Pathophysiology of multiple myeloma bone disease
Pathophysiology of multiple myeloma bone disease
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DOI：
10.1016/j.hoc.2007.08.009
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发表时间：
2007-12-01
影响因子：
2.4
通讯作者：
Roodman, G. David
中科院分区：
文献类型：
--
作者：
Lentzsch, Suzanne;Ehrlich, Lorl A.;Roodman, G. David
多发性骨髓瘤是一种浆细胞恶性肿瘤，其特征是经常发生溶骨性骨病变。多发性骨髓瘤诱导的骨破坏是多发性骨髓瘤细胞附近发生的破骨细胞活性增加的结果。这种活性伴随着成骨细胞分化和活性的抑制，导致骨形成严重受损和破坏性溶骨性病变的发展。近年来，多发性骨髓瘤细胞诱导破骨细胞活化和成骨细胞抑制失衡的生物学机制已开始阐明。本文就多发性骨髓瘤骨重建失衡的病理生理机制及治疗骨病的新策略进行综述。
Multiple myeloma is a plasma cell malignancy characterized by the frequent development of osteolytic bone lesions. The multiple myeloma-induced bone destruction is a result of the increased activity of osteoclasts that occurs adjacent to multiple myeloma cells. This activity is accompanied by suppressed osteoblast differentiation and activity, resulting in severely impaired bone formation and development of devastating osteolytic lesions. Recently the biologic mechanism involved in the imbalance between osteoclast activation and osteoblast inhibition induced by multiple myeloma cells has begun to be clarified. In this article, the pathophysiology underlying the imbalanced bone remodeling and potential new strategies for the treatment of bone disease in multiple myeloma are reviewed.