背景 骨癌性疼痛（bone cancer pain, BCP）或癌性骨痛（cancer-induced bone pain, CIBP）是原发性恶性骨肿瘤或者骨转移癌患者最主要的临床问题，约85%的骨恶性肿瘤患者出现疼痛，从而导致焦虑甚至抑郁，降低其终末期的生活质量[1]。BCP目前临床上难以达到彻底的疼痛缓解[2]。近些年来，随着BCP动物模型的建立和成熟，其病理生理机制正逐渐被人阐述。目的 总结BCP涉及到的病理机制，希望对临床寻找基于病理机制的治疗提供新的思路。内容 综合和总结近5年内的研究文章，阐述BCP涉及的病理机制。趋向 BCP病理机制复杂，涉及到肿瘤—脊髓—大脑的结构性、生理性、药理性等以及细胞因子和通路等的改变，研究建立在机制研究基础上的治疗手段将会给患者带来福音。
Background Bone cancer pain(BCP) or Cancer-induced bone pain(CIBP) is a major clinical problem with up to 85% of paitients with primary bone cancer or bony metastases, often associated with anxiety and depression,reduced performance status, and a poor quality of life. BCP is hard to control. In the last few years, with the development of BCP animal models, its pathological mechanisms has been demonstrated by many researchers. Objective To summarize the pathological mechanisms which may offer the new ideas in the treatment of BCP. Content This article will review the mechanisms implicated in BCP by collecting research articles published in last 5 years. Trend The pathological mechanisms of BCP are so difficult to make clear becaeuse it involves the structural,physiological and pharmalogical alterations of tumor-spine-brain levels and cytokines or cell sign pathways. Traitements based on the pathological mechanisms would be beneficial to the patients suffering from BCP.
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