Pathophysiology
Clinical meaning
Acute rhinosinusitis begins with viral infection of the sinonasal epithelium (rhinovirus, influenza, parainfluenza most common). Viral replication damages ciliated respiratory epithelium, impairing mucociliary clearance - the primary defense mechanism that moves mucus toward the ostia at 1 cm/min. Mucosal edema obstructs the ostiomeatal complex (the narrow drainage pathway between the ethmoid infundibulum, middle meatus, and maxillary/frontal/anterior ethmoid sinuses), creating a closed space with oxygen absorption, pH changes, and mucus stasis. This environment promotes secondary bacterial superinfection in 0.5-2% of viral URI cases. The most common bacterial pathogens are Streptococcus pneumoniae (30-40%), Haemophilus influenzae (20-35%), and Moraxella catarrhalis (15-20%). Bacterial biofilm formation on sinus mucosa contributes to chronic rhinosinusitis by creating antibiotic-resistant bacterial communities encased in extracellular polysaccharide matrix. Chronic rhinosinusitis (>12 weeks) involves persistent inflammation with tissue remodeling: subepithelial fibrosis, basement membrane thickening, goblet cell hyperplasia, and nasal polyp formation (eosinophilic polyposis driven by Th2 cytokines IL-4, IL-5, IL-13 - similar to asthma pathophysiology).