11 Chronic gingivostomatitis – an introduction
Commonly described clinical findings in cats with CGS include elevated serum immunoglobulins (immunoglobulin (Ig) G, IgM and IgA are all raised). They also tend to have raised salivary concentrations of IgG and IgM, but reduced concentration of salivary IgA. It is unclear if the Ig pattern described is a cause or result of the inflammatory disease. Histological examination of affected oral mucosa shows a submucosal inflammatory infiltrate consisting of plasma cells, lymphocytes, macrophages and neutrophils.
The elevated serum globulins in affected cats and the nature of the submucosal inflammatory infiltrate have lead a number of authors to suggest that there may be an immunological basis for the condition. To date, no underlying intrinsic immunological abnormality in cats affected by CGS has been identified; however, the condition may still be immune mediated. Clinical studies have implicated the potential involvement of various viral agents, feline calici virus (FCV) in particular, as well as Gram-negative anaerobic bacterial species. However, attempts to reproduce the disease using these putative infective aetiological agents have been unsuccessful.
The most common sign of feline immunodeficiency virus (FIV) infection is oral inflammation. However, most cats with CGS test negative for FIV, but it needs to be excluded. Feline leukaemia virus (FeLV) also needs to be excluded in the initial work-up. The role of FCV in the development of CGS is unclear. FCV has been isolated from up to 100% of CGS cases, compared with up to 25% of cats in a healthy population, indicating that the carrier state may be a prerequisite for the induction of chronic stomatitis. However, FCV isolated from cats with CGS and then inoculated into specific pathogen-free cats produced signs of acute calici virus infection but not CGS, suggesting that other factors contribute towards the development of the oral inflammation. The fact that CGS often resolves in FCV-positive cats after extraction of all or most teeth and the subsequent reduction in dental plaque suggests that other antigenic stimuli are involved in the pathogenesis of the condition. It is possible that it is the sum of the total antigenic stimulation from plaque bacteria and viruses that is significant in the development of CGS.
Historically, the intractable nature of the disease, in combination with a poor understanding of the aetiopathogenesis of feline CGS, has resulted in the widespread use of empirical symptomatic treatment regimens.
The current treatment recommendations for cats with CGS include a combination of periodontal therapy and a home care regimen whereby plaque accumulation is kept to a minimum. In some cats, this may result in a reduction in inflammation. Unfortunately, most cats will not cooperate adequately with home care measures and plaque reforms beyond a critical level. These cats need extraction of premolar and molar teeth. In some cats, all teeth may require removal. The extraction of all premolar and molar teeth has given the most dependable results, with up to 80% of cats being clinically cured or significantly improved. The 20% that are non-responsive to extraction can be treated with antiseptics, intermittent antibiotics or interferon.
FCV isolation should always be performed prior to using interferon and also to monitor viral status as a consequence of treatment. Interferon should only be used in FCV-positive cats where extraction of at least all premolar and molar teeth has not led to cure. Using interferon without surgical treatment (extraction) has not been shown to have any benefit.
Cats with CGS require a thorough work-up prior to any treatment. The purpose of the work-up is not to reach a diagnosis per se, but rather an attempt to identify possible underlying causes. The minimal work-up includes: testing for FIV and FeLV; routine haematology and blood biochemistry; and a thorough oral and dental examination (including full-mouth radiographs to identify the presence of periodontitis, resorptive lesions, retained root remnants or other lesions). Systemic diseases, e.g. chronic renal failure and diabetes mellitus, which may predispose to the development of severe gingival inflammation in the presence of plaque, must be excluded before any treatment is initiated. Additional investigations include testing for FCV and/or biopsy and microscopic examination of the affected tissues. We do not routinely test for FCV. It is only if the cat does not respond to extraction of all or most teeth that we determine FCV status. Only cats that test positive (virtually 100%) will be treated with interferon therapy. Biopsy and histopathological examination of affected tissue are only performed if the lesions are asymmetrical. There have been recent reports of squamous cell carcinoma developing in cats with GCS. We have seen one case where surgical management lead to cure of the CGS. Two years after the curative treatment, localized intense inflammation of the right glossopalatine mucosa developed (the rest of the oral mucosa was healthy). Biopsy and histopathological examination of the affected mucosa revealed squamous cell carcinoma.