Bone Abstracts

Iron overload due to hemochromatosis or chronic blood transfusions has been implicated in the development of osteoporosis. However, the impact of iron overload or iron deficiency on stromal cell functions and the underlying mechanisms are poorly defined. Since the Wnt signaling pathway is a critical regulator of bone remodelling, we aimed to analyse the effects of iron overload and iron deficiency on osteoblast function and further define the role of Wnt signaling in these pro...

: Glucocorticoid-induced osteoporosis (GIO) is the most frequent secondary osteoporosis in patients undergoing steroid therapy.Recently we demonstrated that the inhibition of bone formation in GIO is occurring in part via the suppression of autocrine cytokines by the glucocorticoid receptor (GR) monomer in osteoblasts (Cell Metab 11, 517–531). Since emerging evidences indicate that microRNAs (miRNAs) play a critical role in the differentiat...

Owing to their anti-inflammatory effects, steroid therapy using glucocorticoids (GCs) is still part of the treatment of rheumatoid arthritis (RA), despite several severe side effects like glucocorticoid-induced osteoporosis (GIO). Until now the molecular mechanisms underlying the beneficial and side effects of GC therapy are poorly understood. GCs exert their actions via the glucocorticoid receptor (GR) that alters gene expression by either binding as a dimer to GC response el...

Osteoporosis is a frequent disease leading to an increased risk of fractures caused by a systemic impairment of bone mass, strength, and microarchitecture. Given the emerging role of the Wnt signaling pathway in bone biology, we focused on the function of the important Wnt inhibitor dickkopf-1 (Dkk-1) and examined how the deletion of Dkk-1 solely in osteoblasts or osteocytes influences bone homeostasis. Therefore, we used the Cre-LoxP recombination system and crossed Dkk-1-flo...

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Glucocorticoids (GCs) are widely used to treat chronic inflammatory diseases such as rheumatoid (RA) and lead to multiple side effects including glucocorticoid induced osteoporosis (GIO). Our work challenges the dogma that transrepression of pro-inflammatory genes by the glucocorticoid receptor (GR) is solely responsible for reducing inflammation, whereas transactivation of genes is causing side effects.Using conditional and function selective mutant mic...