15 Chronic gingivostomatitis with extraction leading to partial cure
The cat was referred to us for management of chronic oral inflammation of 2 years’ duration. Presenting signs had been a progressive reluctance to eat, apathy and weight loss. During the first year, she had been treated with antibiotics and corticosteroids intermittently (five treatments in total). Initially, the combination of a short course of antibiotics and a long-acting steroid had resulted in clinical improvement in that the cat had resumed eating. The effect had only lasted for 3–6 weeks and become shorter for each course. In the last year, the cat had received professional periodontal therapy with extractions twice, as well as four courses of antibiotics and long-acting steroid. There had been short periods of improvement after each episode of therapy. At the second episode of periodontal therapy, it was recorded which teeth had been removed (108, 208, 309, 409 and root remnants from previous extraction) and the extractions had been confirmed radiographically. The procedure had been performed by a veterinarian with a special interest and training in dentistry. She arranged referral to us and did preoperative blood and viral testing. The cat was FeLV and FIV negative, but FCV positive.
ORAL EXAMINATION – CONSCIOUS
The cat allowed conscious oral examination, which revealed the absence of all premolars and molars, and gingivostomatitis of the mucosa overlying the alveolar bone as well as the buccal mucosa and glossopalatine folds.
ORAL EXAMINATION – UNDER GENERAL ANAESTHETIC
A thorough oral examination, including investigating periodontal parameters, was performed and all findings were noted on the dental record.
In summary, examination under general anaesthesia identified the following:
No obvious pathology could be identified. There was no evidence of any retained roots from previous extractions.
ORAL PROBLEM LIST
Chronic gingivostomatitis (CGS) is a common condition of the cat characterized by intense inflammation of gingival and non-gingival oral mucosa. It is thought to be an inappropriate response to oral antigens, namely bacterial plaque present on the tooth surfaces. Affected cats may show mild to severe dysphagia, with slight to absolute reluctance to eat. The decline in food intake leads to progressive apathy and weight loss.
I find it useful in the clinical situation to view CGS as three different types, with some degree of overlap. In one type, an underlying cause that explains the inflammatory response (albeit not the intensity) can be identified, e.g. retained root remnants from previous extraction, periodontitis or other dental pathology. In the second type, concurrent disease that alters the animal’s ability to mount an appropriate inflammatory response can be identified, e.g. chronic renal failure, diabetes mellitus or viral infection (FeLV, FIV, FCV). In the third type, no obvious dental pathology or underlying immune incompetence can be identified, i.e. it is idiopathic.
Cats with chronic stomatitis 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. As a minimum, such a work-up includes testing for FIV and FeLV, and routine haematology and blood biochemistry. A meticulous oral and dental examination, including full-mouth radiographs to identify the presence of periodontitis, resorptive lesions, retained root remnants or other lesions, is mandatory. 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 also be excluded before any treatment is initiated.
The idiopathic type of CGS is refractory to medical management. 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.
In this case, no underlying cause for the inflammatory reaction in the oral mucous membranes was identified, i.e. it is classified as an idiopathic CGS, but an oropharyngeal swab taken from the glossopalatine mucosa for FCV isolation was positive. 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.