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| ORIGINAL RESEARCH |
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| Year : 2020 |
Volume
: 31 | Issue : 2 | Page
: 277-281 |
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PECAM-1 overexpression signifies aggressive biologic behavior of oral lichen planus – A pilot study
A Lavanya, Wafa Khan, Preeti Singh, Dominic Augustine, Roopa S Rao, SV Sowmya, Vanishri C Haragannavar, K Shwetha Nambiar
Department of Oral Pathology and Microbiology, Faculty of Dental Sciences, M S Ramaiah University of Applied Sciences, M S R Nagar, Bangalore, Karnataka, India
Correspondence Address:
Dr. A Lavanya
Department of Oral Pathology and Microbiology, Faculty of Dental Sciences, M S Ramaiah University of Applied Sciences, M S R Nagar, Bangalore . 560 054, Karnataka
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/ijdr.IJDR_653_18
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Context: The etiopathogenesis of oral lichen planus (OLP) is still debatable. According to literature, many studies have illustrated OLP as a T-cell-mediated chronic autoimmune disease. Currently, there is increased evidence of chronic inflammation in OLP and its association with vascular adhesion molecules (VAMs). Aim: The aim of this study was to evaluate the expression of VAM (PECAM-1) in OLP. Setting and Design: Tissue samples involved 20 archival cases of histopathologically confirmed OLP (n = 15) and normal mucosa (n = 5) as controls. Materials and Methods: The sections were subjected to immunohistochemical analysis using antibody to PECAM-1. Brown staining of the endothelial cells of blood vessels was considered positive. The expression of PECAM-1 in OLP was statistically analyzed using Wilcoxon sign-rank test. Results: The expression of PECAM-1 in OLP was statistically significant when compared with normal mucosa (P < 0.05). A statistically significant difference was also observed in PECAM-1 expression between the reticular type and erosive type of OLP. Conclusion: PECAM-1 was found to be overexpressed in OLP; difference in PECAM-1 expression was noted between the reticular and erosive types. The VAMs could be exploited as a possible therapeutic target in OLP to modulate the disease process thereby reducing the dependency on corticosteroids.
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