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dc.contributor.authorJohnson-Lynn, SE
dc.contributor.authorMcCaskie, AW
dc.contributor.authorColl, AP
dc.contributor.authorRobinson, AHN
dc.date.accessioned2018-06-15T09:02:25Z
dc.date.accessioned2018-06-21T07:26:29Z
dc.date.available2018-06-15T09:02:25Z
dc.date.available2018-06-21T07:26:29Z
dc.date.issued2018-05
dc.identifier.issn2046-3758
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/277302
dc.description.abstractCharcot neuroarthropathy is a rare but serious complication of diabetes, causing progressive destruction of the bones and joints of the foot leading to deformity, altered biomechanics and an increased risk of ulceration. Management is complicated by a lack of consensus on diagnostic criteria and an incomplete understanding of the pathogenesis. In this review, we consider recent insights into the development of Charcot neuroarthropathy. It is likely to be dependent on several interrelated factors which may include a genetic pre-disposition in combination with diabetic neuropathy. This leads to decreased neuropeptides (nitric oxide and calcitonin gene-related peptide), which may affect the normal coupling of bone formation and resorption, and increased levels of Receptor activator of nuclear factor kappa-B ligand, potentiating osteoclastogenesis. Repetitive unrecognized trauma due to neuropathy increases levels of pro-inflammatory cytokines (interleukin-1β, interleukin-6, tumour necrosis factor α) which could also contribute to increased bone resorption, in combination with a pre-inflammatory state, with increased autoimmune reactivity and a profile of monocytes primed to transform into osteoclasts - cluster of differentiation 14 (CD14). Increased blood glucose and loss of circulating Receptor for Advanced Glycation End-Products (AGLEPs), leading to increased non-enzymatic glycation of collagen and accumulation of AGLEPs in the tissues of the foot, may also contribute to the pathological process. An understanding of the relative contributions of each of these mechanisms and a final common pathway for the development of Charcot neuroarthropathy are still lacking. Cite this article: S. E. Johnson-Lynn, A. W. McCaskie, A. P. Coll, A. H. N. Robinson. Neuroarthropathy in diabetes: pathogenesis of Charcot arthropathy. Bone Joint Res 2018;7:373-378. DOI: 10.1302/2046-3758.75.BJR-2017-0334.R1.
dc.format.mediumElectronic-eCollection
dc.languageeng
dc.publisherBritish Editorial Society of Bone & Joint Surgery
dc.relation.replaceshttps://www.repository.cam.ac.uk/handle/1810/277069
dc.relation.replaces1810/277069
dc.rightsAttribution-NonCommercial 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by-nc/4.0/
dc.titleNeuroarthropathy in diabetes: pathogenesis of Charcot arthropathy.
dc.typeArticle
prism.endingPage378
prism.issueIdentifier5
prism.publicationDate2018
prism.publicationNameBone Joint Res
prism.startingPage373
prism.volume7
dc.identifier.doi10.17863/CAM.24366
dc.identifier.doi10.17863/CAM.24590
dcterms.dateAccepted2018-03-19
rioxxterms.versionofrecord10.1302/2046-3758.75.BJR-2017-0334.R1
rioxxterms.versionVoR
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserved
rioxxterms.licenseref.startdate2018-05
dc.contributor.orcidMcCaskie, Andrew [0000-0001-6476-0832]
dc.contributor.orcidColl, Anthony [0000-0003-2594-7463]
dc.identifier.eissn2046-3758
rioxxterms.typeJournal Article/Review
cam.issuedOnline2018-06-05
cam.orpheus.successThu Jan 30 12:59:04 GMT 2020 - The item has an open VoR version.
rioxxterms.freetoread.startdate2100-01-01


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Except where otherwise noted, this item's licence is described as Attribution-NonCommercial 4.0 International