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: 3 complete abstracts (665 words), 9 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
Heterogeneous group of arthritic diseases sharing clinical and radiologic features. They are associated with the hla-b27 antigen and some with a triggering infection. Most involve the axial joints in the spine, particularly the sacroiliac joint, but can also involve asymmetric peripheral joints. Subsets include ankylosing spondylitis; reactive arthritis; psoriatic arthritis; and others.
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: Bechterew Syndrome; Syndrome, Bechterew; Marie-Strumpell Spondylitis; Marie Strumpell Spondylitis; Spondylitis, Marie-Strumpell; Spondylarthropathy; Spondyloarthropathy; Spondyloarthropathies.
Where it fits in the MeSH classification
- Broader topics
- Spondylarthritis
- Narrower topics
- Arthritis, Psoriatic; Arthritis, Reactive; Axial Spondyloarthritis
Related concepts
- Hla-B27 Antigen
- Spine
- Sacroiliac Joint
- Ankylosing Spondylitis
- Reactive Arthritis
- Psoriatic Arthritis
Research landscape
PubMed indexes 31,656 records tagged with the MeSH heading “Spondylarthropathies” (counts retrieved 2026-11-04). 7,564 of them (23.9%) were published from 2020 onward, and the busiest period so far is through 1999 with 10,386 records.
Reviews account for 5,341 records (16.9%) and meta-analyses for 548. Randomized controlled trials number 1,045 (3.3%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 10,386 |
| 2000-2009 | 5,127 |
| 2010-2019 | 8,579 |
| 2020 onward | 7,564 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 5,341 | 16.9% |
| Meta-analyses | 548 | 1.7% |
| Randomized controlled trials | 1,045 | 3.3% |
Method: PubMed query "Spondylarthropathies"[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.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Frequency of difficult-to-manage and treatment-refractory axial SpA: insights from the German RABBIT-SpA register using recent ASAS definitions | 2026 | Research article Design not recorded in structured metadata | 7 | cc by PMID 41335412 · DOI · PMC12822491 |
| Linking AIM2 Inflammasome Activation, Mitochondrial Dysfunction and Chronic Inflammation in Ankylosing Spondylitis | 2025 | Review article Design not recorded in structured metadata | 6 | cc by PMID 41369412 · DOI · PMC12691365 |
| HLA-B27-associated gut microbiota and amino acid perturbations promote ankylosing spondylitis through M1 macrophage activation | 2026 | Research article Design not recorded in structured metadata | 4 | cc by PMID 41698880 · DOI · PMC12915779 |
Frequency of difficult-to-manage and treatment-refractory axial SpA: insights from the German RABBIT-SpA register using recent ASAS definitions [1]
Abstract reading summary — source excerpts
- Opening excerpt
- ObjectivesTo determine the frequency of axial SpA (axSpA) patients fulfilling the recently proposed Assessment of SpondyloArthritis International Society (ASAS) definitions for difficult-to-manage (D2M) and treatment-refractory (TR) axSpA, and to characterize these patients at initiation of their first advanced therapy.
- Closing excerpt
- These findings support their clinical utility and highlight the need for phenotype-specific management strategies.
- 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 (241 words)
ObjectivesTo determine the frequency of axial SpA (axSpA) patients fulfilling the recently proposed Assessment of SpondyloArthritis International Society (ASAS) definitions for difficult-to-manage (D2M) and treatment-refractory (TR) axSpA, and to characterize these patients at initiation of their first advanced therapy.MethodsData were derived from the ongoing prospective, multicentre, longitudinal German RABBIT-SpA registry. Patients were eligible if they were biologic and targeted synthetic (b/ts) DMARD-naïve, had initiated a b/tsDMARD and had ≥12 months of follow-up. ASAS definitions were applied to identify cases of D2M and TR.ResultsOf 1850 patients with axSpA, 881 (48%) were b/tsDMARD-naïve at the start of observation. A total of 75/881 patients (8.5%) fulfilled the ASAS criteria for D2M and 22/881 (2.5%) additionally met the criteria for TR. At baseline, D2M patients were more frequently female, more often HLA-B27-negative, and more commonly presented with arthritis and enthesitis compared with not-D2M (nD2M) patients. In addition, they exhibited fewer objective inflammatory markers such as elevated CRP or MRI lesions. Opioid use was higher across D2M patients compared with nD2M patients. In the TR group compared with the D2M/nTR, the proportion of female and of obesity was lower. Even at initiation of first-line b/tsDMARD, these patients showed more frequently signs of inflammation, including sacroiliac/spinal MRI lesions and elevated CRP, while peripheral arthritis was less frequent.ConclusionApplying the ASAS definitions in a large real-world cohort identified clinically relevant subgroups with D2M and TR. These findings support their clinical utility and highlight the need for phenotype-specific management strategies.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41335412 · DOI · PMC12822491
Linking AIM2 Inflammasome Activation, Mitochondrial Dysfunction and Chronic Inflammation in Ankylosing Spondylitis [2]
Abstract reading summary — source excerpts
- Opening excerpt
- The absent in melanoma 2 (AIM2) inflammasome is a cytosolic DNA sensor that links genomic instability, mitochondrial dysfunction, and chronic inflammation.
