Hjertner Ø, Standal T, Børset M, Sundan A, Waage A
Department of Cancer Research and Molecular Medicine, Norwegian University of Science and Technology, Trondheim, Norway.
Curr Drug Targets. 2005 Sep;6(6):701-11. doi: 10.2174/1389450054863716.
One of the most characteristic features of multiple myeloma is the development of osteolytic bone lesions. Myeloma-associated bone disease is caused by an increase in osteoclastic bone resorption and a decrease in osteoblastic new bone formation. Insight into the molecular mechanisms of osteoclastogenesis has been provided by the detection of receptor activator of NF-kappaB ligand (RANKL), its specific receptor (RANK) and its decoy receptor antagonist osteoprotegerin (OPG). The RANK signaling system is abnormally regulated in multiple myeloma and targeting this system may ameliorate myeloma bone disease. Less is known about the development of osteoblastic dysfunction, and further knowledge about the interaction between myeloma cells and osteoblasts is required. The aim of this review is to focus on the principles of bone biology for a better understanding of the development of myeloma bone disease and to identify possible therapeutic targets.
多发性骨髓瘤最典型的特征之一是溶骨性骨病变的发生。骨髓瘤相关骨病是由破骨细胞骨吸收增加和成骨细胞新骨形成减少引起的。通过检测核因子κB受体活化因子配体（RANKL）、其特异性受体（RANK）及其诱饵受体拮抗剂骨保护素（OPG），人们对破骨细胞生成的分子机制有了深入了解。RANK信号系统在多发性骨髓瘤中受到异常调节，针对该系统可能改善骨髓瘤骨病。关于成骨细胞功能障碍的发生了解较少，需要进一步了解骨髓瘤细胞与成骨细胞之间的相互作用。本综述的目的是聚焦于骨生物学原理，以更好地理解骨髓瘤骨病的发生，并确定可能的治疗靶点。
