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Background <p>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.</p> Materials &amp; methods <p>This cross-sectional study analyzed pharyngeal mucosal cells from LPR patients and healthy controls to assess oxidative DNA damage and EMT markers.</p> Results <p>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.</p> Conclusion <p>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.</p>

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

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月23日

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  • Gowtham Sai Ambati,
  • Joy A Ghoshal,
  • Vinoth Kumar Kalidoss,
  • P K Sankaran,
  • Senthil Murugan,
  • Kishore Sesham,
  • Satvinder Singh Bakshi,
  • Yuvaraj Maria Francis,
  • Meivelu Moovendhan

摘要

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.