Pathological investigation of feline chronic gingivostomatitis

In this thesis, the pathogenesis of feline chronic gingivostomatitis (FCGS) and the interrelationships among various molecules and biomarkers were investigated using oral mucosal biopsy tissue blocks obtained from cats affected by FCGS. The aim of the study was to elucidate the role of the mammalian target of rapamycin (mTOR) signaling pathway in the pathogenesis of FCGS and its interaction with the FKBP12 protein, thereby providing a novel perspective on alternative therapeutic strategies involving mTOR inhibitors. For this purpose, oral biopsy tissues from a total of 30 cats, including 5 control animals, were examined using Toluidine Blue (TB), Periodic Acid–Schiff (PAS), Hematoxylin–Eosin (H&E), and immunohistochemical (IHC) staining methods. In histopathological evaluations, mast cells were graded in TB-stained sections, and a marked increase in mast cell numbers was observed in FCGS tissues compared with the control group. In PAS-stained sections, prominent PAS positivity was noted in both the epithelial layer and inflammatory cells in the FCGS group relative to controls. Immunohistochemical analyses demonstrated increased expression of CD3, CD79a, IBA1, mTOR, and FKBP12 in the FCGS group compared with the control group. Statistically positive correlations were identified between CD3 and CD79a, as well as between mTOR and FKBP12; however, although the positive correlation between mTOR and FKBP12 was very close to the threshold of statistical significance, it did not reach a statistically significant level. In conclusion, the demonstration that mTOR and FKBP12 proteins exhibit expression in similar localizations suggests that this similarity may play an important role in the pathogenesis of FCGS. Accordingly, these findings indicate that mTOR inhibitors may be considered as potential therapeutic agents in the management of FCGS.