The mechanisms underlying the bone disease induced by diabetes are complex and not fully understood; and antiresorptive agents, the current standard of care, do not restore the weakened bone architecture. Herein, we reveal the diabetic bone signature in mice at the tissue, cell, and transcriptome levels and demonstrate that three FDA-approved bone-anabolic agents correct it. Diabetes decreased bone mineral density (BMD) and bone formation, damaged microarchitecture, increased porosity of cortical bone, and compromised bone strength.
View Article and Find Full Text PDFContext: Hypoparathyroidism is a rare disease and, as such, its natural history, long-term complications, and correct clinical management remain unclear.
Objective: To describe the natural history and clinical characteristics of the disease.
Design And Setting: To present a retrospective observational analysis from 7 specialized centers in Buenos Aires, Argentina.