Mechanisms of Chronic Pain in Osteoarthritis


Pain is a major clinical problem of osteoarthritis (OA). Recently, OA has been thought to be a disease of the whole joint with both destruction of cartilage and inflammatory components such as synovitis and bone marrow lesions. Clinical studies have documented a significant inflammatory soft tissue contribution to the severity and frequency of OA pain. Both clinical and experimental studies have provided evidence for the sensitization of pain pathways during OA, involving pronounced changes in joint nociceptors and changes of the nociceptive processing in the spinal cord, brainstem, and thalamocortical system. Additionally, evidence has been provided for neuropathic pain components in OA models. Concerning molecular mechanisms of OA pain and potential options for pain therapy, studies on nerve growth factor, cytokines, sodium channel blockers, hyaluronic acid preparations, and others are addressed in this review.

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Correspondence to Hans-Georg Schaible.

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Schaible, HG. Mechanisms of Chronic Pain in Osteoarthritis. Curr Rheumatol Rep 14, 549–556 (2012).

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  • Bone marrow lesion
  • Brain atrophy
  • Cannabinoids
  • Central sensitization
  • COX-2 inhibitor
  • Cytokines
  • Descending facilitation
  • Descending inhibition
  • Endocannabinoids
  • Hyaluronic acid
  • Interleukin-6
  • Interleukin-1β
  • Joint nociceptor
  • Joint pain
  • MIA model
  • Microglial activation
  • Nav1.8
  • Nerve growth factor
  • Neuropathy
  • Osteoarthritis
  • Peripheral sensitization
  • Sodium channel blocker
  • Synovitis
  • TNF-α
  • TRPV1 channel
  • Chronic pain