Association of Anatomical Location of Neuroarthropathic (Charcot’s) Destruction with Age-and Sex-Matched Bone Mineral Density Reduction
Craig J. Verdin, Georgeanne Botek, John D. Miller, J. Derek Kingsley, Danny Plyler
Abstract
Craig J. Verdin, Georgeanne Botek, John D. Miller, J. Derek Kingsley, Danny Plyler
Abstract
BACKGROUND: It is well documented that diabetes has a systemic impact on bone mineral density. Recent literature has evaluated the relationship between the development of Charcot neuroarthropathy and reduced local bone mineral density; however, it is not clear if there is an association between osteoporosis/osteopenia and Charcot onset, or, even further, location of neuroarthropathic breakdown. METHODS: We retrospectively identified and assessed 39 patients with 41 feet (4 bilateral) with a history of Charcot breakdown who underwent a bone mineral density scan over a 15-year period. Demographic, radiographic, and bone mineral density information was analyzed. RESULTS: The average patient age at the time of bone mineral density scan was 53.44 ± 8.09 years, and 52.77 ± 8.19 years at the time of Charcot diagnosis. Four feet were considered Sanders-Frykberg I (9.3%), 17 were Sanders-Frykberg II (39.5%), ten were Sanders-Frykberg III (23.3%), and 12 were Sanders-Frkyberg IV/V (27.9%). Neuroarthropathic breakdown of the rearfoot region (Sanders-Frykberg IV/V) was found to be associated and preceded by osteoporosis and osteopenia at the hip as demonstrated by a lower Z-score (P = 0.05). Charcot neuroarthropathy was not associated with poor bone health or loss of bone mineral density at the femoral neck, forearm, or lumbar spine. CONCLUSIONS: We believe that the present findings suggest a possible relationship between osteoporosis/osteopenia and the location of CN development. With these findings in mind, we conclude that patients with diabetic skeletal fragility may benefit from treatment of underlying poor bone mineral density to prevent the onset of Charcot neuroarthropathy.
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BACKGROUND: It is well documented that diabetes has a systemic impact on bone mineral density. Recent literature has evaluated the relationship between the development of Charcot neuroarthropathy and reduced local bone mineral density; however, it is not clear if there is an association between osteoporosis/osteopenia and Charcot onset, or, even further, location of neuroarthropathic breakdown. METHODS: We retrospectively identified and assessed 39 patients with 41 feet (4 bilateral) with a history of Charcot breakdown who underwent a bone mineral density scan over a 15-year period. Demographic, radiographic, and bone mineral density information was analyzed. RESULTS: The average patient age at the time of bone mineral density scan was 53.44 ± 8.09 years, and 52.77 ± 8.19 years at the time of Charcot diagnosis. Four feet were considered Sanders-Frykberg I (9.3%), 17 were Sanders-Frykberg II (39.5%), ten were Sanders-Frykberg III (23.3%), and 12 were Sanders-Frkyberg IV/V (27.9%). Neuroarthropathic breakdown of the rearfoot region (Sanders-Frykberg IV/V) was found to be associated and preceded by osteoporosis and osteopenia at the hip as demonstrated by a lower Z-score (P = 0.05). Charcot neuroarthropathy was not associated with poor bone health or loss of bone mineral density at the femoral neck, forearm, or lumbar spine. CONCLUSIONS: We believe that the present findings suggest a possible relationship between osteoporosis/osteopenia and the location of CN development. With these findings in mind, we conclude that patients with diabetic skeletal fragility may benefit from treatment of underlying poor bone mineral density to prevent the onset of Charcot neuroarthropathy.
Key concepts: Medicine, Osteopenia, Bone mineral, Osteoporosis, Bone density, Densitometry, Femoral neck, Reduction (mathematics)