Immunohistochemical characterization of oral mucosal lesions in cats with chronic gingivostomatitis

Abstract

Histological and immunohistochemical studies were performed on samples of the glossopalatine mucosa from 30 cats with feline chronic gingivostomatitis (FCGS). Immunohistochemical labelling and computer-assisted morphometric analysis were used to identify expression of CD3, CD4, CD8, CD79a, IgG, IgM, IgA, leucocyte antigen 1 (L1) and class II molecules of the major histocompatibility complex (MHC) in tissue sections. Mast cells were detected by toluidine blue staining. The microscopical lesions were graded by severity of inflammation and although this grading correlated significantly with the severity of mucosal inflammation assessed at clinical examination, sites assessed as clinically normal or mildly inflamed were poorly predictive of the histopathological grade in the corresponding tissue sample. The number of CD79a+ cells (mostly plasma cells), L1+ cells (mostly neutrophils) and CD3+ T cells, and the level of MHC class II expression, tended to correlate with the severity of the inflammation. In general, CD8+ T cells were more numerous than CD4+ T cells. The majority of the plasma cells were of the IgG isotype and fewer IgA+ and IgM+ plasma cells were present. In some cases MHC class II expression by mucosal epithelium, salivary duct epithelium or skeletal muscle fibres was observed. Relative to equivalent oral mucosal samples from healthy cats, the number of cells labelled for CD3, CD4, CD8, CD79a, IgG, IgM, IgA or L1, and the number of mast cells, within the lamina propria/submucosa were significantly increased. Limited analysis of the epithelial compartment also found more CD3+ T cells compared with healthy cats. These findings indicate that the glossopalatine mucosal lesions in FCGS represent a complex, chronic and destructive inflammatory process affecting the epithelium and lamina propria, with frequent extension into submucosal tissues. The predominance of CD8+ cells over CD4+ cells suggests the induction of an underlying cytotoxic cell-mediated immune response, which could be consistent with a viral aetiology.