Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (833 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A spectrum of chronic inflammatory conditions affecting the axial joints (e.g., spine), characterized by pain, stiffness of joints (ankylosis), reduced mobility and inflammation. When joint inflammation and damage are visible on regular X-rays it is called ankylosing spondylitis; otherwise it is referred to as non-radiographic axial spondyloarthritis. hla-b27 antigen is a biomarker and il-23/il-17 pathway a potential therapeutic target for axial and other related spondyloarthritis.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Axial Spondyloarthritides; Spondyloarthritides, Axial; Spondyloarthritis, Axial; AxSpA.
Where it fits in the MeSH classification
- Broader topics
- Spondylarthropathies; Ankylosis
- Narrower topics
- Non-Radiographic Axial Spondyloarthritis; Spondylitis, Ankylosing
Related concepts
- Spine
- Ankylosis
- Ankylosing Spondylitis
- Non-Radiographic Axial Spondyloarthritis
- Hla-B27 Antigen
- Il-23
- Il-17
Research landscape
PubMed indexes 18,659 records tagged with the MeSH heading “Axial Spondyloarthritis” (counts retrieved 2026-11-04). 3,998 of them (21.4%) were published from 2020 onward, and the busiest period so far is through 1999 with 7,452 records.
Reviews account for 2,613 records (14.0%) and meta-analyses for 334. Randomized controlled trials number 609 (3.3%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 7,452 |
| 2000-2009 | 2,710 |
| 2010-2019 | 4,499 |
| 2020 onward | 3,998 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 2,613 | 14.0% |
| Meta-analyses | 334 | 1.8% |
| Randomized controlled trials | 609 | 3.3% |
Method: PubMed query "Axial Spondyloarthritis"[MeSH Terms] with publication-type and date filters, retrieved 2026-11-04.
Reading the evidence in bones, joints, muscles and skin
Joint, bone, muscle and skin conditions are often judged by pain scores, function questionnaires, imaging or photographs, and symptoms can fluctuate, so placebo response and natural improvement matter. Imaging changes are common in people without symptoms. Nothing on this page is advice about treatment. Check how outcomes were measured, whether the comparison group received a placebo or usual care, and how long the benefit lasted.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
The Role of Diet in Modulating Inflammation and Oxidative Stress in Rheumatoid Arthritis, Ankylosing Spondylitis, and Psoriatic Arthritis [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Rheumatic diseases such as rheumatoid arthritis (RA), ankylosing spondylitis (AS), and psoriatic arthritis (PsA) are chronic autoimmune disorders characterized by persistent inflammation and oxidative stress, leading to joint damage and reduced quality of life.
- Closing excerpt
- Collectively, findings suggest that dietary interventions may reduce disease activity, mitigate systemic inflammation, and enhance patients' overall well-being.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (170 words)
Rheumatic diseases such as rheumatoid arthritis (RA), ankylosing spondylitis (AS), and psoriatic arthritis (PsA) are chronic autoimmune disorders characterized by persistent inflammation and oxidative stress, leading to joint damage and reduced quality of life. In recent years, increasing attention has been given to diet as a modifiable environmental factor that can complement pharmacological therapy. This review summarizes current evidence on how key dietary components-such as omega-3 fatty acids, fiber, polyphenols, and antioxidant vitamins-affect inflammatory pathways and oxidative balance. Special emphasis is placed on the Mediterranean diet, low-starch diets, and hypocaloric regimens, which have shown potential in improving disease activity. The gut microbiota emerges as a critical mediator between diet and immune function, with dietary interventions capable of restoring eubiosis and strengthening the intestinal barrier. Additionally, this paper discusses challenges in the clinical implementation of diet therapy, the need for personalized nutritional strategies, and the importance of integrating diet into holistic patient care. Collectively, findings suggest that dietary interventions may reduce disease activity, mitigate systemic inflammation, and enhance patients' overall well-being.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40362911 · DOI · PMC12073256
Exploring difficult-to-manage axial spondyloarthritis: results from a Dutch clinical practice registry [2]
Abstract reading summary — source excerpts
- Opening excerpt
- ObjectivesTo explore (1) the prevalence of difficult-to-manage axial spondyloarthritis (D2M axSpA) in clinical practice according to the Assessment of SpondyloArthritis international Society (ASAS) definition, (2) specific components of this definition contributing most to its fulfilment and (3) associated patient characteristics.
