Changes in nasal epithelium in patients with severe chronic sinusitis: A clinicopathologic and electron microscopic study

Objective: Defective ciliary ultrastructure and impaired mucociliary cleara nce play an important role in the development of respiratory disease and si nusitis, Changes in the ciliary ultrastructure of the sinonasal epithelium have been documented in patients with primary ciliary dyskinesia. However, secondary ciliary dyskinesias and epithelial cytopathologic changes have be en underappreciated as a consequence of respiratory dysfunction and chronic sinusitis. Study Design: Thirty-two patients with severe chronic sinusitis were evaluated for ciliary and epithelial abnormalities. Materials and Met hods: Fourteen patients (44%) were children who underwent full allergy, swe at, and immunologic workups, Eighteen patients (56%) were adults who had se vere refractory sinusitis and had failed previous sinus surgery. All patien ts underwent nasal epithelium biopsies of the middle turbinate and evaluati on by light and transmission electron microscopy. Results: Ciliated cells w ere found in 23 patients (72%) with 9 patients (28%) having no cilia, Foci of normal ciliated epithelium were found in only 19% of the patients, often in epithelial invaginations. Variable numbers (usually a minor population) of cilia in 20 cases (87%) exhibited ultrastructural defects including com pound cilia and microtubule and dynein arm defects. All of the patients sho wed variable loss of differentiated epithelial cells ranging from denuded e pithelium to basal cell, hyperplasia often associated with squamous metapla sia, secondary to chronic sinonasal disease. The lamina propria was often e dematous with dilated capillaries, plasma cells, lymphocytes, and hyperplas tic seromucous glands, Conclusions: This study demonstrates that ciliary dy skinesias are primarily the result rather than the cause of chronic sinusit is. Patients with chronic sinusitis of uncertain origin exhibit a prominent loss of differentiated epithelial cells, as well as ciliary defects, most of which are likely to be secondary to the chronic disease process. These c hanges slow down mucociliary clearance and lead to a vicious cycle leading to chronicity.