Skip to main content
Top
Published in: Current Osteoporosis Reports 1/2014

01-03-2014 | Osteoimmunology (D Novack and G Schett, Section Editors)

Impact of Inflammation on the Osteoblast in Rheumatic Diseases

Authors: Rebecca Baum, Ellen M. Gravallese

Published in: Current Osteoporosis Reports | Issue 1/2014

Login to get access

Abstract

Normal bone remodeling depends upon a balance between the action of bone-resorbing cells, osteoclasts, and bone-forming cells, osteoblasts. When this balance is disrupted, as is seen in inflammatory diseases such as rheumatoid arthritis (RA) and ankylosing spondylitis (AS), abnormal bone loss or bone formation occurs. In RA, proinflammatory cytokines induce osteoclast differentiation and inhibit osteoblast maturation, leading to articular bone erosions. In contrast, the inflammatory milieu in AS leads to excessive osteoblast activation and bone formation at sites of entheses. While much information exists about the effects of proinflammatory cytokines on osteoclast differentiation and function, more recent studies have begun to elucidate the impact of inflammation on the osteoblast. This review will summarize the mechanisms by which inflammation perturbs bone homeostasis, with a specific focus on the osteoblast.
Literature
1.
go back to reference Sims NA, Gooi JH. Bone remodeling: multiple cellular interactions required for coupling of bone formation and resorption. Semin Cell Dev Biol. 2008;19:444–51.PubMedCrossRef Sims NA, Gooi JH. Bone remodeling: multiple cellular interactions required for coupling of bone formation and resorption. Semin Cell Dev Biol. 2008;19:444–51.PubMedCrossRef
2.
go back to reference Kular J et al. An overview of the regulation of bone remodelling at the cellular level. Clin Biochem. 2012;45:863–73.PubMedCrossRef Kular J et al. An overview of the regulation of bone remodelling at the cellular level. Clin Biochem. 2012;45:863–73.PubMedCrossRef
4.
5.
go back to reference Hayden JM, Mohan S, Baylink DJ. The insulin-like growth factor system and the coupling of formation to resorption. Bone. 1995;17:93S–8S.PubMedCrossRef Hayden JM, Mohan S, Baylink DJ. The insulin-like growth factor system and the coupling of formation to resorption. Bone. 1995;17:93S–8S.PubMedCrossRef
7.
go back to reference Martin TJ et al. Communication between ephrinB2 and EphB4 within the osteoblast lineage. Adv Exp Med Biol. 2010;658:51–60.PubMedCrossRef Martin TJ et al. Communication between ephrinB2 and EphB4 within the osteoblast lineage. Adv Exp Med Biol. 2010;658:51–60.PubMedCrossRef
8.
go back to reference Zhao C et al. Bidirectional ephrinB2-EphB4 signaling controls bone homeostasis. Cell Metab. 2006;4:111–21.PubMedCrossRef Zhao C et al. Bidirectional ephrinB2-EphB4 signaling controls bone homeostasis. Cell Metab. 2006;4:111–21.PubMedCrossRef
9.
go back to reference Walker EC et al. Cardiotrophin-1 is an osteoclast-derived stimulus of bone formation required for normal bone remodeling. J Bone Miner Res. 2008;23:2025–32.PubMedCrossRef Walker EC et al. Cardiotrophin-1 is an osteoclast-derived stimulus of bone formation required for normal bone remodeling. J Bone Miner Res. 2008;23:2025–32.PubMedCrossRef
10.
go back to reference Pittenger MF et al. Multilineage potential of adult human mesenchymal stem cells. Science. 1999;284:143–7.PubMedCrossRef Pittenger MF et al. Multilineage potential of adult human mesenchymal stem cells. Science. 1999;284:143–7.PubMedCrossRef
11.
go back to reference Komori T. Regulation of skeletal development by the Runx family of transcription factors. J Cell Biochem. 2005;95:445–53.PubMedCrossRef Komori T. Regulation of skeletal development by the Runx family of transcription factors. J Cell Biochem. 2005;95:445–53.PubMedCrossRef
12.
