Van de Velde Samuel K, Bingham Jeffrey T, Hosseini Ali, Kozanek Michal, DeFrate Louis E, Gill Thomas J, Li Guoan
Massachusetts General Hospital/Harvard Medical School, Boston, Massachusetts 02114, USA.
Arthritis Rheum. 2009 Dec;60(12):3693-702. doi: 10.1002/art.24965.
To investigate the in vivo cartilage contact biomechanics of the tibiofemoral joint following anterior cruciate ligament (ACL) injury.
Eight patients with an isolated ACL injury in 1 knee, with the contralateral side intact, participated in the study. Both knees were imaged using a specific magnetic resonance sequence to create 3-dimensional models of knee bone and cartilage. Next, each patient performed a lunge motion from 0 degrees to 90 degrees of flexion as images were recorded with a dual fluoroscopic system. The three-dimensional knee models and fluoroscopic images were used to reproduce the in vivo knee position at each flexion angle. With this series of knee models, the location of the tibiofemoral cartilage contact, size of the contact area, cartilage thickness at the contact area, and magnitude of the cartilage contact deformation were compared between intact and ACL-deficient knees.
Rupture of the ACL changed the cartilage contact biomechanics between 0 degrees and 60 degrees of flexion in the medial compartment of the knee. Compared with the contralateral knee, the location of peak cartilage contact deformation on the tibial plateaus was more posterior and lateral, the contact area was smaller, the average cartilage thickness at the tibial cartilage contact area was thinner, and the resultant magnitude of cartilage contact deformation was increased. Similar changes were observed in the lateral compartment, with increased cartilage contact deformation from 0 degrees to 30 degrees of knee flexion in the presence of ACL deficiency.
ACL deficiency alters the in vivo cartilage contact biomechanics by shifting the contact location to smaller regions of thinner cartilage and by increasing the magnitude of the cartilage contact deformation.
研究前交叉韧带(ACL)损伤后胫股关节的体内软骨接触生物力学。
8例患者一侧膝关节孤立性ACL损伤,对侧膝关节正常,参与本研究。对双侧膝关节采用特定磁共振序列成像,以创建膝关节骨和软骨的三维模型。接下来,每位患者从0度到90度屈曲进行弓步运动,同时用双荧光透视系统记录图像。利用三维膝关节模型和荧光透视图像再现每个屈曲角度下的体内膝关节位置。通过这一系列膝关节模型,比较正常膝关节和ACL损伤膝关节之间胫股软骨接触的位置、接触面积大小、接触区域的软骨厚度以及软骨接触变形的大小。
ACL断裂改变了膝关节内侧间室在0度至60度屈曲之间的软骨接触生物力学。与对侧膝关节相比,胫骨平台上软骨接触变形峰值的位置更靠后和外侧,接触面积更小,胫骨软骨接触区域的平均软骨厚度更薄,软骨接触变形的合力大小增加。在外侧间室也观察到类似变化,在ACL损伤时,从0度到30度膝关节屈曲时软骨接触变形增加。
ACL损伤通过将接触位置转移到软骨较薄的较小区域并增加软骨接触变形的大小,改变了体内软骨接触生物力学。