ABSTRACT
Multiple myeloma (MM) represents the second most common hematological malignancy with an incidence of 4/100,000 individuals (1). There were approximately 16,000 new cases of MM and 11,000 deaths in 2005 alone (2). MM represents a severely debilitating and essentially fatal neoplastic disease of B-cell origin. One of the major sources of morbidity and mortality for patients with MM results from osteolytic bone lesions throughout the axial skeleton which develop in over 70-80% of patients (3). These lesions are frequently associated with severe and debilitating bone pain, and pathologic fractures can occur in up to 60% of patients (4). Bataille and colleagues have demonstrated that there is a balance between bone destruction and new bone formation, as shown in bone biopsies from patients with MM (5). In more advanced disease this balance is lost, resulting in bone destruction and the development of osteolytic lesions (5). The mechanism involved is increased osteoclast activity and bone destruction which develops adjacent to MM cells, yet not in areas of normal bone marrow. Furthermore new bone formation, which would normally develop at sites of prior bone destruction, is absent with evidence of apoptotic osteoblasts (6). The lack of new bone formation explains why nuclear medicine bone scans can severely underestimate the degree of bone destruction in patients with MM. The bone lesions that develop rarely heal,
even when patients are in a complete remission. As a consequence of increased bone destruction, nearly 15% of patients develop hypercalcemia. Overall, the combination of hypercalcemia, pathologic fractures, potential nerve compression, and severe bone pain frequently results in a significant degree of morbidity and mortality for patients with myeloma (7).
