Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Comment
. 2010;12(3):127.
doi: 10.1186/ar3035. Epub 2010 Jun 25.

The use of glucocorticoids in rheumatoid arthritis--no 'rational' approach yet

Sonali P Desai  1 , Daniel H Solomon
Affiliations
Comment

The use of glucocorticoids in rheumatoid arthritis--no 'rational' approach yet

Sonali P Desai et al. Arthritis Res Ther. 2010.

Abstract

The relationship between glucocorticoids and bone mineral density in rheumatoid arthritis is complex. Further study into the optimal dosing, timing and duration of glucocorticoid use in rheumatoid arthritis is necessary.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Osteoclast formation in the joint. Monocytic cells in the synovium serve as osteoclast precursors. Upon exposure to macrophage colony-stimulating factor (MCSF) and Receptor activator of nuclear factor-kappa B ligand (RANKL) synthesized by T cells and synovial fibroblasts, osteoclasts fuse to polykaryons termed preosteoclasts, which then undergo further differentiation into mature osteoclasts, acquiring specific features such as the ruffled membrane. Inflammatory cytokines such as TNF and IL-1, IL-6, and IL-17 increase the expression of RANKL and thus support osteoclastogenesis in the joint. In contrast, regulatory T cells (Tregs) block osteoclast formation via Cytotoxic T-lymphocyte antigen 4 (CTLA4). Figure obtained with permission from [3].
Figure 2
Figure 2
The direct and indirect effects of glucocorticoids on bone leading to glucocorticoid-induced osteoporosis and fractures. Figure obtained with permission from [4]. CSF, colony stimulating factor; GH, growth hormone; IGF, insulin-like growth factor; RANKL, Receptor activator of nuclear factor-kappa B ligand.
See this image and copyright information in PMC

Comment on

References

    1. Ibanez M, Ortiz AM, Castrejon I, Garcia-Vadillo A, Carvajal I, Castaneda S, Gonzalez-Alvaro I. A rational use of glucocorticoids in patients with early arthritis has a minimal impact on bone mass. Arthritis Res Ther. p. R50. - DOI - PMC - PubMed
    1. Gravallese EM, Harada Y, Wang JT, Gorn AH, Thornhill TS, Goldring SR. Identification of cell types responsible for bone resorption in rheumatoid arthritis and juvenile rheumatoid arthritis. Am J Pathol. 1998;152:943–951. - PMC - PubMed
    1. Schett G. Osteoimmunology in rheumatic diseases. Arthritis Res Ther. 2009;11:210. doi: 10.1186/ar2571. - DOI - PMC - PubMed
    1. Canalis E, Mazziotti G, Giustina A, Bilezikian JP. Glucocorticoid-induced osteoporosis: pathophysiology and therapy. Osteoporos Int. 2007;18:1319–1328. doi: 10.1007/s00198-007-0394-0. - DOI - PubMed
    1. Maurice MM, Nakamura H, van der Voort EA, van Vliet AI, Staal FJ, Tak PP, Breedveld FC, Boers M, Verhoeven AC, Markusse HM, van de Laar MA, Westhovens R, van Denderen JC, van Zeben D, Dijkmans BA, Peeters AJ, Jacobs P, van den Brink HR, Schouten HJ, van der Heijde DM, Boonen A, van der Linden S. Randomised comparison of combined step-down prednisolone, methotrexate and sulphasalazine with sulphasalazine alone in early rheumatoid arthritis. Lancet. 1997;350:309–318. doi: 10.1016/S0140-6736(97)01300-7. - DOI - PubMed

Publication types

MeSH terms