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Joint remodelling in inflammatory disease
Correspondence to:
Georg Schett, Department of Internal Medicine 3 and Institute for Clinical Immunology, University of Erlangen-Nuremberg, Krankenhausstrasse 12, D-91054 Erlangen, Germany; georg.schett{at}med3.imed.uni-erlangen.de
Bone and the immune system share multiple interactions. The skeleton harbours the bone marrow and provides the niche for development of haematopoietic cells including the immune system. The immune system provides cells as well as molecular signals, which regulate bone homeostasis. Understanding the cellular and molecular regulation of the tight interaction between bone and the immune system is crucial for understanding the changes of skeletal architecture during inflammation. Whereas a short and self-limited activation of the immune system has no clinically meaningful effect on bone, prolonged immune activation as found in chronic inflammatory disease inevitably leads to bone wasting.
Abbreviations: AS, ankylosing spondylitis; BMPs, bone morphogenic proteins; DKK, Dickkopf; MCSF, macrophage colony-stimulating factor; OPG, osteoprotegerin; PsA, psoriatic arthritis; RA, rheumatoid arthritis; RANKL, receptor-antagonist of NF-kB ligand; Wnt, wingless proteins
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