Feline stomatitis: How to treat a diseae of unknown etiology

Feline stomatitis: How to treat a diseae of unknown etiology

Treatment goal is to decrease inflammatory response to dental plaque

Feline stomatitis: Extraction is indicated in cats that have retained roots and teeth with periodontitis or feline odontoclastic resorptive lesions.
Feline stomatitis is seen largely in the adult domestic cat. Some adolescent cats may show hyperemia and hyperplasia of the gingiva. Whether this is a separate pathology or represents an early stage of the disease in adult cats is unknown.

Purebred cats and those living in a multi-cat household tend to develop stomatitis at a younger age. The etiology of stomatitis is unknown, and many cases are refractory to treatment. Patients present as a therapeutic challenge, and management is often frustrating for both the veterinarian and owner. Stomatitis is inflammation of the oral mucosa beyond gingivitis. The histological description is compatible with a chronic inflammatory or immunologic response but does not provide a definitive diagnosis as to the primary cause. Based on the major cellular infiltrate present, the disease also has been called lymphocytic-plasmacytic (gingivo) stomatitis. Another term used is faucitis; however, the fauces are the areas surrounding the tonsils or the lateral walls of the pharynx, caudomedial to the palatoglossal folds. Therefore, the term caudal stomatitis instead of faucitis should be used to denote inflammation of the palatoglossal folds.

Figure 1: Stomatitis in a cat involving the gingiva, alveolar, buccal mucosa and the area lateral to the palatoglossal folds.
• Etiology and pathogenesis The etiology of feline stomatitis is poorly understood. Feline calicivirus (FCV) can be isolated from 50 to 100 percent of cats with chronic oral inflammation. A recent investigation found that 88 percent of cats with stomatitis were shedding both FCV and feline herpes virus-1 (FHV-1) in saliva. While 10 to 81 percent of cats with stomatitis may be positive for feline immunodeficiency virus (FIV), the prevalence of feline leukemia virus (FeLV) infection has been consistently low, ranging from 0 to 17 percent. It also has been suggested that stomatitis develops because of an aberrant host response to the presence of plaque bacteria and their toxins. However, bacteria may only play a secondary role in the pathogenesis of the disease, as extensive subepithelial round cell infiltration will result in epithelial breakdown, ulceration and secondary bacterial infection. In one study, cats with oral inflammation were more likely to be infected with Bartonella than healthy cats, but evidence for a cause-effect relationship has not been provided. The presence of a polyclonal gammopathy (with increased serum concentrations of IgG, IgM and IgA; and IgE in about one-third of cats) and the distinct lymphocytic-plasmacytic infiltrate within the oral lesions indicate that feline stomatitis has an immune-mediated basis. In saliva, only IgG and IgM concentrations are increased, while IgA levels are decreased.

• History, clinical signs, oral examination and laboratory evaluation Cats with stomatitis often present with a history of halitosis, pawing at the face, drooling, pain upon eating, anorexia and weight loss. Patients show a preference for soft foods, may be less active, and express aggressive behavior or an aversion to having their face touched. An unkempt hair coat may result from a reluctance to groom. Mandibular lymph nodes may be enlarged, and focal ulceration of the lips can be observed occasionally at the commissures and philtrum. Inflammation involves the gingiva, alveolar and buccal mucosa, the areas lateral to the palatoglossal folds, and — less commonly — the mucosa of sublingual tissues, the tongue and pharynx.

In severe cases, the inflamed tissue becomes erythematous, raised, proliferative and ulcerated and bleeds readily. Various degrees of dental and periodontal disease may be present. Abundant plaque often covers the teeth. A complete blood count, biochemical blood profile and urinalysis are performed to identify concurrent or contributory disease. Leukocytosis, mild to moderate neutrophilia accompanied by a mild left shift, monocytosis, eosinophilia, mild lymphopenia and hyperglobulinemia with an altered albumin/globulin ratio may be observed. Electrophoresis of serum proteins usually reveals a polyclonal elevation in the gamma-globulin region. Serologic evaluation for FeLV antigen and FIV antibody should be performed. Virus isolation studies on specimens obtained from oral swabs of inflamed tissues can be included but are rarely helpful in determining treatment. Although bacterial cultures are not part of a basic evaluation, culture and sensitivity testing can be helpful in chronic cases that do not respond to antibiotics. A Western immunoblot antibody assay has recently been developed to test for Bartonella infection. A specimen for biopsy should be obtained of any lesion that appears neoplastic or of unknown cause.