ABSTRACT
Chronic rhinosinusitis (CRS) can be divided into two mutually exclusive histological subtypes based on the presence of polyps or glandular hypertrophy (1). In CRS with nasal polyps the full thickness and organs of normal nasal mucosa are replaced with an edematous, generally eosinophilic, epithelium-coated “bag” of interstitial matrix “ground substance.” In contrast, the histological findings in CRS without nasal polyps include glandular hypertrophy and a mononuclear and potentially neutrophilic inflammatory pattern that accounts for the thickening of the mucosa in this CRS subset. The pathophysiological processes involved in glandular hypertrophy and nasal polyposis are contrasted in order to highlight the distinct mechanisms that lead to these contrasting phenotypes (1-7).
