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Effect of Posterior Cruciate Ligament Deficiency on In Vivo Translation and Rotation of the Knee During Weightbearing Flexion

Guoan Li, PhD^,*, Ramprasad Papannagari, MS, Meng Li, MS^,, Jeffrey Bingham, MS^,, Kyung W. Nha, MD^,ll, Dain Allred, MD and Thomas Gill, MD

From the Bioengineering Laboratory, Department of Orthopaedic Surgery, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, the Department of Electrical and Computer Engineering, Boston University, Boston, Massachusetts, the Department of Mechanical Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts, and the ^ll Department of Orthopaedic Surgery, Inge University and Ilsanpaik Hospital, Ilsan, South Korea

^* Address correspondence to Guoan Li, PhD, Bioengineering Laboratory, 55 Fruit Street, GRJ 1215, Boston, MA 02114 (e-mail: gli1{at}partners.org).

Background: The effect of posterior cruciate ligament (PCL) deficiency on 6 degrees of freedom in vivo knee-joint kinematics is unclear.

Hypothesis: In addition to constraining anterior-posterior translation, the PCL also functions to constrain the medial-lateral translation and rotation of the knee during weightbearing flexion of the knee.

Study Design: Controlled laboratory study.

Methods: Eight patients with a PCL injury in 1 knee and the other intact were scanned with magnetic resonance imaging, and 3-dimensional models of the femur and tibia were created for both knees. Each knee was imaged during quasistatic weight-bearing flexion (from 0° to 105° ) using a dual-orthogonal fluoroscopic system. The translation and rotation of the PCL-deficient knee were compared with the intact contralateral control.

Results: Posterior cruciate ligament deficiency caused an increase in posterior tibial translation beyond 30° of flexion compared with the intact contralateral knees. At 90° of flexion, PCL deficiency increased posterior tibial translation by 3.5 mm (P < .05). In the medial-lateral direction, PCL deficiency resulted in a 1.1 mm increase in lateral tibial translation at 90° of flexion (P < .05). With regard to rotation, PCL deficiency caused a significantly lower varus rotation (on average, 0.6° lower) at 90° of flexion. Posterior cruciate ligament deficiency caused a decreased internal tibial rotation throughout the range of flexion, but no significant difference was detected.

Conclusions: This study quantitatively describes the effect of PCL injury on 6 degrees of freedom kinematics of the knee during quasistatic weightbearing flexion. Using the intact contralateral side as a control, we found that PCL injuries not only affect anterior-posterior tibial translation but also medial-lateral translation and rotation of the knee.

Clinical Relevance: These data provide baseline knowledge of the in vivo kinematics of the knee after PCL injury. Surgical reconstruction of the injured PCL, either using single-bundle or double-bundle technique, should not only focus on restoration of posterior stability of the knee but also the medial-lateral stability as well as the rotational stability. These findings may help to explain the long-term degenerative changes seen in PCL-deficient knees.

Key Words: posterior cruciate ligament (PCL) • PCL injury • in vivo knee kinematics • PCL reconstruction