ArticleArthritis research & therapy2024
Contribution of inflammation markers and quantitative sensory testing (QST) indices of central sensitisation to rheumatoid arthritis pain.
Article in Arthritis research & therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Beyond Synovitis: Molecular and Neuroimmune Mechanisms Informing Target-Joint Attribution and Pain Phenotyping for Arthroplasty in Inflammatory Arthritis.International journal of molecular sciences · 2026Review
- The Association Between Neuropathic Pain, Pain Intensity, and Inflammatory Activity in Rheumatoid Arthritis.Journal of clinical medicine · 2026Article
- Joint-brain communication in rheumatoid arthritis: glial mechanisms, pain phenotypes, and translational evidence.Frontiers in immunology · 2026Review
- Patient and public involvement in musculoskeletal pain research: using mutual learning to improve research quality.Therapeutic advances in musculoskeletal disease · 2026Review
- Gut dysbiosis in difficult-to-treat rheumatoid arthritis: hypothesized microbial endotypes, persistent inflammation, and pharmacological treatment resistance.Frontiers in pharmacology · 2026Review
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Authors and funding
9 authors.
Funding
Abstract
backgroundPain, the primary complaint in rheumatoid arthritis (RA), is multifaceted, and may be driven by inflammatory disease activity and central sensitisation. We aimed to ascertain what proportion of RA pain severity is explained by markers of inflammation and quantitative sensory testing (QST) indices of central sensitisation.
methodsThis was a cross-sectional analysis of data from individuals with clinically active RA. Pain severity was assessed using numerical rating scales and inflammation via 28-joint Disease Activity Score (DAS28) and Ultrasound (Greyscale, Power Doppler). Pain sensitivity was assessed by 'static' (tibialis anterior or brachioradialis pressure pain detection threshold-PPT-TA/PPT-BR) and 'dynamic' (temporal summation-TS, conditioned pain modulation-CPM) QST. Bivariate associations used Spearman's correlation coefficients, and multivariable linear regression models determined relative contributions to pain severity.
resultsIn bivariate analyses of N = 96 (age 65 ± 10y, 77% females) people with RA, pain severity was significantly associated with inflammation indices (r = 0.20 to 0.55), and CPM (r=-0.26). In multivariable models that included TS, CPM, age, sex, and body mass index, inflammation indices remained significantly associated with pain severity. Multivariable models explained 22 to 27% of pain variance. Heterogeneity was apparent for associations with pain between subscores for pain now, strongest or average over the past 4-weeks.
conclusionsIn individuals with clinically active RA, markers of inflammatory disease activity best explain RA pain with only marginal contributions from QST indices of central sensitisation. Although inflammation plays a key role in the experience of RA pain, the greater proportion of pain severity remains unexplained by DAS28 and ultrasound indices of inflammation.
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