Stromal wound healing explains refractive instability and haze development after photorefractive keratectomy - A 1-year confocal microscopic study
Stromal wound healing explains refractive instability and haze development after photorefractive keratectomy - A 1-year confocal microscopic study
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DOI：
10.1016/s0161-6420(00)00142-1
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发表时间：
2000-07-01
期刊：
影响因子：
13.7
通讯作者：
Jester, JV
中科院分区：
文献类型：
--
作者：
Moller-Pedersen, T;Cavanagh, HD;Jester, JV
目的：评估屈光性角膜切除术 (PRK) 后产生屈光不稳定和角膜混浊的机制。设计：前瞻性、非随机、比较病例系列、自我对照。参与者：包括 17 名低至中度近视患者（-2.88 至 -9.13 屈光度 [D]）的 17 只眼睛。方法：手术干预是采用标准化、直径 6 毫米的 PRK 手术。 Meditec MEL 60 准分子激光器（Aesculap-Meditec，Heroldsberg，德国）。在手术前以及 PRK 后 1、3、6、9 和 12 个月时，使用快速、连续的共焦图像 Z 扫描（称为聚焦共焦显微镜 (CMTF)）对光消融中心进行评估。 主要结果指标：通过 CMTF 扫描的数字图像分析获得上皮和基质厚度的同步分析以及角膜光后向散射的客观评估。在高分辨率体内共焦图像上评估角膜神经支配、前基质角膜细胞密度和伤口愈合形态特征。测量明显屈光度并通过裂隙灯生物显微镜对角膜清晰度进行分级。结果：PRK后1个月时上皮厚度平均为45+/-10μm，3个月时为50+/-8fun，12个月时为52+/-6μm，而术前为51+/-4μm，表明完全恢复了术前厚度，没有代偿性增生。有趣的是，上皮再增厚与屈光退化没有显着相关性。相比之下，基质再生（从 1-12 个月）平均为 6 +/- 12 μm（范围，27 μm 变薄 - 22 μm 再增厚），并且与平均 0.84 +/- 1.23 D 的屈光变化密切相关（r = 0.84，P < 0.001），范围从 -1.63 D（远视偏移）到 +3.38 D （近视回归）。基质再增厚与实际光消融深度成比例增加（r = 0.63，P < 0.01）；线性回归分析表明整个研究组的平均再生率为每年 8%。随着时间的推移，基质再增厚与 CMTF 混浊的发展无关，这表明混浊和消退是由两种独立的伤口愈合机制引起的。与这些发现一致的是，所有“模糊”角膜均显示前基质伤口愈合角膜细胞数量增加，细胞核和细胞体的反射率均增加，这表明与细胞外基质沉积相反，基于细胞的反射是 PRK 后角膜光散射增加的主要根源。 结论：综上所述，这些数据表明，角膜细胞介导的光消融基质再生似乎是接受治疗的人类近视退化的主要原因直径为 6 毫米的 PRK，而远视移位似乎是基质变薄的直接结果。相比之下，角膜上皮似乎恢复了术前的厚度，而对 PRK 后的屈光变化没有显着影响。最后，这项研究还提供了强有力的证据，表明 PRK 后混浊的形成与大量伤口愈合角膜细胞的细胞反射率增加直接相关。 (C) 2000 年由美国眼科学会颁发。
Purpose: To evaluate the mechanism(s) producing refractive instability and corneal haze development after photorefractive keratectomy (PRK).Design: Prospective, nonrandomized, comparative case series, self-controlled.Participants: Seventeen eyes of 17 patients with low- to moderate-grade myopia (-2.88 to -9.13 diopters [D]) were included.Methods: Surgical intervention was a standardized, 6-mm diameter PRK procedure using the Meditec MEL 60 excimer laser (Aesculap-Meditec, Heroldsberg, Germany). The photoablation center was evaluated before surgery and at 1, 3, 6, 9, and 12 months after PRK using rapid, continuous z-scans of confocal images, termed confocal microscopy through focusing (CMTF).Main Outcome Measures: Simultaneous epithelial and stromal thickness analysis and objective assessment of corneal light backscattering were obtained from digital image analysis of the CMTF scans. Corneal reinnervation and anterior stromal keratocyte density and wound healing morphologic features were evaluated on high resolution, in vivo confocal images. Manifest refraction was measured and corneal clarity was graded by slit-lamp biomicroscopy.Results: Epithelial thickness averaged 45 +/- 10 mu m at 1 month, 50 +/- 8 fun at 3 months, and 52 +/- 6 mu m at 12 months after PRK, as compared with 51 +/- 4 mu m before surgery, demonstrating complete restoration of the preoperative thickness without compensatory hyperplasia. interestingly, epithelial rethickening had no significant correlation with refractive regression. By contrast, stromal regrowth (from 1-12 months) averaged 6 +/- 12 mu m (range, 27 mu m thinning-22 mu m rethickening) and correlated closely (r = 0.84, P < 0.001) with changes in refraction that averaged 0.84 +/- 1.23 D, ranging from -1.63 D (hyperopic shift) to +3.38 D (myopic regression). Stromal rethickening increased proportionally with the actual photoablation depth (r = 0.63, P < 0.01); linear regression analysis suggested an average regrowth rate of 8% per year for the entire study group. Stromal rethickening was not associated with CMTF haze development over time, suggesting that haze and regression were caused by two independent wound healing mechanisms. In agreement with these findings, all "hazy" comeas showed increased numbers of anterior stromal wound healing keratocytes with increased reflectivity of both nuclei and cell bodies, suggesting that cellular-based reflections, as opposed to extracellular matrix deposition, ave the major origin of increased corneal light scattering after PRK.Conclusions: Taken together, these data indicate that keratocyte-mediated regrowth of the photoablated stroma appears to be the main cause of myopic regression in humans treated with a 6-mm diameter PRK, whereas hyperopic shifts appear to be a direct consequence of stromal thinning. By contrast, the corneal epithelium appeared to restore its preoperative thickness without contributing significantly to the refractive changes after PRK. Finally, this study also provides strong evidence that the development of haze after PRK is directly associated with increased cellular reflectivity from high numbers of wound healing keratocytes. (C) 2000 by the American Academy of Ophthalmology.