JOINT MECHANORECEPTOR CONTRIBUTIONS TO CONTROL OF KNEE JOINT STABILITY

骨关节炎被认为是由关节软骨的重复性微损伤引起的，尤其是在负重关节，如膝盖。这种微创伤可能是由于软骨关节表面之间的剪切运动和/或压缩载荷造成的。虽然膝关节的前后负荷已被广泛研究，但对膝关节外翻和轴向旋转负荷以及肌肉收缩在促进膝关节外翻平面稳定性中的代偿作用的关注较少。关节稳定性经典地归因于五个主要因素：骨/软骨接触力、韧带和囊刚度、活动肌肉的固有刚度和反射性介导的肌肉刚度。反过来，反射作用可能由肌肉拉伸受体、关节周围组织传入神经（韧带和囊），甚至可能由皮肤机械感受器介导。在关节外翻负荷异常的情况下，后一类反射可能通过肌肉激活来保护关节。在这种情况下，副韧带的损伤将通过破坏来自这些韧带受体的传入神经而剥夺基于还原反射的保护。临床上，一些内侧副韧带（MCL）损伤导致韧带纤维完全断裂，伴有明显的关节不稳定。创伤后膝关节骨关节炎的发展，可能会在MCL损伤后很长一段时间内发生，被认为是由损伤基础不稳定引起的。这些损伤对韧带的“非结构性”影响以及韧带神经感觉功能在促进关节稳定性中的相互作用的关注较少。因此，我们假设创伤后骨关节炎与MCL损伤相关，至少部分归因于韧带受体传入通路的中断。由此可见，对MCL损伤的膝关节施加机械外翻刺激不能引起有针对性的肌肉收缩。我们进一步假设，对对侧正常膝关节施加类似的机械刺激会引起反射反应。显著提高关节外翻方向的刚度。这些假设将在一侧完全MCL损伤而另一侧膝关节正常的受试者身上进行检验。受影响和未受影响的膝盖将在完全伸展和不同程度的关节肌肉预激活（腘绳肌和股四头肌）的情况下进行测试。我们的研究结果将阐明关节稳定性的基本机制，以及MCL损伤膝关节稳定性丧失的不良影响。

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.