Current concepts underlying the pathophysiology of acute Charcot neuroarthropathy in the diabetic foot and ankle.

The interplay between the acute inflammatory response, cytokine signaling, and bone metabolism equilibrium can now be better understood with the aid of several novel immunobiologic mechanisms. The more recently elucidated roles of advanced glycation end-products, neuropeptides, monocyte differentiation, and genomics combine with classical Charcot pathophysiology to aid researchers and clinicians alike in combatting this often puzzling consequence of peripheral neuropathy.