FELINE CHRONIC GINGIVO-STOMATITIS (FCGS)
Synonyms: Feline Lymphocytic- Plasmacytic Stomatitis, Plasma Cell Stomatitis.
The syndrome is characterized by persistent and severe inflammation and ulceration of the oral, lingual and pharyngeal mucosa. The two specific sites are the mucosa lateral to the glossopalatine arches (palatoglossitis) and the mucosa overlying the cheek teeth, known as buccostomatitis. Significant accumulation of calculus is more often not present in the condition. It usually develops much later in life, or it can initially develop around the time of kitten vaccination or temporary teeth eruption.
Purebred cats are over-represented with this syndrome.
This syndrome is best considered as part of a full oral cavity examination and the presence of Feline Tooth Resorption (FTR) lesions frequently adds to and confuses the picture.
Also, a large number of cats is infected with calici virus, 50% of cats infected with FIV also having FCGS, 15% of cats with FCGS are positive to FeLV/FIV. Additionally, there is some concern that it may be a pre-neoplastic lesion. There is also an inverse relationship between the age of onset of disease and the number of cats in the household and this may implicate social stress as predisposing factor.
One consistent feature of all cases is a hyper-gammaglobulinaemia. This implies B-lymphocyte proliferation and therefore no humoral immune response depression. It is probable that affected cats are intolerant to even small quantities of bacterial plaque on the tooth surface and elsewhere in the mouth.
The main problem is that not all cats with FCGS respond alike to periodontal therapy and improved hygiene while others will respond poorly to treatment. 87% of the intractable cases improve with elective tooth extraction and 13% of the cases do not respond to any treatment.
The main sign in all cats is dysphagia and pain due to oral inflammation. Inflammatory lesions can be focal or diffuse and may involve all oral tissues (gingiva, palatine, lingual or buccal mucosa and, possibly, the fauces). Lesions are more commonly found caudally towards the glossopalatine arches where saliva pools. Inflammation crossing the mucogingival line into the buccal or vestibular mucosa is a bad prognostic indicator.
Signs reported are:
1. Ptyalism, dysphagia, halitosis.
2. Weight loss, chronic or acute.
3. Lack of (or inability) to groom.
4. Cachexia. Reluctance to eat food is common.
5. Submandibular lymphadenomegaly. Can be dramatically increased and painful when palpated.
6. Variable accumulation of plaque and calculus.
7. Teeth may be missing, affected by “neck lesions” or suffering from furcation exposure and excessive mobility after recesiion of the periodontal tissues.
1. Breed: Some breeds may appear to have more affected individuals. Purebred cats are anecdotally more often affected with Siames, Burmese, Abyssinian, Persians, Tonkinese, and Main Coons all over represented.
2. Environmental factors: Colony cats or those in multi-cat households appear to be more commonly affected. Stress is considered to be the main factor with also the proximity of animals allowing transmission of micro-organisms also being significant.
3. Plaque Bacteria: The oral bacteria present in the plaque matrix drive the abnormal non-specific inflammatory response.
4. Feline Viruses: Testing at Bristol Veterinary School and elsewhere indicated that 100% of chronically affected individuals (> 6 months) show positive testing for Calici Virus. FIV, FeLV and FHV-1 have also been implicated in the past.
5. Dental Disease: Either periodontal disease or FTR lesions or both can have an exacerbating effect on the syndrome.
A standard clinical approach is advocated for all cats affected. This should comprise:
Virus testing for FIV, FeLV, oral swab for FCV.
Routine Haematology and Biochemistry for underlying systemic disease. 10% of the affected cats has been reported to have renal failure.
Biopsy of affected areas (neoplastic lesions).
Radiography (full mouth dental survey).
Based on three underlying principles:
1. Control Plaque.
2. Control existing disease.
3. Control inflammation.
Base-line treatment for all cases:
2. Dental Surgery
3. Homecare – Hygiene
Cases-additional Selective treatment:
2. Elective tooth extraction
3. Laser therapy
5. Interferon, Cyclosporin treatment
6. Food modification
FCGS at the present time remains a poorly defined syndrome of unknown aetiology characterized by focal or diffuse chronic inflammatory response involving the gingiva, oral mucosa, and often the pharyngeal fauces.
Successful management of this complex requires a logical approach. There is a need for base-line data before considering treatment plan and and prognosis. The role of bacterial plaque is crucial. Professional scaling, polishing and subgingival debridement to eliminate any dental disease plus aggressive homecare by the owner are absolutely necessary. Additional therapy for the unresponsive cases are applied to selective cases.
Girard N, Hennet P. Retrospective Study of Dental Extractions for Treatment of Chronic Caudal Stomatitis in 60 FCV Positive Cats. Proceedings 19th Veterinary Dental Forum 2005 p 447.
Harley R, Helps CR" Harbour DA, et al. Intra-lesional cytokine mRNA expression in chronic gingivostomatitis in cats, Clin Diag Lab Immunol, 1989;6: 471-478.
Harley & Gruffydd-Jones TJ, Day MJ. Salivary and serum immunoglobulin levels in cats with chronic gingivostomatitis, Vet Rec, 2003; 152:125-129.
Harvey CE. Oral inflammatory diseases in cats. J Am Anim Hosp Assoc 1991;27: 585-591.
Hennet P. Chronic gingivostomatitis in cats: Long-term follow-up of 30 cases treated by dental extractions J Vet Dent 1997;14:15-21.
Hennet P, Boucrault-Baralon C. Relationship between oral Calici virus and Herpesvirus carriage and palatoglossitis lesions. Proceedings 19th Veterinary Dental Forum 2005 p 443.
Knowles JO, Gaskell RM, Gaskell CJ, et al. Prevalence of feline calicivirus, feline leukaemia virus and antibodies to FIV in cats with chronic stomatitis. Vet Rec.1989;124:336-338.
Knowles JO, Dawson S, Gaskell RM, et al. Neutralisation patterns among recent British and North American feline calicivirus isolates from different clinical origins. Vet Rec 1990;121:125-127.
Knowles JO, McArdle F, Dawson S, et al. Studies on the role of feline calicivirus in chronic stomatitis in cats. Vet Microbiol 1991;27:205-219.
Lommer MJ, Vershaste FJM (2003). Concurrent oral shedding of feline calicivirus and feline herpesvirus-l in cats with chronic gingivostomatitis. Oral Microbiology and Immunology 18,131-134.
Preshaw PE, Hefti AF et al. Subantimicrobial dose doxycycline as adjunctive treatment for periodontitis. A review. J Clin Periodontol 2004: 3I (9), 697-7O7.
Reubel GII, Hoffinann DE, Pedenen NC. Acute and chronic faucitis of domestic cats: a feline calicivirus-induced disease. Veterinary Clinics of North America-Small Animal Practice 192;22:1347-1360.
Sims TJ, Moncla BJ, Page RC. Serum antibody response to antigens of oral gram-negative bacteria by cats with plasma cell gingivitis-pharyngitis. J Dent Res 1990; 69: 877-882.
Southerden P, Gorrel C. Treatment of a case of refractory feline chronic gingivostomatitis with feline recombinant interferon omega. Journal of Small Animal Practice (2007) 48,104-106.
Williams CA, Aller MS. Gingivitis/stomatitis in cats. Veterinary Clinics of North America Small Animal Practice l992; 22:1361-1383.
Addie DD et al. Cessation of feline calici virus shedding coincident with resolution of chronic gingivostomatitis in a cat. JSAP (2003), 44,112-176
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