Biomechanical consequences of PCL deficiency in the knee under simulated muscle loads--an in vitro experimental study.
The mechanism of chronic degeneration of the knee after posterior cruciate ligament (PCL) injury is still not clearly understood. While numerous biomechanical studies have been conducted to investigate the function of the PCL with regard to antero-posterior stability of the knee, little has been reported on its effect on the rotational stability of the knee. In this study, eight cadaveric human knee specimens were tested on a robotic testing system from full extension to 120 degrees of flexion with the PCL intact and with the PCL resected. The antero-posterior tibial translation and the internal-external tibial rotation were measured when the knee was subjected to various simulated muscle loads. Under a quadriceps load (400 N) and a combined quadriceps/hamstring load (400/200 N), the tibia moved anteriorly at low flexion angles (below 60 degrees). Resection of the PCL did not significantly alter anterior tibial translation. At high flexion angles (beyond 60 degrees), the tibia moved posteriorly and rotated externally under the muscle loads. PCL deficiency significantly increased the posterior tibial translation and external tibial rotation. The results of this study indicate that PCL deficiency not only changed tibial translation, but also tibial rotation. Therefore, only evaluating the tibial translation in the anteroposterior direction may not completely describe the effect of PCL deficiency on knee joint function. Furthermore, the increased external tibial rotations were further hypothesized to cause elevated patello-femoral joint contact pressures. These data may help explain the biomechanical factors causing long-term degenerative changes of the knee after PCL injury. By fully understanding the etiology of these changes, it may be possible to develop an optimal surgical treatment for PCL injury that is aimed at minimizing the long-term arthritic changes in the knee joint.
Li, G; Gill, TJ; DeFrate, LE; Zayontz, S; Glatt, V; Zarins, B
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