- Closing excerpt
- Current smoking and a history of psoriasis are associated characteristics.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (247 words)
ObjectivesTo explore (1) the prevalence of difficult-to-manage axial spondyloarthritis (D2M axSpA) in clinical practice according to the Assessment of SpondyloArthritis international Society (ASAS) definition, (2) specific components of this definition contributing most to its fulfilment and (3) associated patient characteristics.MethodsThis cross-sectional study used data from the SpA-Net registry. Fulfilling the ASAS definition required: (1) treatment failure, (2) insufficient disease control (any of: [A] high disease activity (AxSpA Disease Activity Score [ASDAS] ≥2.1), [B] signs of active disease (e.g. peripheral manifestations) or [C] reduced health-related quality of life) and (3) a problematic management situation in the patient's or rheumatologist's perspective. Three variations of the ASAS definition were investigated, including only subcriterion A, B or C in domain 2. Treatment-refractory axSpA required fulfilment of the primary ASAS definition, an ASDAS ≥2.1 and CRP ≥5 mg/L. The prevalence of D2M axSpA per explored definition was calculated, and associated characteristics were assessed using logistic regression analyses.ResultsData from 263 patients were analysed. Overall, 9.7% had D2M axSpA (variations A-C: 3.6-8.7%) and 1.7% had treatment-refractory disease. 'Treatment failure' affected 9.9-11.6% of patients, 'insufficient disease control' affected 79.7% of patients (variation A: 57.0%, B: 44.6%, C: 51.4%) and 'problematic management' affected 51.4-60.2% of patients. Current smoking (OR = 3.1 [95% CI 1.1-8.7]) and a history of psoriasis (OR = 2.8 [95% CI 1.0-7.6]) were associated characteristics.ConclusionOne in 10 patients with axSpA have D2M disease. Patient-reported outcomes contribute importantly to the classification of D2M axSpA. Current smoking and a history of psoriasis are associated characteristics.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40036773 · DOI · PMC12107025
IL-33-Induced TREM2+ Macrophages Promote Pathological New Bone Formation Through CREG1-IGF2R Axis in Ankylosing Spondylitis [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Pathological new bone formation is the main cause of disability in ankylosing spondylitis (AS), and so far, it lacks a targeted therapy.
- Closing excerpt
- The findings highlight the critical role of IL-33-induced TREM2+ macrophages in pathological new bone formation and provide potential therapeutic targets for halting spinal ankylosis in AS.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (178 words)
Pathological new bone formation is the main cause of disability in ankylosing spondylitis (AS), and so far, it lacks a targeted therapy. Macrophages are central orchestrators of inflammation progression and tissue remodeling, but their contribution to pathological new bone formation has largely not been explored. Here, it is identified that TREM2+ macrophages predominated within the sites of new bone formation and adjacent to osteogenic precursor cells. In vivo, both depletion of macrophages and knockout of Trem2 significantly reduced pathological new bone formation in a collagen antibody-induced arthritis (CAIA) model. Specifically, TREM2+ macrophages promoted osteogenic differentiation of ligament-derived progenitor cells (LDPCs) by secreting CREG1, a secretory glycoprotein involved in cell differentiation and normal physiology. CREG1-IGF2R-PI3K-AKT signaling pathway is involved in TREM2+ macrophage-mediated pathological new bone formation. In addition, it is found that IL-33 promoted TREM2+ macrophage differentiation through phosphorylation of STAT6. Targeting the above signalings alleviated new bone formation in the CAIA model. The findings highlight the critical role of IL-33-induced TREM2+ macrophages in pathological new bone formation and provide potential therapeutic targets for halting spinal ankylosis in AS.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40091508 · DOI · PMC12079337
HLA-B27-associated gut microbiota and amino acid perturbations promote ankylosing spondylitis through M1 macrophage activation [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Ankylosing spondylitis (AS) is strongly associated with the human leukocyte antigen B27 (HLA-B27), yet how this genetic risk factor interacts with the gut microbiome remains unclear.
