Al-Rawi M M, Edelstein D R, Erlandson R A
Department of Otolaryngology, Manhattan Eye, Ear and Throat Hospital, New York, New York 10021, USA.
Laryngoscope. 1998 Dec;108(12):1816-23. doi: 10.1097/00005537-199812000-00010.
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.
Thirty-two patients with severe chronic sinusitis were evaluated for ciliary and epithelial abnormalities.
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.
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.
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.
纤毛超微结构缺陷和黏液纤毛清除功能受损在呼吸系统疾病和鼻窦炎的发生发展中起重要作用。原发性纤毛运动障碍患者鼻窦上皮的纤毛超微结构变化已有文献记载。然而，继发于呼吸功能障碍和慢性鼻窦炎的继发性纤毛运动障碍和上皮细胞病理变化一直未得到充分认识。
对32例严重慢性鼻窦炎患者的纤毛和上皮异常进行评估。
14例（44%）为儿童，接受了全面的过敏、汗液和免疫检查。18例（56%）为成年人，患有严重难治性鼻窦炎且既往鼻窦手术失败。所有患者均接受中鼻甲鼻上皮活检，并通过光镜和透射电镜进行评估。
23例（72%）患者发现有纤毛细胞，9例（28%）无纤毛。仅19%的患者发现正常纤毛上皮灶，通常位于上皮内陷处。20例（87%）患者的纤毛数量不等（通常为少数）呈现超微结构缺陷，包括复合纤毛以及微管和动力蛋白臂缺陷。所有患者均表现出不同程度的分化上皮细胞丢失，从上皮剥脱到基底细胞增生，常伴有化生，继发于慢性鼻窦疾病。固有层常水肿，伴有毛细血管扩张、浆细胞、淋巴细胞和增生的浆液黏液腺。
本研究表明纤毛运动障碍主要是慢性鼻窦炎的结果而非原因。病因不明的慢性鼻窦炎患者表现出显著的分化上皮细胞丢失以及纤毛缺陷，其中大多数可能继发于慢性疾病过程。这些变化会减慢黏液纤毛清除速度，导致恶性循环，进而导致疾病慢性化。
