Osteoarthritis is believed to be induced by repetitive microtrauma to joint cartilage, especially in weight-bearing joints like the knee. This microtrauma can occur both as a result of shear motion between cartilaginous joint surfaces, and/or in compressive loading. While anterior posterior loading of the knee has been studied extensively, there has been less attention paid to knee varus-valgus and axial rotational loading, and to the compensatory role of muscle contractions in promoting knee stability in the varus-valgus plane. Joint stability has been classically attributed to five major factors: bone/cartilaginous contact forces, ligament and capsule stiffness, intrinsic stiffness of active muscles, and reflexively mediated muscle stiffness. Reflex action may, in turn, be mediated either by muscle stretch receptors, by periarticular tissue afferents (ligaments and capsule) and potentially even by skin mechanoreceptors. This latter class of reflexes potentially protects the joint through muscle activation in situations of abnormal valgus loading at the joint. In this setting, an injury of the collateral ligaments will deprive reduce reflex based protection through the disruption of afferents derived from receptors located in these ligaments. Clinically, some injuries to the medial collateral ligaments (MCL) result in complete disruption of the ligament fibers with significant joint instability. The development of posttraumatic osteoarthritis at the knee joint, which may follow long after MCL injury, is believed to be induced by the injury based-instability. There has been less attention paid to the """"""""nonstructural"""""""" effect of these injuries on the ligament, and the interaction of the neurosensory function of the ligament in promoting joint stability. Accordingly, we hypothesize that posttraumatic osteoarthritis associated with MCL injury is attributable, at least in part, to the disruption of afferent pathways originating in ligament receptors. It follows that targeted muscle contractions cannot be elicited by the application of a mechanical valgus stimulus to the MCL injured human knee. We further hypothesize that the application of comparable mechanical stimuli to the contra lateral normal knee elicits reflex responses. which significantly increase the joints stiffness in the valgus direction. These hypotheses will be examined on subjects with complete MCL injuries on one side and a normal knee on the other side. The affected and unaffected knees will be tested at full extension and with different levels of joint muscle preactivation (in hamstrings and quadriceps). Our findings will shed light on fundamental mechanisms of joint stability, and on adverse effects of loss of stability in the MCL injured knee.
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