Oxidative DNA damage and epithelial mesenchymal transition in laryngopharyngeal reflux disease as a pathway to early tumorigenesis

Background Chronic exposure of the upper aerodigestive tract to refluxed gastric contents in laryngopharyngeal reflux (LPR) is associated with mucosal inflammation, oxidative stress, and epithelial-mesenchymal transition (EMT), potentially contributing to early tumorigenesis. Materials & methods This cross-sectional study analyzed pharyngeal mucosal cells from LPR patients and healthy controls to assess oxidative DNA damage and EMT markers. Results Immunohistochemical staining for E-cadherin, N-cadherin, and 8-hydroxy-2-deoxyguanosine (8-OHdG) revealed a significant increase in oxidative DNA damage in LPR patients, correlating with disease severity. While E-cadherin expression remained unchanged, N-cadherin levels were moderately elevated, indicating a shift towards a mesenchymal phenotype. The presence of micro nucleated cells was significantly higher in LPR patients, suggesting genomic instability. The observed cadherin switch, coupled with oxidative stress, supports a mechanistic link between chronic inflammation and mucosal remodeling. Conclusion This study highlights the role of oxidative DNA damage in driving EMT-related tissue changes, emphasizing the need for early intervention to mitigate long-term consequences. Future research should explore targeted therapies, including oxidative stress modulators and (Matrix metalloproteinase) MMP-7 inhibitors, to prevent LPR-associated malignant transformation.