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Multiple myeloma (MM) is a plasma cell disorder, characterized by bone marrow infiltration with clonal plasma cells, production of monoclonal immunoglobulin (paraprotein), and end organ damage including lytic lesions in the bones, renal impairment, hypercalcemia, and anemia. End organ damage is the main differentiating point of symptomatic from asymptomatic MM.

In myeloma bone disease (MBD), lesions could be in the form of a classic discrete lytic lesion (radiolucent, plasmacytoma), widespread osteopenia, or multiple lytic lesions affecting any part of skeleton, preferably spine, skull, and long bones. The higher the number of lesions, the poorer the prognosis.

Increased osteoclastogenesis with suppressed osteoblastic activity is the main mechanism of MBD.4 There are certain factors involved in stimulation and formation of osteoclasts (OCs) and reduction of osteoblastic activity. Recent advances in understanding of MBD showed that the receptor activator of nuclear factor kappa-B ligand (RANKL) and osteoprotegerin (OPG) system plays a key role in this regard.

MBD on one hand results in increased disability, morbidity, and on the other hand leads to increased cost of treatment of these patients.6 MM patients with bone disease not only need standard antimyeloma therapy but also require treatment with bisphosphonates (BPs), pain control, and a subgroup of patients may need radiotherapy and surgical interventions. This article focuses on different factors involved in the development of MBD and treatment modalities to manage this condition.

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