Mechanisms of pain in arthritis

Excerpt

During inflammation in a joint, patients experience hyperalgesia and sometimes resting pain. Hyperalgesia includes stronger pain upon noxious stimulation (e.g. strong pressure or twisting the joint) and the experience of pain when stimuli are applied that are not felt painful under normal conditions (palpation, movements in the working range). Resting pain is felt without intentional stimulation. Neuronal mechanisms involved in arthritic pain are the peripheral sensitization (sensitization of primary afferent fibres supplying the joint) and central sensitization (sensitization of spinal cord neurons). The peripheral sensitization includes the sensitization of so-called polymodal nociceptors (high threshold receptors that are excited under normal conditions by noxious mechanical stimuli) and of silent nociceptors (neurons that are not excited even by noxious mechanical stimuli). When these nociceptors are sensitized in the process of inflammation they are rendered more excitable and then they even respond to normally non-painful stimuli. In addition, the enhanced input from sensitized nociceptors induces hyperexcitability of second-order neurons in the spinal cord. This central sensitization is an increased gain in the spinal nociceptive processing, and sensitized spinal cord neurons show stronger responses to stimulation of inflamed tissue but also to stimulation of adjacent and even remote healthy tissue. Thus the whole pain pathway is sensitized and this explains why, in the inflamed tissue, pain is evoked by stimuli that do not elicit pain under normal conditions [1]. …