Department of Orthopaedic Surgery, University of California at San Francisco, 513 Parnassus Ave., San Francisco, CA, 94143, USA.
Orthopaedic Trauma Institute, Zuckerberg San Francisco General Hospital and Trauma Center, 2550 23rd St, Building 9, San Francisco, CA, 94110, USA.
Curr Osteoporos Rep. 2017 Dec;15(6):601-608. doi: 10.1007/s11914-017-0413-9.
This review summarizes research on the physiological changes that occur with aging and the resulting effects on fracture healing.
Aging affects the inflammatory response during fracture healing through senescence of the immune response and increased systemic pro-inflammatory status. Important cells of the inflammatory response, macrophages, T cells, mesenchymal stem cells, have demonstrated intrinsic age-related changes that could impact fracture healing. Additionally, vascularization and angiogenesis are impaired in fracture healing of the elderly. Finally, osteochondral cells and their progenitors demonstrate decreased activity and quantity within the callus. Age-related changes affect many of the biologic processes involved in fracture healing. However, the contributions of such changes do not fully explain the poorer healing outcomes and increased morbidity reported in elderly patients. Future research should address this gap in understanding in order to provide improved and more directed treatment options for the elderly population.
本篇综述总结了与增龄相关的生理变化及其对骨折愈合的影响。
衰老通过免疫反应的衰老和全身性促炎状态的增加影响骨折愈合过程中的炎症反应。炎症反应的重要细胞,如巨噬细胞、T 细胞和间充质干细胞,表现出内在的与年龄相关的变化,这可能影响骨折愈合。此外,老年人骨折愈合中的血管生成和血管生成受损。最后,软骨细胞和成软骨细胞祖细胞在骨痂中的活性和数量减少。与年龄相关的变化影响骨折愈合过程中许多生物学过程。然而,这些变化的贡献并不能完全解释老年人患者报告的愈合效果较差和发病率增加的情况。未来的研究应该解决这一理解上的差距,以便为老年人群提供更好和更有针对性的治疗选择。