Ivarsen Anders, Laurberg Tinne, Møller-Pedersen Torben
Department of Ophthalmology, Aarhus University Hospital, Denmark.
Invest Ophthalmol Vis Sci. 2004 Oct;45(10):3499-506. doi: 10.1167/iovs.04-0391.
To investigate whether an initial keratocyte loss intensifies central corneal wound repair after LASIK in rabbits.
New Zealand White rabbits received either conventional LASIK (-8 D, 6-mm diameter) or LASIK combined with a 7-mm diameter, epithelial denudation (LASIK-scrape). Animals were examined during 4 months by slit lamp and in vivo confocal microscopy to monitor changes in central corneal morphology, light backscattering (haze), and sublayer thickness. At various time points, corneas were processed for histology and stained for nuclei; F-actin; ED-A fibronectin; alpha-smooth muscle actin; TGF-beta1, -beta2, and -beta receptor II; and connective tissue growth factor (CTGF).
In vivo confocal microscopy identified no major acellular zones or changes in cell morphology or reflectivity after conventional LASIK. By contrast, a complete loss of keratocytes was observed in the anterior 77 +/- 25 microm stroma 1 week after LASIK-scrape. Highly reflective, migratory fibroblasts gradually repopulated the acellular zone, and by week 8, quiescent-appearing keratocytes were observed throughout the stroma. Correspondingly, stromal light backscattering peaked at 2 weeks after LASIK-scrape (2200 +/- 620 U) followed by a decline to approximately 60 U from week 8; comparable to the slightly increased reflectivity (approximately 50 U) observed after conventional LASIK (ns). Stromal thickness appeared stable 8 weeks after both LASIK and LASIK-scrape, after a regrowth of 13 +/- 3 and 20 +/- 11 microm, respectively (ns). In addition, both procedures induced a minor and comparable epithelial hyperplasia of 4 +/- 2 and 7 +/- 5 microm, respectively (ns). No myofibroblast transformation or TGF-beta growth factor expression was observed below the flap after either treatment.
LASIK-scrape induces an anterior keratocyte loss, leading to development of temporary haze during cell repopulation. However, 8 weeks after both LASIK and LASIK-scrape, only a slightly increased reflectivity is noted at the interface. Corneal thickness is stable by week 8, and stromal regrowth and epithelial hyperplasia are comparable after both treatments. Thus, an initial loss of stromal keratocytes does not appear to intensify corneal wound repair after LASIK.
研究兔准分子激光原位角膜磨镶术(LASIK)后初始角膜细胞丢失是否会加剧中央角膜伤口修复。
新西兰白兔接受传统LASIK(-8D,直径6mm)或LASIK联合直径7mm的上皮剥脱术(LASIK-刮除术)。在4个月内通过裂隙灯和体内共聚焦显微镜检查动物,以监测中央角膜形态、光背散射( haze)和亚层厚度的变化。在不同时间点,对角膜进行组织学处理并进行细胞核、F-肌动蛋白、ED-A纤连蛋白、α-平滑肌肌动蛋白、转化生长因子-β1、-β2和-β受体II以及结缔组织生长因子(CTGF)染色。
体内共聚焦显微镜检查显示,传统LASIK后未发现主要的无细胞区或细胞形态或反射率变化。相比之下,LASIK-刮除术后1周,在前部77±25μm基质中观察到角膜细胞完全丢失。高反射性的迁移性成纤维细胞逐渐重新填充无细胞区,到第8周时,在整个基质中观察到静止状态的角膜细胞。相应地,LASIK-刮除术后2周基质光背散射达到峰值(2200±620 U),随后从第8周开始下降至约60 U;与传统LASIK后观察到的反射率略有增加(约50 U)相当(无显著性差异)。LASIK和LASIK-刮除术后8周,基质厚度分别在再生13±3和20±11μm后保持稳定(无显著性差异)。此外,两种手术均分别诱导了轻微且相当的上皮增生,增生厚度分别为4±2和7±5μm(无显著性差异)。两种治疗后在瓣下均未观察到肌成纤维细胞转化或转化生长因子-β生长因子表达。
LASIK-刮除术导致前部角膜细胞丢失,在细胞重新填充期间导致暂时性 haze形成。然而,LASIK和LASIK-刮除术后8周,仅在界面处观察到反射率略有增加。到第8周时角膜厚度稳定,两种治疗后基质再生和上皮增生相当。因此,基质角膜细胞的初始丢失似乎不会加剧LASIK后的角膜伤口修复。