Feline Chronic Gingivostomatitis (FCGS) is a well-known inflammatory condition of the oral cavity in cats. This disease is characterized by ulcers, erosion, and inflammation of the gums, palate, tongue, fauces, periodontal ligament, and other oral cavity structures in affected animals. It is distinguished from more common forms of dental disease by the extent of inflammation. A wide variety of causes have been suggested including viral and bacterial infections, hypersensitivity to plaque antigens, retrovirus infection, and numerous other causes. While the condition may be responsive to antibiotics, steroids, and other drugs in the short term, definitive therapy usually involves surgical extraction of most or all teeth.
The widespread nature of inflammatory change in cats with FCGS has prompted questions regarding concurrent inflammation at other sites. The purpose of this study was to determine if cats with FCGS have concurrent esophageal lesions. It was designed as a prospective observational study at a veterinary school over a 2 year period. 58 cats with FCGS and 12 healthy cats were enrolled. Control cats were healthy with no signs of disease. Study cats had no concurrent disease other than FCGS, were washed out of all medications, and had gross or histologic confirmation of FCGS. Cats with any evidence of esophageal disease (diverticula, strictures, hiatal hernias, etc) were excluded.
Animals from both groups were anesthetized and received esophageal endoscopy by an experienced endoscopist. Oral and esophageal pH were measured and disease scores for the proximal, middle, and distal esophagus were recorded. Endoscopic biopsies were collected from a subset of cats. Stomatitis was also scored using an objective scoring system. Cats with FCGS received appropriate extractions after endoscopy.
pH, stomatitis score, esophagitis score, and histologic changes were compared between groups and statistically analyzed where appropriate.
No changes in oral or esophageal pH were seen between affected and control cats. 98% of cats with FCGS exhibited some degree of esophagitis. The majority of cats had gross inflammation of either the proximal (76%) or distal portion (91%), with less change in the middle esophagus. Esophagitis was most severe in the distal esophagus. The degree of esophagitis did not correlate with the degree of oral inflammation.
There was no correlation of esophagitis severity with salivary pH, duration of disease, or use of previous medications.
Only a small number of cats were histologically examined. None of the control cats had evidence of esophagitis, however all examined cats with FCGS had histologic lesions, including some with no gross evidence of inflammation. Some cats exhibited evidence of squamous metaplasia.
The authors suggest several possible causes for esophagitis in association with FCGS. These include alterations in bacterial populations due to changes in salivary parameters, altered cytokine profiles, gastro-esophageal reflux, or continuation of oral inflammation, among others.
While only a small number of cats were reassessed endoscopically after therapy, two cats that had resolution of FCGS also resolved esophagitis while one cat that maintained oral lesions also had persistent esophagitis.
This manuscript describes a previously unknown condition associated with FCGS in cats. This may help to further our understanding of this poorly understood disease, and provides a new target for therapy of affected cats. Further research should be done to confirm the presence of esophagitis in a large proportion of cats with FCGS, and to determine if standard therapy for this condition also resolves esophagitis. Until this time, instituting therapy for esophagitis for cats with FCGS may be prudent.
