How Bone and the Immune System communicate
A wide variety of chronic inflammatory diseases cause bone loss. To understand this phenomenon, the Bone Lab focuses on two common diseases: rheumatoid arthritis, a chronic inflammation of the joints, and periodontitis, an inflammation of the tooth-supporting structures. In rheumatoid arthritis, which affects 1-2% of the population, joints and bones are damaged and mobility is lost. Periodontitis affects almost 50% of the aging population and leads to tooth loss. Both diseases considerably impair life quality.
Our aim is to better understand the interactions between the immune and skeletal system and identify novel molecular targets that may be used to treat bone loss caused by inflammation. An important topic of this research area is glucocorticoid-induced osteoporosis (GIO). Glucocorticoids are amongst the most commonly described drugs to treat inflammatory diseases. Even though they are very potent and offer patients quick relief of pain and swelling, their long-term use is associated with poor bone quality. Our ambition is to understand what drives bone loss in inflammation and glucocorticoid treatment in order to minimize it in the future.
Martina Rauner, PhD
«Was my first love… the collaborations within the Immunobone consortium really pushed my career»
Ulrike Baschant, PhD
«I would call it my scientific home.»
Paula Goes Pinheiro Dutra, PhD
«I can say it is the core of my career. It is amazing to understand periodontitis through the eyes of immunology.»
Jan Tuckermann, Universität Ulm
Georg Schett, Universität Erlangen-Nürnberg
Maxime Breban, Institut Cochin, Paris, France
Triantaphyllos Chavakis, Technische Universität Dresden
Anke Hannemann, Universität Greifswald
Nicole Horwood, Oxford University, UK
Colditz J, Thiele S, Baschant U, Garbe AI, Niehrs C, Hofbauer LC, Rauner M. Osteogenic Dkk1 mediates glucocorticoid-induced but not arthritis-induced bone loss. J Bone Miner Res. 2019. (in press)
Koenen M, Culemann S, Vettorazzi S, Caratti G, Frappart L, Baum W, Krönke G, Baschant U, Tuckermann JP. Glucocorticoid receptor in stromal cells is essential for glucocorticoid-mediated suppression of inflammation in arthritis. Ann Rheum Dis. 2018; 77:1610-18.
Hildebrandt S, Baschant U, Thiele S, Tuckermann J, Hofbauer LC, Rauner M. Glucocorticoids suppress Wnt16 expression in osteoblasts in vitro and in vivo. Sci Rep. 2018;8:8711.
Geurtzen K, Vernet A, Freidin A, Rauner M, Hofbauer LC, Schneider JE, Brand M, Knopf F. Immune suppressive and bone inhibitory effects of prednisolone in growing and regenerating zebrafish tissues. J Bone Miner Res. 2017;32:2476-2488.
Schulz MC, Kowald J, Estenfelder S, Jung R, Kuhlisch E, Eckelt U, Mai R, Hofbauer LC, Stroszczynski C, Stadlinger B. Site-specific variations in bone mineral density under systemic conditions inducing osteoporosis in minipigs. Front Physiol. 2017;8:426.
Liu P, Baumgart M, Groth M, Wittmann J, Jäck HM, Platzer M, Tuckermann JP, Baschant U. Dicer ablation in osteoblasts by Runx2 driven cre-loxP recombination affects bone integrity, but not glucocorticoid-induced suppression of bone formation. Sci Rep. 2016;6:32112.
Rauner M, Thiele S, Sinningen K, Winzer M, Salbach-Hirsch J, Gloe I, Peschke K, Haegeman G, Tuckermann JP, Hofbauer LC. Effects of the selective glucocorticoid receptor modulator A compound on bone metabolism and inflammation in male mice with collagen-induced arthritis. Endocrinology. 2013;154:3719-28.