Role of p53-mediated apoptotic pathway in oral lichen planus: Relationship among pro-apoptotic, anti-apoptotic, and keratinocytic markers

The aim of the study is to investigate the relationship between oral lichen planus (OLP) pathogenesis, apoptosis and keratinocyte markers. The study employed 98 subjects. In the epithelial portion of OLP biopsies expression of pro-apoptotic molecules, i.e. caspase-3, Bax, p53 and p63, or anti-apopto...

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Published inJournal of Oral and Maxillofacial Surgery, Medicine, and Pathology Vol. 26; no. 2; pp. 221 - 227
Main Authors Calenic, Bogdan, Okamura, Kazuhiko, Yaegaki, Ken, Tovaru, Serban, Tanaka, Tomoko, Imai, Toshio
Format Journal Article
LanguageEnglish
Japanese
Published Elsevier Ltd 01.04.2014
Elsevier BV
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ISSN2212-5558
2212-5566
DOI10.1016/j.ajoms.2013.06.009

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Summary:The aim of the study is to investigate the relationship between oral lichen planus (OLP) pathogenesis, apoptosis and keratinocyte markers. The study employed 98 subjects. In the epithelial portion of OLP biopsies expression of pro-apoptotic molecules, i.e. caspase-3, Bax, p53 and p63, or anti-apoptotic factor such as Bcl-2, involucrin as a keratinocyte-maturation marker and p63 as a keratinocyte stem cell marker were determined immunohistochemically. Anti-apoptotic Bcl-2 expression showed no change. p53 expression rate among examined cells was significantly higher in the OLP group than in control group. p53 expression was significantly correlated with expression of p63 in total OLP group: the both were increased considerably after onset of more than a year. Bax expression was significantly higher in total OLP group. On the other hand, caspoase-3 expression was significantly lower in the total OLP group than in the control group, especially in subjects who were evaluated less than a year after onset. Although pro-apoptotic factors are active, and anti-apoptotic factor is also active, the above results indicate that OLP might be resistant to p53-mediated caspase-3 dependent apoptosis, specially at less than a year following onset.
ISSN:2212-5558
2212-5566
DOI:10.1016/j.ajoms.2013.06.009