Knop E, Knop N
Forschungslabor der Augenklinik, Charité - Universitätsmedizin Berlin, Campus Virchow Klinikum, Ziegelstrasse 5-9, 10117, Berlin, Deutschland.
Ophthalmologe. 2009 Nov;106(11):980-7. doi: 10.1007/s00347-009-2044-8.
Obstructive dysfunction of the meibomian glands (MGD) is surprisingly frequent in the general population and increases with age. Clinically, the focus is mainly on the consequences at the ocular surface in the sense of an evaporative dry eye syndrome. However, in addition, chronic obstruction of the meibomian glands also leads to degeneration of the secretory gland tissue which can result in a secondary hyposecretion even if the primary obstruction is later resolved by therapeutic approaches.Important influencing factors in the pathogenesis of obstructive MGDs and their interaction during the progression of the disease are systematically analyzed and displayed in a flow diagram. Age, hormonal disturbances and environmental influences, such as contact lenses, as well as qualitative alterations in the composition of the meibomian oil (meibum) lead to hyperkeratinization of the ductal epithelium and increased viscosity of the meibum which result, either alone or in combination, in obstruction of the duct and orifice. This leads to a lack of meibum on the lid margin and tear film with downstream hyperevaporative dry eye syndrome. At the same time, obstruction leads to a stasis of meibum inside the meibomian gland with increased pressure and resulting dilatation of the ducts and in atrophy of the acini with rarefaction of the secretory meibocytes and gland dropout. Stasis can also increase the growth of commensal bacteria, their production of oil degrading enzymes (lipases) and release of toxic mediators. These factors can, in return, act as self-enforcing feedback loops in the sense of vicious circles that aggravate the primary hyperkeratinization and compositional disturbance of meibum and can hence lead to a progressive MGD.
睑板腺阻塞性功能障碍(MGD)在普通人群中出奇地常见,且随年龄增长而增加。临床上,主要关注的是其在蒸发型干眼综合征意义上对眼表造成的后果。然而,除此之外,睑板腺的慢性阻塞还会导致分泌腺组织退化,即使原发性阻塞后来通过治疗方法得到解决,也可能导致继发性分泌不足。阻塞性MGD发病机制中的重要影响因素及其在疾病进展过程中的相互作用在流程图中得到了系统分析和展示。年龄、激素紊乱和环境影响,如隐形眼镜,以及睑板腺油脂(睑脂)成分的质性改变,会导致导管上皮过度角化和睑脂粘度增加,单独或共同导致导管和开口阻塞。这会导致睑缘和泪膜上睑脂缺乏,进而引发下游的高蒸发型干眼综合征。与此同时,阻塞会导致睑板腺内睑脂淤积,压力增加,导致导管扩张,腺泡萎缩,分泌性睑板细胞稀疏和腺体脱落。淤积还会增加共生细菌的生长、它们产生的油脂降解酶(脂肪酶)以及有毒介质的释放。这些因素反过来又会形成恶性循环中的自我强化反馈回路,加剧原发性睑脂过度角化和成分紊乱,从而导致MGD病情进展。