Charcot Neuroarthropathy (CN) is a degenerative disease of denervated joints that is most frequently encountered in the feet of patients with diabetic neuropathy. Little is known about etiopathogenesis of CN in diabetes other than that it is usually preceded by the development of moderate to dense diabetic neuropathy and involves a remodeling of bone tissue in the affected foot, usually in the vicinty of several anatomically related joints. Symptoms of CN are usually first notedafter an incident of acute trauma to the foot after which bony disintegration, most often in the tarsal or talonavicular regions, is identifiable by plain radiography. The goal of the present study is to determine if the active bone remodeling found among Cn neuropathic diabetic patients is precipitated by the active CN disease or begins prior to CN fractures. Therefore, we propose to monitor markers of bone remodeling in non-CN neuropathic diabetic patients to determine if any indication of bone remodeling and/or bone disease can be detected among this at-risk population prior to the onset of an active CN process. This study is specifically designed to collect single time-point data on selected biochemical markers of bone regulation and metabolism (Osteocalcin, Collagen, Telopeptides, and Interleukin 1-beta) to determine if patients at risk for CN by virtue of having dense diabetic neuropathy and autonomic neuropathy already show evidence of abnormal bone metabolism prior to actually developing a Charcot fracture.
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