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Additional file 1: The bidirectional relationship between chronic joint pain and frailty: data from the Investigating Musculoskeletal Health and Wellbeing cohort.

ObjectivesTo investigate how social support, financial status and lifestyle influence the development of excess disability in rheumatoid arthritis (RA).MethodsData came from the Étude et Suivi des Polyarthrites Indifférenciées Récentes (ESPOIR) cohort study of people with RA. A previous analysis identified groups with similar inflammation trajectories but markedly different disability over 10 years; those in the higher disability trajectory groups were defined as having “excess disability”. Participants self-reported data on contextual factors (social support, financial situation, lifestyle) and completed patient reported outcome measures (PROMs; pain, fatigue, anxiety, depression) at baseline. The direct effect of the contextual factors on excess disability and the effect mediated by PROMs was assessed using structural equation models. Findings were validated within two independent datasets (Norfolk Arthritis Register [NOAR], Early Rheumatoid Arthritis Network [ERAN]).ResultsOf 538 included ESPOIR participants (mean age [standard deviation (SD)]: 48.3 [12.2] years, 79.2% women), 200 (37.2%) were in the excess disability group. Less social support (β 0.17 [95% CI 0.08, 0.26]), worse financial situation (β 0.24 [95% CI 0.14, 0.34]), less exercise (β 0.17 [95% CI 0.09, 0.25]) and less education (β 0.15 [95% CI 0.06, 0.23]) were associated with excess disability group membership; smoking, alcohol consumption and body mass index were not. Fatigue and depression mediated a small proportion of these effects. Similar results were seen in NOAR and ERAN.ConclusionsGreater emphasis is needed on the economic and social context of people with RA at presentation; these factors might influence disability over the following decade.

Background: Glucocorticosteroids (GCs) are recommended to suppress inflammation in people with active RA. This systematic review and meta-analysis aimed to quantify the effects of systemic GCs on RA pain.Methods: A systematic literature review of randomised controlled trials (RCTs) in RA comparing systemic GCs to inactive treatment. Three databases were and spontaneous pain and evoked pain outcomes were extracted. Standardized mean differences (SMDs) and mean differences (MDs) were meta-analysed. Heterogeneity (I², tau statistics) and bias (funnel plot, Eggers test) were assessed. Subgroup analyses investigated sources of variation. This study was pre-registered (PROSPERO CRD42019111562). Results: 18903 titles, 880 abstracts and 226 full texts were assessed. Thirty three RCTs suitable for the meta-analysis included 2658 participants. Pain scores (spontaneous pain) decreased in participants treated with oral GCs; SMD= -0.65 (15 studies, 95% CI, -0.82, -0.49, p3 to 6 months, and -6mm (95% CI, -10mm, -2mm) at >6 months. Similar findings were obtained when evoked pain outcomes were examined. Data from 5 RCTs suggested improvement also in fatigue during GC treatment.Discussion. Oral GCs are analgesic in RA. The benefit is greatest shortly after initiation and GCs might not achieve clinically important pain relief beyond 3 months. Treatments other than anti-inflammatory GCs should be considered to reduce the long-term burden of pain in RA.

OBJECTIVES: Pain is the prevailing symptom of knee osteoarthritis. Central sensitisation creates discordance between pain and joint pathology. We previously reported a central pain mechanisms trait derived from 8 discrete characteristics: neuropathic-like pain, fatigue, cognitive-impact, catastrophising, anxiety, sleep disturbance, depression, and pain distribution. We here validate and show that an 8-item questionnaire, Central Aspects of Pain in the Knee (CAP-Knee) is associated both with sensory and affective components of knee pain severity.METHODS: Participants with knee pain were recruited from the Investigating Musculoskeletal Health and Wellbeing study in the East Midlands, UK. CAP-Knee items were refined following cognitive interviews. Psychometric properties were assessed in 250 participants using Rasch-, and factor-analysis, and Cronbach’s alpha. Intra-class correlation coefficients tested repeatability. Associations between CAP-Knee and McGill Pain questionnaire pain severity scores using linear regression.RESULTS: CAP-Knee targeted the knee pain sample well. Cognitive interviews indicated that participants interpreted CAP-Knee items in diverse ways aligned to their intended meanings. Fit to the Rasch model was optimised by rescoring each item, producing a summated score from 0-16. Internal consistency was acceptable (Cronbach’s alpha=0.74) and test–retest reliability excellent (ICC2,1=0.91). Each CAP-Knee item contributed uniquely to one discrete `Central Mechanisms trait’ factor. High CAP-Knee scores were associated with worse overall knee pain intensity and with each of sensory and affective McGill Pain Questionnaire scores.CONCLUSION: CAP-Knee is a simple and valid self-report questionnaire, which measures a single `Central Mechanisms’ trait, and may help identify and target centrally-acting treatments aiming to reduce the burden of knee pain.

