Department of Orthopedic Surgery, University of Toledo College of Medicine and Life Sciences, Toledo, OH, USA.
The University of Toledo College of Medicine and Life Sciences, Toledo, OH, USA.
Curr Osteoporos Rep. 2022 Oct;20(5):229-239. doi: 10.1007/s11914-022-00740-z. Epub 2022 Aug 12.
Diabetes mellitus is a chronic metabolic disorder commonly encountered in orthopedic patients. Both type 1 and type 2 diabetes mellitus increase fracture risk and impair fracture healing. This review examines complex etiology of impaired fracture healing in diabetes.
Recent findings point to several mechanisms leading to orthopedic complications in diabetes. Hyperglycemia and chronic inflammation lead to increased formation of advanced glycation end products and generation of reactive oxygen species, which in turn contribute to the disruption in osteoblast and osteoclast balance leading to decreased bone formation and heightening the risk of nonunion or delayed union as well as impaired fracture healing. The mechanisms attributing to this imbalance is secondary to an increase in pro-inflammatory mediators leading to premature resorption of callus cartilage and impaired bone formation due to compromised osteoblast differentiation and their apoptosis. Other mechanisms include disruption in the bone's microenvironment supporting different stages of healing process including hematoma and callus formation, and their resolution during bone remodeling phase. Complications of diabetes including peripheral neuropathy and peripheral vascular disease also contribute to the impairment of fracture healing. Certain diabetic drugs may have adverse effects on fracture healing. The pathophysiology of impaired fracture healing in diabetic patients is complex. This review provides an update of the most recent findings on how key mediators of bone healing are affected in diabetes.
糖尿病是骨科患者常见的慢性代谢性疾病。1 型和 2 型糖尿病都会增加骨折风险并影响骨折愈合。本文综述了糖尿病影响骨折愈合的复杂病因。
最近的研究结果指出了导致糖尿病骨科并发症的几种机制。高血糖和慢性炎症导致晚期糖基化终产物的形成增加和活性氧的产生，进而导致成骨细胞和破骨细胞平衡的破坏，导致骨形成减少，增加了骨折不愈合或延迟愈合以及骨折愈合不良的风险。导致这种失衡的机制是由于促炎介质的增加，导致骨痂软骨过早吸收，以及成骨细胞分化及其凋亡导致骨形成受损。其他机制包括破坏骨骼微环境，骨骼微环境支持愈合过程的不同阶段，包括血肿和骨痂形成，以及在骨重塑阶段的解决。糖尿病的并发症，包括周围神经病变和外周血管疾病，也会影响骨折愈合。某些糖尿病药物可能对骨折愈合有不良影响。糖尿病患者骨折愈合不良的病理生理学很复杂。本文综述了最近关于骨愈合关键介质如何受糖尿病影响的研究结果。
