Injury to the anterolateral ligament (ALL) has been reported to contribute to high-grade anterolateral laxity following anterior cruciate ligament (ACL) injury. Failure to address ALL injury has been suggested as a cause of persistent rotational laxity following ACL reconstruction. However, lateral meniscus posterior root (LMPR) tears have also has been shown to cause increased internal rotation and anterior translation of the knee. Due to the anatomic relationship of the ALL and the lateral meniscus, we hypothesise that the ALL and lateral meniscus work synergistically, and that a tear to the LMPR will have the same effect on anterolateral laxity as an ALL tear in the ACL deficient knee.

Sixteen fresh frozen cadaveric knee specimens were potted into a hip simulator(femur) and a six degree-of-freedom load cell (tibia). Two rigid optical trackers were inserted into the proximal femur and distal tibia, allowing for the motion of the tibia with respect to the femur to be tracked during biomechanical tests. A series of points on the femur and tibia were digitised to create bone coordinate systems that were used to calculate the kinematic variables. Biomechanical testing involved applying a 5Nm internal rotation moment to the tibia while the knee was in full extension and tested sequentially in the following three conditions: i) ACLintact; ii) Partial ACL injury (ACLam) – anteromedial bundle sectioned; iii) Full ACL injury (ACLfull). The specimens were then randomised to either have the ALL sectioned first (ALLsec) followed by the LMPRsec or vice versa. Internal rotation and anterior translation of the tibia with respect to the femur were calculated. A mixed two-way (serial sectioning by ALL section order) repeated measures ANOVA (alpha = 0.05).

Compared to the ACLintact condition, internal rotation was found to be 1.78° (p=0.06), 3.74° (p=0.001), and 3.84° (p=0.001) greater following ACLfull, LMPRsec and ALLsec respectively. LMPRsec and the ALLsec resulted in approximately 20 of additional internal rotation (p=0.004 and p=0.01, respectively) compared with the ACL deficient knee (ACLfull). No difference was observed between the ALL and LMPR sectioned states, or whether the ALL was sectioned before or after the LMPR (p=0.160). A trend of increasing anterior translation was observed when the 5Nm internal rotation moment was applied up until the ACL was fully sectioned; however, these differences were not significant (p=0.070).

The ALL and LMPR seem to have a synergistic relationship in aiding the ACL in controlling anterolateral rotational laxity. High-grade anterolateral laxity following ACL injury may be attributed to injuries of the ALL and/or the LMPR. We suggest that the lateral meniscus should be thought of as part of the anterolateral capsulomeniscal complex (i.e., LM, ITB, and ALL) that acts as a stabiliser of anterolateral rotation in conjunction with the ACL.