go back to reference Biskobing DM, Fan X, Rubin J. Characterization of MCSF-induced proliferation and subsequent osteoclast formation in murine marrow culture. J Bone Miner Res. 1995;10:1025–32.PubMedCrossRef Biskobing DM, Fan X, Rubin J. Characterization of MCSF-induced proliferation and subsequent osteoclast formation in murine marrow culture. J Bone Miner Res. 1995;10:1025–32.PubMedCrossRef
13.
go back to reference Takahashi N, Udagawa N, Suda T. A new member of tumor necrosis factor ligand family, ODF/OPGL/TRANCE/RANKL, regulates osteoclast differentiation and function. Biochem Biophys Res Commun. 1999;256:449–55.PubMedCrossRef Takahashi N, Udagawa N, Suda T. A new member of tumor necrosis factor ligand family, ODF/OPGL/TRANCE/RANKL, regulates osteoclast differentiation and function. Biochem Biophys Res Commun. 1999;256:449–55.PubMedCrossRef
14.
go back to reference Yasuda H et al. Identity of osteoclastogenesis inhibitory factor (OCIF) and osteoprotegerin (OPG): a mechanism by which OPG/OCIF inhibits osteoclastogenesis in vitro. Endocrinology. 1998;139:1329–37.PubMed Yasuda H et al. Identity of osteoclastogenesis inhibitory factor (OCIF) and osteoprotegerin (OPG): a mechanism by which OPG/OCIF inhibits osteoclastogenesis in vitro. Endocrinology. 1998;139:1329–37.PubMed
15.
go back to reference Ma YL et al. Catabolic effects of continuous human PTH (1–38) in vivo is associated with sustained stimulation of RANKL and inhibition of osteoprotegerin and gene-associated bone formation. Endocrinology. 2001;142:4047–54.PubMed Ma YL et al. Catabolic effects of continuous human PTH (1–38) in vivo is associated with sustained stimulation of RANKL and inhibition of osteoprotegerin and gene-associated bone formation. Endocrinology. 2001;142:4047–54.PubMed
18.
go back to reference Regard JB, et al. Wnt signaling in bone development and disease: making stronger bone with Wnts. Cold Spring Harb Perspect Biol. 2012;4. Regard JB, et al. Wnt signaling in bone development and disease: making stronger bone with Wnts. Cold Spring Harb Perspect Biol. 2012;4.
20.
go back to reference Bodine PV et al. The Wnt antagonist secreted frizzled-related protein-1 controls osteoblast and osteocyte apoptosis. J Cell Biochem. 2005;96:1212–30.PubMedCrossRef Bodine PV et al. The Wnt antagonist secreted frizzled-related protein-1 controls osteoblast and osteocyte apoptosis. J Cell Biochem. 2005;96:1212–30.PubMedCrossRef
21.
go back to reference Yao W et al. Overexpression of secreted frizzled-related protein 1 inhibits bone formation and attenuates parathyroid hormone bone anabolic effects. J Bone Miner Res. 2010;25:190–9.PubMedCrossRef Yao W et al. Overexpression of secreted frizzled-related protein 1 inhibits bone formation and attenuates parathyroid hormone bone anabolic effects. J Bone Miner Res. 2010;25:190–9.PubMedCrossRef
22.
go back to reference Bodine PV et al. The Wnt antagonist secreted frizzled-related protein-1 is a negative regulator of trabecular bone formation in adult mice. Mol Endocrinol. 2004;18:1222–37.PubMedCrossRef Bodine PV et al. The Wnt antagonist secreted frizzled-related protein-1 is a negative regulator of trabecular bone formation in adult mice. Mol Endocrinol. 2004;18:1222–37.PubMedCrossRef
23.
go back to reference Pinzone JJ et al. The role of Dickkopf-1 in bone development, homeostasis, and disease. Blood. 2009;113:517–25.PubMedCrossRef Pinzone JJ et al. The role of Dickkopf-1 in bone development, homeostasis, and disease. Blood. 2009;113:517–25.PubMedCrossRef
24.
go back to reference Morvan F et al. Deletion of a single allele of the Dkk1 gene leads to an increase in bone formation and bone mass. J Bone Miner Res. 2006;21:934–45.PubMedCrossRef Morvan F et al. Deletion of a single allele of the Dkk1 gene leads to an increase in bone formation and bone mass. J Bone Miner Res. 2006;21:934–45.PubMedCrossRef
25.
