老龄化影响下骨质疏松性骨折的病理机制及其影响研究  

Study on the Pathological Mechanisms and Impact of Osteoporotic Fractures under the Influence of Aging

作　　者：刘熔 Rong Liu(School of Health Science and Engineering,University of Shanghai for Science and Technology,Shanghai)

机构地区：[1]上海理工大学健康科学与工程学院,上海

出　　处：《老龄化研究》2025年第3期217-222,共6页Aging Research

摘　　要：随着全球老龄化进程的加快,骨质疏松性骨折(OPF)已成为严重威胁老年人健康的公共卫生问题,特别是在绝经后女性和老年男性中,骨折发生率显著上升。本文系统地分析了骨质疏松性骨折的病理机制,重点探讨了破骨细胞与成骨细胞在骨折发生及愈合过程中的关键作用。破骨细胞过度激活和成骨细胞功能受损是导致骨折愈合延迟和骨质量下降的主要原因。衰老、氧化应激、炎症反应以及雌激素缺乏等因素通过多条信号通路共同影响破骨细胞和成骨细胞的功能。为有效治疗骨质疏松性骨折,本文总结了近年来针对破骨细胞和成骨细胞的最新治疗策略,包括靶向RANKL/RANK信号通路抑制破骨细胞活性、应用甲状旁腺激素类药物促进成骨细胞功能、以及基因治疗和纳米技术在骨折治疗中的潜力。综上所述,精准治疗策略有望加速骨折愈合、改善骨质量,并显著减轻骨质疏松性骨折对患者生活质量和社会经济负担的影响。With the acceleration of global aging,osteoporotic fractures(OPF)have become a significant public health issue threatening the health of the elderly,especially with a marked increase in fracture incidence among postmenopausal women and elderly men.This article systematically analyzes the pathological mechanisms of osteoporotic fractures,focusing on the key roles of osteoclasts and osteoblasts in fracture occurrence and healing.Overactivation of osteoclasts and dysfunction of osteoblasts are the main causes of delayed fracture healing and bone quality deterioration.Aging,oxidative stress,inflammatory responses,and estrogen deficiency,among other factors,influence osteoclast and osteoblast functions through various signaling pathways.To effectively treat osteoporotic fractures,this article summarizes the latest therapeutic strategies targeting osteoclasts and osteoblasts,including inhibition of osteoclast activity via the RANKL/RANK signaling pathway,promotion of osteoblast function with parathyroid hormone(PTH)analogs,and the potential application of gene therapy and nanotechnology in fracture treatment.In conclusion,precision treatment strategies are expected to accelerate fracture healing,improve bone quality,and significantly reduce the impact of osteoporotic fractures on patients’quality of life and the socioeconomic burden.

关 键 词：骨质疏松性骨折 病理机制 破骨细胞 成骨细胞 治疗策略 

分 类 号：R683[医药卫生—骨科学]