PURPOSE: Dissatisfaction after total knee arthroplasty (TKA) may be caused by abnormal knee kinematics, and there is concern that 'guided motion' TKAs, designed to replicate normal knee kinematics, cause anterolateral knee pain due to stretching of soft tissues. It was hypothesised that excessive tibial internal rotation and femoral rollback during flexion were to blame. METHODS: Eighteen fresh-frozen specimens were used in two studies. The first study used a knee extension rig and transducers to measure ligament length changes during flexion. The second study used a knee flexion rig and optical trackers to measure tibiofemoral kinematics. Both experiments used the intact knee and were repeated with three TKAs: two guided motion (Journey and Journey II) and a conventional Genesis II PS TKA. RESULTS: TKA did not cause significant elongation of any of the ligaments examined. The medial patellofemoral ligament and the medial collateral ligament tended to be slacker post-TKA, and all three TKAs caused some tightening of the superficial iliotibial band, but these changes were not significant. Normal knee kinematics was not restored by any of the devices. The screw-home mechanism was absent in all three TKAs; anterior laxity was increased in all three devices up to 90° flexion, but tibial internal rotation was not increased. The conventional TKA allowed significantly greater anterior laxity than normal, while the Journey I caused greater tibial anterior translation in flexion. CONCLUSIONS: The hypothesis that over-internal rotation and rollback in the original guided motion knee caused excessive tightening in the soft tissues around the knee was supported; the updated design reduced that tendency. If similar changes occur during real-life activities, these results imply a potential reduction in the incidence of anterolateral knee pain clinically in patients with a guided motion TKA.
PURPOSE: Dissatisfaction after total knee arthroplasty (TKA) may be caused by abnormal knee kinematics, and there is concern that 'guided motion' TKAs, designed to replicate normal knee kinematics, cause anterolateral knee pain due to stretching of soft tissues. It was hypothesised that excessive tibial internal rotation and femoral rollback during flexion were to blame. METHODS: Eighteen fresh-frozen specimens were used in two studies. The first study used a knee extension rig and transducers to measure ligament length changes during flexion. The second study used a knee flexion rig and optical trackers to measure tibiofemoral kinematics. Both experiments used the intact knee and were repeated with three TKAs: two guided motion (Journey and Journey II) and a conventional Genesis II PS TKA. RESULTS: TKA did not cause significant elongation of any of the ligaments examined. The medial patellofemoral ligament and the medial collateral ligament tended to be slacker post-TKA, and all three TKAs caused some tightening of the superficial iliotibial band, but these changes were not significant. Normal knee kinematics was not restored by any of the devices. The screw-home mechanism was absent in all three TKAs; anterior laxity was increased in all three devices up to 90° flexion, but tibial internal rotation was not increased. The conventional TKA allowed significantly greater anterior laxity than normal, while the Journey I caused greater tibial anterior translation in flexion. CONCLUSIONS: The hypothesis that over-internal rotation and rollback in the original guided motion knee caused excessive tightening in the soft tissues around the knee was supported; the updated design reduced that tendency. If similar changes occur during real-life activities, these results imply a potential reduction in the incidence of anterolateral knee pain clinically in patients with a guided motion TKA.
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