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POSSIBILITY OF CARCINOGENESIS IN DRUG-INDUCED GINGIVAL HYPERPLASIA

药物引起的牙龈增生有致癌的可能性

基本信息

批准号：
07807188
负责人：
SAITO Keiichi
金额：
$ 1.34万
依托单位：
TOHOKU UNIVERSITY
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1995
资助国家：
日本
起止时间：
1995 至 1996
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-07807188/
关键词：
GINGIVAL HYPERPLASIA P53 PROTEIN Ki-67 ANTIGEN EGF RECEPTOR IMMUNOHISTOCHEMISTRY p53 Ki-67

项目摘要

The growth factors such as transforming growth factor beta (TGF beta) and basic fibroblast growth factor (bFGF) have been shown to be implicated in the processes of carcinogenesis. We have previously reported that TGF beta, bFGF and their receptors might be related to the pathogenesis of drug-induced gingival hyperplasia. In the present study, we examined immunohistochemically the expression of carcinoma-related markers such as p53 protein, Ki-67 antigen and epidermal growth factor erceptor (EGF-R) in the epithelia of 11 hyperplastic gingival tissues induced by nifedipine and phenytoin as well as 5 control tissues. Two specimens out of 4 nifedipine-induced and 4 out of 7 phenytoin-induced hyperplastic tissues revealed the expression of p53 protein in the nuclei of epithelial cells, while no expression of p53 protein was observed in the epithelia of the 5 non-hyperplastic control tissues. The immunoreactions against p53 protein showed sporadic distribution in the suprabasal layrs of hyperplastic gingival epithelium and was comparable to those in non-neoplastic epithelium adjacent to oral carcinoma indicated in the literatures.The mean percentage of epithelial cells experssing Ki-67 antigen in the hyperplastic gingival tissues was also more than 10% higher than that in the controls. The findings were comparable to those of oral dysplastic epithelia studies. The expression of Ki-67 antigen was suppressed in the rete pegs of hyperplastic gingival tissues. On the other hand, the expression of EGF-R in the hyperplastic gingival tissues was as low as the controls.Although gingival hyperplasia is generally thought to be a non-neoplastic disease and fails to show dysplastic epithelia, our results indicate the possibility that drug-induced gingival hyperplasia may be implcated in the initial changes of carcinogenesis.

生长因子如转化生长因子β（TGF β）和碱性成纤维细胞生长因子（bFGF）已被证明与致癌过程有关。我们以前曾报道TGF β、bFGF及其受体可能与药物性牙龈增生的发病机制有关。本研究采用免疫组化方法检测了11例硝苯地平和苯妥英钠诱导的牙龈增生组织及5例正常牙龈组织上皮中癌相关标志物p53蛋白、Ki-67抗原和表皮生长因子受体（EGF-R）的表达。在4例硝苯地平诱导的增生组织和7例苯妥英钠诱导的增生组织中，有2例上皮细胞核中有p53蛋白表达，而在5例非增生对照组织的上皮细胞中未见p53蛋白表达。p53蛋白在增生牙龈上皮的基底上层呈散在分布，与文献报道的癌旁非肿瘤性上皮相似，增生牙龈组织中Ki-67抗原阳性上皮细胞的平均百分比也比对照组高10%以上。这些结果与口腔异型增生上皮研究的结果相当。Ki-67抗原在增生牙龈组织中的表达受到抑制。虽然牙龈增生通常被认为是一种非肿瘤性疾病，并且不能显示上皮发育不良，但我们的研究结果表明，药物诱导的牙龈增生可能参与了癌变的初始变化。