FLEXOR TENDON HEALING

屈肌腱愈合

• 批准号: 2429569
• 负责人: RICHARD H GELBERMAN
• 金额: $ 29.52万
• 依托单位: WASHINGTON UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 1987
• 资助国家: 美国
• 起止时间: 1987-05-01 至 2000-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/2429569
• 关键词: DNA; autologous transplantation; biomechanics; cell adhesion; collagen; crosslink; dogs; gene expression; high performance liquid chromatography; immunocytochemistry; in situ hybridization; insulinlike growth factor; integrins; joint stiffness; light microscopy; limb movement; messenger RNA; musculoskeletal regeneration; platelet derived growth factor; radiography; scanning transmission electron microscopy; tendon injury; tensile strength; transmission electron microscopy; wound healing

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.

每年，大约 30% 的工人急性损伤发生在上肢 （国家安全委员会，1993 年；凯尔西报告，1994 年）。 之中 这些损伤中，超过 350,000 例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 导致初级肌腱修复后手指活动范围较差 指鞘内自体肌腱移植率很高。 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的负荷 肌腱修复部位偏移，可能会改善愈合反应 滑膜内肌腱和肌腱移植物与受控被动肌腱相比 运动和固定康复技术。我们的中央 假设是促进初级接触肌腱愈合并且 使用增加的药物可以抑制外周粘连的形成 近端肌腱负荷水平和/或更高水平 滑膜内肌腱修复部位偏移。 此外，我们假设 由于无粘连，愈合反应会加速 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 经过加速处理的肌腱和自体肌腱移植物 -康复计划通过内在过程持续愈合， 依赖于表皮细胞的细胞存活和增殖，而无需 外周细胞或血管向内生长的显着贡献 来源。 该提案的目的是确定以下措施的影响： 施加的修复部位力和体内偏移的变化带来 通过改变手腕和手指位置以及肌肉刺激 在康复过程中。形态学、生物力学和 修复滑膜内肌腱和自体肌腱的生化变化 经过精心挑选的增加负荷和更大的肌腱移植物处理 滑动水平将在体内测定。具体来说， 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 显微镜检查、X 线摄影评估、滑动和拉伸 测试以及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）。长期影响（术后 6-12 周） 修复）将通过执行滑行和 拉伸测试。修复肌腱的新生血管反应 将通过血管注射研究和生化检查进行检查 修复后的肌腱基质的表征将通过 检查胶原蛋白浓度、交联胶原蛋白分型和 DNA 内容。