本文基于横观各向同性理论建立关节软骨固液耦合双相三维缺损及修复的有限元模型。本文通过研究邻近修复界面的宿主软骨的应力状态判别其变形类型，探讨致软骨修复界面开裂的原因。研究表明，表层缺损修复时，邻近修复界面的宿主软骨表面节点发生压缩变形；中间层、深层或全层缺损修复时，节点发生拉伸变形，此时软骨径向尺寸增加，修复界面易开裂。若采用全层缺损修复，组织工程化软骨（TEC）的弹性模量较低（0.1 MPa、0.3 MPa）时，邻近修复界面的宿主软骨表层和中间层主要发生拉伸变形；TEC 的弹性模量较高（0.6 MPa、0.9 MPa）时，宿主软骨各层均发生压缩变形。因此，全层缺损修复时，可适当增大 TEC 的弹性模量。本文为评估软骨组织工程修复效果提供了新的思路，或对临床有一定的指导意义。
Based on transversely isotropic theory, a finite element model for three-dimensional solid-liquid coupling defect repair of articular cartilage was established. By studying stress state of host cartilage near the restoration interface, we identified deformation type of cartilage and discussed the cause of restoration interface cracking. The results showed that the host cartilage surface node near the restoration interface underwent compression deformation in the condition of surface layer defect repair. When the middle layer, deep layer or full-thickness defect were repaired, the node underwent tensile deformation. At this point, the radial dimension of cartilage increased, which might cause restoration interface cracking. If elastic modulus of the tissue engineered cartilage (TEC) was lower (0.1 MPa, 0.3 MPa), the host cartilage surface layer and middle layer mainly underwent tensile deformation. While elastic modulus of TEC was higher (0.6 MPa, 0.9 MPa), each layer of host cartilage underwent compression deformation. Therefore, the elastic modulus of TEC could be increased properly for full-thickness defect repair. This article provided a new idea for evaluating the effect of cartilage tissue engineering repair, and has a certain guiding significance for clinical practice.