GENOMICS IN ORAL SUBMUCOUS FIBROSIS: A SCOPING REVIEW

Abstract

Background: Oral submucous fibrosis (OSMF) is a chronic, progressive, potentially malignant oral disorder strongly associated with areca-nut exposure. Although exposure-related mechanisms are well recognised, genetic and epigenetic variation may help explain differences in susceptibility, fibrosis severity, and malignant potential. Objective: To map the available evidence on genomic and molecular mechanisms implicated in OSMF, with emphasis on genetic susceptibility, extracellular-matrix regulation, epigenetic alterations, non-coding RNAs, and progression toward oral squamous cell carcinoma. Methods: This review is organised using a scoping-review framework. Relevant literature domains include genetic association studies, gene-expression investigations, epigenomic studies, non-coding-RNA research, and reviews of OSMF pathogenesis. PubMed/MEDLINE, Scopus, Web of Science, and Embase are proposed as the principal databases, with Google Scholar and reference list screening as supplementary methods. The final manuscript should report the actual search dates, record counts, and study-selection figures after the searches are run and documented. Results: Published evidence implicates variants in xenobiotic-metabolism, antioxidant-defence, inflammatory, DNA-repair, and matrix-remodelling pathways. Epigenomic studies have identified DNA-methylation changes, while microRNA research suggests altered regulation of fibrosis-associated genes and signalling pathways. However, studies vary in population, sample size, methods, and outcome definitions, and many findings have not been independently replicated. Conclusion: Genomic research offers a useful framework for understanding inter-individual differences in OSMF, but current evidence is not sufficiently standardised for routine genetic risk prediction. Larger, well-characterised, multi-ethnic longitudinal studies integrating exposure history, genomic data, transcriptomics, epigenomics, and clinical outcomes are needed.