Introduction

Myeloma bone disease is a major cause of morbidity in patients, the clinical manifestations of which include pain, cord compression, loss of mobility and deformity. The clinical features of myeloma bone disease are due to osteoporosis, or focal lytic lesions leading to pathological fractures, vertebral collapse and hypercalcemia (Figure 8.1). Neurological sequelae secondary to bone disease are commonly caused by compression of nerves by damaged and displaced bone and most dramatically include spinal cord compression, which often presents as a neurosurgical emergency occurring in up to 5% of patients with myeloma (Figure 8.2)[1]. Indeed, consequences of osteolytic bone disease are often the presenting features of myeloma. Approximately 67% of patients with myeloma present with bone pain and up to 90% of patients with myeloma exhibit features of myeloma bone disease at some stage of the disease course[2,3].

The bone marrow micro-environment has long been recognized as a hospitable locale for the growth and rapid expansion of myeloma and other hematological malignancies as well as the metastatic spread of solid tumors including breast and prostate cancers. However, myeloma is uniquely associated with an aggressive and destructive osteolytic bone disease, which not only causes substantial morbidity as a direct result of bone destruction but, owing to the destruction of boney barriers, enables rapid tumor expansion and spread to extra-medullary sites. Once myeloma has escaped from the bone marrow micro-environment, disease enters a leukemic phase and is rapidly fatal.