Role of Renin Angiotensin System in Drug Induced Gingival Overgrowth : Interaction among angiotensin, endothelin, chymase and cyclosporine towards fibroblast proliferation and ECM synthesis

The most common periodontal disease is chronic periodontitis, the inflammatory destructive condition of microbial etiology. Drugs like cyclosporine-A, nifedipine and phenytoin induce overgrowth of the gingiva in 60% of the patients ingesting the drug in the presence of inflammation. During inflammation cytokines derived from inflammatory cells could induce angiotensin II (Ang II) and endothelin-1 (ET-1). Ang II is the effector peptide of renin angiotensin system plays a major role in regulation of collagen synthesis and growth modulating effects on fibroblasts. Endothelin-1 is a powerful vasoconstrictor with mitogenic activity on vascular smooth muscle and fibroblasts. Studies have shown that Ang II and ET-1 were increased in cardiac, renal and pulmonary fibrosis. Since inflammation is prerequisite for drug induced gingival overgrowth (DIGO), mast cells play a major role in the conversion of Ang II and ET-1. This study designed to assess the expression of Ang II, ET-1 and its receptors, mast cell chymase; tryptase and transcription factor c-jun in CsA induced gingival fibroblasts and drug induced gingival overgrowth tissues obtained from kidney transplanted patients.