In vivo knee joint loading and kinematics before and after ACL transection in an animal model
Introduction
Osteoarthritis (OA) of the knee is frequently observed following rupture of the anterior cruciate ligament (ACL) (e.g. Conteducca et al., 1991; Noyes et al., 1983). Although the precise etiology of OA is unknown, it is believed that changes in joint loading play a primary role in initiating OA (Moskowitz, 1984; Radin et al., 1972). To investigate the possible relationship between changes in joint loading and joint degeneration, animal models based on the surgical disruption of the normal joint mechanics have been developed. Transection of the ACL has been associated with joint instability and altered stresses acting on the articular cartilage of the knee. ACL transection is a well-established and reliable model of OA in the dog (e.g. McDevitt et al., 1977; Brandt et al., 1991) and cat (Herzog et al., 1993a).
Whereas full-thickness loss of cartilage in canine knees was observed 4 to 5 years following ACL transection (Brandt et al., 1991), first biochemical and morphological changes of the cartilage have been reported within two to four weeks of ACL transection (Altman and Dean, 1990; Adams and Brandt, 1991; Herzog et al., 1993a). Therefore, it appears that first tissue responses are triggered within days following ACL transection. However, attempts to relate the changes in the joint mechanics to the early biological responses of the joint have been limited to measurements of the external ground reaction forces (GRFs) (O’Connor et al., 1989; Brandt et al., 1991; Herzog et al., 1993a) and hindlimb kinematics (Korvick et al., 1994; Vilensky et al., 1994a). Since joint loading is primarily determined by muscular forces (Morrison, 1970; Radin et al., 1972), measurements of the hindlimb kinematics and GRFs give an indirect, qualitative picture of the joint mechanics. For example, stiffening of the joint through muscular co-contraction may result in an increased loading of the knee after ACL transection despite the apparent unloading in the GRFs (O’Connor et al., 1989; Brandt et al., 1991; Herzog et al., 1993a). To date, systematic measurements of muscle forces determining knee loading have not been performed in an ACL transection model. Specifically, the changes in knee loading immediately following ACL transection, which are likely responsible for the early biological responses of the joint have been ignored. The purpose of this study was to quantify the in vivo loading of the cat knee before and within a few days of ACL transection. We propose that these early changes in knee mechanics are the primary reason for the biologic adaptations seen in the experimental models of OA.
Section snippets
Methods
Six adult cats (body weight 37–49 N) were trained to walk on a motor driven treadmill at speeds ranging from 0.4 to 1.0 m s-1. Training sessions were conducted 4 to 6 times a week for six weeks prior to implantation of force transducers and EMG electrodes. Training was continued after implantation until sacrifice of the animals. The experimental protocol was approved by The University of Calgary Animal Research and Ethics Committee.
Results
PT forces were obtained in four (B, C, D and E) of the six animals: the left hindlimb of cat B, the left and right hindlimbs of cat C, and the left hindlimb of cat E. For the other hindlimbs of cats B, D and E, partial PT data were available, but calibration was not applied due to failure of the IFT in the latter part of testing. Gastrocnemius forces were obtained for six animals before and for five animals after ACL transection in both hindlimbs.
Synchronized muscle forces and joint angles in
Discussion
In order to determine how knee loading changes after ACL injury, forces and EMGs in muscles crossing the knee were measured in the cat before and after ACL transection. We hypothesized that muscle forces and EMGs are increased following ACL transection because of attempts to stabilize and stiffen the ACL-deficient knee through muscular co-contraction. Such co-contraction could produce large contact loads in the knee, despite small GRFs. Until now, in vivo loading of normal injured knees has not
Acknowledgements
This study was supported by The Arthritis Society of Canada, The Whitaker Foundation, and the Medical Research Council of Canada. EMH was supported by a scholarship of ESK Switzerland.
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