Figure 1.

Pathogenesis of ADB. Ageing, diabetes, and genetic factors underlie the pathogenesis of ADB. Scelorstin, DKK1, and sFRP4 inhibits the extracellular binding of wnt to the Frz-LRP5/6 receptor complex blocking the B-catenin-mediated expression of target genes. Hypoparathyrodism precipitated by excessive treatment with cinacalcet and calcitriol therapies together with uremic milieus such as malnutrition, gonadal dysfunction, and uremic toxins all predispose to ADB. The central figure shows acellular bone with bone volume in a patient with ADB. ADB: adynamic bone, DKK-1: Dickkopf-related protein-1, IGF-1: insulin-like growth factor-1, IL-1: interleukin-1, IL-6: interleukin-6, LRP5/6: low-density lipoprotein receptor-related protein 5/6, PTH: parathyroid hormone, sFRP 4: secreted frizzled-related protein 4, TNF-α: tumor necrosis factor-α.