go back to reference Li J et al. Dkk1-mediated inhibition of Wnt signaling in bone results in osteopenia. Bone. 2006;39:754–66.PubMedCrossRef Li J et al. Dkk1-mediated inhibition of Wnt signaling in bone results in osteopenia. Bone. 2006;39:754–66.PubMedCrossRef
26.
go back to reference Wang SY et al. Circulating Dickkopf-1 is correlated with bone erosion and inflammation in rheumatoid arthritis. J Rheumatol. 2011;38:821–7.PubMedCrossRef Wang SY et al. Circulating Dickkopf-1 is correlated with bone erosion and inflammation in rheumatoid arthritis. J Rheumatol. 2011;38:821–7.PubMedCrossRef
27.
go back to reference Heiland GR et al. High level of functional dickkopf-1 predicts protection from syndesmophyte formation in patients with ankylosing spondylitis. Ann Rheum Dis. 2012;71:572–4.PubMedCrossRef Heiland GR et al. High level of functional dickkopf-1 predicts protection from syndesmophyte formation in patients with ankylosing spondylitis. Ann Rheum Dis. 2012;71:572–4.PubMedCrossRef
28.
go back to reference Li X et al. Sclerostin binds to LRP5/6 and antagonizes canonical Wnt signaling. J Biol Chem. 2005;280:19883–7.PubMedCrossRef Li X et al. Sclerostin binds to LRP5/6 and antagonizes canonical Wnt signaling. J Biol Chem. 2005;280:19883–7.PubMedCrossRef
29.
go back to reference Balemans W et al. Increased bone density in sclerosteosis is due to the deficiency of a novel secreted protein (SOST). Hum Mol Genet. 2001;10:537–43.PubMedCrossRef Balemans W et al. Increased bone density in sclerosteosis is due to the deficiency of a novel secreted protein (SOST). Hum Mol Genet. 2001;10:537–43.PubMedCrossRef
30.
go back to reference van Lierop AH et al. Van Buchem disease: clinical, biochemical, and densitometric features of patients and disease carriers. J Bone Miner Res. 2013;28:848–54.PubMedCrossRef van Lierop AH et al. Van Buchem disease: clinical, biochemical, and densitometric features of patients and disease carriers. J Bone Miner Res. 2013;28:848–54.PubMedCrossRef
31.
go back to reference Hamersma H, Gardner J, Beighton P. The natural history of sclerosteosis. Clin Genet. 2003;63:192–7.PubMedCrossRef Hamersma H, Gardner J, Beighton P. The natural history of sclerosteosis. Clin Genet. 2003;63:192–7.PubMedCrossRef
32.
go back to reference Li X et al. Targeted deletion of the sclerostin gene in mice results in increased bone formation and bone strength. J Bone Miner Res. 2008;23:860–9.PubMedCrossRef Li X et al. Targeted deletion of the sclerostin gene in mice results in increased bone formation and bone strength. J Bone Miner Res. 2008;23:860–9.PubMedCrossRef
33.
go back to reference Winkler DG et al. Osteocyte control of bone formation via sclerostin, a novel BMP antagonist. EMBO J. 2003;22:6267–76.PubMedCrossRef Winkler DG et al. Osteocyte control of bone formation via sclerostin, a novel BMP antagonist. EMBO J. 2003;22:6267–76.PubMedCrossRef
34.
go back to reference Costa AG, Bilezikian JP. Sclerostin: therapeutic horizons based upon its actions. Curr Osteoporos Rep. 2012;10:64–72.PubMedCrossRef Costa AG, Bilezikian JP. Sclerostin: therapeutic horizons based upon its actions. Curr Osteoporos Rep. 2012;10:64–72.PubMedCrossRef
35.
go back to reference Spatz JM et al. Sclerostin antibody inhibits skeletal deterioration due to reduced mechanical loading. J Bone Miner Res. 2013;28:865–74.PubMedCrossRef Spatz JM et al. Sclerostin antibody inhibits skeletal deterioration due to reduced mechanical loading. J Bone Miner Res. 2013;28:865–74.PubMedCrossRef
36.
go back to reference Li X et al. Sclerostin antibody treatment increases bone formation, bone mass, and bone strength in a rat model of postmenopausal osteoporosis. J Bone Miner Res. 2009;24:578–88.PubMedCrossRef Li X et al. Sclerostin antibody treatment increases bone formation, bone mass, and bone strength in a rat model of postmenopausal osteoporosis. J Bone Miner Res. 2009;24:578–88.PubMedCrossRef
37.
