Charcot osteoarthropathy or Charcot foot is a disabling complication of diabetes and is associated with poor prognosis and high mortality. Its pathogenesis is not fully understood and its treatment is at best symptomatic. Furthermore, it is not known whether there is a specific type of neuropathy which affects osteoclastic activity, and thereby leads to reduction of bone mineral density and the development of Charcot osteoarthropathy. Recently it has been proposed that there is a difference in the presentation of Charcot osteoarthropathy between type 1 and type 2 diabetes. This article reviews the link between underlying osteopenia, abnormal biomechanical forces and type of neuropathy, and their varying interaction in the pathogenesis of Charcot osteoarthropathy in type 1 and type 2 diabetes. Further attention is drawn to the newly discovered osteoprotegerin/receptor activator of nuclear factor kappaB ligand (OPG/RANKL) cytokine system, which controls bone resorption. Increased osteoclastic activity in the acute Charcot foot may be associated with altered expression of OPG/RANKL signaling pathway and modulation of the OPG/RANKL equilibrium in Charcot osteoarthropathy may provide additional therapeutical option to manage this difficult condition.
Biomedical Reviews 2005; 16: 43-48.
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