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Updated: Sep 10, 2025
Investigating the Three-dimensional Flow Separation Induced by a Model Vocal Fold Polyp
Published on: February 3, 2014
The Role of Environmental and Molecular Factors in the Development of Vocal Cord Polyps: A Scoping Review
Alicja Florczak1, Nicole Witoś1, Natalia Tomala1
1Clinical and Dissecting Anatomy Students' Scientific Club, Medical Faculty, Wroclaw Medical University, Wroclaw, Poland.
Background:
Vocal cord polyps are among the most common benign lesions of the vocal folds, and they can significantly impact quality of life. A comprehensive understanding of factors contributing to vocal cord polyps' formation could serve as a foundation for developing novel prevention, diagnosis, and treatment approaches.
Objective:
We aimed to summarize the available literature describing vocal cord polyps. We described the influence of gastroesophageal reflux and the presence of Helicobacter pylori (HP) on the development of vocal cord polyps as one of the better-described factors that may participate in the pathogenesis of these benign lesions. We also analyzed the overexpression of genes in vocal cord polyps (eg, KRT5, KRT19) and factors such as apolipoproteins, fibroblasts, periostin, and metalloproteinases (MMPs).
Study Design:
Online databases (Scopus, Embase, EBSCOhost, PubMed, and Web of Science) were searched, from which we selected 24 publications.
Results:
Vocal cord polyps are more prevalent in patients with laryngopharyngeal reflux, characterized by elevated pepsin levels in polyps' tissues. The role of HP requires further investigation. Smoking seems to accelerate degenerative changes in polyps. Overexpression of epithelial genes, extracellular matrix remodeling, and increased accumulation of proteoglycans and hyaluronic acid in the extracellular matrix indicate ongoing repair processes in polyps. Lower serum levels of apolipoproteins A-I (ApoA-I) were associated with increased polyp growth. Conversely, reduced APOM levels were linked to laryngeal carcinoma. Fibroblasts from polyps' tissues exhibit heightened immune response, driving chronic inflammation. Periostin and D-β-aspartic acid were highly expressed in polyps, potentially contributing to circulatory disturbances and edema. MMPs, COX-2, and ADAM-33 were implicated in matrix remodeling, angiogenesis, and polyp growth, while Hypoxia inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) expression suggest a role in hypoxia-induced polyp formation.
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