Mechanisms of multiple myeloma bone disease.
Mechanisms of multiple myeloma bone disease.
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DOI：
10.1038/bonekey.2012.135
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发表时间：
2012-01-01
期刊：
影响因子：
--
通讯作者：
Roodman, G David
中科院分区：
文献类型：
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作者：
Galson, Deborah L;Silbermann, Rebecca;Roodman, G David
多发性骨髓瘤是第二常见的血液系统恶性肿瘤，也是累及骨骼的最常见的癌症。多发性骨髓瘤骨病(MMBD)是以骨吸收和骨形成功能障碍为特征的异常骨重建，可作为其他炎症性骨病的范例，以及破骨细胞和成骨细胞在恶性肿瘤中的调控。对MMBD的研究已经发现了新的调节剂，可以增加破骨细胞的生成和破骨细胞的功能，抑制成骨细胞的分化，增加血管生成，或者永久改变基质细胞。本文将讨论MMBD中破骨细胞和成骨细胞调节机制的研究现状，以及目前正在使用和正在开发的针对骨髓瘤患者骨破坏和骨形成抑制介质的治疗方法，包括新的合成代谢疗法。
Multiple myeloma is the second most common hematological malignancy and the most frequent cancer to involve the skeleton. Multiple myeloma bone disease (MMBD) is characterized by abnormal bone remodeling with dysfunction of both bone resorption and bone formation, and thus can be used as a paradigm for other inflammatory bone diseases, and the regulation of osteoclasts and osteoblasts in malignancy. Studies of MMBD have identified novel regulators that increase osteoclastogenesis and osteoclast function, repress osteoblast differentiation, increase angiogenesis, or permanently alter stromal cells. This review will discuss the current understanding of mechanisms of osteoclast and osteoblast regulation in MMBD, and therapeutic approaches currently in use and under development that target mediators of bone destruction and blockade of bone formation for myeloma patients, including new anabolic therapies.