Department of Ophthalmology, Carl Gustav Carus University Hospital, Dresden, Germany.
Ocul Surf. 2013 Apr;11(2):93-108. doi: 10.1016/j.jtos.2013.01.003. Epub 2013 Jan 28.
Changes in the biomechanical properties of the human cornea play an important role in the pathogenesis of corneal ectatic diseases. A variety of conditions in primary acquired (keratoconus and pellucid marginal degeneration) or secondary induced (iatrogenic keratectasia after excimer refractive laser surgery) corneal ectatic disorders lead to reduced biomechanical resistance. Corneal collagen crosslinking (CXL) has emerged as a promising technique to slow or even to stop the progression of these corneal ectatic pathologies. In this procedure, riboflavin (vitamin B2) is administered in conjunction with ultraviolet A light (UVA, 365 nm). This interaction causes the formation of reactive oxygen species, leading to the formation of additional covalent bonds between collagen molecules, with consequent biomechanical stiffening of the cornea. Although this method is not yet accepted as an evidence-based medicine modality for the treatment of corneal primary or secondary ectasias, the results of prospective, randomized studies of CXL used in the treatment of these pathologic entities show significant changes in the properties of corneal tissue. This procedure is currently the only etiopathogenetic approach in ectatic eyes that can delay or stop the process of cornea destabilization, reducing the necessity for keratoplasty. Despite promising results, CXL is associated with issues that include long-term safety and duration of the stabilizing effect. Combination of CXL with vision-improving procedures, such as topography-guided custom ablation and implantation of intracorneal ring segments of phakic intraocular lenses, may expand the indications for this procedure.
人类角膜生物力学特性的变化在角膜扩张性疾病的发病机制中起着重要作用。原发性获得性(圆锥角膜和边缘性角膜营养不良)或继发性诱导性(准分子激光屈光手术后的医源性角膜扩张)角膜扩张性疾病的多种情况导致生物力学抵抗降低。角膜胶原交联(CXL)已成为一种有前途的技术,可以减缓甚至停止这些角膜扩张性病变的进展。在该程序中,同时给予核黄素(维生素 B2)和紫外线 A 光(UVA,365nm)。这种相互作用会导致活性氧的形成,导致胶原分子之间形成额外的共价键,从而导致角膜的生物力学变硬。尽管这种方法尚未被接受为治疗角膜原发性或继发性扩张的循证医学模式,但在这些病变实体的治疗中使用 CXL 的前瞻性、随机研究的结果显示出角膜组织特性的显著变化。该程序目前是唯一可以延迟或停止角膜不稳定过程的病因治疗方法,减少了角膜移植的必要性。尽管有令人鼓舞的结果,但 CXL 与长期安全性和稳定效果的持续时间等问题相关。CXL 与改善视力的程序相结合,如基于地形图的定制消融和植入有晶状体眼眼内环形段,可以扩大该程序的适应证。