Research progress of the relationship between bone bridge formation and inflammation in patients with ankylosing spondylitis

Abstract

Abstract: Ankylosing spondylitis(AS)is a systemic inflammatory diseases. Inflammation and bone bridge formation are two stages of the AS typical pathological changes.Inflammation is the main character and bone bridge formation is the primary cause of joint deformity. It was considered that inflammation contributed to the formation of bone bridge,but clinical studies had found that ankylosis could not been stopped after the control of inflammation. The relationship between them seems be very vague. This article summarized the research of the development about bone bridge formation and the relationship between bone bridge formation and inflammation in recent decades.

Key words: ankylosing spondylitis, inflammation, bone bridge formation

CLC Number:

R593.23

WANG Tian-ling, XU Liang. Research progress of the relationship between bone bridge formation and inflammation in patients with ankylosing spondylitis[J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2015, 20(1): 101-105.

References

[1] Tam LS, Gu J, Yu D. Pathogenesis of ankylosing spondylitis[J]. Nat Rev Rheumatol,2010,6(7):399-405.
[2] Braun J, Sieper J. Ankylosing spondylitis[J]. Lancet,2007,369(9570):1379-1390.
[3] 戴冽,汤美安,尹培达,等.强直性脊柱炎的脊柱外表现[J].中华风湿病学杂志,1998,2(3):168-168.
[4] Benedek TG. How did ankylosing spondylitis become aseparate disease[J] ? Clin Exp Rheumatol,2009,27(4 Suppl 55):S3-S9.
[5] Glinka A, Wu W,Delius H, et al.Dickkopf-1 is a member of a new family of secreted proteins and functions in head induction[J]. Nature,1998, 391(6665):357-362.
[6] Kwon SR, Lim MJ, Suh CH, et al.Dickkopf-1 level is lower in patients with ankylosing spondylitis than in healthy people and is not influenced by anti-tumor necrosis factor therapy[J]. Rheumatol Int,2012,32(8):2523-2527.
[7] Appel H,Ruiz-Heiland G,Listing J,et al.Altered skeletal expression of sclerostin and its link toradiographic progression in ankylosing spondylitis[J]. Arthritis Rheum,2009,60:3257-3262.
[8] Bonewald LF,Johnson ML.Ostepcytes,mechanosensing and Wnt signaling[J].Bone,2008,42(4):606-615.
[9] Wanders A,Heijde D, Landewe R,et al.Nonsteroidal antiinflammatory drugs reduce radiographic progression in patients with ankylosing spondylitis:a randomized clinical trial[J]. Arthritis Rheum,2005,52(6):1756-1765.
[10] 李建明,初同伟,周跃.BMP-2和bFGF在强直性脊柱炎活动期骶髂关节滑膜组织中的表达[J].第三军医大学学报,2008,30(3):25l-253.
[11] Liu T, Gao Y, Sakamoto K et al.BMP-2 promotes differentiation of osteblasts and chondroblasts in Runx2-deficient cell lines[J].J Cell Physiol,2007,211(3):728-735.
[12] Lories RJ,Luyten FP, de Vlam K. Progress in spondyloarthritis. Mechanisms of new bone formation in spondyloarthritis[J]. Arthitis Res Ther,2009,11(2):221.
[13] Uderhardt S, Diarra D, Katzenbeisser J,et al. Blockade of Dickkopf(DKK)-1 induces fusion of sacroiliac joints[J]. Ann Rheum Dis,2010,69(3):592-597.
[14] Cruickshank B.Lesions of cartilaginous joints in ankylosing spondylitis[J].J Pathol Bacteriol,1956,71(1):73-84.
[15] Sieper J, Appel H, Braun J, et al. Critical appraisal of assessment of structural damage in ankylosing spondylitis:implications for treatment outcomes[J]. Arthritis Rheum,2008,58(3):649-656.
[16] Lories RJU, Derses I, Geuppens JL, et al. Bone morphogenetic proteins 2 and 6,expressed in arthritic synovium,are regulated by proinflammatory cytokines and differentially modulate fibroblast like synoviocyte apptosis[J]. Arthritis Rheum,2003,48(10):2807-2818.
[17] Fukui N, Zhu Y, Maloney WJ, et al. Stimulation of BMP-2 expression by pro-inflammatory cytokines IL-1and TNF-alpha in normal and osteoarthritic chondrocytes[J]. J Bone Joint Surg(Am),2003,85A Suppl 3:59-66.
[18] Baraliakos X, Listing J, Rudwaleit M, et al. The relationship between inflammation and new bone formation in patients with ankylosing spondylitis[J]. Arthritis Res Ther,2008,10(5):R104.
[19] Baraliakos X, Listing J, Brandt J, et al. Radiographic progression in patients with ankylosing spondylitis after 4 years oftreatment with the anti-TNF-alpha antibody infliximab[J]. Rheumatology(Oxford),2007,46(9):1450-1453.
[20] Lories RJ, Derses I,de Bari C,et al. Evidence for uncoupling of inflammation and joint remodeling in a mouse model of spondylarthritis[J]. Arthritis Rheum,2007,56(2):489-497.
[21] McGonagle D,Wakefield RJ, Tan AL, et al. Distinct topography of erosion and new bone formation in achilles tendon enthesitis:implications for understanding the link between inflammation and bone formation in spondylarthritis[J]. Arthritis Rheum,2008,58(9):2694-2699.
[22] Van der Heijde D, Landewe R, Einstei S,et al. Radiographic progression of ankylosing spondylitis after up to two years of treatment with etanercept[J]. Arthritis Rheum,2008,58(5):1324-1331.
[23] Van der Heijde D, Landewe R, Baraliakos X,et al. Radiographic findings following two years of infliximab therapy in patients with ankylosing spondylitis[J]. Arthritis Rheum,2008,58(10):3063-3070.
[24] Van der Heijde D, Landewe R, Maksymowych W,et al. Adalimumab(HUMIRA)therapy for ankylosing spondylitis over 2 years does not demonstrate inhibition of radiographic progression compared with a historical control group[J]. Arthritis Rheum,2008,58:S413.
[25] Roux S, Orcel P. Bone loss factors that regulate osteoclast differentiation: an update[J].Arthritis Res,2000,2(6):451-456.
[26] Chiowchanwisawaki P,Pedersen SJ,Lambert R,et a1.Presentation:resolution of inflammation following treatment of ankylosing spondylitis with anti-TNF agents is associated with new bone formation[C].Philadelphia:2009 ACR/ARHP Scientific meeting,2009:1257.
[27] Maksymowych WP, Chiowchanwisawakit P, Clare T,et al. Inflammatory lesions of the spine on magnetic resonance imaging predict the development of new syndesmophytes in ankylosing spondylitis:evidence of a relationship between inflammation and new bone formation[J]. Arthritis Rheum,2009,60(1):93-102.
[28] 雷鹏真,危国军,裴孝鹏,等.Dickkopf-1在强直性脊柱炎病理过程作用研究进展[J].中华实用诊断与治疗杂志,2012,26(12):1149-1151.