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创伤引起的，特别是在像膝盖这样的承重关节中。 这种微创伤可能由于软骨关节表面之间的剪切运动和/或压缩载荷而发生。虽然膝关节的前后负荷已被广泛研究，但对膝关节内翻-外翻和轴向旋转负荷以及肌肉收缩在促进膝关节内翻-外翻平面稳定性中的补偿作用的关注较少。 关节稳定性通常归因于五个主要因素：骨/软骨接触力、韧带和关节囊刚度、活动肌肉的固有刚度和反射介导的肌肉刚度。 反射作用可以反过来由肌肉牵张感受器、关节周围组织传入（韧带和关节囊）以及潜在地甚至由皮肤机械感受器介导。 后一类反射在关节处的异常外翻负荷的情况下通过肌肉激活潜在地保护关节。 在这种情况下，侧副韧带的损伤将通过来自位于这些韧带中的受体的传入神经的破坏来剥夺基于还原反射的保护。临床上，内侧副韧带（MCL）的一些损伤会导致韧带纤维完全断裂，关节明显不稳定。 膝关节创伤后骨关节炎的发展，可能在MCL损伤后很长时间，被认为是由基于损伤的不稳定性引起的。 很少有人关注这些损伤对韧带的“非结构性”影响，以及韧带在促进关节稳定性方面的神经感觉功能的相互作用。 因此，我们推测，创伤后骨关节炎与MCL损伤是可归因的，至少部分，起源于韧带受体的传入通路的中断。由此可见，对MCL损伤的人膝关节施加机械外翻刺激不能引起靶向肌肉收缩。 我们进一步假设，应用可比的机械刺激对侧正常膝关节反射反应。这显著增加了外翻方向上的关节刚度。 这些假设将在一侧MCL完全损伤而另一侧膝关节正常的受试者中进行检验。受影响和未受影响的膝关节将在完全伸展和不同水平的关节肌肉预激活（在腘绳肌和股四头肌中）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.