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.
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