Charcot foot in diabetes: farewell to the neurotrophic theory.

Neuropathic osteoarthropathy is characterised by relatively painless swelling together with extensive damage in bones and joints, predominantly in the feet and ankles. The uncontrolled natural course of the condition leads to gross foot deformity, skin pressure ulceration, spreading infections, and sometimes amputation. Jean-Martin Charcot in 1883 described "Charcot foot" named after him in patients with tabes dorsalis insensitivity. Charcot believed that intrinsic bone weakness was the underlying condition, and was caused by neurogenic deficiencies in bone nutrition. His followers believed such dystrophy to be mediated by sympathetic denervation of the bone vasculature (neurotrophic, or neurovascular theory). Attempts to prove this theory were futile. A neurogenic circulatory disorder potentially relevant to bone nutrition could not be identified. Nowadays, Charcot foot is mostly seen in diabetic neuropathy, which has replaced syphilis as a frequent cause of peripheral nerve dysfunction. Recent studies in the diabetic Charcot foot and bone turnover indicate that the neurotrophic theory is a myth. The assumption of bone resorption due to sympathetic denervation proved to be false--sympathetic activity increases osteoclastic activity and thereby bone loss (sympathomimetic bone resorption). Except for the transient, inflammatory stage of the diabetic Charcot foot, there is no evidence of relevant osteoporosis or demineralisation of the foot skeleton in diabetes.