Kinematics of meniscal- and ACL-transected mouse knees during controlled tibial compressive loading captured using roentgen stereophotogrammetry.

Pre-clinical studies of post-traumatic OA have examined the pathways that lead to disease after injury by using surgical models such as the destabilization of the medial meniscus (DMM) and anterior cruciate ligament transection (ACLT). While the morphological, molecular, and genetic pathways leading to OA have been examined extensively; the effects of these injuries on joint kinematics, and thus disease progression, have yet to be fully characterized. To this end, we sought to understand the kinematics in the DMM and ACLT joints compared to intact joints subjected to controlled tibial compressive loading. We hypothesized that the DMM and ACLT models would result in different patterns of joint instability compared to intact joints, thus explaining the different patterns of OA initiation and severity in these models. Cadaver adult C57BL/6 mice were subjected to either a DMM or ACLT in their right knee joints, while the left limbs remained as intact controls. All limbs were labeled with fiducial markers, and the rigid body kinematics of the tibia and femur were examined using roentgen stereophotogrammetry (RSA) with application of compressive loads from 0 to 9 N. DMM and intact joints demonstrated similar kinematics under compressive loading, in contrast to ACLT joints, which dislocated even before load application. These results demonstrate the importance of rigorous kinematic analysis in defining the role of joint instability in animal models of OA and suggest significant differences in DMM and ACLT joint instabilities in the context of controlled mechanical loading.