Relationship between Charcot joints and Diabetes
A Charcot joint occurs in <1% of all diabetics (both type 1 and type 2). It occurs in both men and women with equal frequency. More than two-thirds of patients are aged >40 years and have had long-standing (>10 years), poorly controlled diabetes complicated by a diabetic peripheral neuropathy. Patients present with relatively painless swelling and deformity of the joint. The foot (most commonly tarsometatarsal joints) and ankle are most commonly involved, although the knee, hip, and spine involvement can occur as well. Occasionally it can be of sudden onset mimicking an infection. With progression of disease, the patient can develop “rocker bottom” feet due to midtarsal collapse. Skin over bony prominences can ulcerate and become infected without the patient’s knowledge as a result of abnormal sensation resulting from the neuropathy.
Radiographs frequently show severe abnormalities characterized by the 5 Ds: destruction, density (increased), debris, disorganization, and dislocation. The increased density and sharp margins of the bony debris can help distinguish a Charcot joint from infection. The exact pathophysiology is uncertain, but an autonomic neuropathy leading to increased blood flow, hyperemia, and osteoclastic resorption of bone is believed to be the primary mechanism, alongside repetitive microtrauma to a desensate foot. Treatment includes protected weight-bearing, soft casts, good shoes and aggressive treatment and prevention of skin ulcerations. Charcot joints, however, usually progress. There is no role for surgery (fusion, arthroplasty) other than amputation for severe cases. DM has replaced neurosyphilis as the most common cause of a Charcot joint.
