Interplay of epigenetics and epistasis drives oral submucous fibrosis

Abstract Persistent injury to oral mucosa due to habitual quid chewing, resulting in the upregulation of inflammatory cytokines and consequential myofibroblastic persistence, emphasizes the role of epigenetic aberration in the pathogenesis of oral submucous fibrosis (OSF). However, there is a dearth...

Full description

Saved in:
Bibliographic Details
Main Authors: Mohit Sharma, Smitha Sammith Shetty, Faisal Alhedyan, Raghu Radhakrishnan
Format: Article
Language:English
Published: Springer 2025-08-01
Series:Discover Applied Sciences
Subjects:
Online Access:https://doi.org/10.1007/s42452-025-07571-4
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1849234621491838976
author Mohit Sharma
Smitha Sammith Shetty
Faisal Alhedyan
Raghu Radhakrishnan
author_facet Mohit Sharma
Smitha Sammith Shetty
Faisal Alhedyan
Raghu Radhakrishnan
author_sort Mohit Sharma
collection DOAJ
description Abstract Persistent injury to oral mucosa due to habitual quid chewing, resulting in the upregulation of inflammatory cytokines and consequential myofibroblastic persistence, emphasizes the role of epigenetic aberration in the pathogenesis of oral submucous fibrosis (OSF). However, there is a dearth of research on the role epistasis plays in the pathophysiology of OSF. Among the important epistatic interactions in the pathophysiology of OSF are those between Phosphatase and Tensin Homologue (PTEN) and Insulin-Like Growth Factor 1, Transforming Growth Factor-β (TGF-β), Cyclooxygenases, and lipoxygenases (LOX). Additionally, PTEN and Nuclear Factor Kappa B (NF-κB) have an epistatic relationship that is particularly mediated by the p65 subunit of NF-κB. Given the importance of epigenetic modification in the pathogenesis of OSF, the potential use of DNA methyltransferase and Histone deacetylase inhibitors as a therapeutic option holds promise. Another in vivo epigenetic therapeutic option for treating OSF is using stimulatory microRNAs against antifibrotic genes and inhibitory microRNAs against profibrotic genes. This review aims to connect numerous epigenetic and epistatic components to the mechanism of OSF. A better understanding of the disease process may provide OSF management with newer therapeutic options. Graphical Abstract
format Article
id doaj-art-68d1f145c9e34bd2ae739da28da2c5d8
institution Kabale University
issn 3004-9261
language English
publishDate 2025-08-01
publisher Springer
record_format Article
series Discover Applied Sciences
spelling doaj-art-68d1f145c9e34bd2ae739da28da2c5d82025-08-20T04:03:06ZengSpringerDiscover Applied Sciences3004-92612025-08-017812310.1007/s42452-025-07571-4Interplay of epigenetics and epistasis drives oral submucous fibrosisMohit Sharma0Smitha Sammith Shetty1Faisal Alhedyan2Raghu Radhakrishnan3Department of Oral Pathology and Microbiology, Faculty of Dental Sciences, SGT UniversityDepartment of Oral and Maxillofacial Pathology and Oral Microbiology, Manipal College of Dental Sciences, Manipal Academy of Higher EducationDepartment of Oral and Maxillofacial Surgery and Diagnostic Sciences, College of Dentistry, Prince Sattam Bin Abdulaziz UniversityDepartment of Oral and Maxillofacial Pathology and Oral Microbiology, Manipal College of Dental Sciences, Manipal Academy of Higher EducationAbstract Persistent injury to oral mucosa due to habitual quid chewing, resulting in the upregulation of inflammatory cytokines and consequential myofibroblastic persistence, emphasizes the role of epigenetic aberration in the pathogenesis of oral submucous fibrosis (OSF). However, there is a dearth of research on the role epistasis plays in the pathophysiology of OSF. Among the important epistatic interactions in the pathophysiology of OSF are those between Phosphatase and Tensin Homologue (PTEN) and Insulin-Like Growth Factor 1, Transforming Growth Factor-β (TGF-β), Cyclooxygenases, and lipoxygenases (LOX). Additionally, PTEN and Nuclear Factor Kappa B (NF-κB) have an epistatic relationship that is particularly mediated by the p65 subunit of NF-κB. Given the importance of epigenetic modification in the pathogenesis of OSF, the potential use of DNA methyltransferase and Histone deacetylase inhibitors as a therapeutic option holds promise. Another in vivo epigenetic therapeutic option for treating OSF is using stimulatory microRNAs against antifibrotic genes and inhibitory microRNAs against profibrotic genes. This review aims to connect numerous epigenetic and epistatic components to the mechanism of OSF. A better understanding of the disease process may provide OSF management with newer therapeutic options. Graphical Abstracthttps://doi.org/10.1007/s42452-025-07571-4Oral submucous fibrosisEpigenomicsEpistasisDNA methyltransferasesHistone deacetylase inhibitors
spellingShingle Mohit Sharma
Smitha Sammith Shetty
Faisal Alhedyan
Raghu Radhakrishnan
Interplay of epigenetics and epistasis drives oral submucous fibrosis
Discover Applied Sciences
Oral submucous fibrosis
Epigenomics
Epistasis
DNA methyltransferases
Histone deacetylase inhibitors
title Interplay of epigenetics and epistasis drives oral submucous fibrosis
title_full Interplay of epigenetics and epistasis drives oral submucous fibrosis
title_fullStr Interplay of epigenetics and epistasis drives oral submucous fibrosis
title_full_unstemmed Interplay of epigenetics and epistasis drives oral submucous fibrosis
title_short Interplay of epigenetics and epistasis drives oral submucous fibrosis
title_sort interplay of epigenetics and epistasis drives oral submucous fibrosis
topic Oral submucous fibrosis
Epigenomics
Epistasis
DNA methyltransferases
Histone deacetylase inhibitors
url https://doi.org/10.1007/s42452-025-07571-4
work_keys_str_mv AT mohitsharma interplayofepigeneticsandepistasisdrivesoralsubmucousfibrosis
AT smithasammithshetty interplayofepigeneticsandepistasisdrivesoralsubmucousfibrosis
AT faisalalhedyan interplayofepigeneticsandepistasisdrivesoralsubmucousfibrosis
AT raghuradhakrishnan interplayofepigeneticsandepistasisdrivesoralsubmucousfibrosis