The role of the medial collateral ligament (MCL) and the posterior oblique ligament (POL) in restraining valgus and anteromedial rotation has been extensively studied. However, the individual role of each part of these broad structures have not been evaluated yet. Thus, the goal of the present study was to investigate the role of the individual fiber region of the MCL and POL. It was hypothesized that each MCL and POL fiber region have similar roles in restraining medial knee laxity.
Eight fresh-frozen cadaveric knee specimens were mounted onto a six degree of freedom robotic testing setup (KUKA KR60/3) with a force-moment sensor(ATI-Theta FT-sensor; Schunk). The knees were aligned according to the coordinate system of Grood and Suntay and the following simulated clinical laxity tests were performed at 0/30/60/90° knee flexion: 1) 134N anterior tibial translation (ATT) performed at 5Nm external tibial rotation (ER) to simulate anteromedial rotatory knee instability (AMRI), 2) internal tibial rotation, and 3) 10Nm valgus rotation. These simulated laxity tests were applied to the intact knee and after sequentially resecting the 1) anterior- , 2) middle-, and 3) posterior portion of the MCL and the 1) central- and 2) capsular arm of the POL. Therefore, the femoral and tibial insertion site of the MCL was divided into 3 parts from anterior to posterior and each portion was longitudinally resected. Similarly, the POL was divided macroscopically into the central and capsular arm and was also resected. The contribution of each portion was recorded using a position controlled setup and was presented as percentage from the total MCL and POL contribution, respectively. A 2-way repeated measure ANOVA with post-hoc Bonferroni correction was performed.
The anterior portion of the MCL was the major restraint (more than 50% of the whole MCL) at 30-90° knee flexion (p<0.01) in restraining AMRI, which was the highest at 90° knee flexion (63.1% of the whole MCL and 23.2±9.8% total). The middle portion also had a significant contribution, but never exceeded 30% contribution of the whole MCL.
The central arm of the POL primarily contributed in restraining internal tibial rotation at 0 and 30° knee flexion, presenting 72% (0°) and 92% (30°) of the POL, which showed a 46.5±13.1% and 30.4±17.7% overall contribution in restraining internal rotation. The MCL only showed a relevant contribution at 30° (21.7±11.9), with the posterior portion contributing for 55.8%. All parts of the MCL had a similar contribution in restraining valgus rotation at 0 and 30°, with the middle part as highest contributor (38.4 and 42.1%). At higher flexion angles the anterior portion of the MCL was the major restraint(p< 0.01).Only the central arm of the POL showed a statistically significant(p<0.05) contribution in restraining valgus rotation at early flexion angles(0-30°).
Contrary to our hypothesis, each of the MCL/POL portions had individual contribution in restraining medial knee laxity, where the anterior portion was the major restraint to AMRI at high flexion angles and the posterior portion and the central arm of the POL were the major restraint to internal rotation at early flexion angles.
Reconstructing only one part of the MCL may not be sufficient in restoring the entire medial knee kinematic.