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 然而肌腱的分子生物学研究 治愈被忽视了。 细胞的主要反应是 肌腱是产生新的胶原蛋白和非胶原蛋白。 胶原蛋白是 这种关键的结构蛋白质使肌腱能够 抵抗张力。 胶原交联的含量和位置主要是 测定抗拉力的强度。 已知 受伤肢体的固定会导致关节僵硬， 韧带和肌腱中的顽固性粘连，影响活动性。 一个 亚稳态、可还原胶原交联的增加伴随着 迁移率 受伤肌腱的中期锻炼， 手术修复有利于愈合， 可还原和稳定的吡啶啉交联可能不会形成限制 议案 肌腱细胞如何对胶原蛋白做出反应并调节它们， 非胶原蛋白对创伤的反应，以及固定或 改变这些反应？ 鞘、滑膜细胞和内 肌腱成纤维细胞相互作用， 量的适当的胶原蛋白，具有正确的质量？ 是 这些细胞的某些组合参与基质重组， 哪种细胞的作用最大？ 过程中 本研究发现，纤维连接蛋白的产生和分泌是 在体内，与内部成纤维细胞相比，滑膜细胞增加 在vitro？ 纤连蛋白是否单独用作细胞粘附分子， 这些细胞和异常分泌是否会促进粘附形成？ 是 纤连蛋白与其他一些分子如 透明质酸在肌腱表面作为润滑剂？ 将 固定和运动改变纤连蛋白合成和分泌 肌腱细胞群？ 本研究的总体目标是 识别正在愈合的肌腱中胶原蛋白结构的变化 并已受到固定或运动，并调查 肌腱细胞在体内和体外的生化反应 力. 根据动物实验的结果，我们希望应用一种 涉及物理和化学干预的人类医学战略， 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.