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Collagenase-mediated tissue modeling of corneal ectasia and collagen cross-linking treatments

机译:胶原酶介导的角膜扩张的组织建模和胶原蛋白交联治疗

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PURPOSE. Corneal collagen cross-linking (CXL) is a method for modifying the natural history of keratoconus and other corneal ectatic diseases. The authors evaluated the use of collagenase for generating an experimental model of ectasia to evaluate the topographic effects of CXL interventions. METHODS. Nine human corneoscleral specimens unsuitable for transplantation were used. After epithelial debridement, mounting, and pressurization on an artificial anterior chamber, a solution of 10 mg/mL collagenase type II with 15% dextran was applied to five corneas for three hours. Three of these corneas subsequently underwent riboflavin/UV-A CXL. Scheimpflug-based tomography was performed before collagenase exposure, after collagenase exposure, and after CXL to evaluate changes in maximum axial curvature of the anterior surface (K max) at three IOP levels. Results were compared to four control eyes exposed to dextran alone. RESULTS. A statistically significant increase in K max was seen across all IOP levels in the collagenase group compared to the control group (+6.6 ± 1.1 diopters [D] and +0.3 ± 0.8 D, respectively, at physiological IOP). After CXL, K max decreased (+6 6 ± 2.0 D at physiological IOP). Anterior corneal aberrations increased after collagenase exposure and decreased after CXL. Light microscopy showed loss of normal stromal collagen architecture and localized edema after collagenase exposure. CONCLUSIONS. A method for generating topographic features of corneal ectasia in human tissue is demonstrated. No significant sensitivity of K max to IOP was observed. CXL caused regression of steepening and induced aberrations in this model, consistent with clinical trends. The model may be useful for testing modifications to standard CXL techniques.
机译:目的。角膜胶原蛋白交联(CXL)是一种改变圆锥角膜和其他角膜直肠疾病的自然病史的方法。作者评估了胶原酶在产生扩张性实验模型中的作用,以评估CXL干预措施的地形效应。方法。使用了九个不适合移植的人角膜巩膜标本。在上皮清创术,固定和在人工前房加压后,将具有15%葡聚糖的10 mg / mL II型胶原酶溶液施加到五个角膜上三个小时。这些角膜中的三个随后接受了核黄素/ UV-A CXL。在胶原酶暴露之前,胶原酶暴露之后和CXL之后进行基于Scheimpflug的层析成像,以评估三种IOP水平下前表面最大轴向曲率(K max)的变化。将结果与仅暴露于右旋糖酐的四只对照眼进行比较。结果。与对照组相比,胶原酶组所有IOP水平的K max均具有统计学上的显着提高(生理IOP分别为+6.6±1.1屈光度[D]和+0.3±0.8 D)。 CXL后,K max降低(在生理学IOP下为+6 6±2.0 D)。胶原酶暴露后,前角膜畸变增加,CXL后降低。光学显微镜显示,胶原酶暴露后,正常的基质胶原结构消失,局部水肿消失。结论。证明了一种在人体组织中产生角膜扩张的地形特征的方法。没有观察到K max对IOP的显着敏感性。 CXL导致该模型的变陡回归并引起像差,与临床趋势一致。该模型可用于测试对标准CXL技术的修改。

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