go back to reference Padhi D et al. Single-dose, placebo-controlled, randomized study of AMG 785, a sclerostin monoclonal antibody. J Bone Miner Res. 2011;26:19–26.PubMedCrossRef Padhi D et al. Single-dose, placebo-controlled, randomized study of AMG 785, a sclerostin monoclonal antibody. J Bone Miner Res. 2011;26:19–26.PubMedCrossRef
39.
go back to reference Lories RJ, Derese I, Luyten FP. Modulation of bone morphogenetic protein signaling inhibits the onset and progression of ankylosing enthesitis. J Clin Invest. 2005;115:1571–9.PubMedCentralPubMedCrossRef Lories RJ, Derese I, Luyten FP. Modulation of bone morphogenetic protein signaling inhibits the onset and progression of ankylosing enthesitis. J Clin Invest. 2005;115:1571–9.PubMedCentralPubMedCrossRef
40.
go back to reference Li P et al. Systemic tumor necrosis factor alpha mediates an increase in peripheral CD11bhigh osteoclast precursors in tumor necrosis factor alpha-transgenic mice. Arthritis Rheum. 2004;50:265–76.PubMedCrossRef Li P et al. Systemic tumor necrosis factor alpha mediates an increase in peripheral CD11bhigh osteoclast precursors in tumor necrosis factor alpha-transgenic mice. Arthritis Rheum. 2004;50:265–76.PubMedCrossRef
41.
go back to reference Kotake S et al. IL-17 in synovial fluids from patients with rheumatoid arthritis is a potent stimulator of osteoclastogenesis. J Clin Invest. 1999;103:1345–52.PubMedCentralPubMedCrossRef Kotake S et al. IL-17 in synovial fluids from patients with rheumatoid arthritis is a potent stimulator of osteoclastogenesis. J Clin Invest. 1999;103:1345–52.PubMedCentralPubMedCrossRef
42.
go back to reference Lam J et al. TNF-alpha induces osteoclastogenesis by direct stimulation of macrophages exposed to permissive levels of RANK ligand. J Clin Invest. 2000;106:1481–8.PubMedCentralPubMedCrossRef Lam J et al. TNF-alpha induces osteoclastogenesis by direct stimulation of macrophages exposed to permissive levels of RANK ligand. J Clin Invest. 2000;106:1481–8.PubMedCentralPubMedCrossRef
43.
go back to reference Walsh NC, Gravallese EM. Bone remodeling in rheumatic disease: a question of balance. Immunol Rev. 2010;233:301–12.PubMedCrossRef Walsh NC, Gravallese EM. Bone remodeling in rheumatic disease: a question of balance. Immunol Rev. 2010;233:301–12.PubMedCrossRef
44.
45.
go back to reference Gravallese EM et al. Identification of cell types responsible for bone resorption in rheumatoid arthritis and juvenile rheumatoid arthritis. Am J Pathol. 1998;152:943–51.PubMed Gravallese EM et al. Identification of cell types responsible for bone resorption in rheumatoid arthritis and juvenile rheumatoid arthritis. Am J Pathol. 1998;152:943–51.PubMed
46.
go back to reference Bromley M, Woolley DE. Chondroclasts and osteoclasts at subchondral sites of erosion in the rheumatoid joint. Arthritis Rheum. 1984;27:968–75.PubMedCrossRef Bromley M, Woolley DE. Chondroclasts and osteoclasts at subchondral sites of erosion in the rheumatoid joint. Arthritis Rheum. 1984;27:968–75.PubMedCrossRef
47.
go back to reference Suzuki Y et al. Osteoclast-like cells in murine collagen induced arthritis. J Rheumatol. 1998;25:1154–60.PubMed Suzuki Y et al. Osteoclast-like cells in murine collagen induced arthritis. J Rheumatol. 1998;25:1154–60.PubMed
48.
go back to reference Romas E et al. Expression of osteoclast differentiation factor at sites of bone erosion in collagen-induced arthritis. Arthritis Rheum. 2000;43:821–6.PubMedCrossRef Romas E et al. Expression of osteoclast differentiation factor at sites of bone erosion in collagen-induced arthritis. Arthritis Rheum. 2000;43:821–6.PubMedCrossRef
49.
go back to reference Kuratani T et al. Induction of abundant osteoclast-like multinucleated giant cells in adjuvant arthritic rats with accompanying disordered high bone turnover. Histol Histopathol. 1998;13:751–9.PubMed Kuratani T et al. Induction of abundant osteoclast-like multinucleated giant cells in adjuvant arthritic rats with accompanying disordered high bone turnover. Histol Histopathol. 1998;13:751–9.PubMed
