OA39 Assessment of pain types in recently diagnosed patients with inflammatory arthritis

Up to 40% of patients with inflammatory arthritis (IA) experience persistent pain which, as the disease progresses, is likely to be underpinned by distinct peripherally versus centrally mediated mechanisms. This study assessed the sensory profiles of recently diagnosed individuals with IA, hypothesising that pain at this early stage is primarily driven by peripheral joint inflammation.

Patients with a recent IA diagnosis and a pain numerical rating scale (NRS) score of ≥ 3 were recruited for the study. Data collected included demographics, Disease Activity Score-28 (DAS28CRP), quality of life (measured by MSK-HQ and EQ-5D), mental health status (PHQ-ADS), musculoskeletal ultrasound findings, and pain characteristics (using painDETECT, fibromyalgia criteria, and static and dynamic quantitative sensory testing [QST]).

61 participants (57% female, 62% with rheumatoid arthritis) were analysed, with a mean age of 49.8 ± 15 years and an average time since diagnosis of 1.2 ± 2.3 months. The mean DAS28 score was 3.8 ± 1, and the mean NRS pain score was 5.5 ± 2.1. Criteria for anxiety, depression, and somatic symptoms were fulfilled in 62%, 66%, and 80% of participants, respectively. As expected, 97% had peripheral joint inflammation confirmed by clinical assessment and ultrasound. Unexpectedly, in addition, 20% had a tender-minus-swollen joint count of ≥ 7, 25% had a painDETECT score of ≥ 19, and 21% met the fibromyalgia criteria, indicating potential centrally mediated pain. These outcomes significantly correlated with DAS28, MSK-HQ, and PHQ-ADS scores. QST findings showed evidence of abnormal central pain processing in a subset of participants, where enhanced pain facilitatory and reduced pain inhibitory mechanisms were recorded.

This work provides the first detailed study of sensory profiles in individuals in the early stages of IA. Evidence of centrally mediated pain, present even at the time of diagnosis, was obtained. Our findings challenge the notion that, at the early stage of disease, pain is driven only by peripheral mechanisms. This has implications for pain relief therapeutic targets.

Z. Rutter-Locher: Grants/research support; NIHR301674. S. Norton: None. J. Taylor: None. B. Menon: None. T. Esterine: None. R. Williams: None. L. Taams: None. K. Bannister: None. B. Kirkham: None.