Trends in the pathophysiology of Charcot neuroarthropathy

Dured Dardari

doi:10.1016/j.tem.2022.12.003

Trends in the pathophysiology of Charcot neuroarthropathy

Trends Endocrinol Metab. 2023 Feb;34(2):61-62. doi: 10.1016/j.tem.2022.12.003. Epub 2022 Dec 15.

Author

Dured Dardari¹

Affiliation

¹ Diabetology Department, Centre, Hopitalier Sud Francilien, Corbeil-Essonnes, France; LBEPS, Université d'Evry, IRBA, Université Paris Saclay, 91025 Evry, France. Electronic address: dured.dardari@chsf.fr.

PMID: 36528439
DOI: 10.1016/j.tem.2022.12.003

Abstract

The pathophysiology of Charcot neuroarthropathy (CN) includes a number of gray areas, particularly regarding the onset of inflammation which induces the disruption of the bone remodeling factor responsible for the onset of bone lysis. This clinical insight highlights a potential link between this inflammation and the rapid correction of chronic hyperglycemia (Dardari et al., 2022), which is known to be responsible for a particular type of neuropathy known as treatment-induced neuropathy of diabetes (TIND). Our description makes an additional contribution to shed light on the mysterious physiopathology of CN.

Keywords: Charcot neuroarthropathy; RANKL/OPG; inflammation; rapid correction of chronic hyperglycemia.

MeSH terms

Humans
Inflammation*