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一次严重骨折:骨折后急慢性疼痛的机制与评估

A bad break: mechanisms and assessment of acute and chronic pain after bone fracture.

作者信息

Nishimura Haruki, Layne Jonathan, Yamaura Kohei, Marcucio Ralph, Morioka Kazuhito, Basbaum Allan I, Weinrich Jarret A P, Bahney Chelsea S

机构信息

Center for Regenerative and Personalized Medicine, Steadman Philippon Research Institute, Vail, CO, United States.

Department of Orthopaedic Surgery, University Hospital of Occupational and Environmental Health, Fukuoka, Japan.

出版信息

Pain. 2025 May 21. doi: 10.1097/j.pain.0000000000003646.

DOI:10.1097/j.pain.0000000000003646
PMID:40408239
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12354150/
Abstract

Pain is one of the primary indicators of a bone fracture and serves both a functional and practical role in guiding recovery. However, fracture pain can persist long after the fracture itself has clinically healed. The neural and molecular mechanisms that drive acute pain postfracture, and how these mechanisms are pathologically usurped to trap patients into persistent, debilitating, and often difficult to treat, chronic pain, are not well understood. The aim of this review is to provide insight into the risk factors for pain persistence after fracture, review the physiological and pathophysiological mechanisms of fracture pain, and critically evaluate the literature around fracture pain assessment techniques/models. Taken together, the concepts covered herein will provide a strong foundation to support the development of more effective treatments to better alleviate postfracture pain.

摘要

疼痛是骨折的主要指标之一,在指导康复过程中兼具功能和实际作用。然而,骨折疼痛可能在骨折本身临床愈合后仍长期存在。导致骨折后急性疼痛的神经和分子机制,以及这些机制如何在病理上被篡夺,使患者陷入持续的、使人衰弱且往往难以治疗的慢性疼痛,目前尚不清楚。本综述的目的是深入了解骨折后疼痛持续的危险因素,回顾骨折疼痛的生理和病理生理机制,并严格评估有关骨折疼痛评估技术/模型的文献。综上所述,本文涵盖的概念将为支持开发更有效的治疗方法以更好地缓解骨折后疼痛提供坚实基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8852/12519537/497e4b62e3aa/jop-166-e491-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8852/12519537/7cc63c1ba613/jop-166-e491-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8852/12519537/497e4b62e3aa/jop-166-e491-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8852/12519537/7cc63c1ba613/jop-166-e491-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8852/12519537/497e4b62e3aa/jop-166-e491-g002.jpg

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本文引用的文献

1
Polytrauma impairs fracture healing accompanied by increased persistence of innate inflammatory stimuli and reduced adaptive response.多发伤会损害骨折愈合,同时伴有先天性炎症刺激持续时间延长和适应性反应降低。
J Orthop Res. 2025 Mar;43(3):603-616. doi: 10.1002/jor.26015. Epub 2024 Nov 17.
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Innate immune response to bone fracture healing.对骨折愈合的先天免疫反应。
Bone. 2025 Jan;190:117327. doi: 10.1016/j.bone.2024.117327. Epub 2024 Nov 8.
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BDNF sensitizes bone and joint afferent neurons at different stages of MIA-induced osteoarthritis.
BDNF 可使 MIA 诱导的骨关节炎不同阶段的骨和关节传入神经元敏化。
Bone. 2024 Dec;189:117260. doi: 10.1016/j.bone.2024.117260. Epub 2024 Sep 17.
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Sensory nerve regulation of bone homeostasis: Emerging therapeutic opportunities for bone-related diseases.感觉神经对骨稳态的调节:骨相关疾病的新兴治疗机会。
Ageing Res Rev. 2024 Aug;99:102372. doi: 10.1016/j.arr.2024.102372. Epub 2024 Jun 14.
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Nerve growth factor receptor limits inflammation to promote remodeling and repair of osteoarthritic joints.神经生长因子受体限制炎症反应,促进骨关节炎关节的重塑和修复。
Nat Commun. 2024 Apr 15;15(1):3225. doi: 10.1038/s41467-024-47633-6.
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Sensory neuron transient receptor potential vanilloid-1 channel regulates angiogenesis through CGRP .感觉神经元瞬时受体电位香草酸亚型1通道通过降钙素基因相关肽调节血管生成。
Front Bioeng Biotechnol. 2024 Mar 21;12:1338504. doi: 10.3389/fbioe.2024.1338504. eCollection 2024.
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Silencing p75NTR regulates osteogenic differentiation and angiogenesis of BMSCs to enhance bone healing in fractured rats.沉默 p75NTR 可调节 BMSCs 的成骨分化和血管生成,从而增强骨折大鼠的骨愈合。
J Orthop Surg Res. 2024 Mar 20;19(1):192. doi: 10.1186/s13018-024-04653-8.
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OsteoMac: A new player on the bone biology scene.OsteoMac:骨生物学领域的新玩家。
Ann Anat. 2024 Jun;254:152244. doi: 10.1016/j.aanat.2024.152244. Epub 2024 Mar 14.
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Temporal dynamics of immune-stromal cell interactions in fracture healing.骨折愈合中免疫-基质细胞相互作用的时空动态
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Med Res Rev. 2024 Jul;44(4):1867-1903. doi: 10.1002/med.22031. Epub 2024 Feb 29.