Additional file 1.

Additional file 2: Supplement 2. CAP-RA PIS final version 1.218082020. CAP-RA Participant Information Sheet, describing the study protocol to potential participants and members of the public in lay language.

Additional file 1: Supplement 1. SPIRIT Checklist describing protocol items for clinical trials.

Additional file 2.

Additional file 3: Supplement 3. CAP-RA consent form final version 1.423092020 CAP-RA study participant consent form.

Additional file 2.

Additional file 1.

© 2019, American College of Rheumatology Objective: Subchondral bone and the osteochondral junction are thought to contribute to osteoarthritis (OA) knee pain. We undertook this study to identify osteochondral pathologies specifically associated with symptomatic human knee OA. Methods: Medial tibial plateau samples from 2 groups of subjects (n = 31 per group) were matched for macroscopic chondropathy scores. The symptomatic chondropathy group had undergone total knee replacement for OA knee pain, at which time specimens of the medial tibial plateau were obtained. The asymptomatic chondropathy group included subjects who died of unrelated illness (specimens were obtained at postmortem examination) and who had not previously sought help for knee pain. OA histopathology, immunoreactivity for nerve growth factor (NGF) and CD68 (macrophages), tartrate-resistant acid phosphatase–positive subchondral osteoclasts, and synovitis were compared between groups. Results: Mankin scores, subchondral bone density, and subchondral CD68-immunoreactive macrophage infiltration were similar between the 2 groups. NGF-like immunoreactivity was found in subchondral mononuclear cells and osteoclasts, as well as in chondrocytes. NGF in osteochondral channels and osteoclast densities in subchondral bone were higher in the symptomatic chondropathy group than in the asymptomatic chondropathy group (P < 0.01 and P = 0.02, respectively), as were synovitis scores (P < 0.01). Osteochondral pathology was not significantly associated with synovitis score. The differences in NGF expression and in osteoclast density remained significant after adjustment for age and synovitis score (P = 0.01 and P = 0.04, respectively). Osteochondral NGF and osteoclast densities, together with synovitis scores, explained ~28% of sample allocation to symptomatic or asymptomatic groups. Conclusion: Subchondral pathology was associated with symptomatic knee OA, independent of chondropathy and synovitis. Increased NGF expression in osteochondral channels and increased osteoclast density appear to be key features associated with bone pain in knee OA.

Background:\ud Knee pain results from a combination of nociceptive input from the joint, and processing by the central nervous system. Pressure pain detection thresholds (PPTs) are lower and pain is more severe in people with greater central sensitisation. \ud \ud Objective:\ud We hypothesised that lower PPTs predicted worse pain prognosis in people with knee pain.\ud \ud Methods:\ud KPIC participants were people aged >40 years recruited from Nottingham, UK. Participants were mailed questionnaires at baseline and 1 year. This study reports a sample of responders who attended baseline and 1 year clinical assessment, had self-reported knee pain (within the last 4 weeks) and underwent PPT. PPTs were measured at the knee, anterior tibia and the sternum. Radiographic knee OA was classified using an atlas. Questionnaires measured ICOAP (constant and intermittent knee pain), painDETECT (neuropathic-like) and average knee pain severity over 4 weeks (0-10).\ud The presence of pain at baseline and 1 year (persistent pain), or pain severity were predicted from baseline anterior tibia PPT. Additional analyses adjusted for baseline pain score, age, sex, BMI, or for radiographic knee OA. Pain persistence (Yes/No) was analysed using t tests, odds ratios (OR) and logistic regression. Pain severity was analysed using linear regression.\ud \ud Results:\ud The sample for this study contained n=419 people at baseline, and n=182 people reported knee pain persistent over both time points. The mean (SD) values were age 61 (9) years, BMI 30.1 (5.8) kg m-2, 59% female, and 36% fulfilled radiographic OA criteria at the index knee, for those with persistent knee pain at 1 year.\ud In univariate analysis, persistent knee pain was associated with a lower PPT at baseline (461 vs 424 kPa; OR (95% CI) 0.58 (0.34-0.97) p=0.020). Adjustments for age, sex and BMI removed the significance from the association (adjusted OR (95% CI) 0.64 (0.36-1.13) p=0.120). \ud In those with persistent pain, worse 1 year ICOAP-constant, ICOAP-intermittent, painDETECT and knee pain severity were correlated with lower baseline anterior tibia PPT ( r= -0.28 to -0.24; p