FLEXOR TENDON HEALING

在美国，每年有超过30万的上肢损伤需要手术治疗，以修复在其中间物质或插入部位受伤的肌腱。这些伤害造成的损失估计为400万个工作日。最近屈肌腱中物质损伤治疗的改进是由对修复和康复变量的科学理解的进步推动的。相比之下，几十年来屈肌腱插入部位损伤的治疗没有明显的变化，部分原因是很少有科学研究支持这种变化。因此，许多患者在屈肌腱止点修复后临床效果不佳，表现为活动范围减小和握力丧失。我们的长期目标是确定修复和康复技术，这些技术将始终如一地为屈肌腱插入部位损伤的即时和延迟治疗提供出色的临床功能。在这个项目中，我们将应用一个犬屈肌腱插入部位损伤和修复模型来研究几个以前没有解决的临床相关变量：1)缝合技术用于肌腱与骨的再附着，2)在康复期间增加肌腱的力量和偏移，3)从损伤到修复的时间间隔，以及4)生长因子增强肌腱-骨愈合。我们的主要假设是，通过在早期被动运动康复中增加肌腱力，修复部位的刚度和强度得到改善。此外，我们假设肌腱-骨修复部位的愈合可以通过在修复时递送靶向基因产物来加速，这些基因产物可以增强对早期组织愈合很重要的生长因子的表达。这些包括：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）。将采用多学科方法评估实验变量，并分析生物力学、组织学和生化结果。最终确定的实际效益将基于生物力学评估的数字活动范围和修复部位的刚度和力量在关键的前6周愈合。确定插入部位损伤的改进修复和康复技术将是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.