IMMUNOHISTOCHEMICAL LOCALIZATION OF TRANSFORMING GROWTH-FACTOR-BETA, BASIC FIBROBLAST GROWTH-FACTOR AND HEPARAN-SULFATE GLYCOSAMINOGLYCAN IN GINGIVAL HYPERPLASIA INDUCED BY NIFEDIPINE AND PHENYTOIN

Although drug-induced gingival hyperplasia has been extensively studie d, the pathogenesis of this disorder has not been clarified to date. T ransforming growth factor beta (TGF beta) and basic fibroblast growth factor (bFGF) have been shown to be implicated in diverse fibrotic and hyperplastic diseases. Heparan sulphate proteoglycan (HSPG), which is composed of heparan sulphate glycosaminoglycan (HSGAG), has also been shown to;play an important role in the pathogenesis of tissue overgro wth by enhancing the functions of bFGF. However, the possible implicat ion of these growth factors in gingival hyperplasia has not been studi ed. Immunohistochemical localization of TGF beta, bFGF, their receptor s and HSGAG was studied in 4 nifedipine-induced and 5 phenytoin-induce d hyperplastic gingival tissues, and 5 non-hyperplastic control gingiv al tissues to elucidate the pathogenesis of this disease. Significant immunostaining against TGF beta, bFGF, the receptors of these two grow th factors and HSGAG was observed in the lamina propria of hyperplasti c gingival tissues while less immunostaining was observed in the contr ols. The mean numbers of immunostained cells against TGF beta, bFGF, t heir receptors in a square unit (0.1 x 0.1 mm) of the lamina propria, which were counted to 10 units of each hyperplastic gingival tissue, w ere significantly higher than those of the controls. The results sugge st that the increased synthesis of TGF beta, bFGF, their receptors and HSGAG may be related to the pathogenesis of drug-induced gingival hyp erplasia.