Impact of Ostiomeatal Complex Anatomical Variants on Histological Remodeling and Radiological Severity: A Retrospective Cross-Sectional Study.

Background The anatomical integrity of the ostiomeatal complex (OMC) is critical in the pathophysiology of chronic rhinosinusitis (CRS). While individual structural deformities are known to impede sinus drainage, the cumulative "dose-response" impact of concurrent OMC variants on microscopic mucosal remodeling remains under-investigated. Objective To quantitatively map the correlation between specific OMC anatomical variants - nasal septal deviation (NSD), concha bullosa (CB), and agger nasi (AN) cells - and the severity of histological tissue remodeling and radiological opacification. Methods This retrospective cross-sectional study evaluated archived medical, radiological, and histopathological records of 80 adult patients (January 2024 to February 2026). The cohort comprised an experimental group (n=60) with CT-confirmed OMC variants and a normal control group (n=20). To isolate anatomical effects, patients with a history of severe atopy or heavy smoking were excluded. Data extracted included the Lund-Mackay score, subepithelial basement membrane (SBM) thickness, eosinophil count/high-power field (HPF), and goblet cell density/HPF. Statistical evaluation utilized one-way analysis of variance (ANOVA) to determine the dose-response effect of single versus multiple anatomical variants. Results All individual OMC variants significantly exacerbated pathological markers compared to controls (p<0.001). A highly significant linear dose-response relationship (p for trend <0.001) demonstrated that mucosal degradation worsened with increasing structural complexity. In the triple variant group (n=24), where NSD, CB, and AN coexisted, radiological and histopathological severity peaked significantly compared to controls (n=20): the Lund-Mackay score advanced to 14.6 ± 2.5 (vs. 3.6 ± 1.1), SBM thickness increased to 15.3 ± 1.8 μm (vs. 10.1 ± 1.0 μm), mucosal eosinophil influx escalated to 9.8 ± 2.2 cells/HPF (vs. 2.4 ± 0.8 cells/HPF), and goblet cell density expanded to 34.2 ± 5.0 cells/HPF (vs. 21.3 ± 3.4 cells/HPF). Transitioning from a single variant (n=19) to the full triad significantly accelerated tissue fibrosis and inflammatory infiltration (p<0.01). Conclusions Anatomical complexity within the OMC acts as a direct, cumulative driver of chronic sinus pathology and severe mucosal remodeling. The linear escalation of tissue degradation highlights the clinical necessity of early surgical or medical intervention in patients presenting with multiple concurrent variants to prevent irreversible structural damage.