Role of delayed cellular apoptosis in the pathogenesis of nasal polyps

Abstract

Rationale Epithelial proliferation and differentiation have been implicated in the pathogenesis of nasal polyposis, but the underlying mechanisms remain unknown. Though polyps are reported to contain inflammatory cells which could play important roles, development of nasal polyposis is likely to involve several other factors. The role of epithelial cells is still uncertain. We hypothesized that delayed cellular apoptosis has a major role in the pathogenesis of nasal polyps. Methods The study group comprised polyps removed endoscopically from 20 consecutive patients. Ethmoid mucosa from 4 patients who underwent orbital decompression for Graves' opthalmopathy was used as controls. Human subjects committee approved the study. Apoptosis in fixed polyp or tissue sections was assessed by labeling free 3'-hydroxyl groups of DNA using a Trevigen terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling (TUNEL) peroxidase assay kit and counterstaining with hematoxylin. TUNEL-positive cells were counted within the epithelial layer of these tissue sections and were normalized to the length of the basement membrane. Data were expressed as the mean ± SEM. Differences were considered significant at a P value of less than .05. Results Overall, polyps contained significantly fewer apoptotic cells compared to controls (5.2 ± 4.4% vs 22.7 ± 5.6%; p<0.001). Among the study group, there were however no significant differences in the percentage of apoptotic cells between polyps obtained from patients with or without Samster's triad (6.3 ± 5.4% vs 4.3 ± 4.6%, p=0.5), and allergic fungal sinusitis (6.5 ± 2.8% vs 4.3 ± 4.6%, p=0.4). Conclusions Delayed cellular apoptosis is involved in the pathogenesis of nasal polyps irrespective of etiology.