Anterior Cruciate Ligament Deficiency Alters the In Vivo Motion of the Tibiofemoral Cartilage Contact Points in Both the Anteroposterior and Mediolateral Directions

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Background: Quantifying the effects of anterior cruciate ligament deficiency on joint biomechanics is critical in order to better understand the mechanisms of joint degeneration in anterior cruciate ligament-deficient knees and to improve the surgical treatment of anterior cruciate ligament injuries. We investigated the changes in position of the in vivo tibiofemoral articular cartilage contact points in anterior cruciate ligament-deficient and intact contralateral knees with use of a newly developed dual orthogonal fluoroscopic and magnetic resonance imaging technique.

Methods: Nine patients with an anterior cruciate ligament rupture in one knee and a normal contralateral knee were recruited. Magnetic resonance images were acquired for both the intact and anterior cruciate ligament-deficient knees to construct computer knee models of the surfaces of the bone and cartilage. Each patient performed a single-leg weight-bearing lunge as images were recorded with use of a dual fluoroscopic system at full extension and at 15°, 30°, 60°, and 90° of flexion. The in vivo knee position at each flexion angle was then reproduced with use of the knee models and fluoroscopic images. The contact points were defined as the centroids of the areas of intersection of the tibial and femoral articular cartilage surfaces.

Results: The contact points moved not only in the anteroposterior direction but also in the mediolateral direction in both the anterior cruciate ligament-deficient and intact knees. In the anteroposterior direction, the contact points in the medial compartment of the tibia were more posterior in the anterior cruciate ligament-deficient knees than in the intact knees at full extension and 15° of flexion (p < 0.05). No significant differences were observed with regard to the anteroposterior motion of the contact points in the lateral compartment of the tibia. In the mediolateral direction, there was a significant lateral shift of the contact points in the medial compartment of the tibia toward the medial tibial spine between full extension and 60° of flexion (p < 0.05). The contact points in the lateral compartment of the tibia shifted laterally, away from the lateral tibial spine, at 15° and 30° of flexion (p < 0.05).

Conclusions: In the presence of anterior cruciate ligament injury, the contact points shift both posteriorly and laterally on the surface of the tibial plateau. In the medial compartment, the contact points shift toward the medial tibial spine, a region where degeneration is observed in patients with chronic anterior cruciate ligament injuries.

Clinical Relevance: This in vivo measurement technique may be useful for assessing the ability of an anterior cruciate ligament reconstruction to restore normal tibiofemoral cartilage contact biomechanics. The observed altered motions of the tibiofemoral contact points might change contact stress distributions in the cartilage and predispose the joint to degenerative changes.

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