McBrien Neville A, Gentle Alex
Department of Optometry and Vision Sciences, The University of Melbourne, Victoria 3010, Australia.
Prog Retin Eye Res. 2003 May;22(3):307-38. doi: 10.1016/s1350-9462(02)00063-0.
Myopia is one of the most prevalent ocular conditions and is the result of a mismatch between the power of the eye and axial length of the eye. As a result images of distant objects are brought to a focus in front of the retina resulting in blurred vision. In the vast majority of cases the structural cause of myopia is an excessive axial length of the eye, or more specifically the vitreous chamber depth. In about 2% of the general population, the degree of myopia is above 6 dioptres (D) and is termed high myopia. The prevalence of sight-threatening ocular pathology is markedly increased in eyes with high degrees of myopia ( > -6 D). This results from the excessive axial elongation of the eye which, by necessity, must involve the outer coat of the eye, the sclera. Consequently, high myopia is reported as a leading cause of registered blindness and partial sight. Current theories of refractive development acknowledge the pivotal role of the sclera in the control of eye size and the development of myopia. This review considers the major biochemical mechanisms that underlie the normal development of the mammalian sclera and how the scleral structure influences the rate of eye growth during development. The review will characterise the aberrant mechanisms of scleral remodelling which underlie the development of myopia. In describing these mechanisms we highlight how certain critical events in both the early and later stages of myopia development lead to scleral thinning, the loss of scleral tissue, the weakening of the scleral mechanical properties and, ultimately, to the development of posterior staphyloma. This review aims to build on existing models to illustrate that the prevention of aberrant scleral remodelling must be the goal of any long-term therapy for the amelioration of the permanent vision loss associated with high myopia.
近视是最常见的眼部疾病之一，是眼球屈光力与眼轴长度不匹配的结果。因此，远处物体的图像聚焦在视网膜前方，导致视力模糊。在绝大多数情况下，近视的结构原因是眼轴过长，或者更具体地说是玻璃体腔深度过长。在普通人群中，约2%的人近视度数高于6屈光度（D），称为高度近视。高度近视（>-6D）患者发生威胁视力的眼部病变的患病率显著增加。这是由于眼球过度的轴向伸长必然涉及眼球的外层——巩膜。因此，高度近视被认为是登记失明和视力部分丧失的主要原因。目前的屈光发育理论承认巩膜在控制眼球大小和近视发展中的关键作用。本综述探讨了哺乳动物巩膜正常发育的主要生化机制，以及巩膜结构如何影响发育过程中眼球的生长速度。该综述将描述近视发展过程中巩膜重塑的异常机制。在描述这些机制时，我们强调近视发展早期和后期的某些关键事件如何导致巩膜变薄、巩膜组织丧失、巩膜机械性能减弱，最终导致后巩膜葡萄肿的形成。本综述旨在在现有模型的基础上进行拓展，以说明预防异常的巩膜重塑必须成为任何旨在改善与高度近视相关的永久性视力丧失的长期治疗的目标。
