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硝苯地平和苯妥英钠所致牙龈增生中转化生长因子β、碱性成纤维细胞生长因子及硫酸乙酰肝素糖胺聚糖的免疫组化定位

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

作者信息

Saito K, Mori S, Iwakura M, Sakamoto S

机构信息

Department of Preventive Dentistry, School of Dentistry, Tohoku University, Sendai, Japan.

出版信息

J Periodontal Res. 1996 Nov;31(8):545-55. doi: 10.1111/j.1600-0765.1996.tb00519.x.

DOI:10.1111/j.1600-0765.1996.tb00519.x
PMID:8971653
Abstract

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.

摘要

尽管药物性牙龈增生已得到广泛研究,但迄今为止,这种疾病的发病机制尚未阐明。转化生长因子β(TGF-β)和碱性成纤维细胞生长因子(bFGF)已被证明与多种纤维化和增生性疾病有关。硫酸乙酰肝素蛋白聚糖(HSPG)由硫酸乙酰肝素糖胺聚糖(HSGAG)组成,也已被证明通过增强bFGF的功能在组织过度生长的发病机制中起重要作用。然而,这些生长因子在牙龈增生中的可能作用尚未得到研究。对4例硝苯地平诱导的和5例苯妥英诱导的增生性牙龈组织以及5例非增生性对照牙龈组织进行了TGF-β、bFGF、它们的受体和HSGAG的免疫组织化学定位研究,以阐明这种疾病的发病机制。在增生性牙龈组织的固有层中观察到针对TGF-β、bFGF、这两种生长因子的受体和HSGAG的显著免疫染色,而在对照中观察到的免疫染色较少。在增生性牙龈组织的每个10个单位的固有层一平方单位(0.1×0.1毫米)中,针对TGF-β、bFGF及其受体的免疫染色细胞的平均数显著高于对照。结果表明,TGF-β、bFGF、它们的受体和HSGAG合成增加可能与药物性牙龈增生的发病机制有关。

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Immunohistochemical localization of transforming growth factor beta, basic fibroblast growth factor and heparan sulphate glycosaminoglycan in gingival hyperplasia induced by nifedipine and phenytoin.硝苯地平和苯妥英钠所致牙龈增生中转化生长因子β、碱性成纤维细胞生长因子及硫酸乙酰肝素糖胺聚糖的免疫组化定位
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