Lentzsch Suzanne, Ehrlich Lori A, Roodman G David
Division of Hematology/Oncology, Department of Medicine, University of Pittsburgh, and Division of Hematology/Oncology, Veterans Administration Pittsburgh Healthcare System, Research and Development, PA 15232, USA.
Hematol Oncol Clin North Am. 2007 Dec;21(6):1035-49, viii. doi: 10.1016/j.hoc.2007.08.009.
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.
多发性骨髓瘤是一种浆细胞恶性肿瘤，其特征是频繁出现溶骨性骨病变。多发性骨髓瘤诱导的骨破坏是由于骨髓瘤细胞附近破骨细胞活性增加所致。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毁灭性溶骨性病变的发展。最近，由多发性骨髓瘤细胞诱导的破骨细胞激活与成骨细胞抑制之间失衡所涉及的生物学机制已开始得到阐明。本文综述了多发性骨髓瘤骨重塑失衡的病理生理学以及治疗骨病的潜在新策略。
