Evidence map›Paper›PMID 39825398›Full record

ArticleArthritis research & therapy2025

The serum level of sclerostin decreases in radiographic axial spondyloarthritis patients with fatty lesions.

Xuegang Li, Haijian Jiang, Xu Wang, Shuping Zhong

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Article in Arthritis research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

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3citing papers in PubMed
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3 citing papers in PubMed.

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5 · Who and what money

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4 authors.

Xuegang Li *Department of Rheumatology, the Fifth Affiliated Hospital of Sun Yat-sen University, 52 Meihua East Road, Zhuhai, People's Republic of China.ORCID 0000-0002-1557-7369
Haijian Jiang *Department of Rheumatology, the Fifth Affiliated Hospital of Sun Yat-sen University, 52 Meihua East Road, Zhuhai, People's Republic of China.ORCID 0009-0009-1953-1948
Xu Wang *Department of Rheumatology, the Fifth Affiliated Hospital of Sun Yat-sen University, 52 Meihua East Road, Zhuhai, People's Republic of China.ORCID 0009-0009-2188-1138
Shuping ZhongDepartment of Rheumatology, the Fifth Affiliated Hospital of Sun Yat-sen University, 52 Meihua East Road, Zhuhai, People's Republic of China. zhshup@mail.sysu.edu.cn.ORCID 0000-0003-1803-0948

Funding

Guangdong Medical Research Foundation A2021237Zhuhai Science and Technology Innovation Bureau 2220004000250
6 · The paper itself

Abstract

backgroundCurrently, the pathophysiology of new bone formation in radiographic axial spondyloarthritis (r-axSpA) remains unclear. Cellular elements and their secreted bone turnover markers might be one of the underlying mechanisms that drive the new bone formation. Our study aimed to investigate the role of bone turnover markers in r-axSpA patients with fatty lesions.

methods73 r-axSpA patients were enrolled in this study. 48 and 25 patients were divided into r-axSpA group with and without fatty lesions. Clinical variables were collected and all patients received comprehensive rheumatologic assessment for disease activity, including Modified Stoke Ankylosing Spondylitis Spine Score (mSASSS), Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) and Axial Spondyloarthritis Disease Activity Score (ASDAS). Fatty lesions in the sacroiliac joints (SIJs) were scored independently by two radiologists. Serum levels of bone turnover markers, including sclerostin, osteoprotegerin (OPG), procollagen I N-terminal propeptide (PINP), cross linked C-telopeptide of type I collagen (CTX-I), osteocalcin (OC), were measured using enzyme-linked immunosorbent assays.

resultsThere were no significant differences between two groups in terms of gender, age, body mass index (BMI), duration, smoking, HLA-B27 positivity rate, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), BASDAI, ASDAS-ESR, ASDAS-CRP, biological disease-modifying anti-rheumatic drugs (bDMARDs) rate. No significant differences were observed in terms of OPG, PINP, CTX-I or OC between two groups. The mSASSS were higher in fatty lesions group than in those without fatty lesions (p < 0.001). The serum sclerostin levels were significantly lower in r-axSpA patients with fatty lesions than in those without fatty lesions (p < 0.001). There were correlations between BMI, mSASSS and sclerostin with the comprehensive Berlin scoring method (CBM) scores in the univariate analysis (ρ = 0.311, ρ = 0.306, ρ = -0.920, respectively). However, only sclerostin had correlation with the CBM scores in multivariate analysis (ρ = -0.040, p < 0.001).

conclusionsIn the r-axSpA patients with fatty lesions, serum sclerostin levels are declined. Serum sclerostin might be useful as a biomarker to predict the progression of the chronic inflammation in SIJs in r-axSpA.

Indexed as

Axial SpondyloarthritisBone Morphogenetic ProteinsAdaptor Proteins, Signal TransducingAdultBiomarkersBone RemodelingFemaleGenetic MarkersHumansMaleMiddle AgedRadiographySacroiliac JointAdaptor Proteins, Signal TransducingBiomarkersBone Morphogenetic ProteinsGenetic MarkersSOST protein, humanFatty lesionsRadiographic axial spondyloarthritisSclerostin

Identifiers

PMID39825398
PMCPMC11740347

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