Sandra Manfra Marretta, DVM, Diplomate ACVS, AVDC
Management of feline oral pathologic conditions include several specific problems, including: (1) variation in dentition and dental abnormalities, (2) abnormalities of occlusion, (3) periodontal disease, (4) odontoclastic resorptive lesions, (5) fractured teeth, (6) lymphocytic-plasmacytic stomatitis, (7) eosinophilic granuloma, and (8) nasopharyngeal polyps.
Clinical signs associated with oral pain include: (1) changes in eating habits, (2) halitosis, (3) pawing at the mouth, (4) abnormal salivation, (5) oral hypersensitivity, (6) facial swelling, (7) oral hemorrhage, (8) sneezing, (9) nasal discharge, and (10) behavioral changes.2 Thorough oral examination will frequently reveal the source of discomfort. Recognition of normal as well as abnormal oral structures are important in the management of feline oral pain. Normal anatomic structures that may be mistaken for pathologic conditions include the incisive papilla, a small eminence located just caudal to the central incisor teeth, and the lingual molar gland, a small salivary gland, located adjacent to the lingual aspect of the mandibular molar.
Variation in Numbers of Teeth and Dental Abnormalities
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. In the cat all the incisors and canine teeth have 1 root, the maxillary 2nd premolar has 1 root, the 3rd premolar has 2 roots, and the 4th premolar has 3 roots while the maxillary 1st molar has 2 roots. The mandibular cheek teeth in a cat (3rd and 4th premolars and 1st molars) all have 2 roots.
Abnormalities in the number of teeth in cats can be inherited, or can result from disturbances during the initial stages of tooth formation. Complete absence of all teeth, anodontia, and decreased number of teeth, oligodontia, are uncommon in cats. Supernumerary teeth are more common, and may result in crowding and malalignment of teeth with development of premature periodontal disease. The mandibular fourth premolars appear to be the most common supernumerary teeth in the cat. Supernumerary teeth that result in crowding should be extracted early.
Retention of deciduous teeth rarely occurs in cats. Retained deciduous teeth should be extracted as soon as they are diagnosed so that permanent teeth may erupt into their normal position. When retained deciduous teeth are not removed, permanent teeth are deflected lingually, except maxillary canine teeth, which are deflected rostrally.
Abnormalities in development of teeth occur rarely in cats. Gemination is a disorder in which the developing tooth bud attempts to split but fails to do so completely, resulting in duplication of part of the tooth but not complete twinning. Gemination teeth commonly have two crowns, each with a separate pulp chamber merging into a common root canal system which can be demonstrated radiographically.
Abnormalities of Occlusion
Abnormalities of occlusion in cats include: (1) prognathic malocclusions, (2) brachygnathic malocclusions, (3) wry mouth (4) rostromesial inclination of the maxillary canine tooth, and (5) lingual displacement of mandibular canine teeth. Prognathic malocclusions occur most frequently in Persians. Occasionally, excessive dolichocephalism in Siamese cats may result in brachygnathic malocclusions. Wry mouth is a skeletal malocclusion in which one or more of the four quadrants of the jaw grow disproportionately to the others, resulting in improper alignment of the midlines of the dental arcades. Wry mouth occurs most frequently in extreme flat-nosed brachycephalic cats that have a malpositioned mandibular canine tooth that remains exposed when the mouth is closed. A maxillary canine tooth that is displaced rostrally may occlude traumatically with the mandibular canine, causing labial displacement of the mandibular canine tooth and secondary traumatic occlusion of the mandibular canine with the lip. This is known as rostromesial inclination of the maxillary canine tooth (Figure 3). This traumatic occlusion by the mandibular canine tooth may cause a lesion resembling an eosinophilic granuloma. Retained deciduous mandibular canine teeth may result in lingual displacement of the permanent mandibular canine teeth resulting in traumatic occlusion with the hard palate. When abnormalities of occlusion result in traumatic occlusion including soft tissue trauma and tooth-to-tooth trauma treatment in the form of exodontia, orthodontia or endodontia is recommended.
The primary cause of periodontal disease is accumulation of bacterial plaque on tooth surfaces. Periodontal disease can be divided into two categories: Gingivitis and periodontitis. Gingivitis is confined to gingival soft tissue, while periodontitis is a more severe form of disease involving loss of bone supporting the tooth. Cats with periodontitis, in addition to having gingivitis, may have gingival recession or increased pocket depth, alveolar bone loss, exposure of roots and furcations, tooth mobility, and eventual tooth loss. A periodontal probe is used to access the level of attachment loss, and measure pocket depth.
The prevention and treatment of feline periodontal disease consists of regular dental prophylaxis every 6 to 12 months. A thorough dental prophylaxis can only be performed under general anesthesia and consists of supragingival and subgingival scaling, subgingival currettage, root planing and polishing the teeth. Broad spectrum perioperative antibiotic therapy such as clavulanic acid/amoxicillin (Clavamox) is recommended.
Two additional abnormalities may be associated with feline periodontal disease, and can complicate treatment significantly. These abnormalities are oral inflammatory diseases and odontoclastic resorptive lesions. When periodontal disease is complicated by either of these conditions, exodontia is the treatment of choice. In cats, hard dry-food diets, especially tartar control diets, result in improved gingival health compared to a soft-food or semi-moist diet. In addition, daily brushing to remove plaque is ideal.
