Wang Xuejuan, Li Li, Wang Yun
Department of Anesthesiology, Beijing Friendship Hospital, Capital Medical University, Beijing, People's Republic of China.
J Pain Res. 2025 Jan 20;18:315-326. doi: 10.2147/JPR.S498466. eCollection 2025.
Bone is a common site of advanced cancer metastasis, second only to the lungs and liver. Cancer-induced bone pain (CIBP) is a persistent and intense pain that is caused by a combination of inflammatory and neuropathic factors. As CIBP progresses, the degree of pain intensifies. Despite advancements in medical technology, the treatment outcomes of patients with CIBP remain unsatisfactory, and severe pain can typically only be controlled with opioid medications. However, patients treated with opioid medications often develop tolerance. Therefore, they may require dose increases, which can increase the severity of opioid-induced side effects, in turn influencing quality of life. The peripheral mechanisms of CIBP primarily involve bone tissue damage, tumor microenvironment formation, and changes in the dorsal root ganglion. The central mechanisms usually involve biochemical and electrophysiological changes in the spinal cord and brain. The spinal cord is the main processing center for nociceptive signals. When tumor cells produce inflammatory mediators that acidify the microenvironment or damage nerve endings, the spinal cord becomes excessively stimulated, resulting in increased or prolonged pain signals that propagate to the higher central nervous system through the ascending pathway. There are substantial differences in the pain generation mechanisms between CIBP and common inflammatory and neuropathic pain. Therefore, understanding the mechanisms underpinning CIBP development at the level of the spinal cord is crucial for optimizing pain management. This study explores the pathogenesis of CIBP at the level of the spinal cord and describes recently proposed treatment methods for CIBP.
骨骼是晚期癌症转移的常见部位，仅次于肺和肝。癌症诱发的骨痛（CIBP）是一种由炎症和神经病理性因素共同引起的持续性剧痛。随着CIBP的进展，疼痛程度会加剧。尽管医疗技术有所进步，但CIBP患者的治疗效果仍不尽人意，严重疼痛通常只能用阿片类药物控制。然而，接受阿片类药物治疗的患者往往会产生耐受性。因此，他们可能需要增加剂量，这会增加阿片类药物引起的副作用的严重程度，进而影响生活质量。CIBP的外周机制主要涉及骨组织损伤、肿瘤微环境形成以及背根神经节的变化。中枢机制通常涉及脊髓和大脑的生化和电生理变化。脊髓是伤害性信号的主要处理中心。当肿瘤细胞产生使微环境酸化或损伤神经末梢的炎症介质时，脊髓会受到过度刺激，导致疼痛信号增加或延长，并通过上行通路传播到更高的中枢神经系统。CIBP与常见的炎症性和神经病理性疼痛在疼痛产生机制上存在很大差异。因此，在脊髓水平了解CIBP发生发展的机制对于优化疼痛管理至关重要。本研究探讨了脊髓水平上CIBP的发病机制，并描述了最近提出的CIBP治疗方法。
