Kelly D J, Prendergast P J
Centre for Bioengineering, Department of Mechanical Engineering, Trinity College, Dublin, Ireland.
J Biomech. 2005 Jul;38(7):1413-22. doi: 10.1016/j.jbiomech.2004.06.026. Epub 2004 Oct 2.
Cartilage defects that penetrate the subchondral bone can undergo spontaneous repair through the formation of a fibrous or cartilaginous tissue mediated primarily by mesenchymal stem cells from the bone marrow. This tissue is biomechanically inferior to normal articular cartilage, and is often observed to degrade over time. Whether or not biomechanical factors control the type and quality of the repair tissue, and its subsequent degradation, have yet to be elucidated. In this paper, we hypothesise a relationship between the mechanical environment of mesenchymal stem cells and their subsequent dispersal, proliferation, differentiation and death. The mechano-regulation stimulus is hypothesised to be a function of strain and fluid flow; these quantities are calculated using biphasic poroelastic finite element analysis. A finite element model of an osteochondral defect in the knee was created, and used to simulate the spontaneous repair process. The model predicts bone formation through both endochondral and direct intramembranous ossification in the base of the defect, cartilage formation in the centre of the defect and fibrous tissue formation superficially. Greater amounts of fibrous tissue formation are predicted as the size of the defect is increased. Large strains are predicted within the fibrous tissue at the articular surface, resulting in significant cell apoptosis. This result leads to the conclusion that repair tissue degradation is initiated in the fibrous tissue that forms at the articular surface. The success of the mechano-regulation model in predicting many of the cellular events that occur during osteochondral defect healing suggest that in the future it could be used as a tool for optimising scaffolds for tissue engineering.
穿透软骨下骨的软骨缺损可通过主要由骨髓间充质干细胞介导形成的纤维组织或软骨组织进行自发修复。这种组织在生物力学性能上低于正常关节软骨，并且经常观察到会随时间退化。生物力学因素是否控制修复组织的类型和质量及其随后的退化，尚未阐明。在本文中，我们假设间充质干细胞的力学环境与其随后的分散、增殖、分化和死亡之间存在关联。机械调节刺激被假设为应变和流体流动的函数；这些量使用双相多孔弹性有限元分析来计算。创建了膝关节骨软骨缺损的有限元模型，并用于模拟自发修复过程。该模型预测在缺损底部通过软骨内成骨和直接膜内成骨形成骨组织，在缺损中心形成软骨组织，在表面形成纤维组织。随着缺损尺寸增加，预测会形成更多的纤维组织。预计关节表面的纤维组织内会出现大应变，导致大量细胞凋亡。这一结果得出结论，修复组织的退化始于关节表面形成的纤维组织。机械调节模型在预测骨软骨缺损愈合过程中发生的许多细胞事件方面的成功表明，未来它可作为优化组织工程支架的工具。
