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Sylvia Thiele, Anke Hannemann, Maria Winzer, Ulrike Baschant, Heike Weidner, Matthias Nauck, Rajesh V Thakker, Martin Bornhäuser, Lorenz C Hofbauer and Martina Rauner

glucocorticoid-induced osteoporosis (GIO) involves many organ systems. At the skeletal level, GCs stimulate osteoclastogenesis and profoundly inhibit bone formation ( 3 , 4 ). While an increased receptor activator of NF-κB ligand (RANKL)/osteoprotegerin (OPG