobile teeth are beneficial for treatment planning.

Myth—Pulse dosing of antimicrobials is recom-mended for treatment of animals with periodontal disease.

Reality—Periodontal disease is an infectious, in-flammatory, and often progressive disease process. As periodontal disease progresses, destruction of the periodontium often becomes extensive as a result of the interaction of pathogens, toxins, and host defense mechanisms. Periodontal disease has been described in 4 stages, which characterize gingivitis followed by

an increasing severity of periodontitis and periodon-tal destruction. Stage 1 is considered reversible (ie, gingivitis) and does not involve bone loss. Stage 2 of periodontal disease involves periodontal bone loss of 0% to 25%. Stages 3 and 4 involve bone loss of 25% to 50% and > 50%, respectively. Microbial populations appear to become increasingly more pathogenic as the disease progresses and can be categorized as anaerobic, gram-negative bacteria with spirochetes. These organ-isms hide in deep pockets and can elude host immune defenses. Bacteria in plaque biofilm can be 1,500 times as resistant to antimicrobials, compared with suscepti-bility of the same bacteria in a monoculture.38

With increasing severity, periodontal disease is more difficult to treat. Pulse dosing of antimicrobi-als, such as clindamycin, has been advocated by some veterinarians, with anecdotal success. However, the authors were unable to find peer-reviewed scientific reports to support the use of this treatment. Concern has been expressed with regard to the potential for the development of antimicrobial-resistant pathogens as a result of pulse-dosing antimicrobial treatment because this technique is at odds with the principles of correct antimicrobial usage.41

Clindamycin is used for the treatment of hu-mans with anaerobic infections.42 The most common mechanism of resistance is via rRNA methylases, and resistance has been reported42 for a number of aero-bic gram-positive bacteria and aerobic and anaerobic gram-negative bacteria. In addition, cross-resistance to other lincosamides, macrolides, and streptogramins is possible.42 Clearly, research is needed to determine the benefits and risks of pulse dosing of antimicrobials.

Daily teeth brushing along with periodic profes-sional cleaning and periodontal assessment are current-ly the most effective treatment strategy for periodontal disease. Pulse dosing of antimicrobials is not a long-term treatment strategy. Animals with extensive peri-odontitis may benefit from the use of clindamycin before anesthesia and periodontal treatment; however, antimicrobials should never be used as a monotherapy.2

Myth—When planning treatment for maxillary or mandibular fractures resulting from trauma, teeth in the fracture line should always be extracted at the time of stabilization of the fracture.

Reality—It is common for an alveolus to be in-volved in a fracture line. The tooth involved may be luxated and loose. In those situations, it is preferable to remove the tooth. When there is still sufficient healthy periodontal attachment (as evidenced by the fact that the tooth is immobile), it is usually an indication to leave the tooth in place because it will contribute to stability of the fracture fixation. Leaving a tooth in the fracture line increases morbidity and, in particular, infectious complications, but the immediate removal of the tooth involved cannot reverse those effects.43,44 When rigid internal fixation is used in humans, teeth can be (and typically are) retained.45-47 When the apex of a tooth is involved in the fracture, the tooth will probably be devitalized, especially when located rostral to the fracture line. When a tooth involved in the frac-ture line is retained, it should be carefully monitored


for subsequent evidence of periodontal or endodontal lesions and appropriate treatment should be instituted as soon as those conditions are recognized.48,49

In some animals, the tooth involved in a fracture line will be fractured. Again, an attending veterinar-ian has the discretion of whether to retain the tooth or remove it. However, deep crown-root fractures, root fractures, and comminuted fractures are indications for extraction.43

Myth—Intramedullary pins in the mandibular ca-nal are an option for treatment of fractures of the man-dibular body.

