Hyperalgesia and allodynia: peripheral mechanisms.
Nociceptive signals are generated by peripheral sensory organs called nociceptors, which are endings of small-diameter nerve fibers responsive to the tissue environment. The myriad chemical mediators capable of activating, sensitizing, or arousing nociceptors include kinins, proinflammatory and anti-inflammatory cytokines, prostanoids, lipooxygenases, the "central immune response mediator" NF-kappaB, neurotrophins and other growth factors, neuropeptides, nitric oxide, histamine, serotonin, proteases, excitatory amino acids, adrenergic amines, and opioids. These mediators may act in combination or at a given time in the inflammatory process, producing subtle changes that result in hyperalgesia or allodynia. We will review the most extensively studied molecular and cellular mechanisms underlying these two clinical abnormalities. The role of the peripheral nervous system in progression of inflammatory joint disease to chronicity is discussed.
Coutaux
Anne
A
Rheumatology Department, Pitié-Salpêtrière Teaching Hospital, 91, Boulevard de l'Hôpital, 75013 Paris, France.
Adam
Frédéric
F
Willer
Jean-Claude
JC
Le Bars
Daniel
D
D006801:Humans; D006930:Hyperalgesia / Q000503:physiopathology*; D007249:Inflammation / Q000503:physiopathology; D018836:Inflammation Mediators / Q000502:physiology*; D009619:Nociceptors / Q000503:physiopathology*; D010146:Pain / Q000209:etiology / Q000503:physiopathology*; D017933:Peripheral Nervous System / Q000503:physiopathology; D015222:Sodium Channels / Q000502:physiology
D018836:Inflammation Mediators; D015222:Sodium Channels