Korhonen Rami K, Laasanen Mikko S, Töyräs Juha, Lappalainen Reijo, Helminen Heikki J, Jurvelin Jukka S
Department of Applied Physics, University of Kuopio, 70211, Kuopio, Finland.
J Biomech. 2003 Sep;36(9):1373-9. doi: 10.1016/s0021-9290(03)00069-1.
Degradation of collagen network and proteoglycan (PG) macromolecules are signs of articular cartilage degeneration. These changes impair cartilage mechanical function. Effects of collagen degradation and PG depletion on the time-dependent mechanical behavior of cartilage are different. In this study, numerical analyses, which take the compression-tension nonlinearity of the tissue into account, were carried out using a fibril reinforced poroelastic finite element model. The study aimed at improving our understanding of the stress-relaxation behavior of normal and degenerated cartilage in unconfined compression. PG and collagen degradations were simulated by decreasing the Young's modulus of the drained porous (nonfibrillar) matrix and the fibril network, respectively. Numerical analyses were compared to results from experimental tests with chondroitinase ABC (PG depletion) or collagenase (collagen degradation) digested samples. Fibril reinforced poroelastic model predicted the experimental behavior of cartilage after chondroitinase ABC digestion by a major decrease of the drained porous matrix modulus (-64+/-28%) and a minor decrease of the fibril network modulus (-11+/-9%). After collagenase digestion, in contrast, the numerical analyses predicted the experimental behavior of cartilage by a major decrease of the fibril network modulus (-69+/-5%) and a decrease of the drained porous matrix modulus (-44+/-18%). The reduction of the drained porous matrix modulus after collagenase digestion was consistent with the microscopically observed secondary PG loss from the tissue. The present results indicate that the fibril reinforced poroelastic model is able to predict specifically characteristic alterations in the stress-relaxation behavior of cartilage after enzymatic modifications of the tissue. We conclude that the compression-tension nonlinearity of the tissue is needed to capture realistically the mechanical behavior of normal and degenerated articular cartilage.
胶原蛋白网络和蛋白聚糖（PG）大分子的降解是关节软骨退变的标志。这些变化损害了软骨的力学功能。胶原蛋白降解和PG损耗对软骨随时间变化的力学行为的影响是不同的。在本研究中，使用纤维增强多孔弹性有限元模型进行了数值分析，该模型考虑了组织的压缩-拉伸非线性。本研究旨在增进我们对正常和退变软骨在无侧限压缩下应力松弛行为的理解。分别通过降低排水多孔（非纤维状）基质和纤维网络的杨氏模量来模拟PG和胶原蛋白的降解。将数值分析结果与用软骨素酶ABC（PG损耗）或胶原酶（胶原蛋白降解）消化的样品的实验测试结果进行比较。纤维增强多孔弹性模型预测，软骨素酶ABC消化后，排水多孔基质模量大幅降低（-64±28%），纤维网络模量小幅降低（-11±9%），从而得出软骨的实验行为。相比之下，胶原酶消化后，数值分析预测，纤维网络模量大幅降低（-69±5%），排水多孔基质模量降低（-44±18%），从而得出软骨的实验行为。胶原酶消化后排水多孔基质模量的降低与组织微观观察到的继发性PG损失一致。目前的结果表明，纤维增强多孔弹性模型能够特异性地预测组织酶促修饰后软骨应力松弛行为的特征性改变。我们得出结论，需要组织的压缩-拉伸非线性来真实地捕捉正常和退变关节软骨的力学行为。
