Abstract

Mast cells (MCs) expressing serine proteases; tryptase and chymase, are associated with fibrosis in various diseases. However, little is known about their involvement in oral submucous fibrosis (OSF). Our goal was to evaluate the role of MC tryptase and chymase in the pathogenesis of OSF and its malignant transformation. Immunohistochemical expression of MC tryptase and chymase was evaluated in 20 cases of OSF, 10 cases of oral squamous cell carcinoma (OSCC) and 10 cases of healthy controls. Subepithelial zone of Stage 1 and 2 while deep zone of Stage 3 and 4 OSF demonstrated increased tryptase positive MCs. OSCC revealed a proportionate increase in tryptase and chymase positive MCs irrespective of areas of distribution. An altered balance in the subepithelial and deep distribution of tryptase and chymase positive MCs play an important role in the pathogenesis of OSF and its malignant transformation.

Highlights

  • Oral submucous fibrosis (OSF) is a chronic progressive, areca nut chewing habit related, precancerous condition of the oral mucosa predominantly affecting Indians and South Asians

  • Mast cells (MCs) activation is a characteristic feature of chronic inflammation that may lead to fibrosis as a result of increased collagen synthesis by fibroblasts [37]

  • To the best of our knowledge this is the first study to emphasize the possible role of MC tryptase and chymase in OSF and its malignant transformation

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Summary

Introduction

Oral submucous fibrosis (OSF) is a chronic progressive, areca nut chewing habit related, precancerous condition of the oral mucosa predominantly affecting Indians and South Asians. It is clinically characterized by burning sensation of the oral mucosa accompanied by pallor and progressive, irreversible fibrosis leading to difficulty in opening mouth, speech and swallowing [1]. Characteristic histopathologic features of this disease include epithelial atrophy with loss of rete ridges, reduced vascularity, chronic inflammatory infiltrate and hyalinization of the submucosal tissue. The pathogenic mechanism in OSF begins primarily in the connective tissue and epithelial response secondarily. The characteristic fibro-elastic changes observed in the connective tissue are almost entirely due to abnormal accumulation of collagen. OSF is regarded as a collagen related disorder induced by betel nut/betel quid chewing habit often resulting in an overall increased production of collagen with decreased collagen degradation [2]

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