Abstract

Charcot neuroarthropathy, or, as it is also known, neuropathic joint disease (NJD), is a particularly severe form of osteoarthritis. It is recognized by severe joint damage in the context of relatively little pain in the presence of neuropathy and associated with characteristic radiographic changes in well-established disease. Patients with diabetes are at particular risk of NJD; permanent disability through foot deformity or amputation as a consequence of peripheral neuropathy (1) and diabetes is now the leading cause of NJD. The midfoot or ankle joints are most commonly affected in diabetic patients (2). The limited epidemiologic data on NJD suggest that ∼0.1–0.4% of patients with diabetes develop NJD (3), usually 10–15 years after the onset of diabetes, and up to 16% of diabetic patients with peripheral neuropathy have been reported to be affected by NJD (4), which therefore represents a considerable cause of diabetic ankle- and foot-related morbidity. NJD often presents acutely, resulting in misdiagnosis and inappropriate treatment and consequently leading to disastrous damage and possible loss of the affected limb (3). Typically, in the acute phase, NJD presents as a warm, edematous, and erythematous joint (5,6). As a result of sensory neuropathy, there may be little pain or tenderness, and the patient may not even seek medical assistance. During examination, a bounding pedal pulse compared with the other limb is found (7). The radiographic changes of chronic NJD include florid new bone formation, joint space loss, and severe joint destruction and deformity, but these characteristic changes are usually absent in early NJD. In this clinical context, cellulitis, osteomyelitis, or infection may be diagnosed instead and treated accordingly, and the window of opportunity for the initiation of treatment designed to minimize subsequent NJD joint …

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