多发性骨髓瘤骨病发生机制研究进展  

Cellular Mechanisms of Multiple Myeloma Bone Disease

作　　者：李强[1] 高秀娟[2] 高磊[1] 

机构地区：[1]聊城市人民医院血液科,山东聊城252000 [2]聊城市人民医院麻醉科,山东聊城252000

出　　处：《医学综述》2016年第9期1697-1700,共4页Medical Recapitulate

摘　　要：多发性骨髓瘤(MM)是一种恶性浆细胞疾病,其中骨痛是其最常见的临床症状,部分患者出现病理性骨折,甚至截瘫,严重影响了患者的生活质量。尽管最近的治疗进展使患者平均生存时间翻了一倍,但是骨髓瘤仍然是无法治愈的疾病。现已证实有多种途径和调节成骨细胞和破骨细胞活性的因子参与了MM骨病的发生与恶化。其中核因子κB受体激活蛋白/核因子κB受体激活蛋白配体/骨保护素系统、泛素-蛋白酶体途径、Wnt信号途径和骨髓微环境中细胞间的相互作用对MM骨病的发生、发展起了至关重要的作用。Multiple myeloma（MM） is a hematologic malignancy caused by clonal expansion of malignant plasma cells and bone pain is the most common clinical symptom, some patients may have pathologic fracture and even paraplegina which affect the quality of life of the patients severely. Despite recent therapeutic advances, which have doubled the median survival time, myeloma continues to be a mostly incurable disease. Recent studies have revealed that numerous pathways and regulating factors of esteoblast and osteoclast activity interfere with the pathogenesis of MM bone disease, for example, RANK/RANKL/OPG system, ubiquitin-pre- teasome pathway, Wnt signal pathway, and interactions between cells in bone marrow microenvirenment play key roles.

关 键 词：多发性骨髓瘤 骨病 成骨细胞 破骨细胞 细胞因子 

分 类 号：R733.3[医药卫生—肿瘤]