Reality—The term intramedullary pinning in ref-erence to the body of the mandible is a misnomer be-cause the mandible does not have a true medullary cavity.50 Review of the case reports51-54 describing in-tramedullary pinning revealed that the pins used in these animals were largely placed in the mandibular canal. The confined space within the mandibular ca-nal is occupied by the inferior alveolar nerve, artery, and vein, and inserting a sizable pin in the canal will unavoidably cause damage to these neurovascular structures. A pin placed more dorsally in the body of the mandible will damage tooth roots, which occupy most of the dorsal two thirds of the mandible. Experi-mentally, inserting pins into the body of the mandible results in delayed healing and considerable damage to many tooth roots,55 whereas clinically, malalignment is a common complication.51,56 Therefore, this method cannot be recommended.57

Myth—The lower jaw consists of a left and right hemimandible.

Reality—All vertebrates have 2 mandibles, each of which develops separately.58,59 The 2 mandibles are joined on the rostral midline by the intermandibular joint, which can vary from an intermandibular suture that allows little movement to an intermandibular syn-chondrosis that consists primarily of cartilage.60 In do-mestic dogs and cats, the intermandibular joint consists of fibrocartilage, and hence, symphysis would appear to be the most appropriate term.61,62 Therefore, the jaw consists of a left and right mandible, rather than hemi-mandibles. The surgical removal of 1 mandible would be most correctly termed a unilateral mandibulectomy, rather than a hemimandibulectomy, which strictly speaking would refer to the excision of half of 1 man-dible. Humans ontogenetically have 2 mandibles; how-ever, the suture of the 2 mandibles ossifies at an early stage (end of the first postnatal year), which results in the 2 mandibles forming a single functional entity.63 Be-cause of this, the term mandible to indicate the entire lower jaw is deeply entrenched in the human medical and lay literature.63,64

Myth—Coronectomy (often referred to as crown amputation in the veterinary literature) is always an ac-ceptable treatment for cats whose teeth have resorptive lesions.

Reality—Tooth resorption continues to be one of the most common dental diseases affecting cats. Coro-nectomy with intentional root retention may be a suit-

able alternative to extraction in selected cats with re-sorptive lesions.65,66 Prior to performing this procedure, radiography must be performed to verify that the dis-ease process is causing root resorption-replacement.65,67 Coronectomy allows for removal of the portion of a tooth that is causing pain to a patient and allows the re-sorption process to be completed without creating the potential complications of full root pulverization. The technique involves raising an envelope gingival flap, removal of the crown below the gingival margin, alveo-loplasty to remove rough edges, and closure of the flap with absorbable sutures.13

Coronectomy is contraindicated in teeth with clearly demarcated roots and no radiographic signs of root resorption and also in animals with periodontal or endodontic disease. In the latter, coronectomy may be associated with long-term root retention and persistent periodontal or endodontic disease.65,67 Coronectomy is contraindicated in cats with chronic gingivostomatitis or infected with FeLV or FIV.13

Myth—A fractured tooth with vital pulp exposure (complicated fracture) is always treated with partial coronal pulpectomy and direct pulp capping (vital pulp therapy).

Reality—Vital pulp therapy has a relatively high success rate (88%) when the duration of pulp expo-sure is < 48 hours at the time of treatment. The long-term (> 1 year) success rate decreases with an increase in the interval between time of the fracture and time of treatment.68 In 1 study,69 all of the teeth treated with vital pulp therapy at > 7 days after pulp exposure were nonvital during follow-up examinations conducted 6 months to 6 years later. The optimal time for treat-ment of complicated fractures is during the first 24 hours after pulp exposure, when the pulp inflamma-tion is superficial.29

Myth—Crown reduction of canine teeth in dogs, cats, and nonhuman primates (which is often referred to as disarming) is a safe and effective method to de-crease bite wounds.

