Ellis Benjamin J, Lujan Trevor J, Dalton Michelle S, Weiss Jeffrey A
Department of Bioengineering, University of Utah, Salt Lake City, Utah 84112, USA.
J Orthop Res. 2006 Apr;24(4):800-10. doi: 10.1002/jor.20102.
The objectives of this research were to determine the effects of anterior cruciate ligament (ACL) deficiency on medial collateral ligament (MCL) insertion site and contact forces during anterior tibial loading and valgus loading using a combined experimental-finite element (FE) approach. Our hypothesis was that ACL deficiency would increase MCL insertion site forces at the attachments to the tibia and femur and increase contact forces between the MCL and these bones. Six male knees were subjected to varus-valgus and anterior-posterior loading at flexion angles of 0 degrees and 30 degrees. Three-dimensional joint kinematics and MCL strains were recorded during kinematic testing. Following testing, the MCL of each knee was removed to establish a stress-free reference configuration. An FE model of the femur-MCL-tibia complex was constructed for each knee to simulate valgus rotation and anterior translation at 0 degrees and 30 degrees, using subject-specific bone and ligament geometry and joint kinematics. A transversely isotropic hyperelastic material model with average material coefficients taken from a previous study was used to represent the MCL. Subject-specific MCL in situ strain distributions were used in each model. Insertion site and contact forces were determined from the FE analyses. FE predictions were validated by comparing MCL fiber strains to experimental measurements. The subject-specific FE predictions of MCL fiber stretch correlated well with the experimentally measured values (R2 = 0.95). ACL deficiency caused a significant increase in MCL insertion site and contact forces in response to anterior tibial loading. In contrast, ACL deficiency did not significantly increase MCL insertion site and contact forces in response to valgus loading, demonstrating that the ACL is not a restraint to valgus rotation in knees that have an intact MCL. When evaluating valgus laxity in the ACL-deficient knee, increased valgus laxity indicates a compromised MCL.
本研究的目的是采用实验与有限元（FE）相结合的方法，确定前交叉韧带（ACL）缺失对胫骨前负荷和外翻负荷期间内侧副韧带（MCL）附着点及接触力的影响。我们的假设是，ACL缺失会增加MCL在胫骨和股骨附着处的附着点力，并增加MCL与这些骨骼之间的接触力。对6个男性膝关节在0度和30度屈曲角度下进行内翻-外翻和前后负荷试验。在运动学测试过程中记录三维关节运动学和MCL应变。测试后，切除每个膝关节的MCL以建立无应力参考构型。利用个体特异性的骨骼和韧带几何形状以及关节运动学，为每个膝关节构建股骨-MCL-胫骨复合体的有限元模型，以模拟0度和30度时的外翻旋转和胫骨前移。使用从先前研究中获取的平均材料系数的横观各向同性超弹性材料模型来代表MCL。每个模型中使用个体特异性的MCL原位应变分布。通过有限元分析确定附着点和接触力。通过将MCL纤维应变与实验测量值进行比较来验证有限元预测。MCL纤维拉伸的个体特异性有限元预测与实验测量值相关性良好（R2 = 0.95）。ACL缺失导致在胫骨前负荷时MCL附着点和接触力显著增加。相比之下，ACL缺失在应对外翻负荷时并未显著增加MCL附着点和接触力，这表明在MCL完整的膝关节中，ACL对外翻旋转并非限制因素。在评估ACL缺失膝关节的外翻松弛度时，外翻松弛度增加表明MCL受损。
