Department of Pharmacology, University of Arizona, 1501 N. Campbell Ave., PO Box 245050, Tucson, AZ, 85724, USA.
Cancer Center, University of Arizona, Tucson, AZ, 85724, USA.
Curr Osteoporos Rep. 2018 Aug;16(4):325-332. doi: 10.1007/s11914-018-0446-8.
This paper describes recent advances in understanding the mechanisms that drive fracture pain and how these findings are helping develop new therapies to treat fracture pain.
Immediately following fracture, mechanosensitive nerve fibers that innervate bone are mechanically distorted. This results in these nerve fibers rapidly discharging and signaling the initial sharp fracture pain to the brain. Within minutes to hours, a host of neurotransmitters, cytokines, and nerve growth factor are released by cells at the fracture site. These factors stimulate, sensitize, and induce ectopic nerve sprouting of the sensory and sympathetic nerve fibers which drive the sharp pain upon movement and the dull aching pain at rest. If rapid and effective healing of the fracture occurs, these factors return to baseline and the pain subsides, but if not, these factors can drive chronic bone pain. New mechanism-based therapies have the potential to fundamentally change the way acute and chronic fracture pain is managed.
本文描述了人们对导致骨折痛的机制的理解的最新进展，以及这些发现如何帮助开发治疗骨折痛的新疗法。
骨折后，支配骨骼的机械敏感神经纤维会被机械性扭曲。这会导致这些神经纤维快速放电，并将最初的剧烈骨折痛信号发送到大脑。在数分钟到数小时内，骨折部位的细胞会释放出大量的神经递质、细胞因子和神经生长因子。这些因子会刺激、敏化并诱导感觉神经和交感神经纤维的异位神经发芽，从而导致运动时的剧烈疼痛和休息时的隐隐作痛。如果骨折能够快速有效地愈合，这些因子会恢复到基线水平，疼痛会缓解，但如果没有，这些因子可能会导致慢性骨痛。基于新机制的治疗方法有可能从根本上改变急性和慢性骨折痛的管理方式。
