AFFECTS OF IMMOBILIZATION & MOTION IN THE INJURED TENDON

肌腱损伤在创伤病例中所占比例越来越大 在我们医院有报道，但对肌腱的分子生物学研究 医治一直被忽视。损伤后细胞的主要反应 肌腱是产生新的胶原蛋白和非胶原蛋白。胶原蛋白是 持续存在的关键结构蛋白，使肌腱有能力 抵抗拉力。胶原蛋白的交联量和位置很大 测定抗拉力的大小。这是众所周知的 固定受伤的肢体会导致关节僵硬和 韧带和肌腱的顽固性粘连，影响活动能力。一个 亚稳的、可还原的胶原交联物的增加伴随着 机动性。肌腱损伤后应尽早进行中期锻炼 外科修复有利于愈合，因为某些亚稳态， 可还原的、稳定的吡啶酚交联物不能形成极限 动议。肌腱细胞如何反应和调节其胶原蛋白和 非胶原蛋白对创伤的反应，以及固定化或 运动改变了这些反应吗？鞘、滑膜细胞和内部是如何 肌腱成纤维细胞相互作用，产生足够的 有合适质量的合适的胶原蛋白的数量？是 这些细胞的某些组合参与了基质的重组 在这些细胞中，哪种细胞的作用最大？在课程期间 在这项研究中，我们发现纤维连接蛋白的产生和分泌 与体内成纤维细胞相比，滑膜细胞增加 那么在体外呢？纤维连接蛋白是否单独用作细胞黏附分子 这些细胞以及异常分泌是否会促进黏附的形成？是 Fibonectin与其他一些分子如 透明质酸在肌腱表面起到润滑剂的作用？将要 固定化和运动改变纤维连接蛋白的合成和分泌 肌腱细胞群？这项研究的总体目标是 识别正在愈合的肌腱中胶原蛋白结构的变化 并已被固定或移动，并调查 肌腱细胞对外用药物的体内和体外生化反应 力量。根据动物实验的结果，我们希望应用一种 人类医学涉及物理和化学干预的策略 促进肌腱愈合。

Tendon injuries constitute an increasing proportion of trauma cases reported at our hospital, yet research in the molecular biology of tendon healing has been neglected. The major response of cells in an injured tendon is to produce new collagen and noncollagen proteins. Collagen is the key structural protein that persists, giving tendon its ability to resist tensile forces. The collagen crosslink content and location largely determine themagnitude of the resistance to tensile force. It is known that immobilization of an injured limb leads to joint stiffness and intractable adhesions in ligaments and tendons that impair mobility. An increase in metastable, reducible collagen crosslinks accompanies loss of mobility. Middle exercise of an injured tendon as early as possible after surgical repair is favorable to healing because certain metastable, reducible, and stable pyridinoline crosslinks may not form to limit motion. How do tendon cells react to and regulate their collagen and noncollagen protein responses to wounding, and how does immobiliztion or motion alter these responses? How do sheath, synovial cells, and inner tendon fibroblasts interact with each other to produce sufficient quantities of the appropriate collagen that has the right qualities? Are certain combinations of these cells involved in matrix reorganiztion during healing and which of these cells has the greatest role? During the course of this research, we have found tht fibronectin production and secretion is increased in synovial cells compared to internal fibroblasts both in vivo and in vitro? Is fibronectin used as a cell attachment molecule alone by these cells and could abnormal secretion promote adhesion formation? Is firbonectin found in conjunction with some other molecule such as hyaluronic acid on the tendon surface to act as a lubricant? Will immobilization and motion alter fibronectin synthesis and secretion by tendon cell populations? The overall objectives of this study are to identify changes in the structure of collagen in tendons that are healing and have been subjected to immobilization or motion and to investigate the biochemical responses of tendon cells in vivo and in vitro to applied forces. Based on results of animal experimentation, we hope to apply a strategy to human medicine involving physical and chemical intervention to improve tendon healing.