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

OBJECTIVE

Defective ciliary ultrastructure and impaired mucociliary clearance play an important role in the development of respiratory disease and sinusitis. 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 been 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 METHODS

Fourteen patients (44%) were children who underwent full allergy, sweat, and immunologic workups. Eighteen patients (56%) were adults who had severe refractory sinusitis and had failed previous sinus surgery. All patients underwent nasal epithelium biopsies of the middle turbinate and evaluation by light and transmission electron microscopy.

RESULTS

Ciliated cells were 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 compound cilia and microtubule and dynein arm defects. All of the patients showed variable loss of differentiated epithelial cells ranging from denuded epithelium to basal cell hyperplasia often associated with squamous metaplasia, secondary to chronic sinonasal disease. The lamina propria was often edematous with dilated capillaries, plasma cells, lymphocytes, and hyperplastic seromucous glands.

CONCLUSIONS

This study demonstrates that ciliary dyskinesias are primarily the result rather than the cause of chronic sinusitis. 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 changes slow down mucociliary clearance and lead to a vicious cycle leading to chronicity.