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Exp Brain Res. 2009 Jun;196(1):153-62. doi: 10.1007/s00221-009-1782-9. Epub 2009 Apr 11.

Joint pain.

Author information

1
Institute of Physiology 1/Neurophysiology, University Hospital Jena, Teichgraben 8, 07740 Jena, Germany. Hans-Georg.Schaible@mti.uni-jena.de

Abstract

Both inflammatory and degenerative diseases of joints are major causes of chronic pain. This overview addresses the clinical problem of joint pain, the nociceptive system of the joint, the mechanisms of peripheral and central sensitization during joint inflammation and long term changes during chronic joint inflammation. While the nature of inflammatory pain is obvious the nature and site of origin of osteoarthritic pain is less clear. However, in both pathological conditions mechanical hyperalgesia is the major pain problem, and indeed, both joint nociceptors and spinal nociceptive neurons with joint input show pronounced sensitization for mechanical stimulation. Molecular mechanisms of mechanical sensitization of joint nociceptors are addressed with an emphasis on cytokines, and molecular mechanisms of central sensitization include data on the role of excitatory amino acids, neuropeptides and spinal prostaglandins. The overview will also address long-term changes of pain-related behavior, response properties of neurons and receptor expression in chronic animal models of arthritis.

PMID:
19363606
DOI:
10.1007/s00221-009-1782-9
[Indexed for MEDLINE]
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