Evaluation of p53, bcl-2, and interleukin-15 levels in gingival crevicular fluid of cyclosporin A-treated patients.

Abstract

Apoptosis plays an important role in the maintenance of tissue homeostasis. Considering that apoptosis mediators may play a role in the pathogenesis of drug-induced gingival overgrowth, this study was conducted to evaluate p53, bcl-2, and interleukin-15 (IL-15) levels in gingival crevicular fluid (GCF) of cyclosporin A (CsA)-treated patients. Twenty renal transplant patients exhibiting CsA-induced gingival overgrowth and 15 systemically healthy gingivitis patients were included in the study; 15 systemically and periodontally healthy volunteer subjects served as the healthy control group. GCF samples were obtained from one interdental site with gingival overgrowth (GO+) and one site without (GO-) from each CsA-treated patient; hyperplasia index, probing depth, papilla bleeding index, and plaque presence were recorded. One site from each gingivitis patient and healthy control was selected, GCF samples were obtained, and the same clinical parameters were recorded. GCF p53, bcl-2, and IL-15 levels were analyzed by enzyme-linked immunosorbent assay. The results were tested statistically. p53 and bcl-2 levels were below the minimum detectable level in all GCF samples analyzed. CsA GO+ and CsA GO- sites, as well as gingivitis sites, exhibited significantly higher GCF levels of IL-15 compared to healthy controls (P<0.05). The difference between CsA GO+ sites and gingivitis sites was not statistically significant, although the total amount of IL-15 in CsA GO+ sites was lower than gingivitis sites (P>0.05). The total amount of IL-15 in CsA GO- sites was significantly lower than gingivitis sites (P<0.05). No significant correlation was found between the clinical parameters and GCF IL-15 levels (P>0.05). The pathogenesis of CsA-induced gingival overgrowth is multifactorial. The findings of the present study indicate that IL-15 may play a role in the pathogenesis of CsA-induced gingival overgrowth due to its interactions with CsA and its role in apoptosis and inflammation.