FLEXOR TENDON HEALING

在美国，每年有超过30万例上肢损伤需要手术治疗，以修复在肌腱中间或止点受伤的肌腱。这些伤害估计造成400万个工作日的损失。对修复和康复变量的科学理解的进步推动了屈肌腱中间物质损伤治疗的最新进展。相比之下，屈肌腱插入部位损伤的治疗几十年来没有显著变化，部分原因是很少有科学研究支持这种变化。因此，许多患者在修复屈肌腱附着点后的临床结果很差，表现为活动范围减少和握力丧失。我们的长期目标是确定修复和康复技术，这些技术将持续产生良好的临床功能，用于立即和延迟治疗屈肌腱插入部位损伤。在这个项目中，我们将应用犬屈肌腱插入部位损伤和修复的模型来研究几个以前没有被解决的临床相关变量：1)肌腱与骨重新连接的缝合技术，2)在康复过程中应用的更大的肌腱作用力和漂移，3)从损伤到修复的时间间隔，以及4)生长因子促进肌腱-骨愈合。我们的基本假设是，在早期的被动运动康复中，通过应用增加的肌腱力来改善修复部位的硬度和强度。此外，我们假设肌腱-骨修复部位的愈合可以通过在修复时交付靶向基因产品来加速，这些基因产品可以增强对早期组织愈合至关重要的生长因子的表达。它们包括：碱性成纤维细胞生长因子(BFGF)、血小板衍生生长因子(PDGF)和血管内皮生长因子(VEGF)。将利用多学科方法对实验变量进行评估，并对生物力学、组织学和生化结果进行分析。实际效益的最终确定将基于关键的前6周愈合期间手指活动范围和修复部位的硬度和强度的生物力学评估。确定改进的插入部位损伤的修复和康复技术将是迈向现代化临床治疗和改善患者预后的第一步。

Annually, more than 300,000 upper extremity injuries in the U.S. require operative treatment for repair of tendons injured in their midsubstance or at their insertion sites. These injuries lead to an estimated loss of 4 million workdays. Recent improvements in the treatment of flexor tendon midsubstance injuries have been driven by advances in the scientific understanding of repair and rehabilitation variables. By contrast, there have been no significant changes in the treatment of flexor tendon insertion-site injuries in several decades, in part because there have been few scientific investigations to support such changes. As a result, many patients have a poor clinical outcome after repair of the flexor tendon insertion site, as evidenced by decreased range of motion and loss of grip strength. Our long-term objective is to identify repair and rehabilitation techniques that will consistently produce excellent clinical function for immediate and delayed treatment of flexor tendon insertion-site injuries. In this project, we will apply a canine model of flexor tendon insertion-site injury and repair to investigate several clinically relevant variables that have not been previously addressed: 1) suture technique for reattachment of tendon to bone, 2) increased tendon force and excursion applied during rehabilitation, 3) time interval from injury to repair, and 4) growth factor enhancement of tendon-bone healing. Our primary hypothesis is that the stiffness and strength of the repair site are improved by application of increased tendon force during early, passive motion rehabilitation. In addition, we hypothesize that healing of the tendon-bone repair site can be accelerated by delivery, at the time of repair, of targeted gene products that enhance expression of growth factors that are important to early tissue healing. These include: basic fibroblast growth factor (bFGF), platelet- derived growth factor (PDGF) and vascular endothelial growth factor (VEGF). A multidisciplinary approach will be utilized for evaluation of the experimental variables, with biomechanical, histological and biochemical outcomes analyzed. The final determination of practical benefit will be based on biomechanical assessment of digital range of motion and repair-site stiffness and strength during the critical first 6 weeks of healing. Identification of improved repair and rehabilitation techniques for insertion-site injuries will be an initial step toward modernizing clinical treatment and improving patient outcomes.