2019 ISAKOS Biennial Congress ePoster #1503
Experimental Analysis of Medial Structures on Kinematics of PCL-Deficient Knees
Alireza Moslemian, BSc, London, ON CANADA
Philip P. Roessler, MD, MHBA, Bonn GERMANY
Ryan M. Degen, MD, FRCSC, London, ON CANADA
Alan Getgood, MD, FRCS(Tr&Orth), DipSEM, London, ON CANADA
Ryan Willing, PhD, London, ON CANADA
Western University, London, ON, CANADA
FDA Status Not Applicable
This study looks at role of dMCL and POL in stabilization of PCL-deficient knees.
Studies show between 50% and 90 % of PCL injuries occur in combination with injuries to other structures of knee. While it is commonly accepted that the posterolateral structures need to be addressed surgically in high grade PCL injuries, it is unclear which medial structures need to be addressed and when. The posterior oblique ligament (POL) and deep medial collateral ligament (dMCL) are two medial ligamentous structures whose behavior in the PCL-deficient knee are not well characterized. We hypothesize that by dissecting either of these two structures in combination with the PCL, more posteromedial tibial laxity will be observed than in an isolated PCL injury.
Six intact cadaver knees were used in this study. Knees were mounted onto a VIVO joint motion simulator (Advanced Mechanical Technologies, Inc.). Once installed, specimens were subjected to a baseline loading scenario which consisted of prescribed flexion from 0 to 90 degrees with simulated muscle forces applied and all remaining degrees of freedom unconstrained. Muscle forces were simulated using a 50 N quadricep tension applied via a pneumatic actuator, and two 25 N hamstring forces applied via virtual springs in the VIVO control system. The motion was repeated with additional loads applied to the tibia, including: (1) a posterior-directed force of 67 N, (2) a 2.5 Nm internal torque and (3) a posterior-directed force of 50 N combined with a 2.5 Nm internal torque. The tests were repeated following sequential ligament dissections. The PCL was first dissected arthroscopically, followed by dissection of either the POL or dMCL, performed in a randomized order (3 POL first, 3 dMCL first). All data were processed to calculate the anterior/posterior position of the center of the medial tibial plateau with respect to the femoral flexion axis (line connecting the epicondyles).
With a posterior-directed load applied to the tibia, dissection of dMCL increased the posterior translation of the medial side of the tibia by 2.7 +/- 5.0 mm at 0 degree and 1.6 +/- 3.4 mm at 30 degrees. With an internal torque applied, the medial tibia moved significantly more posterior at 90 degrees after dissecting the POL and more posterior at 0, 30 and 60 degrees after dissecting dMCL, with the largest change happening at 0 degrees (increase of 2.2 +/- 4.3 mm). With a posterior-directed force and internal torque applied to the tibia, dissection of POL increased medial side posterior translation significantly (by 0.5 +/- 4.2 mm at 90 degrees). Dissection of the dMCL increased posterior translation significantly at 0, 30 and 60 degrees, with the largest increase occurring at 0 degree (increase of 2.5 +/- 5.8 mm).
There was an observed trend of more posterior relative translation of the medial side of the tibia after the dMCL was dissected at 0, 30 and 60 degrees. Dissection of POL allowed increased posterior translation only when the knee was at 90 degrees and an internal torque was applied. Therefore, these results agree with our hypotheses that these structures act as secondary stabilizers in PCL-deficient knees.