IMMUNOPROBES FOR LUBRICIN FROM HUMAN SYNOVIAL FLUID

尽管进行了大量的研究，骨关节炎发病机制的具体或相关原因仍不清楚。这证明了对涉及退行性关节疾病的其他因素进行研究的新场所。关节润滑的研究，生物摩擦学，一直充满了相互矛盾的理论，未能充分利用分子技术，标准化的商业分析，并赋予临床滑膜液润滑的重要性。本研究探讨了动物关节滑膜润滑的分子机制。大量文献表明，这些摩擦和加压表面（即轴承）具有低摩擦特性（1-4）。这些特性部分源于关节软骨的光滑性。大多数报告实际上是处理滑液的流变学，并可能错误地认为其粘度是关节润滑的基础（5-10）。直接测量证明，滑液降低了软骨轴承和某些人造表面之间的摩擦系数。来自滑液的一种称为“润滑素”的润滑糖蛋白负责这一点，但没有人提出它是如何起作用的机制或如何在体外研究它。PI使用的由乳胶振荡对抗玻璃组成的关节关节计再现了先前使用软骨轴承研究的关键发现。它隔离了以前被其他人采用的边界模式润滑测量装置。滑液、唾液和洗涤剂是唯一显示这种活性的物质（11）。润滑油润滑乳胶玻璃轴承是PI最近的一项发现。这提供了一个实验机会，暗示润滑失败在退行性关节疾病的发生在大量患者中，并将这一措施与润滑剂因果联系起来。低摩擦系数（mu）不一定是磨损保护的衡量标准，但滑液确实赋予软骨这种特性（12）。目前尚不清楚润滑剂的缺乏或缺乏是否对骨关节炎或类风湿关节炎的初始或持续发病有重要意义。本研究的主要目的是开发新的免疫探针，并利用这些探针鉴定从健康和患有关节炎的人关节中提取的滑液中润滑素的浓度。

Specific or related causes in the pathogenesis of osetoarthritis remain unclear despite a great deal of investigation. This justifies a new venue of research into other factors involved in degenerative joint disease . The study of joint lubrication, biotribology, has been fraught with conflicting theories, failure to adequately use molecular techniques, standardize merchanical assays and assign clinical importance to lubrication by synovial fluid. This investigation addresses the molecular of synovial lubrication of animal joints. A considerable literature has demonstrated that these rubbing and pressurized surfaces (i.e., bearings) have low frictional properties (1-4). These properties arise in part from the slippery nature of articular cartilage. Most reports actually deal with the rheology of synovial fluid and may incorrectly assume that its viscosity is the basis for joint lubrication (5-10). Direct measurements documents that synovial fluid lowers the coefficient of friction between cartilage bearings and certain artificial surfaces. A lubricating glycoprotein termed "lubricin" from synovial fluid is responsible for this but no one has proposed a mechanism of how it does so or how to study it in vitro. An arthrotripsometer composed of latex oscillating against glass employed by the PI reproduced critical findings of previous studies using cartilage bearings. It isolated boundary mode lubrication measuring devices previously employed by others. Synovial fluid, saliva, and detergents are the only substances which display this activity (11). The observation that lubricin lubricated the latex: glass bearing is a recent discovery by the PI. This provides an experimental opportunity to implicate failed lubrication in the occurrence of degenerative joint disease in a large number of patients and to causally link this measure to lubricin. A low coefficient of friction (mu) is no necessarily a measure of wear protection but synovial fluid does in fact confer this property to cartilage (12). It is unknown if the absence or paucity of lubricin is significant to the initial or continued pathogenesis of either osteoarthritis or rheumatoid arthritis. This principal goal of this investigation is to develop new immunological probes and with these identify the concentration of lubricin in synovial fluid extracted from healthy and arthritic human joints.