title: Hyperalgesia and allodynia: peripheral mechanisms.
abstract: 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.
authors.affiliation: Rheumatology Department, Pitié-Salpêtrière Teaching Hospital, 91, Boulevard de l'Hôpital, 75013 Paris, France.
authors.forename: Anne
authors.initials: A
authors.lastname: Coutaux
authors.forename: Frédéric
authors.initials: F
authors.lastname: Adam
authors.forename: Jean-Claude
authors.initials: JC
authors.lastname: Willer
authors.forename: Daniel
authors.initials: D
authors.lastname: Le Bars
mesh_terms: 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
chemical_list: D018836:Inflammation Mediators; D015222:Sodium Channels