50.
go back to reference Gravallese EM et al. Synovial tissue in rheumatoid arthritis is a source of osteoclast differentiation factor. Arthritis Rheum. 2000;43:250–8.PubMedCrossRef Gravallese EM et al. Synovial tissue in rheumatoid arthritis is a source of osteoclast differentiation factor. Arthritis Rheum. 2000;43:250–8.PubMedCrossRef
51.
go back to reference Pettit AR et al. TRANCE/RANKL knockout mice are protected from bone erosion in a serum transfer model of arthritis. Am J Pathol. 2001;159:1689–99.PubMedCrossRef Pettit AR et al. TRANCE/RANKL knockout mice are protected from bone erosion in a serum transfer model of arthritis. Am J Pathol. 2001;159:1689–99.PubMedCrossRef
53.
go back to reference Moller Dohn U et al. Erosive progression is minimal, but erosion healing rare, in patients with rheumatoid arthritis treated with adalimumab. A 1 year investigator-initiated follow-up study using high-resolution computed tomography as the primary outcome measure. Ann Rheum Dis. 2009;68:1585–90.PubMedCrossRef Moller Dohn U et al. Erosive progression is minimal, but erosion healing rare, in patients with rheumatoid arthritis treated with adalimumab. A 1 year investigator-initiated follow-up study using high-resolution computed tomography as the primary outcome measure. Ann Rheum Dis. 2009;68:1585–90.PubMedCrossRef
54.•
go back to reference Dohn UM et al. No overall progression and occasional repair of erosions despite persistent inflammation in adalimumab-treated rheumatoid arthritis patients: results from a longitudinal comparative MRI, ultrasonography, CT, and radiography study. Ann Rheum Dis. 2011;70:252–8.PubMedCrossRef Dohn UM et al. No overall progression and occasional repair of erosions despite persistent inflammation in adalimumab-treated rheumatoid arthritis patients: results from a longitudinal comparative MRI, ultrasonography, CT, and radiography study. Ann Rheum Dis. 2011;70:252–8.PubMedCrossRef
55.
go back to reference Haavardsholm EA et al. Magnetic resonance imaging findings in 84 patients with early rheumatoid arthritis: bone marrow edema predicts erosive progression. Ann Rheum Dis. 2008;67:794–800.PubMedCrossRef Haavardsholm EA et al. Magnetic resonance imaging findings in 84 patients with early rheumatoid arthritis: bone marrow edema predicts erosive progression. Ann Rheum Dis. 2008;67:794–800.PubMedCrossRef
56.
go back to reference Hetland ML et al. MRI bone edema is the strongest predictor of subsequent radiographic progression in early rheumatoid arthritis. Results from a 2-year randomized controlled trial (CIMESTRA). Ann Rheum Dis. 2009;68:384–90.PubMedCrossRef Hetland ML et al. MRI bone edema is the strongest predictor of subsequent radiographic progression in early rheumatoid arthritis. Results from a 2-year randomized controlled trial (CIMESTRA). Ann Rheum Dis. 2009;68:384–90.PubMedCrossRef
57.
go back to reference Gilbert L et al. Expression of the osteoblast differentiation factor RUNX2 (Cbfa1/AML3/Pebp2alpha A) is inhibited by tumor necrosis factor-alpha. J Biol Chem. 2002;277:2695–701.PubMedCrossRef Gilbert L et al. Expression of the osteoblast differentiation factor RUNX2 (Cbfa1/AML3/Pebp2alpha A) is inhibited by tumor necrosis factor-alpha. J Biol Chem. 2002;277:2695–701.PubMedCrossRef
59.
go back to reference Jilka RL et al. Osteoblast programmed cell death (apoptosis): modulation by growth factors and cytokines. J Bone Miner Res. 1998;13:793–802.PubMedCrossRef Jilka RL et al. Osteoblast programmed cell death (apoptosis): modulation by growth factors and cytokines. J Bone Miner Res. 1998;13:793–802.PubMedCrossRef
60.
go back to reference Stashenko P et al. Interleukin-1 beta is a potent inhibitor of bone formation in vitro. J Bone Miner Res. 1987;2:559–65.PubMedCrossRef Stashenko P et al. Interleukin-1 beta is a potent inhibitor of bone formation in vitro. J Bone Miner Res. 1987;2:559–65.PubMedCrossRef
