Review

Experimental Brain Research

, Volume 196, Issue 1, pp 153-162

First online:

Joint pain

  • Hans-Georg SchaibleAffiliated withInstitute of Physiology 1/Neurophysiology, University Hospital Jena Email author 
  • , Frank RichterAffiliated withInstitute of Physiology 1/Neurophysiology, University Hospital Jena
  • , Andrea EbersbergerAffiliated withInstitute of Physiology 1/Neurophysiology, University Hospital Jena
  • , Michael K. BoettgerAffiliated withInstitute of Physiology 1/Neurophysiology, University Hospital Jena
  • , Horacio VanegasAffiliated withInstitute of Physiology 1/Neurophysiology, University Hospital Jena
  • , Gabriel NaturaAffiliated withInstitute of Physiology 1/Neurophysiology, University Hospital Jena
  • , Enrique VazquezAffiliated withInstitute of Physiology 1/Neurophysiology, University Hospital Jena
  • , Gisela Segond von BanchetAffiliated withInstitute of Physiology 1/Neurophysiology, University Hospital Jena

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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.

Keywords

Arthritis Osteoarthritis Cytokines Central sensitization Peripheral sensitization