Reality—Crown reduction of canine teeth is often requested when there is a history of animal-to-animal aggression or animal-to-human aggression that has resulted in bite wounds. Crown reductions in canine teeth require endodontic treatment (vital pulp therapy or pulpectomy and restoration) at the time of crown reduction. In a study70 in primates, there was a 21% fail-ure rate for crown reduction of canine teeth and vital pulp therapy performed under controlled and aseptic conditions. Failure leads to chronic inflammation and pulp necrosis.70

We are not aware of any controlled studies indicat-ing that the types or frequencies of aggressive behaviors are diminished by crown reductions in any species. The AVMA is opposed to removal of healthy teeth of dogs as a treatment for aggression. This approach to manag-ing aggression does not address the cause of the behav-ior. The welfare of a patient may be adversely affected because the animal is subjected to dental procedures that cause pain, are invasive, and do not address the behavioral problem. In addition, dogs may still cause


severe injury with the remaining teeth, and removal or reduction of teeth may provide owners with a false sense of security. Preventing injuries and welfare of the dogs are best addressed through behavioral assessment and modification by a qualified veterinary behaviorist.71 Disarming is not a safe treatment method in nonhuman primates or an effective method of decreasing aggres-sion in dogs and cats, nor is it approved by the AVMA.

Myth—Dentistry is an ancillary service veterinary practitioners provide for their patients.

Reality—An epidemiologic study1 conducted in 1995 at the University of Minnesota revealed that oral disease was the most common disease in all age groups of cats and dogs. In human medicine, periodontal dis-ease causes increased insulin resistance, decreased gly-cemic control, cardiovascular disease, myocardial in-farction, pneumonia, and other systemic diseases.26,72,73 There is now evidence that periodontal disease also affects the systemic health of veterinary patients. In 1 study,74 investigators detected a positive correlation between severity of periodontal disease and histolog-ic changes in the kidneys, myocardium, and liver. In another studya of 38 dogs, it was concluded that peri-odontal disease leads to systemic inflammation that is significantly reduced with appropriate periodontal treatments. Concentrations of blood glucose and renal indices were also affected by severity of periodontal disease and periodontal treatment in that study.a In ad-dition, there are case reports of insulin resistance in a dog with dental disease that responded after receiving treatment for the dental disease75 and morbidity in a cat with dental and periodontal infection.76

With the prevalence of oral disease and the evi-dence for the systemic effects on patient health, vet-erinary dentistry is a primary service that practitioners can provide as part of a general wellness program. Rec-ognition and appropriate treatment of oral and dental disease in companion animals are important to overall patient well-being and comfort. It is the obligation of veterinary practitioners to provide the oral cavity with the same attentiveness that is given to the rest of the patient’s body.

a. Rawlinson JE, Goldstein RE, Reiter AM, et al. Tracking systemic parameters in dogs with periodontal disease (abstr), in Proceed-ings. 19th Annu Vet Dental Forum 2005;429.

References1. Lund EM, Armstrong PJ, Kirk CA, et al. Health status and

population characteristics of dogs and cats examined at private veterinary practices in the United States. J Am Vet Med Assoc 1999;214:1336–1341.

2. Harvey CE. Management of periodontal disease: understanding the options. Vet Clin North Am Small Anim Pract 2005;35:819–836.

3. DeBowes LJ. The effects of dental disease on systemic disease. Vet Clin North Am Small Anim Pract 1998;28:1057–1062.

4. Wagner AE, Wright BD, Hellyer PW. Myths and misconceptions in small animal anesthesia. J Am Vet Med Assoc 2003;223:1426–1432.

5. Holowaychuk MK, Martin LG. Misconceptions about emer-gency and critical care: cardiopulmonary, cerebral resuscitation, fluid therapy, shock and trauma. Compend Contin Educ Pract Vet 2006;28:420–431.

6. Holowaychuk MK, Martin LG. Misconceptions about emer-gency and critical care: metabolic disease and intensive care medicine. Compend Contin Educ Pract Vet 2006;28:434–447.

7. Murison P. Prevention and treatment of perioperative hypother-mia in animals under 5 kg body-weight. In Pract 2001;23:412–418.

8. Oncken A, Kirby R, Rudloff E. Hypothermia in critically ill dogs and cats. Compend Contin Educ Pract Vet 2001;23:506–520.

