Submitted: 18 Mar 2014
Accepted: 18 Mar 2014
ePublished: 18 Mar 2014
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J Iran Dent Assoc. 2014;26(2): 114-121.
  Abstract View: 24

Original

Correlation of Bcl-2 and COX-2 Expression in Oral Lichen Planus

Nasim Taghavi, Nazanin Mahdavi*, Maryam Shahla
*Corresponding Author: Email: mahdavinazanin@yahoo.com

Abstract

 Background and Aim : Lichen planus is a common immune-mediated disease that is associated with an increased risk of malignant transformation in the oral cavity. Synchronous up-regulation of COX-2 and down-regulation of Bcl-2 have been demonstrated in some malignancies. The aim of this study was to assess the correlation between COX-2 and Bcl-2 expression and their role in dysplastic changes of oral lichen planus (OLP ).
Materials and Methods : This study was performed on 47 paraffin blocks with the diagnosis of OLP and 16 blocks with the diagnosis of focal fibrous hyperplasia (control group). Immunohistochemical staining was performed using antibodies against COX-2 and Bcl-2. Spearman’s rank correlation coefficient and Mann-Whitney test were used for data analysis .

 Results : A significant correlation was observed between the intensity of sub-epithelial inflammation and the severity of basal cell layer degeneration (P=0.048). Significant up-regulation of Bcl-2 and COX-2 was detected in sub-epithelial inflammatory infiltration (P<0.001, P=0,003). The amount and intensity of Bcl-2 and COX-2 expression were significantly correlated in sub-epithelial lymphocytic infiltration (P=0.013, P=0.019 ).

 Conclusion : Our findings indicated the effective role of Bcl-2 expression in decreasing the apoptosis in the inflammator y infiltrate unlike the epithelium. The significant correlation of the intensity of Bcl-2 expression in the epithelium and the sub-epithelial inflammatory infiltrate with COX-2 expression and also the correlation of the intensity of inflammation with the severity of basal layer hydropic degeneration may imply that these two markers can induce malignant transformation in the affected epithelium in an indirect manner by the continuation of inflammation and activation of carcinogenic mechanisms .

  

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