1996 Volume 59 Issue 3 Pages 252-258
We conducted a clinical and histopathological study of a patient taking Cyclosporin to evaluate both the pathogenesis and treatment of gingival hyperplasia induced by this madication. We evaluated the plaque control record (PCR), probing depth (PD), gingival index (GI), gingival bleeding index (GBI), gingival overgrowth index (GOI) and tooth mobility (TM). Evaluations were made during the patient's initial examination, after initial preparation, after periodontal surgery and during the maintenance recall phase. PCR, GI and GBI improved markedly follwing initial preparation, although no changes were detected in either GOI or TM. GOI and TM subsequently improved with resectioning of the hyperplastic gingiva. However, gingival hyperplasia recurred during the maintenance recall phase.
These observations suggest that the primary cause of Cyclosporin-induced gingival hyperplasia may be the pharmacological activity of the drug. Regional factors such as plaque may only play a secondary role, exacerbating the hyperplasia. Histopathological study of the gingival specimens obtained during surgery revealed chronic inflammation characterized by parakeratinization of the gingival epithelium, thickening of the prickle-cell layer, hyperplasia of the collagen fibers, and infiltration of both plasma cells and lymphocytes into the subepithelial connective tissue.
These results indicate the importance of not only plaque control, scaling and root planing, but also of periodontal surgery when treating Cyclosporin-induced gingival hyperplasia. Sahika lgaku（J Osaka Odontol Soc) 1996 Sept; 59(3): 252− 258.
