title: Charcot neuro-osteoarthropathy.
abstract: The classical neurotraumatic and neurotrophic theories for the pathogenesis of the acute Charcot neuro-osteoarthropathy (CN) in diabetes, do not address certain key features of the disease. These features include the facts that the condition usually affects just one side, that it is self-limiting, and that it is also very uncommon. Similarly, it is not known to what extent the condition may depend, as suggested by Jean-Martin Charcot, on pre-morbid osteopenia. Recent advances in understanding the mechanisms underlying the pathogenesis of osteopenia and osteoporosis and the central role of the RANKL/OPG signalling system have, however, suggested the possible involvement of other factors in the evolution of the disease. Specifically, it has been suggested that acute CN may be triggered in a susceptible individual by any event that leads to localized inflammation in the affected foot. This local inflammation leads to a vicious cycle in which there is increasing inflammation, increasing expression of RANKL, and increasing bone breakdown. The likely central role for the RANKL/OPG pathway suggests new possibilities for future treatments.
authors.affiliation: Department of Diabetes and Endocrinology, Nottingham University Hospitals Trust, City Hospital Campus, Nottingham NG5 1PB, UK. wjeffcoate@futu.co.uk
authors.forename: William J
authors.initials: WJ
authors.lastname: Jeffcoate
mesh_terms: D001177:Arthropathy, Neurogenic / Q000503:physiopathology* / Q000628:therapy; D001851:Bone Diseases, Metabolic / Q000503:physiopathology*; D018450:Disease Progression; D006801:Humans; D007249:Inflammation / Q000503:physiopathology