Experimental glucocorticoid induced osteoporosis: differences between mouse strains

Abstract

Event Abstract Back to Event Experimental glucocorticoid induced osteoporosis: differences between mouse strains Y Vattakuzhi1*, AR Clark1 and NJ Horwood1 1 Imperial College Faculty of Medicine, Kennedy Institute of Rheumatology, United Kingdom Glucocorticoids (GCs) are frequently used in inflammatory diseases like rheumatoid arthritis, asthma and inflammatory bowel disease. Long term use of GCs, however, can lead to the development of GC induced osteoporosis (GIO). GIO is characterised by increased osteoclast (OCL) activity and decreased osteoblast activity leading to bone loss; paradoxically, GCs are also reported to inhibit p38 MAPK activity and to directly inhibit OCL function. Experimental models of GIO are well established in the outbred Swiss Webster mice and show loss of bone volume and trabecular connectivity. However, most genetically modified mice are on C57BL/6 background and the aim of this study was to induce GIO in this strain. {BR}CD1 mice were used instead of Swiss Webster mice in these experiments; they are an outbred strain similarly derived from the original Swiss mice. Bone marrow cells of C57BL/6 and CD1 mice were used to investigate the effect of GCs on OCL formation and activity in vitro and to assess p38 activity. To determine the in vivo effects of GCs in the two mouse strains, slow release pellets containing the GC prednisolone were implanted subcutaneously into C57BL/6 and CD1 mice to induce GIO. 3.2mg/kg/day of prednisolone was released over a 58 day period. Lumbar vertebrae and tibiae were then analysed by bone histomorphometry and micro CT analysis. Bone marrow cells were harvested for colony forming assays to determine differences in the progenitor cell populations after GC treatment as well as for in vitro OCL assays.{BR}GCs inhibited p38 activity after RANKL stimulation in C57BL/6 mice; however, in vitro OCL formation and activity was not affected. Long term treatment with prednisolone did not reduce trabaecular volume and bone mineral density compared to placebo in C57BL/6 mice in contrast to CD1 mice. In addition no differences were observed in progenitor cell populations in C57BL/6 mice.{BR}Experimental models of GIO are therefore dependent on the genetic background of the mice with CD1 mice being more susceptible than C57BL/6 mice to glucocorticoid induced bone loss. Keywords: Bones, Bone Research Conference: 2011 joint meeting of the Bone Research Society & the British Orthopaedic Research Society, Cambridge, United Kingdom, 27 Jun - 29 Jun, 2011. Presentation Type: Poster Topic: Abstracts Citation: Vattakuzhi Y, Clark A and Horwood N (2011). Experimental glucocorticoid induced osteoporosis: differences between mouse strains. Front. Endocrinol. Conference Abstract: 2011 joint meeting of the Bone Research Society & the British Orthopaedic Research Society. doi: 10.3389/conf.fendo.2011.02.00070 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 30 Sep 2011; Published Online: 30 Sep 2011. * Correspondence: Prof. Y Vattakuzhi, Imperial College Faculty of Medicine, Kennedy Institute of Rheumatology, London, W6 8LH, United Kingdom, yv07@ic.ac.uk Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Y Vattakuzhi AR Clark NJ Horwood Google Y Vattakuzhi AR Clark NJ Horwood Google Scholar Y Vattakuzhi AR Clark NJ Horwood PubMed Y Vattakuzhi AR Clark NJ Horwood Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.