Immunohistochemical localization of transforming growth factor beta, basic fibroblast growth factor and heparan sulphate glycosaminoglycan in gingival hyperplasia induced by nifedipine and phenytoin

• Published in: Journal of periodontal research Vol. 31; no. 8; p. 545
• Main Authors: Saito, K, Mori, S, Iwakura, M, Sakamoto, S
• Format: Journal Article
• Language: English
• Published: United States 01.11.1996
• Subjects: Adolescent; Adult; Aged; Anticonvulsants - adverse effects; Calcium Channel Blockers - adverse effects; Cell Count; Coloring Agents; Female; Fibroblast Growth Factor 2 - analysis; Fibroblast Growth Factor 2 - biosynthesis; Fibroblast Growth Factor 2 - drug effects; Gingiva - metabolism; Gingiva - pathology; Gingival Hyperplasia - chemically induced; Gingival Hyperplasia - pathology; Heparitin Sulfate - analysis; Heparitin Sulfate - biosynthesis; Humans; Immunohistochemistry; Male; Nifedipine - adverse effects; Phenytoin - adverse effects; Receptors, Fibroblast Growth Factor - analysis; Receptors, Fibroblast Growth Factor - biosynthesis; Receptors, Fibroblast Growth Factor - drug effects; Receptors, Growth Factor - analysis; Receptors, Growth Factor - biosynthesis; Receptors, Growth Factor - drug effects; Receptors, Transforming Growth Factor beta - analysis; Receptors, Transforming Growth Factor beta - biosynthesis; Receptors, Transforming Growth Factor beta - drug effects; Transforming Growth Factor beta - analysis; Transforming Growth Factor beta - biosynthesis; Transforming Growth Factor beta - drug effects
• ISSN: 0022-3484
• DOI: 10.1111/j.1600-0765.1996.tb00519.x

Although drug-induced gingival hyperplasia has been extensively studied, the pathogenesis of this disorder has not been clarified to date. Transforming 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 overgrowth by enhancing the functions of bFGF. However, the possible implication of these growth factors in gingival hyperplasia has not been studied. Immunohistochemical localization of TGF beta, bFGF, their receptors and HSGAG was studied in 4 nifedipine-induced and 5 phenytoin-induced hyperplastic gingival tissues, and 5 non-hyperplastic control gingival tissues to elucidate the pathogenesis of this disease. Significant immunostaining against TGF beta, bFGF, the receptors of these two growth factors and HSGAG was observed in the lamina propria of hyperplastic gingival tissues while less immunostaining was observed in the controls. The mean numbers of immunostained cells against TGF beta, bFGF, their 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, were significantly higher than those of the controls. The results suggest that the increased synthesis of TGF beta, bFGF, their receptors and HSGAG may be related to the pathogenesis of drug-induced gingival hyperplasia.