A Quantitative Assessment of Laryngeal Polyp Morphology Using Stereological Techniques
Kamyar Iravani1, Saeid Karbalay-Doust1, Mahsan Nadgaran1
1Shiraz University of Medical Sciences, Zand ave, Shiraz City, Fars Province, Iran.
Background:
The underlying histopathological drivers of vocal fold polyp formation remain incompletely characterized, with quantitative stereological data being scarce. While factors like phonotrauma and inflammation are implicated, the precise structural alterations in epithelium, stroma, and vasculature are poorly quantified. This study aimed to provide an unbiased, stereological quantification of these key tissue components to clarify the pathogenesis of this common lesion.
Methods:
In a case-control study, five polyp and five normal vocal fold tissue samples were analyzed. Using unbiased stereological methods on H&E-stained sections, volume densities of the epithelium, lamina propria, collagen bundles, and blood vessels were calculated via point counting. The numerical density of fibroblasts within the lamina propria was estimated using the optical disector. Statistical comparisons were performed using the Mann-Whitney U test.
Results:
Significant structural remodeling was observed in polyp tissues. Volume densities increased substantially in the epithelium (70%), lamina propria (66%), collagen bundles (66%), and blood vessels (55%) compared to controls (all P < 0.05). The numerical density of fibroblasts also showed a significant 24% increase (P < 0.03). However, no statistically significant difference was found in the density of neutrophils or lymphocytes between the groups.
Conclusion:
This stereological study quantifies profound structural remodeling in vocal fold polyps, driven by fibrovascular proliferation. Key findings include significant expansion of the epithelium, lamina propria, collagen, and vasculature. Notably, this occurs without increased inflammatory cell infiltration. This dissociation suggests polypogenesis may be primarily fueled by dysregulated fibroproliferative and angiogenic pathways rather than active inflammation, highlighting stromal remodeling as central to the disease and pointing toward potential antifibrotic/antiangiogenic therapies.
