Osipov Benjamin, Emami Armaun J, Christiansen Blaine A
Lawrence J. Ellison Musculoskeletal Research Center, Department of Orthopaedic Surgery, University of California Davis Medical Center, 4635 2nd Avenue, Suite 2000, Sacramento, CA 95817.
Clin Rev Bone Miner Metab. 2018 Dec;16(4):116-130. doi: 10.1007/s12018-018-9253-0. Epub 2018 Dec 6.
A history of prior fracture is the most reliable indicator of prospective fracture risk. Increased fracture risk is not confined to the region of the prior fracture, but is operant at all skeletal sites, providing strong evidence of systemic bone loss after fracture. Animal and human studies suggest that systemic bone loss begins shortly after fracture and persists for several years in humans. In fact, bone quantity and bone quality may never fully return to their pre-fracture levels, especially in older subjects, demonstrating a need for improved understanding of the mechanisms leading to systemic bone loss after fracture in order to reduce subsequent fracture risk. Although the process remains incompletely understood, mechanical unloading (disuse), systemic inflammation, and hormones that control calcium homeostasis may all contribute to systemic bone loss. Additionally, individual factors can potentially affect the magnitude and time course of systemic bone loss and recovery. The magnitude of systemic bone loss correlates positively with injury severity and age. Men may also experience greater bone loss or less recovery than women after fracture. This review details the current understanding of systemic bone loss following fracture, including possible underlying mechanisms and individual factors that may affect this injury response.
既往骨折史是未来骨折风险最可靠的指标。骨折风险增加并不局限于既往骨折部位,而是在所有骨骼部位都起作用,这有力地证明了骨折后全身性骨质流失。动物和人体研究表明,全身性骨质流失在骨折后不久就开始,并在人类中持续数年。事实上,骨量和骨质量可能永远无法完全恢复到骨折前的水平,尤其是在老年受试者中,这表明需要更好地理解导致骨折后全身性骨质流失的机制,以降低后续骨折风险。尽管这一过程仍未完全了解,但机械性失用(废用)、全身性炎症以及控制钙稳态的激素都可能导致全身性骨质流失。此外,个体因素可能会影响全身性骨质流失和恢复的程度及时间进程。全身性骨质流失的程度与损伤严重程度和年龄呈正相关。骨折后,男性可能比女性经历更大程度的骨质流失或恢复更慢。本综述详细阐述了目前对骨折后全身性骨质流失的理解,包括可能的潜在机制以及可能影响这种损伤反应的个体因素。