The knee joints of mice can be used as a model for studying the effects of interventions on knee laxity. The goal of this study was to quantify knee joint laxity in vitro. Three devices were developed: a positioning-and cemcnting device, an anterior-posterior (AP) laxity tester and a varus-valgus (VV) laxity tester. The positioningand cementing device was used to position the joint in a reproducible way and to attach clamping pins to the proximal femur and distal tibia using PMMA. The clamping pins were used to fix the joint to the AP-and VV-testers. In both testers the load was applied by means of a spindle-actuated spring while load and displacements were measured simultaneously. The load-displacement data were used to calculate displacement and compliance parameters, The performance of the testers was evaluated by testing 5 normal knee joints of 5 mice.

The aim of this study was to validate a device developed previously to measure laxity of murine knee joints and to investigate whether experimentally induced pathological conditions result in measurable laxity. The laxity characteristics of normal murine knee joints were derived from measurements of 25 left knees of normal mice. Reproducible, nonlinear s-shaped load-displacement curves were determined, and parameters of anterior-posterior translation, varus-valgus rotation, and compliance were calculated from the curves. No differences were found between the left and right knee joints of eight mice. The average displacement between 0.8 N of anterior force and 0.8 N of posterior force was 0.47 +/- 0.10 mm. The endpoint compliances for anterior and posterior displacements were 0.16 +/- 0.03 and 0.16 +/- 0.04 mm/N, respectively. The average rotation between a 4 Nmm valgus moment and a 4 Nmm varus moment was 17.4 +/- 3.3 degrees. The endpoint compliances for varus and valgus rotations were 1.1 +/- 0.7 and 1.0 +/- 0.3 degrees/Nmm, respectively. Storage of the joints at -70 degrees C had no effect on laxity. We also studied the parameters of laxity after pathology of the knee joint was induced. Zymosan-induced or antigen-induced arthritis did not increase laxity of the joint. In an osteoarthritis model induced by injection of collagenase, laxity was markedly increased. In conclusion, laxity in the knees of mice can be measured reproducibly and changes in the characteristics of laxity due to pathological conditions can be quantified.