FLEXOR TENDON HEALING

每年，大约30%的工人急性损伤发生在上腹部。 极端（国家安全理事会，1993;凯尔西报告，1994）。 之间 超过350，000例受伤需要进行广泛的肌腱手术， 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差 指鞘内自体肌腱移植的比例很高。 最近的临床研究表明，两个因素，增加水平， 近端肌肉肌腱负荷和滑膜内更大幅度的 肌腱修复部位偏移，可能会改善 滑膜内肌腱和肌腱移植物与对照被动 运动和固定康复技术。我们的中央 假设是促进了初级接触肌腱愈合， 外周粘连的形成被抑制， 近端肌肉肌腱负荷水平和/或更高水平的 滑膜内肌腱修复部位偏移。 另外，我们假设 愈合反应加速， 新血管形成增强，肌腱表面细胞迁移和 I型胶原沉积增加。我们建议修复 肌腱和自体肌腱自体移植物， 康复计划通过内在过程持续愈合， 依赖于细胞的存活和增殖， 来自外周细胞或血管向内生长的显著贡献 源 本提案的目的是确定 在体内施加的修复部位力和偏移的变化 通过改变手腕和手指的位置， 在康复过程中。形态学、生物力学和 修复后滑膜内肌腱和自体肌腱的生化变化 肌腱移植物经过精心选择的增加负荷和更大的 将在体内确定滑动水平。具体而言是 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 显微镜检查，X线评价，滑动和拉伸 测试，并通过细胞受体的免疫组织化学分析 (i.e.整合素）和生长因子（即PDGF-BB和IGF-I）， 修复后早期（6-18天）。长期影响（术后6-12周） 修复）将通过进行滑动和 拉伸试验修复肌腱的新生血管反应 将进行血管注射研究和生化检查 修复后的肌腱基质的表征将通过 检测胶原蛋白浓度、交联胶原蛋白分型和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.