Abstract

Charcot neuroarthropathy is defined by painful or relatively painless bone and joint deformity in limbs that have lost sensory innervation (1). The incidence is ∼0.1–5% in diabetic patients with peripheral neuropathy (2,3). The pathogenesis of Charcot neuroarthropathy is unknown (1,4). In acute Charcot neuroarthropathy, osteoclast activity increases (5). Alendronate is a bisphosphonate that induces the apoptosis of the osteoclasts (6). The utilization of the alendronate could improve the clinical signs of acute Charcot neuroarthropathy and stop bone reabsorption. A total of 20 consecutive patients with a new diagnosis of acute painful Charcot neuroarthropathy were enrolled after the approval of the ethics committee. The patients gave informed consent. Acute Charcot neuroarthropathy was defined on the basis of at least three of the following clinical signs: edema, erythema, and skin temperature increase of 2°C compared with contralateral foot (temperature was measured using an infrared thermometer [Riester] at the site of the maximum deformity of the affected foot and on a similar site on the contralateral foot), deformity, tenderness, abnormal motility, and palpatory crunches. According to a blinded randomization, 11 patients, who were treated with 70 mg alendronate by mouth once a week (test group), and 9 control subjects were followed for 6 months. All patients received a total contact cast boot for the first 2 months and pneumatic walker for …

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call