FLEXOR TENDON HEALING

每年，大约30%的工人急性伤害发生在上层 《极端》(国家安全委员会，1993年；凯尔西报告，1994年)。其中 这些损伤超过350,000人，需要进行广泛的肌腱手术，包括 肌腱修复和重建。粘连形成的发生率 导致初次肌腱修复后手指活动范围较差 而指鞘内的自体肌腱移植一直很高。 最近的临床研究表明，有两个因素，水平升高 近端肌腱负荷和滑膜内更大幅度的 肌腱修复部位远足，可提高肌腱愈合反应 滑膜内肌腱和肌腱移植与受控被动移植的比较 运动和制动康复技术。我们的中央 假设初次接触肌腱愈合是容易的，并且 使用增强型药物可抑制外周粘连形成 近端肌腱负荷水平和/或更高水平 滑膜内肌腱修复部位游览。此外，我们假设 愈合反应被加速为无粘连 新生血管得到增强，肌腱表面细胞迁移和 I型胶原沉积增多。我们建议修好 加速型自体肌腱及肌腱移植 康复计划-通过内在过程持续康复， 依赖于没有外膜的细胞的生存和增殖 来自外周细胞或血管内生的显著贡献 消息来源。 这项提案的目标是确定 体内修复部位作用力和漂移的变化 关于通过改变手腕和手指位置以及肌肉刺激 在康复过程中。形态、生物力学和 滑膜内肌腱和自体肌腱修复后的生化变化 肌腱移植物经过精心选择的增加负荷和更大的 滑行的程度将在体内确定。具体地说， 修复时发生的形态、功能和结构变化 部位和肌腱残端将通过光和电子进行评估 显微镜，通过X-射线摄影术评价，滑动和拉伸 检测并通过细胞受体的免疫组织化学分析 (即整合素)和生长因子(即PDGF-BB和IGF-I) 修复后早期(6-18天)。较长期影响(6-12周后 修复)将通过执行滑行和 拉伸测试。肌腱修复后的新生血管反应 将通过血管注射研究和生化检查进行检查 修复的肌腱基质的特征将通过以下方式进行 检测胶原浓度、交联型胶原分型和DNA 内容。

Annually, approximately 30% of acute injuries in workers are to the upper extremity (National Safety Council, 1993; Kelsey Report, 1994). Among those injuries, over 350,000 require extensive tendon surgery including tendon repair and reconstruction. The incidence of adhesion formation resulting in poor digital range of motion following primary tendon repair and autogenous tendon grafting within the digital sheath has been high. Recent clinical studies have suggested that two factors, increased levels of proximal musculotendinous load and greater magnitudes of intrasynovial tendon repair site excursion, may improve the healing response of intrasynovial tendons and tendon grafts compared to controlled passive motion and immobilization rehabilitation techniques. Our central hypothesis is that primary contact tendon healing is facilitated and peripheral adhesion formation is inhibited with the use of increased levels of proximal musculotendinous load and/or greater levels of intrasynovial tendon repair site excursion. In addition, we hypothesize that the healing response is accelerated as adhesion-free neovascularization is enhanced, and tendon surface cell migration and type I collagen deposition are increased. We propose that repaired tendons and autogenous tendon autografts treated with an accelerated program of -rehabilitation heal consistently by intrinsic processes, relying on cellular survival and proliferation from the epitenon without significant contributions from peripheral cellular or vascular ingrowth sources. The objectives of this proposal are to determine the effects of variations in applied repair site force and excursion in vivo brought about by altering wrist and digital position and by muscle stimulation during the rehabilitation process. Morphological, biomechanical and biochemical changes in repaired intrasynovial tendons and autogenous tendon grafts treated with carefully selected increased loads and greater levels of gliding will be determined in vivo. Specifically, the morphological functional and structural changes occurring at the repair site and in the tendon stumps will be evaluated by light and electron microscopy, by roentgenographic evaluation, by gliding and tensile testing, and by immunohistochemical analysis of the cell's receptors (i.e. integrins) and growth factors (i.e. PDGF-BB and IGF-I) during the early term (6-18 days) post repair. Longer term effects (6-12 weeks post repair) will be evaluated biomechanically by performing gliding and tensile testing. The neovascularization response of the repaired tendons will be examined with vascular injection studies and biochemical characterization of the repaired tendon matrix will be carried out by examining collagen concentration, crosslinking collagen typing and DNA content.