Abstract
Cancer-induced bone pain is a common complication of bone metastases and consists of a triad of continuous pain, spontaneous pain and incident pain. It can considerably compromise social functioning, quality of life and survival. Through the use of animal models, it has been suggested that cancer-induced bone pain differs from other pain states, including inflammatory and neuropathic pain; it is increasingly considered to be a complex, mixed-mechanism pain, rather than a single neuropathic, visceral or inflammatory pain state. A variety of possible mechanisms by which bone metastases may cause pain have been reported. These mechanisms likely include local production of growth factors and cytokines (either tumour-induced or tumour-produced), tumour-induced osteolysis, stimulation of ion channels on nerve cell endings, and direct infiltration. However, the exact mechanism by which a bone metastasis induces pain is not completely understood. The understanding of its pathophysiology continues to evolve and further research is required into the complex basis of cancer-induced bone pain and its mechanisms.
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