62.
go back to reference Liu XH et al. Cross-talk between the interleukin-6 and prostaglandin E(2) signaling systems results in enhancement of osteoclastogenesis through effects on the osteoprotegerin/receptor activator of nuclear factor-{kappa}B (RANK) ligand/RANK system. Endocrinology. 2005;146:1991–8.PubMedCrossRef Liu XH et al. Cross-talk between the interleukin-6 and prostaglandin E(2) signaling systems results in enhancement of osteoclastogenesis through effects on the osteoprotegerin/receptor activator of nuclear factor-{kappa}B (RANK) ligand/RANK system. Endocrinology. 2005;146:1991–8.PubMedCrossRef
63.
go back to reference Walsh NC et al. Osteoblast function is compromised at sites of focal bone erosion in inflammatory arthritis. J Bone Miner Res. 2009;24:1572–85.PubMedCrossRef Walsh NC et al. Osteoblast function is compromised at sites of focal bone erosion in inflammatory arthritis. J Bone Miner Res. 2009;24:1572–85.PubMedCrossRef
64.••
go back to reference Matzelle MM et al. Resolution of inflammation induces osteoblast function and regulates the Wnt signaling pathway. Arthritis Rheum. 2012;64:1540–50.PubMedCrossRef Matzelle MM et al. Resolution of inflammation induces osteoblast function and regulates the Wnt signaling pathway. Arthritis Rheum. 2012;64:1540–50.PubMedCrossRef
65.
66.
go back to reference Heiland GR et al. Neutralisation of Dkk-1 protects from systemic bone loss during inflammation and reduces sclerostin expression. Ann Rheum Dis. 2010;69:2152–9.PubMedCrossRef Heiland GR et al. Neutralisation of Dkk-1 protects from systemic bone loss during inflammation and reduces sclerostin expression. Ann Rheum Dis. 2010;69:2152–9.PubMedCrossRef
67.••
68.
go back to reference Finzel S et al. Repair of bone erosions in rheumatoid arthritis treated with tumour necrosis factor inhibitors is based on bone apposition at the base of the erosion. Ann Rheum Dis. 2011;70:1587–93.PubMedCrossRef Finzel S et al. Repair of bone erosions in rheumatoid arthritis treated with tumour necrosis factor inhibitors is based on bone apposition at the base of the erosion. Ann Rheum Dis. 2011;70:1587–93.PubMedCrossRef
69.••
go back to reference Finzel S et al. Interleukin-6 receptor blockade induces limited repair of bone erosions in rheumatoid arthritis: a micro CT study. Ann Rheum Dis. 2013;72:396–400.PubMedCrossRef Finzel S et al. Interleukin-6 receptor blockade induces limited repair of bone erosions in rheumatoid arthritis: a micro CT study. Ann Rheum Dis. 2013;72:396–400.PubMedCrossRef
70.
go back to reference Lories RJ, Schett G. Pathophysiology of new bone formation and ankylosis in spondyloarthritis. Rheum Dis Clin North Am. 2012;38:555–67.PubMedCrossRef Lories RJ, Schett G. Pathophysiology of new bone formation and ankylosis in spondyloarthritis. Rheum Dis Clin North Am. 2012;38:555–67.PubMedCrossRef
71.••
go back to reference Uderhardt S et al. Blockade of Dickkopf (DKK)-1 induces fusion of sacroiliac joints. Ann Rheum Dis. 2010;69:592–7.PubMedCrossRef Uderhardt S et al. Blockade of Dickkopf (DKK)-1 induces fusion of sacroiliac joints. Ann Rheum Dis. 2010;69:592–7.PubMedCrossRef
72.
go back to reference Haynes KR et al. Excessive bone formation in a mouse model of ankylosing spondylitis is associated with decreases in Wnt pathway inhibitors. Arthritis Res Ther. 2012;14:R253.PubMedCentralPubMedCrossRef Haynes KR et al. Excessive bone formation in a mouse model of ankylosing spondylitis is associated with decreases in Wnt pathway inhibitors. Arthritis Res Ther. 2012;14:R253.PubMedCentralPubMedCrossRef
73.
