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Mechanoadaptation: articular cartilage through thick and thin

机译:机械齿面:通过厚且薄的关节软骨

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Abstract The articular cartilage is exquisitely sensitive to mechanical load. Its structure is largely defined by the mechanical environment and destruction in osteoarthritis is the pathophysiological consequence of abnormal mechanics. It is often overlooked that disuse of joints causes profound loss of volume in the articular cartilage, a clinical observation first described in polio patients and stroke victims. Through the 1980s, the results of studies exploiting experimental joint immobilisation supported this. Importantly, this substantial body of work was also the first to describe metabolic changes that resulted in decreased synthesis of matrix molecules, especially sulfated proteoglycans. The molecular mechanisms that underlie disuse atrophy are poorly understood despite the identification of multiple mechanosensing mechanisms in cartilage. Moreover, there has been a tendency to equate cartilage loss with osteoarthritic degeneration. Here, we review the historic literature and clarify the structural, metabolic and clinical features that clearly distinguish cartilage loss due to disuse atrophy and those due to osteoarthritis. We speculate on the molecular sensing pathways in cartilage that may be responsible for cartilage mechanoadaptation.
机译:摘要关节软骨对机械负荷有敏感。其结构主要由机械环境而定义,并且骨关节炎的破坏是异常力学的病理生理结果。它常常被忽略,滥用关节导致关节软骨中的体积丧失,脊髓灰质炎患者和中风受害者首先描述的临床观察。通过20世纪80年代,研究利用实验联合固定的研究结果支持了这一点。重要的是,这种实质性的工作也是第一个描述导致基质分子的合成,特别是硫酸化蛋白多糖的合成的代谢变化。尽管有软骨中的多机械损伤机制,但脱脂萎缩的分子机制很差。此外,已经倾向于与骨关节炎变性等同于软骨损失。在这里,我们审查了历史文学,并阐明了结构,代谢和临床特征,清楚地区分布式萎缩和由于骨关节炎而导致的结构。我们推测软骨中的分子传感途径,可能负责软骨机械面。

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