9. Armstron SR, Roberts BK, Aronsohn M. Perioperative hypother-mia. J Vet Emerg Crit Care 2005;15:32–37.

10. Cookson BA, Di Palma JR. Severe bradycardia of profound hy-pothermia in the dog. Am J Physiol 1955;182:447–453.

11. Waterman A. Accidental hypothermia during anaesthesia in dogs and cats. Vet Rec 1975;96:308–313.

12. Marshall M. Capnography in dogs. Compend Contin Educ Pract Vet 2004;26:761–777.

13. Holmstrom SE, Frost P, Eisner ER. Exodontics—general com-ments. In: Veterinary dental techniques for the small animal practi-tioner. 3rd ed. Philadelphia: Elsevier-Saunders, 2004;292–293.

14. Smith MM. Exodontics. Vet Clin North Am Small Anim Pract 1998;28:1297–1319.

15. Peterson LJ. Principles of complicated exodontia. In: Peterson LJ, Ellis E III, Hupp JR, et al, eds. Contemporary oral and maxil-lofacial surgery. 4th ed. Philadelphia: Mosby, 2003;156–183.

16. Wiggs RB, Lobprise HB. Oronasal fistula. In: Veterinary dentistry: principles and practice. Philadelphia: Lippincott-Raven Publish-ers, 1997;241–242.

17. Manfra Marretta S. Maxillofacial surgery. Vet Clin North Am Small Anim Pract 1998;28:1285–1296.

18. Harvey CE, Emily PP. Endodontics. In: Harvey CE, Emily PP, eds. Small animal dentistry. St Louis: Mosby Year Book Inc, 1993;156–212.

19. Golden AL, Stoller N, Harvey CE. A survey of oral and dental diseases in dogs anesthetized at a veterinary hospital. J Am Anim Hosp Assoc 1982;18:891–899.

20. Simison WG. Sialadenitis associated with periorbital disease in a dog. J Am Vet Med Assoc 1993;202:1983–1985.

21. Verstraete FJM. Self-assessment color review of veterinary den-tistry. Ames, Iowa: Iowa State University Press, 1999;145–146.

22. Martin CL. Ophthalmic disease in veterinary medicine. London: Manson Publishing, 2005;120–122.

23. Gorrel C. Tooth extraction. In: Veterinary dentistry for the gen-eral practitioner. Edinburgh: Saunders, 2004;157–174.

24. Lye KW, Wee J, Gao F, et al. The effect of prior radiation therapy for treatment of nasopharyngeal cancer on wound healing fol-lowing extractions: incidence of complications and risk factors. Int J Oral Maxillofac Surg 2007;36:315–320.

25. Chang DT, Sandow PR, Morris CG, et al. Do pre-irradiation dental extractions reduce the risk of osteoradionecrosis of the mandible? Head Neck 2007;29:528–536.

26. Mealey BL, Klokkevold PR, Otomo-Corgel J. Periodontal treat-ment of medically compromised patients. In: Newman MG, Takei HH, Carranza FA, eds. Clinical periodontology. 9th ed. Philadelphia: WB Saunders Co, 2002;527–550.

27. Regezi JA, Sciubba JJ, Jordan RC. Therapeutic radiation com-plications. In: Regezi JA, Sciubba JJ, Jordan RC, eds. Oral pa-thology–clinical pathologic correlations. 4th ed. Philadelphia: WB Saunders Co, 2003;67–70.

28. American College of Veterinary Anesthesiologists. American College of Veterinary Anesthesiologists’ position paper on the treatment of pain in animals. J Am Vet Med Assoc 1998;213:628–630.

29. Trope M, Chivian N, Sigurdsson A, et al. Traumatic injuries. In: Cohen S, Burns RC, eds. Pathways of the pulp. 8th ed. St Louis: Mosby, 2002;603–649.

