Department of Orthopaedic and Trauma Surgery, Campus Biomedico University of Rome, Via Alvaro del Portillo, Rome, Italy.
Int J Immunopathol Pharmacol. 2011 Jan-Mar;24(1 Suppl 2):45-50. doi: 10.1177/03946320110241S209.
Overuse tendinopathies are a common cause of pain and disability in athletes. According to histological findings, it is a failed healing response to overuse tendon injury. In obesity, macrophages and mast cells migrate to adipose tissue, and the resulting decreased availability of immune circulating cells should be responsible for less effective immune responses to acute tendon injury. In diabetic patients, free glucose molecules attach to collagen, alter collagen solubility, increase resistance to enzymatic degradation, and impair cross linking, contributing to the subsequent development of chronic tendinopathy secondary to a failed healing response to a tendon insult. Prolonged systemic, low-grade inflammation and impaired insulin sensitivity act as a risk factor for a failed healing response after an acute tendon insult, and predispose to the development of chronic overuse tendinopathies. Further studies may reveal novel therapeutic treatment approaches.
过度使用性肌腱病是运动员疼痛和残疾的常见原因。根据组织学发现，这是对过度使用肌腱损伤的失败愈合反应。在肥胖症中，巨噬细胞和肥大细胞迁移到脂肪组织，导致免疫循环细胞的可用性减少，这应该是对急性肌腱损伤的免疫反应不那么有效的原因。在糖尿病患者中，游离葡萄糖分子附着在胶原蛋白上，改变胶原蛋白的溶解度，增加对酶降解的抵抗力，并损害交联，导致继发于对肌腱损伤的愈合反应失败的慢性肌腱病。长期全身性低度炎症和胰岛素敏感性受损是急性肌腱损伤后愈合反应失败的危险因素，并易发生慢性过度使用性肌腱病。进一步的研究可能会揭示新的治疗方法。
