慢性角膜损伤与圆锥角膜发病机制研究进展

Analysis on pathogenesis of keratoconus with chronic corneal trauma

圆锥角膜是一种双眼进展的,非炎症性的角膜基质变薄的疾病,它以角膜锥形扩张及一系列角膜曲率改变为特征。与它发生相关的可疑因素包括遗传机制、家族相关、过敏性疾病及特异性疾病等,但是环境因素比如非正常性揉眼、角膜接触镜的配戴及紫外线的暴露等却往往易被忽视,虽然对于圆锥角膜的发生、发展普遍认为是一种多因素介导的多种病理过程共同作用的结果,但是这些慢性损伤可能在疾病的发生发展中起着关键性作用。即使现在对它的定义仍然是一种非炎症型的角膜扩张性营养不良性病变,但近年来越来越多的临床证据及实验结果表明圆锥角膜的发生是由于角膜表面长期持续存在的慢性损伤,导致角膜上皮细胞炎性因子过度释放及角膜基质金属蛋白酶的过度表达,从而使角膜基质的酶代谢失调和细胞凋亡程序的启动,最终导致角膜基质细胞的丢失,角膜抗张强度下降和角膜锥形扩张。在此,对目前已知的一些关于角膜慢性损伤与圆锥角膜关系的文章进行综述,并对其可能存在的因果关系进行阐述及讨论。

Keratoconus is a progressive, non- inflammatory corneal thinning disorder that produces a unique spectrum of change in the surface curvature of the cornea. The suspected factors associated with the cause of keratoconus include genetic mechanisms, familial associations,allergy,atopy and so on,but environmental factors,such as abnormal rubbing,contact lens wearing and ultraviolet radiation may be easily ignored. Although it is commonly thought that keratoconus is a result of various pathological progress mediated by multiple factors,those chronic trauma could play important roles in the pathological progress. The classic definition of keratoconus is still referred as a non- inflammation disorder with malnutrition of keratectasia,more and more clinical evidences and experimental results that may refute this concept. It may be due to the long- term persistent chronic trauma resulted from eye rubbing,contact lens or ultraviolet radiation. Under this conditions,the increased release of inflammatory mediators and matrix metalloproteinases may accelerate keratocyte apoposis and enzyme metabolism disorders, with the result of matrix cell lost, tensile strength decreased and keratectasia. Here, for some papers known about the relationship between chronic cornea trauma and keratoconus were reviewed and discussed its possible causal relationship.