30. Hale FA. Localized intrinsic staining of teeth due to pulpitis and pulp necrosis in dogs. J Vet Dent 2001;18:14–20.

31. American Veterinary Dental College. American Veterinary Den-tal College—position statement: the use of antibiotics in veteri-nary dentistry. Available at: www.avdc.org/position-statements.html#AB. Accessed Jun 10, 2007.

32. Armitage GC. Diagnosis of periodontal diseases. J Periodontol 2003;74:1237–1247.


33. Hoffman S. Diagnostic imaging in veterinary dental prac-tice. Focal advanced periodontal disease. J Am Vet Med Assoc 2006;228:1683–1684.

34. Carranza FA. Clinical diagnosis. In: Newman MG, Takei HH, Carranza FA, eds. Clinical periodontology. 9th ed. Philadelphia: WB Saunders Co, 2002;432–453.

35. Harvey CE, Shofer FS, Laster L. Association of age and body weight with periodontal disease in North American dogs [erra-tum published in J Vet Dent 1994;11:133]. J Vet Dent 1994;11:94–105.

36. Theilade E, Wright WH, Jensen SB, et al. Experimental gingivi-tis in man. II. A longitudinal clinical and bacteriological investi-gation. J Periodontal Res 1966;1:1–13.

37. Loe H, Theilade E, Jensen SB. Experimental gingivitis in man. J Periodontol 1965;36:177–187.

38. DuPont GA. Understanding dental plaque; biofilm dynamics. J Vet Dent 1997;14:91–94.

39. Polson AM, Southard GL, Dunn RL, et al. Periodontal pocket treatment in beagle dogs using subgingival doxycycline from a biodegradable system. I. Initial clinical responses. J Periodontol 1996;67:1176–1184.

40. American Veterinary Dental College. American Veterinary Den-tal College—veterinary dental nomenclature. Available at: www.avdc.org/position-statements.html#AB. Accessed Jun 10, 2007.

41. Peterson LJ. Principles of antibiotic therapy. In: Topazian RG, Goldberg MH, eds. Oral and maxillofacial infections. 3rd ed. Philadelphia: WB Saunders Co, 1994;160–197.

42. Roberts MC. Antibiotic resistance in oral/respiratory bacteria. Crit Rev Oral Biol Med 1998;9:522–540.

43. Andreasen JO. Injuries to the supporting bone. In: Andreasen JO, Andreasen FM, eds. Textbook and color atlas of traumatic in-juries to the teeth. 3rd ed. Copenhagen: Munksgaard, 1994;427–455.

44. Neal DC, Wagner WF, Alpert B. Morbidity associated with teeth in the line of mandibular fractures. J Oral Surg 1978;36:859–862.

45. Berg S, Pape HD. Teeth in the fracture line. Int J Oral Maxillofac Surg 1992;21:145–146.

46. Gerbino G, Tarello F, Fasolis M, et al. Rigid fixation with teeth in the line of mandibular fractures. Int J Oral Maxillofac Surg 1997;26:182–186.

47. Thaller SR, Mabourakh S. Teeth located in the line of mandibu-lar fracture. J Craniofac Surg 1994;5:16–19.

48. Shields Henney LH, Galburt RB, Boudrieau RJ. Treatment of dental injuries following craniofacial trauma. Semin Vet Med Surg (Small Anim) 1992;7:21–35.

49. Smith MM, Kern DA. Skull trauma and mandibular fractures. Vet Clin North Am Small Anim Pract 1995;25:1127–1148.

50. Evans HE. The skull. In: Evans HE, ed. Miller’s anatomy of the dog. 3rd ed. Philadelphia: WB Saunders Co, 1993;128–166.

51. Cechner PE. Malocclusion in the dog caused by intramedul-lary pin fixation of mandibular fractures: two case reports. J Am Anim Hosp Assoc 1980;16:79–85.

52. Hosek JJ. Surgical approach to difficult reduction of a mandib-ular fracture in a dog. Vet Med Small Anim Clin 1968;63:392–393.

