Palliative Care and Pain Therapy Unit, University Hospital of Careggi, Florence, Italy.
Department of Surgery and Translational Medicine, University of Florence, AOU Careggi Largo Brambilla n.3, 50134, Florence, Italy.
Osteoporos Int. 2018 Jul;29(7):1477-1491. doi: 10.1007/s00198-018-4476-y. Epub 2018 Apr 4.
Osteoporosis, a disorder that affects millions of people worldwide, is characterized by decreased bone mass and microstructural alterations giving rise to an increased risk of fractures. Osteoporotic fractures can cause acute and chronic pain that mainly affects elderly patients with multiple comorbidities and commonly on different drug regimens. The aim of this paper is to summarize the pathogenesis and systemic treatment of osteoporotic pain. This narrative review summarizes the main pathogenetic aspects of osteoporotic pain and the cornerstones of its treatment. Osteoporotic fractures induce both acute and chronic nociceptive and neuropathic pain. Central sensitization seems to play a pivotal role in developing and maintaining chronicity of post-fracture pain in osteoporosis. Antiosteoporosis drugs are able to partially control pain, but additional analgesics are always necessary for pain due to bone fractures. Nonsteroidal anti-inflammatory drugs (NSAIDs) and selective COX-2 inhibitors reduce acute pain but with a poor effect on the chronic neuropathic component of pain and with relevant side effects. Opioid drugs can control the whole spectrum of acute and chronic bone pain, but they differ with respect to their efficacy on neuropathic components, their tolerability and safety. Chronic pain after osteoporotic fractures requires a multifaceted approach, which includes a large spectrum of drugs (antiosteoporosis treatment, acetaminophen, NSAIDs, selective COX-2 inhibitors, weak and strong opioids) and non-pharmacological treatment. Based on a better understanding of the pathogenesis of osteoporotic and post-fracture pain, a guided stepwise approach to post-fracture osteoporotic pain will also better meet the needs of these patients.
骨质疏松症是一种影响全球数百万人的疾病，其特征是骨量减少和微观结构改变，导致骨折风险增加。骨质疏松性骨折可引起急性和慢性疼痛，主要影响患有多种合并症的老年患者，且通常使用不同的药物治疗方案。本文旨在总结骨质疏松性疼痛的发病机制和系统治疗。这篇综述总结了骨质疏松性疼痛的主要发病机制和治疗的基石。骨质疏松性骨折可引起急性和慢性伤害性和神经性疼痛。中枢敏化似乎在骨质疏松性骨折后疼痛的发展和维持慢性方面起着关键作用。抗骨质疏松药物能够部分控制疼痛，但对于骨折引起的疼痛，还需要额外的镇痛药。非甾体抗炎药（NSAIDs）和选择性 COX-2 抑制剂可减轻急性疼痛，但对疼痛的慢性神经性成分效果不佳，且存在相关副作用。阿片类药物可以控制急性和慢性骨痛的整个谱，但它们在治疗神经性成分、耐受性和安全性方面存在差异。骨质疏松性骨折后慢性疼痛需要多方面的治疗方法，包括广泛的药物（抗骨质疏松治疗、对乙酰氨基酚、NSAIDs、选择性 COX-2 抑制剂、弱阿片类药物和强阿片类药物）和非药物治疗。基于对骨质疏松症和骨折后疼痛发病机制的更好理解，对骨折后骨质疏松性疼痛的有指导的逐步治疗方法也将更好地满足这些患者的需求。
