The pathophysiological mechanism of pain in patients with bone metastases in the absence of a fracture is poorly understood. The presence of pain is not correlated with the type of tumor, location, number and size of metastases, gender or age of patients (Oster et al., 1978). While about 80% of patients with breast cancer will develop osteolytic or osteoblastic metastases, about two-thirds of demonstrated sites of bone metastases are painless (Front et al., 1979). The resorption of bone due to the increased osteoclastic activation decreases bone density and disrupts skeletal architecture, either at focal sites or generally throughout the skeleton. Many nerves are found in the periosteum and others enter bones via the blood vessels. Microfractures occur in bony trabeculae at the site of metastases resulting in bone distortion. The stretching of periosteum by tumor expansion, mechanical stress of the weakened bone, nerve entrapment by the tumor or direct destruction of the bone with a consequent collapse are possibly associated mechanisms (Bjurholm et al., 1988; Campa and Payne, 1992; Foley, 1993). The weakening of bone trabecolate and the cytokines, which mediate osteoclastic bone destruction, may activate pain receptors. The release of algesic chemicals within the marrow probably accounts for the observation that pain produced by tumors is often disproportionate to their size or degree of bone involvement. A secondary pain may be caused by reactive muscle spasm (Twycross, 1995). Nerve root infiltration and the compression of nerves by the collapse of osteolytic vertebrae are other sources of pain (Bruera, 1993).