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An Official Publication of the Indian Association of Oral and Maxillofacial Pathologists

ORIGINAL ARTICLE Table of Contents   
Year : 2021  |  Volume : 25  |  Issue : 3  |  Page : 430-436
Role of programmed cell death 4 in myofibroblast differentiation in oral submucous fibrosis

1 Department of Oral Pathology and Microbiology, KLE VK Institute of Dental Sciences, KLE University, Belagavi, Karnataka, India
2 Department of Oral Pathology and Microbiology, Bharati Vidyapeeth University, Dental College and Hospital, Sangli, Maharashtra, India
3 Department of Oral Biology and Biomedical Engineering, School of Dental Medicine, Engineering and Applied Sciences, University at Buffalo, Buffalo, NY, USA

Correspondence Address:
Karishma Madhusudan Desai
KLE VK Institute of Dental Sciences, KLE University, JNMC Campus, Nehru Nagar, Belagavi - 590 010, Karnataka
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jomfp.jomfp_86_21

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Background: Fibrosis is an uncontrolled healing process, led by persistent differentiation of fibroblast to alpha-smooth muscle actin (αSMA) positive activated fibroblast or myofibroblast. Oral submucous fibrosis (OSMF) is one such condition that is associated with areca nut use. Recently, Programmed Cell Death 4 (PDCD4), a pro-apoptotic marker, has been shown to modulate fibroblast differentiation in various organ fibrosis. The present study aimed to evaluate the role of PDCD4 in the regulation of fibroblast differentiation in OSMF. Materials and Methods: Paraffin-embedded tissue sections from 45 cases of the normal oral mucosa, early OSMF and advanced OSMF were examined for PDCD4 and αSMA expression by immunostaining. Co-expression of PDCD4 and αSMA in fibroblasts was examined using Spearman's correlation test. Results: The stromal fibroblasts showed minimal expression of αSMA in the normal mucosa and early OSMF, while advanced OSMF groups demonstrated a higher frequency of αSMA myofibroblasts. The PDCD4 expression was noted in the normal stromal fibroblasts. However, this expression appeared to progressively reduce with an increasing grade of OSMF. Thus, a negative correlation was noted between stromal PDCD4 and αSMA expression with progressive OSMF. Conclusion: This study demonstrated a putative role for PDCD4 in oral fibrosis consistent with its role in other tissues. The lack of PDCD4 expression with increasing myofibroblast expression in OSMF suggests that targeting its dysregulation may be an attractive translational therapeutic target.

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Journal of Oral and Maxillofacial Pathology | Published by Wolters Kluwer - Medknow
Online since 15th Aug, 2007