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. 2012 Feb;8(1):26-8.
doi: 10.1007/s11420-011-9263-7. Epub 2012 Feb 23.

Mechanisms of pain in osteoarthritis

Bruce Kidd  1
Affiliations

Mechanisms of pain in osteoarthritis

Bruce Kidd. HSS J. 2012 Feb.
No abstract available

Keywords: Anesthesiology; Imaging / Radiology; Medicine & Public Health; Orthopedics; Rheumatology; Sports Medicine; Surgical Orthopedics; central sensitization; inflammatory mediators; osteoarthritis; pain; peripheral sensitization.

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Figures

Fig. 1
Fig. 1
Peripheral sensitization. Contribution of peripheral nociceptors to pain. a Acute pain: Noxious stimuli activate high threshold ion channels with resultant propagation of axon potentials. b Early phase sensitization: Mediators, including prostaglandin E2, activate kinases to phosphorylate receptors/ion channels and lower threshold for activation. c Late phase sensitization: Gene induction in response to growth factors resulting in changes to cell phenotype. Adapted from [16]. Adapted with permission of John Wiley & Sons, Inc.
Fig. 2
Fig. 2
Central sensitization. Contribution of spinal cord neurones to pain. a Acute pain: Activation of AMPA receptor by glutamate. NMDA receptor blocked. b Early phase sensitization: Activation of NMDA receptor following removal of magnesium ion block [mediated by substance P (SP) acting on NK1 receptors—black spheres and triangle, respectively]. c Late phase sensitization: Gene induction with enhanced production of prostaglandins and other local mediators. Modulation by descending facilitatory/inhibitory pathways. Adapted from [16]. Adapted with permission of John Wiley & Sons, Inc.
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