Interaction of pain and chronic inflammation.

Abstract

Rheumatic diseases are characterized by chronic inflammation of synovial joints and are often associated with persistent pain and increased pain sensitivity. The inflammatory process is acomplex cascade of events involving several mediators, which can lead to achronic condition of pain. Inflammation can stimulate angiogenesis, and angiogenesis can facilitate inflammation. Inflammatory pain arises from tissue damage via the sensitization of pain receptors (nociceptors). The main peripheral mechanism underlying nociceptive pain is achange in the activity of the nociceptors located in the affected anatomical structures (joints, tendons, and ligaments), which renders them more sensitive to normally painful stimuli (hyperalgesia) or normally non-painful stimuli (allodynia). Neuroimmune interaction has been considered to play an essential role in rheumatic disease. Neurogenic inflammation, which influences normal central nervous system signaling, leads to insufficient signaling/bioavailability of various cytokines. These central mechanisms play an important role in the increased pain sensitivity following inflammation and are responsible for the development of secondary hyperalgesia in regions beyond the injured tissue. Reduction of pain in rheumatic disease requires familiarity with various pain mechanisms.