Odontoclastic Resorptive Lesions
Odontoclastic resorptive lesions are the most common dental lesions in cats. A recent report reviewing 10 independent surveys of odontoclastic resorptive lesions revealed that 20 to 67 per cent of all cats have 1 or more lesions with a mean of 2.3 to 4.1 lesions per affected cat. Odontoclastic resorptive lesions have been classified into 5 stages based on thorough examination with a dental explorer and radiographic evaluation. Stage I lesions are shallow and involve only the enamel or cementum. Stage II lesions penetrate into the dentin. Stage III lesions have pulpal exposure. Stage IV lesions result in major structural instability and Stage V lesions progress to the point where only the roots of teeth remain. Treatment modalities vary depending on the stage of the lesion and include the following treatment options as the lesions progress: fluoride varnish, glass ionomer restoration, endodontic therapy and glass ionomer restoration and exodontia. Because these lesions are painful, progressive, and successful treatment is limited, exodontia should be considered a viable alternative in many cases.
Fractured teeth usually result from external trauma. In cats, the tooth most frequently fractured because of trauma is the canine tooth. Fractured canine teeth usually result in pulpal exposure because of the extension of the pulp canal into the coronal tip of the canine tooth in felines. Pulpal exposure is confirmed if a fine dental explorer, penetrates into the canal. Teeth with confirmed pulpal exposure should be extracted or treated endodontically. Prior to endodontic therapy radiographs must be taken to ensure that the apex is intact. Failure to treat fractured teeth with pulpal exposure may result in periapical abscessation, mucosal or cutaneous fistulation, chronic rhinitis, and ocular discharge.
Lymphocytic Plasmacytic Stomatitis
Cats with lymphocytic plasmacytic stomatitis (LPS) typically present with a history of halitosis, ptyalism, dysphagia, inappetence and weight loss. Oral examination reveals a hyperemic, proliferative, ulcerative mucosa with a raspberry red, cobblestone appearance . These lesions may be primarily around the dentition but may extend onto the palatoglossal folds and fauces. The etiology is unknown. Histologically, this condition is characterized by infiltration of affected tissue with large numbers of lymphocytes and plasmacytes. Polyclonal hypergammaglobulinemia is a consistent hematologic finding. It has been suggested that LPS result from atypical immune responses, either deficiencies or exaggerated responses, and that gram-negative anaerobes that are present in plaque may be major contributing factors.
Cats with lymphocytic plasmacytic stomatitis should be tested for feline leukemia virus and feline immunodeficiency virus, although many test negative. Cats with LPS lack a permanent response to conventional oral hygiene, antibiotics, anti-inflammatory drugs, and immunomodulators. Refractory cases frequently necessitate extraction of at least all the premolars and molars and in some cases extraction of the entire dentition including removal of all root tips and debridement of reactive bone is required. Lack of a known causative agent, severe disease with possible underlying naturally occurring or acquired immunopathologies necessitates aggressive treatment.
Two types of eosinophilic granulomas occur in the feline oral cavity. The first is a mild to severe ulcerative cheilitis and the second is a proliferative (nodular), ulceroproliferative, or plaque-like lesion involving any structure in the oral cavity. The etiology is unknown. Clinically, the lesions can be mistaken for neoplasia. Diagnosis of eosinophilic granuloma is confirmed by deep incisional biopsy. The treatment of choice for eosinophilic granulomas is early and aggressive use of systemic glucocorticoids, such as oral prednisolone or subcutaneous (SQ) methylprednisolone acetate at 20mg/cat SQ every 2 weeks for 3 doses. Breeding cats with a history of eosinophilic granulomas should be avoided since the stress of pregnancy may result in exacerbation of lesions.
Nasopharyngeal polyps are an uncommon upper respiratory problem that is unique to cats, and occur most frequently in young cats. Nasopharyngeal polpys are non-neoplastic soft tissue growths that originate from the mucous membrane of the auditory tube or middle ear. The polyp may extend into the external ear canal, osseous bullae, or nasopharynx. Clinical signs associated with nasopharyngeal polyps include inspiratory stridor, sneezing, rhinitis, dysphagia, voice change, and head tilt or nystagmus. Diagnosis of nasopharyngeal polyps generally is based on history, clinical signs, and direct visualization of the polyp in the anesthetized patient. Forward displacement of the soft palate frequently reveals a firm smooth pink mass in the nasopharynx. Otoscopic examination also may reveal extension of the polyp into the external ear canal.
The cause of nasopharyngeal polyps in cats is unknown. Nasopharyngeal polyps may develop secondary to chronic inflammation and local tissue irritation. Feline calicivirus has been identified in cats with nasopharyngeal polyps. The common occurrence of this virus in cats makes it difficult to support a cause and effect relationship. Because nasopharyngeal polyps occur most frequently in young cats, congenital origin has also been suspected.
Treatment options for nasopharyngeal polyps is dependent upon radiographic evaluation and localization of the polyp. Computerized tomography of the bullae are benefical in assessing bullae involvement. If the polyp does not involve the bulla when assessed radiographically, it may be removed with gentle traction through the oral cavity or external ear canal. Unfortunately, many polyps invade the middle ear, necessitating ventral bulla osteotomy for complete removal. The feline tympanic bulla contains a septum that separates it into dorsolateral and ventromedial compartments. This septum must be opened to permit curettage and drainage of both compartments. Complete removal of a polyp warrants a favorable long-term prognosis.
Postoperative complications that may occur following removal of nasopharyngeal polyps include transient Horner's syndrome that resolves spontaneously 3 to 6 weeks postoperatively, persistent otitis media possibly related to rupture of the tympanic membrane, regrowth of the polyp, and facial nerve palsy.