Differential Diagnosis: Bone Pain and Fractures

Abstract

Bone pain is a very common feature of many metabolic bone diseases such as metastatic bone disease, osteoporosis and Paget’s disease of bone. The bone pain that accompanies such diseases can very often be severe and debilitating. Attempts to relieve pain in these conditions can dominate the management of the overall disease. A common factor in many metabolic bone diseases is increased bone resorption, mediated by activated osteoclasts, a pathophysiological process that often results in pain by a variety of direct and indirect mechanisms. The mechanism of pain is complex and depends on an increasing number of interrelated pathways and mediators. The sensation of pain from bone is still poorly understood, although it is believed to depend mainly on the action of nociceptors in the periosteum and around joint surfaces, whilst areas such as the cortex and bone marrow are believed to be insensitive to pain. In general terms bone pain can be categorized as arising from one of the following mechanisms: a direct action on bone nociceptors or a secondary mechanical effect. A number of chemical mediators can directly affect bone nociceptors, in addition to structural damage to nerve fibres by direct compression of tissue. Often mechanical pressures on an area of bone that is pain insensitive may alter the shape of a nearby joint and cause pain. For instance, a vertebral compression fracture may distort a nearby apophyseal joint, triggering nociceptors and resulting in pain. Although the mechanisms of bone pain, in a variety of different diseases, may have common pathways, the role of certain mediators in the cause of the pain may differ and this may have therapeutic implications.