Esquenazi Salomon, Esquenazi Isi, Grunstein Lev, He Juicheng, Bazan Haydee
Department of Ophthalmology, LSU Eye and Neuroscience Center, Louisiana State University Health Sciences Center, New Orleans 70112, USA.
J Refract Surg. 2009 Aug;25(8):739-46. doi: 10.3928/1081597X-20090707-09.
To evaluate the healing response at the flap interface in corneas with LASIK ectasia that required penetrating keratoplasty (PK).
Corneas of five patients who developed corneal ectasia after LASIK (range: 2.5 to 5 years postoperative) were collected after corneal transplant surgery. The corneas were bisected and processed for conventional histologic analysis and immunofluorescence.
Light microscopy showed a hypocellular fibrotic scar at the wound margin compared with the adjacent corneal stroma in all eyes. All corneas had positive staining for alpha-smooth muscle actin (SMA), a myofibroblast marker. In one eye, alpha-SMA cells were located in the fibrotic scar region in the area of the semicircular ring of haze along the margin of the LASIK flap corresponding to an area of epithelial ingrowth. In all other eyes, alpha-SMA positive cells were fewer and mainly located in the superficial stroma under the epithelial wound margin surface. Type III collagen was minimal or absent in the central zone and wound margin of all corneas except for the cornea with epithelial ingrowth present in the hypercellular fibrotic scar region. Chondroitin sulfate was stronger in the periphery of the flap wound coinciding with a higher presence of alpha-SMA-positive cells in that region. Positive staining for matrix metalloproteinase 9 (MMP-9) in the paracentral wound margin scar was seen.
A wound-healing process characterized by absence of significant fibrosis and myofibroblasts at the wound edge in the flap interface was noted in all keratectatic eyes. However, changes in the composition of collagen and the presence of MMP-9 at the wound edge several years after LASIK indicates active wound remodeling that may explain the ongoing loss of tissue and tendency of the cornea to bulge.
评估接受穿透性角膜移植术（PK）的准分子激光原位角膜磨镶术（LASIK）后角膜扩张患者角膜瓣界面的愈合反应。
收集5例LASIK术后发生角膜扩张患者（术后2.5至5年）角膜移植术后的角膜。将角膜切成两半，进行常规组织学分析和免疫荧光检测。
光学显微镜检查显示，与所有患眼相邻的角膜基质相比，伤口边缘有细胞成分较少的纤维化瘢痕。所有角膜的α-平滑肌肌动蛋白（SMA，一种肌成纤维细胞标志物）染色均为阳性。在一只眼中，α-SMA细胞位于LASIK瓣边缘对应上皮内生区域的沿雾状半圆环区域的纤维化瘢痕区。在所有其他眼中，α-SMA阳性细胞较少，主要位于上皮伤口边缘表面下方的浅层基质中。除了在细胞成分较多的纤维化瘢痕区存在上皮内生的角膜外，所有角膜的中央区和伤口边缘III型胶原极少或不存在。硫酸软骨素在瓣伤口周边较强，与该区域较高的α-SMA阳性细胞存在一致。在旁中央伤口边缘瘢痕中可见基质金属蛋白酶9（MMP-9）阳性染色。
在所有角膜扩张患眼中均观察到伤口愈合过程，其特征为角膜瓣界面伤口边缘无明显纤维化和肌成纤维细胞。然而，LASIK术后数年伤口边缘胶原成分的变化和MMP-9的存在表明存在活跃的伤口重塑，这可能解释了持续的组织丢失和角膜膨隆的趋势。
