Presence and quantification of mast cells in the gingiva of cats with tooth resorption, periodontitis and chronic stomatitis.

OBJECTIVE: Mast cells are tissue-dwelling granule-containing immune cells that play a pivotal role in the pathogenesis of inflammation and other processes. The three most common orodental disorders in cats are periodontitis, feline resorptive lesions (FRL), and chronic gingivostomatitis (FCGS). The presence and density of mast cells in the gingiva has been established in healthy cats but not in cats affected by FRL, FCGS or periodontitis. The aim of the present study was to document and quantify the presence of mast cells in the gingiva adjacent to teeth affected by FRL, FCGS or chronic periodontitis. METHODS: Samples from the gingiva of 32 cats affected by FRL, FCGS or periodontitis were obtained and compared to samples obtained from 7 specific pathogen-free (SPF) cats. Evaluation of mast cells and the inflammatory infiltrate were performed on hematoxylin and eosin, and toluidine blue stained sections. RESULTS: Mast cells densities were significantly increased in gingival tissues adjacent to teeth affected by FRL, FCGS or periodontitis in comparison to SPF samples. There were no significant differences between gingival tissues of the FRL, FCGS and periodontitis groups. However, the relative inflammatory score in the FRL group was significantly lower as compared to the FCGS or periodontitis groups, yet with similar density of mast cells. CONCLUSION: In the gingiva of cats affected with FRL, FCGS or periodontitis, there is an increase in the number of mast cells. The high number of mast cells in the FRL group and concurrent mild inflammatory reaction suggests the notion that mast cells may potentially play role in the pathogenesis of FRL.

Inflammatory cytokines and the nuclear vitamin D receptor are implicated in the pathophysiology of dental resorptive lesions in cats.

Dental resorptive lesions (RL) are a common oral disease in cats (Felis catus) associated with pain and tooth destruction. The aetiology of RL in cats is unknown, but inflammation is often seen in conjunction with RL. Vitamin D involvement has been suggested because 1,25-dihydroxyvitamin D (1,25(OH)(2)D) stimulates osteoclastogenesis, through up-regulation of the nuclear vitamin D receptor (nVDR). The aim of this study is to determine the involvement of inflammatory cytokines and the possible role of vitamin D in the pathophysiology of RL using quantitative PCR. We measured the mRNA expression of cytokines with stimulatory (IL-1beta, IL-6, and TNF-alpha) and inhibitory effects (IL-10 and IFN-gamma) on osteoclastogenesis, and the mRNA expression of the receptor activator of nuclear factor-kappaB ligand (RANKL), osteoprotegerin (OPG), and nVDR in RL samples. We found increased expression of mRNA levels for inflammatory cytokines and nVDR, but not for RANKL and OPG, in tissue from RL-affected cats compared with tissue from radiological confirmed healthy controls. The mRNA levels of nVDR were positively correlated with mRNA levels of pro-inflammatory (IL-1beta, IL-6, TNF-alpha, and IFN-gamma), anti-inflammatory (IL-10), pro-resorptive (IL-1beta, IL-6, and TNF-alpha), and anti-resorptive (IFN-gamma and IL-10) cytokines in the course of resorptive lesions. These data are consistent with our view that both inflammation and an overexpression of the nVDR are likely to be involved in RL in cats.