Bone disease in multiple myeloma (MM) is characterized by lytic bone lesions, which can cause severe bone pain, pathologic fractures and hypercalcemia. However, the lytic bone disease in MM differs from that in other cancer patients who have lytic bone metastases. Although increased osteoclastic bone destruction is involved in MM and other tumors involving bone, in contrast to other tumors, once the MM tumor burden exceeds 50% in a local area, osteoblast activity is either suppressed or absent.1 The basis for this severe imbalance between increased osteoclastic bone resorption and decreased bone formation has been a topic of intensive investigation over the last several years and will be reviewed in this article.
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Preparation of this article was made possible by research funds from the Multiple Myeloma Research Foundation and from the Department of Veteran's Affairs (VA Merit Review Award). The materials are the result of work supported with resources and the use of facilities at the VA Pittsburgh Healthcare System, Research and Development.
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