IMMUNOPROBES FOR LUBRICIN FROM HUMAN SYNOVIAL FLUID

尽管进行了大量的研究，但骨性关节炎发病机制中的特定或相关原因仍不清楚。 这证明了一个新的研究场所涉及退行性关节疾病的其他因素。 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，标准化的商业测定和分配滑液润滑的临床重要性。本研究涉及动物关节滑液润滑的分子。 相当多的文献已经证明，这些摩擦和加压表面（即，轴承）具有低摩擦性能（1-4）。这些特性部分是由于关节软骨的光滑特性引起的。 大多数报告实际上涉及滑液的流变学，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工表面之间的摩擦系数。 滑液中一种称为润滑素的润滑糖蛋白对此负责，但没有人提出它如何这样做或如何在体外研究它的机制。 PI使用的由乳胶对玻璃振荡组成的关节测振仪再现了先前使用软骨关节面研究的关键结果。 它隔离边界模式润滑测量装置以前采用的其他人。 滑液、唾液和洗涤剂是唯一显示这种活性的物质（11）。 润滑素润滑乳胶：玻璃轴承的观察结果是PI最近发现的。 这提供了一个实验的机会，牵连失败的润滑在退行性关节疾病的发生在大量的患者，并因果联系这一措施润滑。 低摩擦系数（mu）不一定是磨损保护的量度，但滑液实际上确实赋予软骨这种性质（12）。 目前尚不清楚润滑素的缺乏或缺乏是否对骨关节炎或类风湿性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学探针，并利用这些探针鉴定从健康和关节炎患者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.