摘要
多发性骨髓瘤骨病(MMBD)是由浆细胞恶性增殖引起的一系列溶骨性改变,包括骨骼疼痛、高钙血症、骨质疏松、病理性骨折等,起病隐匿、误诊率高,预后差。其核心机制主要是破骨细胞活性增强,成骨细胞被抑制导致的骨模型稳态失衡。近期越来越多的研究认为骨细胞是调节破骨细胞和成骨细胞活性的中心,且MMBD的发生受某些因子调控。文章对MMBD的发生机制进行综述。
Multiple myeloma bone diseases (MMBD) is a series of osteolytic changes caused by plasma cells malignant proliferation,including bone pain,hypercalcemia,osteoporosis,pathological fracture,etc.MMBD has insidious onset,high misdiagnosis rate and poor prognosis.The broken-up bone homeostasis model due to the activated osteoclasts and inhibited osteoblasts is considered as the core mechanism.More and more studies suggest that osteocyte is the key to regulate the activity of osteoclasts and osteoblasts,and the occurrence of MMBD is regulated by some cytokines.This article reviews the mechanisms of MMBD.
作者
杨世伟
朱尊民
Yang Shiwei;Zhu Zunmin(Department of Hematology,Zhengzhou University People's Hospital,Hematology Institute of Henan Provincial People's Hospital,Zhengzhou 450003,China)
出处
《白血病．淋巴瘤》
CAS
2019年第3期190-192,共3页
Journal of Leukemia & Lymphoma
关键词
多发性骨髓瘤
骨髓瘤骨病
预后
Multiple myeloma
Myeloma bone diseases
Prognosis
