Bone metabolism in the healthy, young adult is identified as a relatively stable process. Normal bone turnover is a dynamic state, which is conferred through intracellular signaling and complex cellular pathways. It has been well described in the literature that Charcot neuro-osteoarthropathy is a disease state, which is marked by intense bone turnover leading to structural collapse and dissolution of skeletal features of the foot and ankle. Within the last two decades, extensive interest has been placed in characterizing the metabolic pathogenesis of Charcot bone metabolism. Despite this work, there remains an incomplete understanding of this devastating disorder. In this article, we review bone histology, physiologic bone metabolism, biomarkers of bone metabolism, pathologic bone metabolism in Charcot diabetics, and potential avenues for intervention.
Keywords: Charcot foot; Diabetic neuropathic osteoarthropathy; Pathogenesis; Receptor activator of nuclear factor k-β ligand (RANKL).
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