The Charcot Foot Reflects a Response to Injury That Is Critically Distorted by Preexisting Nerve Damage: An Imperfect Storm

Abstract

It has been recognized since comprehensive descriptions by Jean-Martin Charcot in 1868 and 1883 that development of what is usually known as neuropathic osteoarthropathy (or the Charcot foot) requires the coincidence of neuropathy and inflammation. Despite this, detailed understanding of the causes has remained remarkably limited in the succeeding century and a half. The aim of this descriptive account is to draw particular attention to the processes involved in both the onset and resolution of the inflammation that is an essential component of active disease. The principal observation is that while neuropathy is common in people with diabetes, the inflammation and secondary skeletal damage that characterize neuropathic osteoarthropathy are observed in only a small minority of people with diabetes and with neuropathy. We therefore argue that the key to understanding the causes of the Charcot foot is to focus equally on those who have active disease as well as those who do not. Although neuropathy is essential for development of the disorder, neuropathy also has an adverse impact on the mechanisms involved in the onset of inflammation, and these may be critically affected in the majority of those who are susceptible. The Charcot foot is uncommon in people with diabetes (or any other cause of neuropathy) because the large majority of those with neuropathy may have also lost the capacity to mount the specific inflammatory reaction that is essential for its development.