An Update on Feline Chronic Gingivostomatitis

Abstract

Feline chronic gingivostomatitis is a frustrating disease to manage owing to its elusive etiopathogenesis and its subsequently suboptimal treatment options. Nevertheless, efforts to shed light on the disease over the past few decades have advanced the knowledge on its potential etiopathogenesis and the success rates of available treatment options. Further research is ongoing, with promising attempts to better understand and treat this, likely, multifactorial disease.

Keywords: Feline; Gingivostomatitis; Inflammation; Medical therapy; Oral mucosa; Surgical therapy.

Fig. 1

The hallmark of FCGS is inflammation in the caudal oral cavity in the area lateral to the palatoglossal folds. Ulcerative (A) and proliferative (B) phenotypes can be observed.

Fig. 2

Occasionally, the proliferative inflammation can be so severe as to prevent the tongue from retracting into its normal and functional position.

Fig. 3

On histology, the healthy oral mucosa of cats is composed of squamous epithelium with a rare presence of inflammatory cells (A). However, in cats affected by FCGS, ulceration of the squamous epithelium is observed with profound inflammatory infiltration comprising mostly granulocytes, lymphocytes, plasma cells, and mast cells (B) (hematoxylin-eosin [H&E] staining, original magnification ×10). Immunohistochemistry of FCGS mucosal inflammation indicates that most of the T lymphocytes (CD3 cells) are present in the epithelium (C) and most of the B lymphocytes (CD20 cells) are present in the submucosa (D) (original magnification ×10 ).