Abstract
Ankylosing spondylitis is a chronic and severe inflammatory disease of the axial skeleton and the joints. Inflammation is associated with trabecular bone loss leading to osteoporosis but also with corcal new bone formation leading to progressive ankylosis of the spine and sacroiliac joints. This results in an apparent paradox of bone formation and loss taking place at sites closesly located to each other. Osteoporosis can be explained by the impact of inflammation of the bone remodeling cycle. In contrast, new bone formation has been linked to aberrant acvaon of bone morphogenec protein and Wnt signaling. In this commentary, we review recent data on this bone paradox and highlight recent advances including the effect of current drug therapies and the idenfication of new therapeutic targets.
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References
Appel H et al. Immunohistologic analysis of zygapophyseal joints in patients with ankylosing spondylitis. Arthritis Rheum. 2006;54(9):2845–51.
Schett G. Structural bone changes in spondyloarthritis: mechanisms, clinical impact and therapeutic considerations. Am J Med Sci. 2011;341(4):269–71.
El Maghraoui A. Osteoporosis and ankylosing spondylitis. Joint Bone Spine. 2004;71(4):291–5.
El Maghraoui A et al. Osteoporosis, body composition, and bone turnover in ankylosing spondylitis. J Rheumatol. 1999;26(10):2205–9.
Hanson CA, Shagrin JW, Duncan H. Vertebral osteoporosis in ankylosing spondylitis. Clin Orthop Relat Res. 1971;74:59–64.
Magrey M, Khan MA. Osteoporosis in ankylosing spondylitis. Curr Rheumatol Rep. 2010;12(5):332–6.
Maillefert JF et al. Changes in bone density in patients with ankylosing spondylitis: a two-year follow-up study. Osteoporos Int. 2001;12(7):605–9.
Karberg K et al. Bone loss is detected more frequently in patients with ankylosing spondylitis with syndesmophytes. J Rheumatol. 2005;32(7):1290–8.
Rubinstein HM. Osteoporosis in ankylosing spondylitis. Br J Rheumatol. 1991;30(2):160.
Will R et al. Osteoporosis in early ankylosing spondylitis: a primary pathological event? Lancet. 1989;2(8678–8679):1483–5.
Franck H, Meurer T, Hofbauer LC. Evaluation of bone mineral density, hormones, biochemical markers of bone metabolism, and osteoprotegerin serum levels in patients with ankylosing spondylitis. J Rheumatol. 2004;31(11):2236–41.
Ghozlani I et al. Prevalence and risk factors of osteoporosis and vertebral fractures in patients with ankylosing spondylitis. Bone. 2009;44(5):772–6.
Dasgupta B et al. Serial estimation of interleukin 6 as a measure of systemic disease in rheumatoid arthritis. J Rheumatol. 1992;19(1):22–5.
Roche NE et al. Correlation of interleukin-6 production and disease activity in polymyalgia rheumatica and giant cell arteritis. Arthritis Rheum. 1993;36(9):1286–94.
Gratacos J et al. Serum cytokines (IL-6, TNF-alpha, IL-1 beta and IFN-gamma) in ankylosing spondylitis: a close correlation between serum IL-6 and disease activity and severity. Br J Rheumatol. 1994;33(10):927–31.
Melis L et al. Systemic levels of IL-23 are strongly associated with disease activity in rheumatoid arthritis but not spondyloarthritis. Ann Rheum Dis. 2010;69(3):618–23.
Lubberts E et al. IL-17 promotes bone erosion in murine collagen-induced arthritis through loss of the receptor activator of NF-kappa B ligand/osteoprotegerin balance. J Immunol. 2003;170(5):2655–62.
Jovanovic DV et al. IL-17 stimulates the production and expression of proinflammatory cytokines, IL-beta and TNF-alpha, by human macrophages. J Immunol. 1998;160(7):3513–21.
Kim HR, Lee SH, Kim HY. Elevated serum levels of soluble receptor activator of nuclear factors-kappaB ligand (sRANKL) and reduced bone mineral density in patients with ankylosing spondylitis (AS). Rheumatology (Oxford). 2006;45(10):1197–200.
Vis M et al. Evaluation of bone mineral density, bone metabolism, osteoprotegerin and receptor activator of the NFkappaB ligand serum levels during treatment with infliximab in patients with rheumatoid arthritis. Ann Rheum Dis. 2006;65(11):1495–9.
Appel H et al. Immunohistochemical analysis of osteoblasts in zygapophyseal joints of patients with ankylosing spondylitis reveal repair mechanisms similar to osteoarthritis. J Rheumatol. 2010;37(4):823–8.
Lories RJ, Derese I, Luyten FP. Inhibition of osteoclasts does not prevent joint ankylosis in a mouse model of spondyloarthritis. Rheumatology (Oxford). 2008;47(5):605–8.
Obermayer-Pietsch BM et al. Vitamin D receptor initiation codon polymorphism, bone density and inflammatory activity of patients with ankylosing spondylitis. Osteoporos Int. 2003;14(12):995–1000.
De Keyser F et al. Gut inflammation and spondyloarthropathies. Curr Rheumatol Rep. 2002;4(6):525–32.
Uderhardt S et al. Blockade of Dickkopf (DKK)-1 induces fusion of sacroiliac joints. Ann Rheum Dis. 2010;69(3):592–7.
Visvanathan S et al. Effects of infliximab on markers of inflammation and bone turnover and associations with bone mineral density in patients with ankylosing spondylitis. Ann Rheum Dis. 2009;68(2):175–82.
Toussirot E, Wendling D. Anti-inflammatory treatment with bisphosphonates in ankylosing spondylitis. Curr Opin Rheumatol. 2007;19(4):340–5.
Disclosure
Conflicts of interest: S. Carter: none; R.J. Lories: has been a consultant for MSD, Pfizer, Abbott Laboratories, Roche, and Cellgene; has been on the speakers’ bureaus for Pfizer, MSD, and Abbott Laboratories; and has received travel/accommodations expenses for Pfizer, MSD, and Abbott Laboratories.
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Carter, S., Lories, R.J. Osteoporosis: A Paradox in Ankylosing Spondylitis. Curr Osteoporos Rep 9, 112–115 (2011). https://doi.org/10.1007/s11914-011-0058-z
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DOI: https://doi.org/10.1007/s11914-011-0058-z