ABSTRACT
We have determined that chronic rhinosinusitis (CRS) can be divided into two mutually exclusive histological subtypes based on the presence of polyps or glandular hypertrophy (1). CRS with nasal polyps (CRSwNP) destroy the full thickness and organs of normal nasal mucosa and replace it with an edematous, generally eosinophilic, epithelium-coated ‘‘bag’’ of interstitial matrix ‘‘ground substance.’’ This macromolecular content has not been fully characterized. The other histological finding has been designated ‘‘hyperplastic rhinosinusitis’’ or CRS without nasal polyps (CRSsNP). We have demonstrated that glandular hypertrophy is responsible for the thickening of the mucosa in this syndrome (1-4). The typical mucosal structures of subbasement membrane superficial vasculature, submucosal glands, nerves, and deep venous sinusoids are maintained. However, there is a transition away from the usual mixed leukocytic infiltrate found in normal inferior turbinates with an expansion of the mucosal area containing submucosal serous and mucous cells. Examination of patterns of mRNA (5,6) and protein (7,8) expression has begun to accelerate our understanding of potential mechanisms that may explain these two distinct pathological processes. This histopathological distinction is clinically important because CRS is truly a chronic disorder that persists for over 20 years of follow-up despite current surgical and topical glucocorticoid treatment (9). Different treatments may be required for each phenotype. In the early stages of CRS, there may be discriminate complaints of idiopathic rhinitis, other forms of nonallergic rhinitis (NAR), CRSwNP (small polyps or limited to very early middle turbinate changes), and CRS with mucosal thickening due to glandular hypertrophy. The clinical diagnosis of ‘‘turbinate hypertrophy’’ may represent one aspect of this overlapping spectrum of illnesses.
