Pathophysiology of multiple myeloma bone disease.

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.
Hematology/Oncology Clinics of North America (Impact Factor: 2.08). 01/2008; 21(6):1035-49, viii. DOI: 10.1016/j.hoc.2007.08.009
Source: PubMed

ABSTRACT 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.

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