Effects of joint load on the stiffness and laxity of ligament-deficient knees. An in vitro study of the anterior cruciate and medial collateral ligaments.

We measured the effects of serial section of the medial collateral ligament and anterior cruciate ligament and of the anterior cruciate ligament and medial collateral ligament on anterior-posterior force-versus-displacement and tibial torque-versus-rotation response curves for seven fresh frozen cadaver knees at zero and 20 degrees of flexion before and after application of as much as 925 newtons of compressive load on the tibiofemoral joint. Section of the anterior cruciate ligament always increased anterior laxity in an unloaded specimen; joint load reduced this increase by a greater amount at zero degrees than at 20 degrees of flexion. Joint load was more effective in limiting anterior laxity in anterior cruciate-deficient specimens at low levels of applied anterior force; at higher levels of applied force, the effects of joint congruency were overcome and ligament restraints came into play. Section of the medial collateral ligament increased anterior laxity in an unloaded knee only for specimens in which the anterior cruciate ligament had been previously sectioned; joint load eliminated this increase at full extension but did not do so at 20 degrees of flexion. The medial collateral ligament was the more important of the two ligaments in controlling torsional laxity. Secondary section of either ligament (the other ligament having been sectioned first) produced a greater increase in laxity than did primary section of that ligament in an intact knee. Increases in torsional laxity due to primary section of either ligament were unaffected by the application of joint load. Joint load reduced increases in laxity that were due to secondary section of the medial collateral ligament.