David R Sinacore1, Kathryn L Bohnert2, Kirk E Smith3, Mary K Hastings2, Paul K Commean4, David J Gutekunst5, Jeffrey E Johnson6, Fred W Prior3. 1. Applied Kinesiology Laboratory, Program in Physical Therapy, Campus Box 8502, Washington University School of Medicine, St. Louis, MO, 63108. Electronic address: sinacored@wustl.edu. 2. Applied Kinesiology Laboratory, Program in Physical Therapy, Campus Box 8502, Washington University School of Medicine, St. Louis, MO, 63108. 3. Department of Biomedical Informatics, University of Arkansas for Medical Sciences, Little Rock, AK. 4. Electronic Radiology Laboratory, Mallinckrodt Institute of Radiology, Washington University School of Medicine, St. Louis, MO. 5. Musculoskeletal Biomechanics Laboratory, Program in Physical Therapy, Doisy College of Health Sciences, Saint Louis University, St. Louis, MO. 6. Foot & Ankle Service, Department of Orthopaedic Surgery, Washington University School of Medicine, St. Louis, MO.
Abstract
AIMS: To determine local and systemic markers of inflammation and bone mineral density (BMD) in the foot and central sites in participants with diabetes mellitus and peripheral neuropathy (DMPN) with and without acute Charcot neuropathic osteoarthropathy (CN). METHODS: Eighteen participants with DMPN and CN and 19 participants without CN had foot temperature assessments, serum markers of inflammation [C-reactive protein, (CRP) and erythrocyte sedimentation rate, (ESR)] and BMD of the foot, hip and lumbar spine at baseline and 1year follow-up. RESULTS: CN foot temperature difference was higher compared to DMPN controls at baseline (4.2±1.9°F vs. 1.2±0.9°F, P<0.01) and after 1year (2.9±3.2°F vs. 0.9±1.1°F, P<0.01). Serum inflammatory markers in the CN group were greater at baseline and remained elevated 1year later compared to DMPN controls (CRP, P=0.02, ESR, P=0.03). All pedal bones' BMD decreased an average of 3% in the CN foot with no changes in hip or lumbar spine. DMPN controls' foot, hip and lumbar spine BMD remained unchanged. CONCLUSIONS: Local and systemic inflammation persists 1 year after CN with an accompanying pedal osteolysis that may contribute to mid foot deformity which is the hallmark of the chronic Charcot foot.
AIMS: To determine local and systemic markers of inflammation and bone mineral density (BMD) in the foot and central sites in participants with diabetes mellitus and peripheral neuropathy (DMPN) with and without acute Charcot neuropathic osteoarthropathy (CN). METHODS: Eighteen participants with DMPN and CN and 19 participants without CN had foot temperature assessments, serum markers of inflammation [C-reactive protein, (CRP) and erythrocyte sedimentation rate, (ESR)] and BMD of the foot, hip and lumbar spine at baseline and 1year follow-up. RESULTS: CN foot temperature difference was higher compared to DMPN controls at baseline (4.2±1.9°F vs. 1.2±0.9°F, P<0.01) and after 1year (2.9±3.2°F vs. 0.9±1.1°F, P<0.01). Serum inflammatory markers in the CN group were greater at baseline and remained elevated 1year later compared to DMPN controls (CRP, P=0.02, ESR, P=0.03). All pedal bones' BMD decreased an average of 3% in the CN foot with no changes in hip or lumbar spine. DMPN controls' foot, hip and lumbar spine BMD remained unchanged. CONCLUSIONS: Local and systemic inflammation persists 1 year after CN with an accompanying pedal osteolysis that may contribute to mid foot deformity which is the hallmark of the chronic Charcot foot.
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