53. Thirloway L. Retrograde pinning of a mandibular fracture. Vet Med 1984;89:1362–1364.

54. Legendre L. Maxillofacial fracture repairs. Vet Clin North Am Small Anim Pract 2005;35:985–1008.

55. Roush JK, Wilson JW. Healing of mandibular body oste-otomies after plate and intramedullary pin fixation. Vet Surg 1989;18:190–196.

56. Umphlet RC, Johnson AL. Mandibular fractures in the dog. A retrospective study of 157 cases. Vet Surg 1990;19:272–275.

57. Verstraete FJM. Maxillofacial fractures. In: Slatter DH, ed. Text-book of small animal surgery. 3rd ed. Philadelphia: WB Saunders Co, 2003;2190–2207.

58. Hildebrand M. Head skeleton. In: Analysis of vertebrate struc-ture. 4th ed. New York: John Wiley & Sons, 1995;119–147.

59. Hillson S. Jaws, teeth and dentitions. In: Teeth. 2nd ed. Cam-bridge, England: Cambridge University Press, 2005;9–13.

60. International Committee on Veterinary Gross Anatomical No-menclature. Osteologia. In: Nomina anatomica veterinaria. 5th ed. Hannover, Germany: World Association of Veterinary Anat-omists, 2005;14–50.

61. Scapino RP. The third joint of the canine jaw. J Morphol 1965;116:23–50.

62. Scapino R. Morphological investigation into functions of the jaw symphysis in carnivorans. J Morphol 1981;167:339–375.

63. Avery JK. Embryology of the head, face, and oral cavity. In: Oral development and histology. 3rd ed. New York: Thieme, 2002;15-44.

64. Federative Committee on Anatomical Terminology. Terminolo-gia anatomica. New York: Georg Thieme Verlag, 1998.

65. DuPont G. Crown amputation with intentional root retention for advanced feline resorptive lesions—a clinical study. J Vet Dent 1995;12:9–13.

66. Lommer MJ, Verstraete FJ. Prevalence of odontoclastic resorp-tion lesions and periapical radiographic lucencies in cats: 265 cases (1995–1998). J Am Vet Med Assoc 2000;217:1866–1869.

67. DuPont GA, DeBowes LJ. Comparison of periodontitis and root replacement in cat teeth with resorptive lesions. J Vet Dent 2002;19:71–75.

68. Clarke DE. Vital pulp therapy for complicated crown fracture of permanent canine teeth in dogs: a three-year retrospective study. J Vet Dent 2001;18:117–121.

69. Niemiec BA. Assessment of vital pulp therapy for nine compli-cated crown fractures and fifty-four crown reductions in dogs and cats. J Vet Dent 2001;18:122–125.

70. Lommer MJ, Verstraete FJ. Results of crown-height reduction and partial coronal pulpectomy in rhesus monkeys (Macaca mu-latta). Comp Med 2001;51:70–74.

71. AVMA. Executive board coverage. AVMA: removing, reducing teeth as treatment for canine aggression inappropriate. J Am Vet Med Assoc 2005;226:167.

72. Beck JD, Offenbacher S. Systemic effects of periodontitis: epi-demiology of periodontal disease and cardiovascular disease. J Periodontol 2005;76:2089–2100.

73. Noack B, Genco RJ, Trevisan M, et al. Periodontal infections contribute to elevated systemic C-reactive protein level. J Periodontol 2001;72:1221–1227.

74. DeBowes LJ, Mosier D, Logan E, et al. Association of periodon-tal disease and histologic lesions in multiple organs from 45 dogs. J Vet Dent 1996;13:57–60.

75. Van Nice E. Management of multiple dental infections in a dog with diabetes mellitus. J Vet Dent 2006;23:18–25.

76. Reiter AM, Brady CA, Harvey CE. Local and systemic complica-tions in a cat after poorly performed dental extractions. J Vet Dent 2004;21:215–221.

Documents

Myths and misconceptions in veterinary dentistry