- Closing excerpt
- This approach offers new insight into disease control through re-establishing the balance between mitochondrial dysfunction and autoimmunity.
- 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 (186 words)
The absent in melanoma 2 (AIM2) inflammasome is a cytosolic DNA sensor that links genomic instability, mitochondrial dysfunction, and chronic inflammation. Unlike the nucleotide-binding domain, leucine-rich repeat (NLR) family pyrin domain-containing protein 3 (NLRP3) inflammasome, AIM2 is activated directly by double-stranded Deoxyribonucleic Acid (dsDNA), including mitochondrial DNA (mtDNA) released under stress conditions. This positions AIM2 at the intersection of oxidative stress, impaired mitophagy, and innate immune dysregulation. Current therapies for ankylosis spondylitis (AS), such as anti-tumor necrosis factor (TNF), anti-interleukin 17 (IL-17), and Janus kinase (JAK) inhibitors, improve clinical outcomes; however, they do not address upstream mitochondrial dysfunction or DNA-driven inflammasome activation. By contrast, other inflammasomes, such as AIM2, remain comparatively less studied. Since autoimmune diseases, including AS, are frequently accompanied by uncontrolled innate immune responses to self-DNA, these findings provide a framework for comprehending the mechanisms of AIM2 activation and its interaction with inflammation, mitophagy, and oxidative stress. Here, we review the current evidence on AIM2 inflammasome involvement in AS pathogenesis and its potential as a therapeutic target. This approach offers new insight into disease control through re-establishing the balance between mitochondrial dysfunction and autoimmunity.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41369412 · DOI · PMC12691365
HLA-B27-associated gut microbiota and amino acid perturbations promote ankylosing spondylitis through M1 macrophage activation [3]
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 Prevalence of psoriatic arthritis in patients with psoriasis: A systematic review and meta-analysis of observational and clinical studies [4]
- 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 undiagnosed psoriatic arthritis among psoriasis patients: Systematic review and meta-analysis [6]
- Research article Prevalence, Incidence, and Risk of Cancer in Patients With Psoriasis and Psoriatic Arthritis: A Systematic Review and Meta-analysis [7]
- Research article Prevalence and incidence of psoriatic arthritis: A systematic review and meta-analysis [8]
- Research article Prevalence of Post-Chikungunya Infection Chronic Inflammatory Arthritis: A Systematic Review and Meta-Analysis [9]
References
- Proft F, Lembke S, Weiß A, Kellner H, Baraliakos X, Poddubnyy D, et al.. Frequency of difficult-to-manage and treatment-refractory axial SpA: insights from the German RABBIT-SpA register using recent ASAS definitions. . 2026. PMID 41335412 · DOI · PMC12822491
- Boengiu CA, Barbulescu AL, Dragomirescu CC, Buga AM, Mirea AA. Linking AIM2 Inflammasome Activation, Mitochondrial Dysfunction and Chronic Inflammation in Ankylosing Spondylitis. . 2025. PMID 41369412 · DOI · PMC12691365
- 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
- Alinaghi F, Calov M, Kristensen LE, Gladman DD, Coates LC, Jullien D, et al.. Prevalence of psoriatic arthritis in patients with psoriasis: A systematic review and meta-analysis of observational and clinical studies. J Am Acad Dermatol. 2019. PMID 29928910 · DOI
- 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
- Villani AP, Rouzaud M, Sevrain M, Barnetche T, Paul C, Richard MA, et al.. Prevalence of undiagnosed psoriatic arthritis among psoriasis patients: Systematic review and meta-analysis. J Am Acad Dermatol. 2015. PMID 26054432 · DOI
- Vaengebjerg S, Skov L, Egeberg A, Loft ND. Prevalence, Incidence, and Risk of Cancer in Patients With Psoriasis and Psoriatic Arthritis: A Systematic Review and Meta-analysis. JAMA Dermatol. 2020. PMID 32074260 · DOI · PMC7042857
- Scotti L, Franchi M, Marchesoni A, Corrao G. Prevalence and incidence of psoriatic arthritis: A systematic review and meta-analysis. Semin Arthritis Rheum. 2018. PMID 29398124 · DOI
- Rodríguez-Morales AJ, Cardona-Ospina JA, Fernanda Urbano-Garzón S, Sebastian Hurtado-Zapata J. Prevalence of Post-Chikungunya Infection Chronic Inflammatory Arthritis: A Systematic Review and Meta-Analysis. Arthritis Care Res (Hoboken). 2016. PMID 27015439 · DOI
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.