Increased tibiofemoral cartilage contact deformation in patients with anterior cruciate ligament deficiency.

Increased tibiofemoral cartilage contact deformation in patients with anterior cruciate ligament deficiency.
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DOI:
10.1002/art.24965
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发表时间:
2009-12
影响因子:
--
通讯作者:
Li, Guoan
Li, Guoan
中科院分区:
其他
文献类型:
--
作者:
Van de Velde, Samuel K.;Bingham, Jeffrey T.;Hosseini, Ali;Kozanek, Michal;DeFrate, Louis E.;Gill, Thomas J.;Li, Guoan

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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 one knee and the contralateral side intact participated in the study. Both knees were imaged using a specific MR sequence to create three-dimensional knee models of bone and cartilage. Next, each patient performed a lunge as images were recorded with a dual fluoroscopic system from 0° to 90° of flexion. The three-dimensional knee models and fluoroscopic images were used to reproduce the in-vivo knee position at each flexion angle. With these series of knee models, the location of tibiofemoral cartilage contact, size of contact area, cartilage thickness at the contact area, and magnitude of cartilage contact deformation were compared between the intact and ACL-deficient knees. Rupture of the ACL changed the cartilage contact biomechanics from 0° to 60° of flexion in the medial knee compartment. 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, compared with the contralateral knee. Similar changes were observed in the lateral compartment, with increased cartilage contact deformation from 0° to 30° of knee flexion in ACL deficiency. ACL deficiency alters the in-vivo cartilage contact biomechanics, by shifting the contact location to smaller regions of thinner cartilage, and increasing the magnitude of cartilage contact deformation.
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