Review Article| Volume 21, ISSUE 6, P1035-1049, December 2007

Pathophysiology of Multiple Myeloma Bone Disease

  • Suzanne Lentzsch
    Corresponding author. Division of Hematology/Oncology, Department of Medicine, University of Pittsburgh, 5150 Centre Avenue, #568, Pittsburgh, PA 15232.
    Division of Hematology/Oncology, Department of Medicine, University of Pittsburgh, 5150 Centre Avenue, Pittsburgh, PA 15232, USA
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  • Lori A. Ehrlich
    Division of Hematology/Oncology, Veterans Administration Pittsburgh Healthcare System, Research and Development, 151-U, University Drive C, Pittsburgh, PA 15240, USA
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  • G. David Roodman
    Division of Hematology/Oncology, Department of Medicine, University of Pittsburgh, 5150 Centre Avenue, Pittsburgh, PA 15232, USA

    Division of Hematology/Oncology, Veterans Administration Pittsburgh Healthcare System, Research and Development, 151-U, University Drive C, Pittsburgh, PA 15240, USA
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      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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