| Project/Area Number |
07807188
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
矯正・小児・社会系歯学
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| Research Institution | TOHOKU UNIVERSITY |
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Principal Investigator |
SAITO Keiichi TOHOKU UNIVERSITY SCHOOL OF DENTISTRY RESEARCH ASSISTANT, 歯科部, 助手 (00178477)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1996: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1995: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | GINGIVAL HYPERPLASIA / P53 PROTEIN / Ki-67 ANTIGEN / EGF RECEPTOR / IMMUNOHISTOCHEMISTRY / p53 / Ki-67 |
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| Research Abstract |
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.
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