Osteopontin might be involved in bone remodelling rather than in inflammation in ankylosing spondylitis

被引:112
作者
Choi, S. T. [1 ]
Kim, J. H. [1 ]
Kang, E. -J. [1 ]
Lee, S. -W. [1 ]
Park, M. -C. [1 ]
Park, Y. -B. [1 ]
Lee, S. -K. [1 ]
机构
[1] Yonsei Univ, Dept Internal Med, Coll Med,Brain Korea Project Med Sci 21, Inst Immunol & Immunol Dis,Div Rheumatol, Seoul 120752, South Korea
关键词
D O I
10.1093/rheumatology/ken385
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objectives. To determine whether osteopontin (OPN) is increased in patients with AS and to investigate its relationship to inflammatory disease activity and bone remodelling process. Methods. This cross-sectional study included 30 patients with AS and 23 age- and sex-matched healthy controls. We assessed clinical characteristics and laboratory parameters including the ESR, CRP, lipid profiles, the Bath AS disease activity index (BASDAI) and the Bath AS radiographic index (BASRI). To evaluate bone metabolism, we tested ALP, OCN and C-telopeptide of type I collagen (CTX-I). Plasma levels of OPN, TNF- and IL-6 were measured by ELISA, and mRNA expression in peripheral blood mononuclear cells (PBMCs) was performed by RTPCR. Changes in OPN level were also evaluated in eight patients after the treatment with a TNF- blocker. Results. Patients with AS had significantly higher plasma OPN, TNF- and IL-6 levels and more mRNA expression than healthy controls. Plasma OPN levels were correlated with serum ALP, OCN and CTX-I levels, but not with ESR, CRP, lipid profiles, BASDAI or BASRI. Treatment with a TNF- blocker did not alter OPN levels, although it reduced the disease activity. Conclusions. Patients with AS had higher levels of OPN compared with controls. The plasma OPN level was correlated with serum ALP, OCN and CTX-I levels, but not with disease activity in AS. OPN might be involved in bone remodelling rather than in inflammation in AS.
引用
收藏
页码:1775 / 1779
页数:5
相关论文
共 33 条
[1]   Comparison of serum IL-1β, sIL-2R, IL-6, and TNF-α levels with disease activity parameters in ankylosing spondylitis [J].
Bal, A. ;
Unlu, E. ;
Bahar, G. ;
Aydog, E. ;
Eksioglu, E. ;
Yorgancioglu, R. .
CLINICAL RHEUMATOLOGY, 2007, 26 (02) :211-215
[2]   Noncollagenous bone matrix proteins, calcification, and thrombosis in carotid artery atherosclerosis [J].
Bini, A ;
Mann, KG ;
Kudryk, BJ ;
Schoen, FJ .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 1999, 19 (08) :1852-1861
[3]   Treatment of spondyloarthropathies with antibodies against tumour necrosis factor α:: first clinical and laboratory experiences [J].
Braun, J ;
Xiang, J ;
Brandt, J ;
Maetzel, H ;
Haibel, H ;
Wu, PH ;
Kohler, S ;
Rudwaleit, M ;
Siegert, S ;
Radbruch, A ;
Thiel, A ;
Sieper, J .
ANNALS OF THE RHEUMATIC DISEASES, 2000, 59 :85-89
[4]   Ankylosing spondylitis [J].
Braun, Juergen ;
Sieper, Joachim .
LANCET, 2007, 369 (9570) :1379-1390
[5]   Osteopontin deficiency produces osteoclast dysfunction due to reduced CD44 surface expression [J].
Chellaiah, MA ;
Kizer, N ;
Biswas, R ;
Alvarez, U ;
Strauss-Schoenberger, J ;
Rifas, L ;
Rittling, SR ;
Denhardt, DT ;
Hruska, KA .
MOLECULAR BIOLOGY OF THE CELL, 2003, 14 (01) :173-189
[6]  
Denhardt DT, 1998, J CELL BIOCHEM, P92, DOI 10.1002/(SICI)1097-4644(1998)72:30/31+<92::AID-JCB13>3.0.CO
[7]  
2-A
[8]   OSTEOPONTIN - A PROTEIN WITH DIVERSE FUNCTIONS [J].
DENHARDT, DT ;
GUO, XJ .
FASEB JOURNAL, 1993, 7 (15) :1475-1482
[9]   Differential expression of bone matrix regulatory proteins in human atherosclerotic plaques [J].
Dhore, CR ;
Cleutjens, JPM ;
Lutgens, E ;
Cleutjens, KBJM ;
Geusens, PPM ;
Kitslaar, PJEHM ;
Tordoir, JHM ;
Spronk, HMH ;
Vermeer, C ;
Daemen, MJAP .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2001, 21 (12) :1998-2003
[10]  
DODDS RA, 1995, J BONE MINER RES, V10, P1666