Advancements in understanding the malignant transformation pathways of oral submucous fibrosis: Implications for early detection and intervention

• OSMF Pathogenesis: Chronic inflammation, fibrosis, and epithelial dysplasia contribute to the development of OSMF, primarily associated with betel quid chewing. • Molecular Mechanisms: Dysregulated signaling pathways, including the TGF-β pathway, promote fibrosis and carcinogenesis in OSMF, with aberrant TGF-β signaling driving fibroblast activation and epithelial-mesenchymal transition (EMT). • Role of Inflammation: Inflammatory cytokines such as IL-6, TNF-α, and IL-1β mediate fibroblast activation and collagen synthesis, creating a microenvironment conducive to tumorigenesis in OSMF. • Biomarkers for Early Detection: MicroRNAs (miRNAs) and DNA methylation patterns serve as potential biomarkers for the early detection and risk stratification of malignant transformation in OSMF, offering non-invasive diagnostic tools for clinicians. • Therapeutic Strategies: Emerging therapeutic strategies target key molecular pathways implicated in OSMF pathogenesis, including the inhibition of TGF-β signaling and modulation of inflammatory mediators, offering potential avenues for disease modification and prevention of malignant transformation.