Marino Gustavo K, Santhiago Marcony R, Torricelli Andre A M, Santhanam Abirami, Wilson Steven E
J Refract Surg. 2016 Feb;32(2):118-25. doi: 10.3928/1081597X-20160105-02.
To provide an overview of the recent advances concerning the corneal molecular and cellular biology processes involved in the wound healing response after excimer laser surface ablation and LASIK surgery.
Literature review.
The corneal wound healing response is a complex cascade of events that impacts the predictability and stability of keratorefractive surgical procedures such as photorefractive keratectomy and LASIK. The generation and persistence of corneal myofibroblasts (contractile cells with reduced transparency) arise from the interaction of cytokines and growth factors such as transforming growth factor beta and interleukin 1 produced by epithelial and stromal cells in response to the corneal injury. Myofibroblasts, and the opaque extracellular matrix they secrete into the stroma, disturb the precise distribution and spacing of collagen fibers related to corneal transparency and lead to the development of vision-limiting corneal opacity (haze). The intact epithelial basement membrane has a pivotal role as a structure that regulates corneal epithelial-stromal interactions. Thus, defective regeneration of the epithelial basement membrane after surgery, trauma, or infection leads to the development of stromal haze. The apoptotic process following laser stromal ablation, which is proportional to the level of attempted correction, leads to an early decrease in anterior keratocyte density and the diminished contribution of these non-epithelial cells of components such as perlecan and nidogen-2 required for normal regeneration of the epithelial basement membrane. Haze persists until late repair of the defective epithelial basement membrane.
Defective regeneration of the epithelial basement membrane has a critical role in determining whether a cornea heals with late haze after photorefractive keratectomy or with scarring at the flap edge in LASIK.
概述准分子激光表面切削术和准分子原位角膜磨镶术（LASIK）术后角膜伤口愈合反应中涉及的分子和细胞生物学过程的最新进展。
文献综述。
角膜伤口愈合反应是一系列复杂的事件，会影响屈光性角膜手术（如准分子激光角膜切削术和LASIK）的可预测性和稳定性。角膜肌成纤维细胞（具有降低透明度的收缩细胞）的产生和持续存在源于细胞因子和生长因子（如上皮细胞和基质细胞在角膜损伤后产生的转化生长因子β和白细胞介素1）之间的相互作用。肌成纤维细胞以及它们分泌到基质中的不透明细胞外基质会干扰与角膜透明度相关的胶原纤维的精确分布和间距，并导致限制视力的角膜混浊（ haze）的形成。完整的上皮基底膜作为调节角膜上皮-基质相互作用的结构起着关键作用。因此，手术、创伤或感染后上皮基底膜的再生缺陷会导致基质 haze的形成。激光基质消融后的凋亡过程与预期矫正水平成正比，导致前角膜细胞密度早期降低，以及这些非上皮细胞对正常上皮基底膜再生所需的诸如基底膜聚糖和巢蛋白-2等成分的贡献减少。haze会持续到有缺陷的上皮基底膜的晚期修复。
上皮基底膜的再生缺陷在决定角膜在准分子激光角膜切削术后是否会出现晚期 haze或在LASIK中是否会在瓣边缘形成瘢痕方面起着关键作用。
