Purpose of review: When tissue is destroyed, pain arises. Tissue destruction is associated with an inflammatory reaction. This leads to activation of nociceptors. The following review will concentrate on pro-algesic and analgesic mediators, which arise from immune cells or resident cells in the periphery or the circulation during inflammation.
Recent findings: In early inflammation endogenous hyperalgesic mediators are produced, including cytokines, chemokines, nerve growth factor as well as bradykinin, prostaglandins and ATP. Simultaneously, analgesic mediators are secreted: opioid peptides, somatostatin, endocannabinoids and certain cytokines. Inflammation increases the expression of peripheral opioid receptors on sensory nerve terminals and enhances their signal transduction, as well as the amount of opioid peptides in infiltrating immune cells. Interference with the recruitment of opioid-containing immune cells into inflamed tissue by blockade of adhesion molecules or by intrathecal morphine injection reduces endogenous analgesia.
Summary: Inflammatory pain is the result of the interplay between pro-algesic and analgesic mediators. To avoid central side effects, future analgesic therapy should be targeted at either selectively blocking novel pro-algesic mediators or at enhancing endogenous peripheral analgesic effects.