Abstract

The histopathological assessment of Oral Lichen Planus (OLP) and oral lichenoid lesions is relatively subjective. The distinguishing criteria established by WHO effectively reproducible when all selection criteria were fulfilling but sometimes fail to provide a reliable diagnosis. The aim of the present study was to evaluate mast cell counts and their distribution among OLP and lichenoid lesions. The density and localization of mast cells was examined in 22 patients with a diagnosis of OLP (11 patients) or oral lichenoid reactions (11 patients) by c-kit/CD117 immunohistochemical and toluidine blue histochemical staining. Data were analyzed using either the Kruskal-Wallis or Mann-Whitney U tests. No significant difference in the total number of mast cells was observed between the two groups (P = 0.599); however, a significant difference was observed in mast cell counts between reticular and junctional zones (P<0.05). The findings of the present study suggest that mast cells play a key role in the pathogenesis of oral inflammation; however, the ability of mast cell measurements to reliably differentiate between lichen planus and other lichenoid mimickers was limited as the number of mast cells was found to be increased in both the conditions.

Highlights

  • Oral lichenoid tissue reaction, known as an interface mucositis, is an inflammatory disorder characterized by dense subepithelial lympho-histiocytic infiltrates, increased numbers of intra-epithelial lymphocytes and degeneration of basal keratinocytes (Sugerman et al, 2002; Sugerman and Savage, 2002)

  • The precise mechanism underlying the initiation of inflammatory destruction remains unknown, it is believed that Oral Lichen Planus (OLP) represents a cell-mediated immunological reaction to antigenic alterations of keratinocytes

  • The expression of a self-peptide by keratinocytes has been posited as an early event leading to the development of two hypotheses regarding the initiation of basal keratinocyte apoptosis: The “chance encounter” hypothesis, i.e., the epithelium and specific CD8 T cells encounter each other by chance during routine surveillance; and the “directed migration” hypothesis, i.e., attraction of lymphocytes to the epithelium by keratinocyte-derived chemokines (Sugerman et al, 2002; Zhou et al, 2002)

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Summary

Introduction

Known as an interface mucositis, is an inflammatory disorder characterized by dense subepithelial lympho-histiocytic infiltrates, increased numbers of intra-epithelial lymphocytes and degeneration of basal keratinocytes (Sugerman et al, 2002; Sugerman and Savage, 2002) This disorder has a unique histopathological presentation, it comprises a wide range of lesions with different managements and etiopathogenesis similar to its skin counterpart and the most recognized type of lesion is lichen planus, a T cell-mediated immunopathological response to antigenic alterations in keratinocytes of the skin and mucosal tissues (Sugerman et al, 2002; Sugerman and Savage, 2002; Roopashree et al, 2010; Srinivas et al, 2011). The expression of a self-peptide by keratinocytes has been posited as an early event leading to the development of two hypotheses regarding the initiation of basal keratinocyte apoptosis: The “chance encounter” hypothesis, i.e., the epithelium and specific CD8 T cells encounter each other by chance during routine surveillance; and the “directed migration” hypothesis, i.e., attraction of lymphocytes to the epithelium by keratinocyte-derived chemokines (Sugerman et al, 2002; Zhou et al, 2002)

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