Meibomian gland dysfunction: hyperkeratinization or atrophy?
Meibomian gland dysfunction: hyperkeratinization or atrophy?
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DOI：
10.1186/s12886-015-0132-x
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发表时间：
2015-12-17
影响因子：
2
通讯作者：
Brown DJ
中科院分区：
文献类型：
--
作者：
Jester JV;Parfitt GJ;Brown DJ
睑板腺功能障碍（MGD）是蒸发性干眼病（EDED）的主要原因，并且功能障碍被广泛认为在机械上涉及导管过度角化、堵塞和阻塞。这篇综述重新评估角化过度在MGD中的作用，基于最近的研究结果，从小鼠模型。在这些研究中，通过免疫荧光断层扫描和三维重建评价正常年轻和老年小鼠或暴露于干燥应激的小鼠的眼睑，以评价腺体体积、过度角化标记物的表达和细胞增殖，或通过受激拉曼散射（SRS）显微镜评价脂质质量。结果表明，衰老小鼠表现出睑板腺脱落，腺体体积减少，粘膜皮肤连接向前迁移到腺体口;与人类受试者中检测到的年龄相关变化相似。萎缩性腺体也显示出上皮堵塞口的证据，而不存在角化过度。暴露于干燥应激的小鼠表现出睑板腺过度增生和导管扩张，表明脂质合成显着增加。在EDED小鼠中，脂质质量也受到影响，腺体导管内脂质的蛋白质含量增加。总体而言，小鼠的年龄相关变化显示出与临床MGD中观察到的相似的结构和功能相关性，而没有过度角化的证据，表明腺体萎缩可能是EDED的主要原因。睑板腺对干燥胁迫的反应也表明环境条件可能加速或加强与年龄相关的变化。
Meibomian gland dysfunction (MGD) is the major cause of evaporative dry eye disease (EDED) and dysfunction is widely thought to mechanistically involve ductal hyperkeratinization, plugging and obstruction. This review re-evaluates the role of hyperkeratinization in MGD based on more recent findings from mouse models. In these studies, eyelids from normal young and old mice or mice exposed to desiccating stress were evaluated by immunofluorescent tomography and 3-dimensional reconstruction to evaluate gland volume, expression of hyperkeratinization markers and cell proliferation or stimulated Raman scattering (SRS) microscopy to assess lipid quality. Results indicate that aging mice show dropout of meibomian glands with loss of gland volume and a forward migration of the mucocutaneous junction anterior to the gland orifice; similar age-related changes that are detected in human subjects. Atrophic glands also showed evidence of epithelial plugging of the orifice without the presence of hyperkeratinization. Mice exposed to desiccating stress showed hyperproliferation of the meibomian gland and ductal dilation suggesting a marked increase in lipid synthesis. Lipid quality was also affected in EDED mice with an increase in the protein content of lipid within the duct of the gland. Overall, age-related changes in the mouse show similar structural and functional correlates with that observed in clinical MGD without evidence of hyperkeratinization suggesting that gland atrophy may be a major cause of EDED. The response of the meibomian gland to desiccating stress also suggest that environmental conditions may accelerate or potentiate age-related changes.