In this work, a hyperelastic model accounting for cross-linking and microstructural damage is proposed for corneal stroma, where the strengthening mechanisms of the matrix materials, collagen fibers and cross-links, as well as the softening behaviors induced by the damage of collagen fibers and cross-links are systematically addressed. In order to quantitatively characterize the stiffening behavior related to riboflavin/ultraviolet A (UVA)-induced collagen cross-linking, a novel microstructure-based model is proposed that the strain energy function is specified as a function of the density and orientation of cross-links. When addressing the stress softening behavior with respect to the damage of fibers and cross-links, two individual damage variables in an exponential form are considered in the strain energy function as inspired by the pseudo-elastic model. In order to verify the accuracy and rationality of the developed model, uniaxial tensile results of corneal lenticule strips until materials failure are compared between the experimental data and theoretical results at different UVA irradiation doses, and a good agreement is achieved for both the calibrated and predicted results. The unveiled stiffening and damage mechanisms could help assess the clinically relevant issues for corneal stroma, especially from a biomechanical point of view.

在这项工作中，提出了一种解释角膜基质交联和微观结构损伤的超弹性模型，其中基质材料、胶原纤维和交联的强化机制，以及胶原纤维损伤引起的软化行为。并系统地解决了交叉链接问题。为了定量表征与核黄素/紫外线 A (UVA) 诱导的胶原交联相关的硬化行为，提出了一种新的基于微结构的模型，该模型将应变能函数指定为交联的密度和方向的函数。链接。在解决与纤维和交联损坏有关的应力软化行为时，在拟弹性模型的启发下，应变能函数中考虑了指数形式的两个单独的损伤变量。为了验证所建​​立模型的准确性和合理性，将不同UVA照射剂量下的实验数据与理论结果进行了比较，比较了角膜微透镜条的单轴拉伸结果，直到材料失效，校准结果与预测结果吻合良好。结果。揭示的硬化和损伤机制可以帮助评估角膜基质的临床相关问题，特别是从生物力学的角度来看。比较了不同UVA照射剂量下的实验数据和理论结果，比较了角膜微透镜条直到材料失效的单轴拉伸结果，校准结果和预测结果都达到了很好的一致性。揭示的硬化和损伤机制可以帮助评估角膜基质的临床相关问题，特别是从生物力学的角度来看。比较了不同UVA照射剂量下的实验数据和理论结果，比较了直到材料失效的角膜微透镜条的单轴拉伸结果，校准结果和预测结果都达到了很好的一致性。揭示的硬化和损伤机制可以帮助评估角膜基质的临床相关问题，特别是从生物力学的角度来看。