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Expression of p53 Protein and Ki‐67 Antigen in Gingival Hyperplasia Induced by Nifedipine and Phenytoin
Author(s) -
Saito Keiichi,
Mori Shiro,
Tanda Naoko,
Sakamoto Seizaburo
Publication year - 1999
Publication title -
journal of periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.036
H-Index - 156
eISSN - 1943-3670
pISSN - 0022-3492
DOI - 10.1902/jop.1999.70.6.581
Subject(s) - hyperplasia , carcinogenesis , pathogenesis , antigen , pathology , immunohistochemistry , phenytoin , nifedipine , lamina propria , chemistry , medicine , cancer , epithelium , immunology , calcium , epilepsy , psychiatry
Background: Although it has been thought that drug‐induced gingival hyperplasia is not related to tumorigenesis, recent case reports have shown that squamous cell carcinomas may arise in gingival hyperplasia induced by cyclosporin and phenytoin. The possible implications between the pathogenesis of this disease and tumorigenesis have not been elucidated and remain to be studied. Methods: We immunohistochemically examined the expression of tumor‐related markers such as p 53 protein and Ki‐67 antigen in 11 hyperplastic gingival tissues induced by nifedipine and phenytoin, as well as 5 control tissues using an avidin‐biotin‐peroxidase complex method. Results: Two specimens out of 4 nifedipine‐induced and 4 out of 7 phenytoin‐induced hyperplastic gingival tissues revealed the expression of p 53 protein in the nuclei of epithelial cells, while no expression of p 53 protein was observed in the epithelia of the 5 non‐hyperplastic control tissues. The immunoreactions against p 53 protein showed sporadic distribution in the suprabasal layers of hyperplastic epithelia. The mean percentage of epithelial cells expressing Ki‐67 antigen in the hyperplastic gingival tissues was more than 10% higher than that in the controls. The expression of Ki‐67 antigen was suppressed in the typical rete pegs deeply elongated into lamina propria of hyperplastic gingival tissues. Intense immunostaining of Ki‐67 antigen was found in fibroblasts of hyperplastic gingival tissues, while that of the control tissues was negligible. Conclusions: The expression of p 53 protein in gingival hyperplasia suggests that the pathogenesis of this disease is involved with impaired DNA, while the growth arrest observed in the hyperplastic epithelia with typically elongated rete pegs as expressed with Ki‐67 antigen may prevent the invasive expansion of epithelial cells undergoing DNA damage within gingival tissues and may consequently suppress tumorigenic progression. J Periodontol 1999;70:581‐586.