Abstract
In developed nations Charcot arthropathy is most commonly caused by diabetes mellitus. Worldwide, leprosy remains the primary cause. All evidence points to a relationship between neurologic loss, continued loading activities and the development of unrecognized bone fragmentation. In type 2 diabetes, dysregulation of leptin biology causes bone loss and may be an important factor in precipitating Charcot events. Bone density studies show massive loss of bone in patients with ankle and hindfoot Charcot problems, but not midfoot problems. This suggests a different mechanism for collapse. Stable collapse with ulcer development in the midfoot can be treated with exostectomy. Realignment and fusion remain the mainstays of treatment for diabetic Charcot neuropathy, especially in the ankle and hindfoot. Bone mineralization deficiencies require special consideration of fixation techniques. Thin wire external fixation – either as primary fixation or to reinforce/neutralize other methods can be very helpful. Large bridging screws and carefully selected bridging plates are frequently also valuable to consider. Excessive immobilization periods (often double the normal amount of time) are generally required. The goal may be limited to a braceable, plantigrade foot.
