2019 ISAKOS Biennial Congress ePoster #793
Contribution of the Anterolateral Complex to Rotational Stability of the Knee: A Biomechanical Analysis
Thomas Neri, MD, PhD, Asst. Prof., Saint-Etienne FRANCE
Aaron Beach, PhD, Sydney, NSW AUSTRALIA
Danè Dabirrahmani, PhD, Sydney, NSW AUSTRALIA
Sven Edward Putnis, MBChB, FRCS(Orth), Bristol UNITED KINGDOM
Samuel Grasso, PhD, B. Engineering (Mechanical), Sydney, NSW AUSTRALIA
Joseph Cadman, PhD, Sydney, NSW AUSTRALIA
Takeshi Oshima, MD, PhD, Sydney, NSW AUSTRALIA
Brett A. Fritsch, MBBS, BMedSc, Hunters Hill, NSW AUSTRALIA
Myles R. J. Coolican, FRACS, Sydney, NSW AUSTRALIA
Brian M. Devitt, MD, FRCS, FRACS, Melbourne, VIC AUSTRALIA
Richard Appleyard, PhD, Sydney, NSW AUSTRALIA
David A. Parker, MBBS, BMedSc, FRACS, Sydney, NSW AUSTRALIA
Sydney Orthopaedic Research Institute, Sydney, NSW, AUSTRALIA
FDA Status Not Applicable
The objective was to evaluate the contribution of ALC injury, and specific injuries to its individual anatomical components, to rotational instability in ACL-deficient knees.
The individual functions of the extra-articular structures of the anterolateral complex (ALC) including the anterolateral ligament (ALL), the anterolateral capsule, and the iliotibial band Kaplan fibres, in the setting of the anterior cruciate ligament (ACL) deficient knee, are still controversial and unclear. Their potential individual contribution to the residual anterolateral rotational laxity after an isolated ACLR requires furthers investigation. The objective was to evaluate the contribution of ALC injury, and specific injuries to its individual anatomical components, to rotational instability in ACL-deficient knees.
A controlled laboratory study was performed using 10 fresh-frozen cadaveric knees. Kinematics were recorded using a Motion Analysis® 3D optoelectronic system (Vicon, LA, USA). Joint centres and bone landmarks were calculated from 3D bone models obtained from CT scans and 3D rotations and translations of the joints were calculated based on the Grood and Suntay joint coordinate system. Kinematics were recorded with different conditions of testing: 5 Nm - internal rotation applied with a dynamometric torque rig (from 0 to 90° of flexion), 90 Nm - anterior tibial load (at 30 and 90° of flexion) and simulated Pivot shift test. Testing was first performed in ACL-intact. After ACL sectioning, sectioning was randomly performed for the ALC anatomical components, either ALL plus anterolateral capsule or Kaplan fibres (distal and proximal).
Compared to the intact state, ACL section significantly increased internal tibial rotation (from 0 to 90°) and anterior tibial translation (at 30 and 90°). Sectioning of the ALC led to significantly increased tibial internal rotation and to increased positive PS test; but did not change the anterior tibial translation. ALL-capsule sectioning led to significantly greater internal rotation at 30° of flexion when compared with Kaplan fibres sectioning. At higher flexion angles (50° to 90°), the effect of Kaplan fibres sectioning on increased internal rotation was greater than ALL-capsule sectioning.
The anterolateral complex contributes to restraint of tibial internal rotation and the pivot shift in the ACL deficient knee, but does not contribute to control of anterior tibial translation. The ALL and the anterolateral capsule restrain internal rotation close to 30° of flexion, whilst Kaplan fibres sectioning has a greater effect on rotational control at higher degrees of flexion. By highlighting the increased rotational knee laxity with combined ACL and anterolateral complex knee injuries, these findings suggest that these extra articular injuries should be taken into account when managing patient with ACL deficient knee, with consideration given to addressing the injuries to these structures as well as the intra-articular reconstruction.