- Closing excerpt
- Together, these findings support a model in which HLA-B27-associated gut dysbiosis and metabolic reprogramming promote AS pathogenesis through macrophage-mediated inflammation and osteocatabolic signaling, highlighting microbial-metabolic pathways as potential therapeutic targets.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (238 words)
Ankylosing spondylitis (AS) is strongly associated with the human leukocyte antigen B27 (HLA-B27), yet how this genetic risk factor interacts with the gut microbiome remains unclear. We integrated fecal gut microbiota analysis, untargeted metabolomics, and clinical phenotyping in 88 participants, including HLA-B27-positive patients with AS (n = 28), HLA-B27-positive healthy controls (n = 30), and HLA-B27-negative healthy controls (n = 30). HLA-B27 positivity, particularly in AS, was associated with marked alterations in gut microbial composition and metabolic profiles, with forty bacterial species showing progressive disease-related shifts across cohorts. Integrated pathway and metabolomic analyses identified three amino acid-related pathways consistently disrupted in AS: tryptophan metabolism, cysteine metabolism, and pyruvate-centered biosynthesis of branched-chain amino acids, ornithine, and lysine. Correlation network analyses linking differential taxa, metabolites, and clinical indices revealed previously unrecognized microbial and metabolic signatures that robustly distinguished AS from both control groups. To explore causality, fecal microbiota transplantation (FMT) from clinical donors into antibiotic-treated mice recapitulated key disease-relevant features, including impaired intestinal barrier function, systemic inflammation, trabecular bone loss, and polarization of macrophages toward a proinflammatory M1 phenotype. Mechanistic validation identified cinnabarinic acid as a critical microbial-derived metabolite that suppresses M1 macrophage polarization via activation of the aryl hydrocarbon receptor (AhR) pathway and confers protection in the FMT model. Together, these findings support a model in which HLA-B27-associated gut dysbiosis and metabolic reprogramming promote AS pathogenesis through macrophage-mediated inflammation and osteocatabolic signaling, highlighting microbial-metabolic pathways as potential therapeutic targets.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41698880 · DOI · PMC12915779
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Safety of Janus Kinase Inhibitors in Patients With Inflammatory Bowel Diseases or Other Immune-mediated Diseases: A Systematic Review and Meta-Analysis [5]
- Research article Prevalence of peripheral and extra-articular disease in ankylosing spondylitis versus non-radiographic axial spondyloarthritis: a meta-analysis [6]
- Research article Efficacy of TNFα blockers in patients with ankylosing spondylitis and non-radiographic axial spondyloarthritis: a meta-analysis [7]
- Research article Cardiovascular profile in ankylosing spondylitis: a systematic review and meta-analysis [8]
- Research article Diagnostic delay in axial spondyloarthritis: a systematic review and meta-analysis [9]
- Research article Efficacy and Safety of Curcumin and Curcuma longa Extract in the Treatment of Arthritis: A Systematic Review and Meta-Analysis of Randomized Controlled Trial [10]
References
- Kupczyk D, Bilski R, Szeleszczuk Ł, Mądra-Gackowska K, Studzińska R. The Role of Diet in Modulating Inflammation and Oxidative Stress in Rheumatoid Arthritis, Ankylosing Spondylitis, and Psoriatic Arthritis. . 2025. PMID 40362911 · DOI · PMC12073256
- Smits ML, Webers C, Vonkeman HE, van Tubergen A. Exploring difficult-to-manage axial spondyloarthritis: results from a Dutch clinical practice registry. . 2025. PMID 40036773 · DOI · PMC12107025
- Hao W, Chen S, Chao H, Li Z, Yang H, Chen D, et al.. IL-33-Induced TREM2+ Macrophages Promote Pathological New Bone Formation Through CREG1-IGF2R Axis in Ankylosing Spondylitis. . 2025. PMID 40091508 · DOI · PMC12079337
- Huang T, Yang H, Zhang L, Wang X, Chen Y, Dai H, et al.. HLA-B27-associated gut microbiota and amino acid perturbations promote ankylosing spondylitis through M1 macrophage activation. . 2026. PMID 41698880 · DOI · PMC12915779
- Olivera PA, Lasa JS, Bonovas S, Danese S, Peyrin-Biroulet L. Safety of Janus Kinase Inhibitors in Patients With Inflammatory Bowel Diseases or Other Immune-mediated Diseases: A Systematic Review and Meta-Analysis. Gastroenterology. 2020. PMID 31926171 · DOI
- de Winter JJ, van Mens LJ, van der Heijde D, Landewé R, Baeten DL. Prevalence of peripheral and extra-articular disease in ankylosing spondylitis versus non-radiographic axial spondyloarthritis: a meta-analysis. Arthritis Res Ther. 2016. PMID 27586785 · DOI · PMC5009714
- Callhoff J, Sieper J, Weiß A, Zink A, Listing J. Efficacy of TNFα blockers in patients with ankylosing spondylitis and non-radiographic axial spondyloarthritis: a meta-analysis. Ann Rheum Dis. 2015. PMID 24718959 · DOI
- Mathieu S, Gossec L, Dougados M, Soubrier M. Cardiovascular profile in ankylosing spondylitis: a systematic review and meta-analysis. Arthritis Care Res (Hoboken). 2011. PMID 20890982 · DOI
- Zhao SS, Pittam B, Harrison NL, Ahmed AE, Goodson NJ, Hughes DM. Diagnostic delay in axial spondyloarthritis: a systematic review and meta-analysis. Rheumatology (Oxford). 2021. PMID 33428758 · DOI
- Zeng L, Yang T, Yang K, Yu G, Li J, Xiang W, et al.. Efficacy and Safety of Curcumin and Curcuma longa Extract in the Treatment of Arthritis: A Systematic Review and Meta-Analysis of Randomized Controlled Trial. Front Immunol. 2022. PMID 35935936 · DOI · PMC9353077
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-11-04; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-11-04.
See how EvidenceLib is built. Spotted an error? Email support@evidencehelix.com.
Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.