go back to reference Appel H et al. Altered skeletal expression of sclerostin and its link to radiographic progression in ankylosing spondylitis. Arthritis Rheum. 2009;60:3257–62.PubMedCrossRef Appel H et al. Altered skeletal expression of sclerostin and its link to radiographic progression in ankylosing spondylitis. Arthritis Rheum. 2009;60:3257–62.PubMedCrossRef
74.
go back to reference Chen HA et al. Association of bone morphogenetic proteins with spinal fusion in ankylosing spondylitis. J Rheumatol. 2010;37:2126–32.PubMedCrossRef Chen HA et al. Association of bone morphogenetic proteins with spinal fusion in ankylosing spondylitis. J Rheumatol. 2010;37:2126–32.PubMedCrossRef
75.
go back to reference van der Heijde D et al. Assessment of radiographic progression in the spines of patients with ankylosing spondylitis treated with adalimumab for up to 2 years. Arthritis Res Ther. 2009;11:R127.PubMedCentralPubMedCrossRef van der Heijde D et al. Assessment of radiographic progression in the spines of patients with ankylosing spondylitis treated with adalimumab for up to 2 years. Arthritis Res Ther. 2009;11:R127.PubMedCentralPubMedCrossRef
76.
go back to reference Schett G et al. Tumor necrosis factor alpha and RANKL blockade cannot halt bony spur formation in experimental inflammatory arthritis. Arthritis Rheum. 2009;60:2644–54.PubMedCrossRef Schett G et al. Tumor necrosis factor alpha and RANKL blockade cannot halt bony spur formation in experimental inflammatory arthritis. Arthritis Rheum. 2009;60:2644–54.PubMedCrossRef
77.
go back to reference Mei Y et al. Increased serum IL-17 and IL-23 in the patient with ankylosing spondylitis. Clin Rheumatol. 2011;30:269–73.PubMedCrossRef Mei Y et al. Increased serum IL-17 and IL-23 in the patient with ankylosing spondylitis. Clin Rheumatol. 2011;30:269–73.PubMedCrossRef
78.
go back to reference Duan Z et al. Interleukin-23 receptor genetic polymorphisms and ankylosing spondylitis susceptibility: a meta-analysis. Rheumatol Int. 2012;32:1209–14.PubMedCrossRef Duan Z et al. Interleukin-23 receptor genetic polymorphisms and ankylosing spondylitis susceptibility: a meta-analysis. Rheumatol Int. 2012;32:1209–14.PubMedCrossRef
79.••
go back to reference Sherlock JP et al. IL-23 induces spondyloarthropathy by acting on ROR-gammat+ CD3+CD4-CD8- entheseal resident T cells. Nat Med. 2012;18:1069–76.PubMedCrossRef Sherlock JP et al. IL-23 induces spondyloarthropathy by acting on ROR-gammat+ CD3+CD4-CD8- entheseal resident T cells. Nat Med. 2012;18:1069–76.PubMedCrossRef
80.
go back to reference Sherlock JP, Buckley CD, Cua DJ. The critical role of interleukin-23 in spondyloarthropathy. Mol Immunol. 2013;57:38–43.PubMedCrossRef Sherlock JP, Buckley CD, Cua DJ. The critical role of interleukin-23 in spondyloarthropathy. Mol Immunol. 2013;57:38–43.PubMedCrossRef
Metadata
Title
Impact of Inflammation on the Osteoblast in Rheumatic Diseases
Authors
Rebecca Baum
Ellen M. Gravallese
Publication date
01-03-2014
Publisher
Springer US
Published in
Current Osteoporosis Reports / Issue 1/2014
Print ISSN: 1544-1873
Electronic ISSN: 1544-2241
DOI
https://doi.org/10.1007/s11914-013-0183-y

Other articles of this Issue 1/2014

Current Osteoporosis Reports 1/2014 Go to the issue

Osteoimmunology (D Novack and G Schett, Section Editors)

Bone and the Innate Immune System

Skeletal Biology and Regulation (MR Forwood and A Robling, Section Editors)

Regulatory Mechanisms of RANKL Presentation to Osteoclast Precursors

Skeletal Biology and Regulation (MR Forwood and A Robling, Section Editors)

Osteoblast-Chondrocyte Interactions in Osteoarthritis

Epidemiology and Pathophysiology (PR Ebeling and EF Eriksen, Section Editors)

Review: Epidemiology and Pathophysiology of Atypical Femur Fractures

Regenerative Biology and Medicine in Osteoporosis (EM Schwartz and RE Guldberg, Section Editors)

Pharmacologic Augmentation of Implant Fixation in Osteopenic Bone

Epidemiology and Pathophysiology (PR Ebeling and EF Eriksen, Section Editors)

Bone Metabolism in Anorexia Nervosa