Oral Submucous Fibrosis Pathogenesis and Management

Oral submucous fibrosis is a chronic, progressive condition of the oral cavity and oropharynx characterised by excessive collagen deposition and stiffening of the mucosa. Predominantly linked to habitual betel quid chewing, it manifests with burning sensations, ulceration and progressive trismus, and carries a significant risk of malignant transformation. Pathogenesis begins with epithelial injury induced by alkaloids and polyphenols in areca nut, leading to chronic inflammation and release of profibrotic mediators such as transforming growth factor-β. Activated fibroblasts differentiate into contractile myofibroblasts, depositing dense extracellular matrix and altering tissue architecture. Additional factors, including oxidative stress, immune cell crosstalk and epigenetic modifications, further drive fibrogenesis. Management encompasses primary prevention through cessation of areca nut exposure, nutritional support and close surveillance for dysplasia. Symptomatic relief is offered by intralesional corticosteroids, hyaluronidase and antioxidants, while physiotherapy and device-assisted mouth opening maintain function. Emerging strategies include targeted molecular inhibitors of profibrotic pathways and cell-based therapies utilising dental pulp stem cells to restore immune homeostasis and promote remodelling. Surgical intervention remains reserved for advanced cases with refractory trismus or dysplastic change. Despite advances, standardised treatment guidelines and high-quality clinical trials are needed to translate mechanistic insights into routine care.

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Oral Submucous Fibrosis Pathogenesis and Management publication trend

The graph below shows the total number of articles in oral submucous fibrosis pathogenesis and management across all publications each year (not limited to Nature Index journals).

Technical terms

Fibrosis: The formation of excess fibrous connective tissue in an organ or tissue as a reparative response to injury.

Extracellular matrix: A complex network of proteins and polysaccharides secreted by cells that provides structural support and regulates cell behaviour.

Myofibroblast: A specialised cell with contractile properties that differentiates from fibroblasts during wound healing and fibrotic processes.

Epithelial–mesenchymal transition: A biological process in which epithelial cells acquire mesenchymal characteristics, enhancing motility and extracellular matrix production.

Transforming growth factor-β: A multifunctional cytokine that regulates cell proliferation, differentiation and the production of extracellular matrix.

Betel quid: A chewing mixture typically containing areca nut, betel leaf, slaked lime and sometimes tobacco, implicated in oral submucous fibrosis.

Dental pulp stem cell: A mesenchymal stem cell population derived from the dental pulp that exhibits anti-inflammatory and regenerative capabilities.

PI3K/Akt pathway: A signalling cascade involving phosphatidylinositol 3-kinase and protein kinase B that regulates cell survival, proliferation and metabolism.

Vascular endothelial growth factor: A signal protein that stimulates the formation of new blood vessels and modulates vascular permeability.

References

1. DPSCs regulate epithelial-T cell interactions in oral submucous fibrosis. Stem Cell Research & Therapy (2024).
2. Expression and correlation of the Pi3k/Akt pathway and VEGF in oral submucous fibrosis. Cell Proliferation (2023).
3. Malignant Transformation Rate of Oral Submucous Fibrosis: A Systematic Review and Meta-Analysis. Journal of Clinical Medicine (2022).
4. Oral submucous fibrosis: a contemporary narrative review with a proposed inter-professional approach for an early diagnosis and clinical management. Journal of Otolaryngology (2020).