Correspondence on Role of joint damage, malalignment and

1Ann Rheum Dis Month 2021 Vol 0 No 0

Correspondence on ‘Role of joint damage, malalignment and inflammation in articular tenderness in rheumatoid arthritis, psoriatic arthritis and osteoarthritis’

With great interest we read the article of Gessl et al that studied whether tenderness of non- swollen small hand joints was explained by subclinical inflammation as detected by ultrasound (US). Interestingly, the findings in rheumatoid arthritis (RA) were dependent on the disease stage: tender-ness in longstanding RA (mean disease duration 7.2 years) was not associated with subclinical inflammation, while in early RA (disease duration <2 years) tenderness of hand joints was associated with subclinical inflammation (54.5% of tender joints vs 48.4% of non- tender joints showed inflammation; OR 2.22).1 Since validation of research findings is of utmost importance, we hypothesised that the findings observed in early clinical RA would correspond to similar findings in the symptomatic phase that precedes clinical inflammatory arthritis and RA.2 It is important to understand whether joint tenderness in patients with clinically suspect arthralgia (CSA) is related to subclinical inflammation, since joint swelling is per definition absent in this phase.

This prompted us to perform a validation study in CSA patients. We studied the association of joint tenderness in metacarpophalangeal (MCP) joints with subclinical inflam-mation as determined by MRI. We focused on MCP joints since these joints are included in the EULAR definition of arthralgia suspicious for progression to RA.3 On the contrary to Gessl et al, who used US examination for determining the presence of subclinical inflammation, we used MRI. According to the EULAR imaging taskforce, both MRI and US have an added value when diagnosing patients in the early disease phases of RA.4 US has advantages in terms of costs and availability. MRI in contrast is more sensitive; especially for tenosynovitis, the sensitivity of US compared with MRI is moderate- low.5 To prevent false negative findings due to missing subtle subclinical inflammation in the phase of CSA, MRI was implemented in our study.

Between April 2012 and February 2019, 602 patients were consecutively included in the Leiden CSA cohort and assessed for MCP tenderness by physical examination at base-line. Patient- reported joint pain was also assessed by using a

mannequin. Unilateral MRI of the MCP (2–5) joints was made and scored for subclinical inflammation (synovitis, tenosyno-vitis, osteitis) by two experienced readers, blinded for clinical data, as described previously and in the online supplemental file.2 Presence of subclinical inflammation was determined after referring to MRI findings of MCP joints of symptom- free controls of the same age.6 Data of tenderness and inflam-mation in ipsilateral MCP joints were studied. Analyses were done in all patients presenting with CSA and in the subgroup that progressed to inflammatory arthritis within 2 years follow- up (in retrospect these patients were truly ‘pre- RA’ when presenting with arthralgia). A flowchart of the studied population and baseline characteristics are presented online supplemental figure 1 and table 1.

In all CSA patients, 38% of patients with tender MCP joints had subclinical inflammation compared with 25% of patients with non- tender MCP joints (OR 1.84 (95% CI: 1.29 to 2.63); figure 1A, online supplemental table 2A). At patient level, MCP tenderness was associated with subclinical synovitis and tenosynovitis (OR 1.76 (95% CI: 1.10 to 2.81), OR 1.69 (95% CI: 1.12 to 2.55), online supplemental table 2A) but not with osteitis. In the subgroup of patients who progressed to clinical arthritis (n=87), 61% of patients with tender MCP joints had subclinical inflammation compared with 46% of patients with non- tender joints (OR subclinical inflammation 1.79 (95% CI: 0.74 to 4.30), figure 1B, online supplemental table 2A). Studying the 39% of patients who presented with MCP tenderness without subclinical inflammation at MRI and who later on developed IA revealed that clinical arthritis had mostly (85%) developed in joints that were not scanned, hence being left unanswered whether these patients had subclinical inflammation at presentation with CSA in joints that were not imaged. The remaining patients (15%) did develop clin-ical arthritis in MCP joints that were imaged but were normal at first presentation, suggesting that subclinical inflammation developed after CSA onset. Evaluating patient- reported MCP pain (mannequin) instead of MCP joint tenderness at phys-ical examination showed similar associations with subclinical inflammation (online supplemental figure 2, table 2B).

Concluding, associations of joint tenderness with subclin-ical inflammation in the symptomatic phase preceding clin-ical arthritis had roughly similar effect sizes as observed in the phase of clinical arthritis. Hereby, we validated and expanded the findings of Gessl et al in early RA.

Correspondence

Figure 1 (A) Association of subclinical inflammation with tender MCP joints (N=226 with tenderness vs N=376 without tenderness): OR 1.84, 95% CI 1.29 to 2.63. (B) Association of subclinical inflammation with tender MCP joints in patients who developed inflammatory arthritis (N=33 with tenderness vs N=54 without tenderness): OR 1.79, 95% CI 0.74 to 4.30.

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2 Ann Rheum Dis Month 2021 Vol 0 No 0

Correspondence

Quirine A Dumoulin ,1 Xanthe M E Matthijssen ,1 Fenne Wouters ,1 Doortje I Krijbolder,1 Ellis Niemantsverdriet ,1 Annette H M van der Helm- van Mil 1,2

1Rheumatology, Leiden University Medical Center, Leiden, The Netherlands2Rheumatology, Erasmus Medical Center, Rotterdam, The Netherlands

Correspondence to Quirine A Dumoulin, Rheumatology, Leiden University Medical Center, 2333 ZA Leiden, Netherlands; q. a. dumoulin@ lumc. nl

Contributors QAD, XMEM and AHMvdH- vM contributed to the conception and study design. QAD analysed the data. All authors contributed to the interpretation of the data and read and approved the final version of the document. XMEM, FW, DIK and EN contributed to the acquisition of the data. QAD, EN and AHMvdH- vM wrote the first version of the manuscript. XMEM, FW and DIK contributed to the critical revision of the manuscript.

Funding This work was supported by the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation programme and the Dutch Arthritis Foundation.

Competing interests None declared.

Patient consent for publication Not required.

Ethics approval The Medical Ethics Committee of the Leiden University Medical Center (METC LUMC) has approved this study. Participants gave informed consent to participate before taking part in the studied cohort.

Provenance and peer review Not commissioned; internally peer reviewed.

Data availability statement Data are available upon reasonable request.

Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer- reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.

© Author(s) (or their employer(s)) 2021. No commercial re- use. See rights and permissions. Published by BMJ.

► Additional supplemental material is published online only. To view, please visit the journal online (http:// dx. doi. org/ 10. 1136/ annrheumdis- 2021- 220511).

To cite Dumoulin QA, Matthijssen XME, Wouters F, et al. Ann Rheum Dis Epub ahead of print: [please include Day Month Year]. doi:10.1136/annrheumdis-2021-220511

Received 9 April 2021Accepted 4 June 2021

► http:// dx. doi. org/ 10. 1136/ annrheumdis- 2021- 220922

Ann Rheum Dis 2021;0:1–2. doi:10.1136/annrheumdis-2021-220511

ORCID iDsQuirine A Dumoulin http:// orcid. org/ 0000- 0003- 0318- 096XXanthe M E Matthijssen http:// orcid. org/ 0000- 0001- 7332- 8072Fenne Wouters http:// orcid. org/ 0000- 0002- 4375- 4043Ellis Niemantsverdriet http:// orcid. org/ 0000- 0002- 5781- 3817Annette H M van der Helm- van Mil http:// orcid. org/ 0000- 0001- 8572- 1437

REFERENCES 1 Gessl I, Popescu M, Schimpl V, et al. Role of joint damage, malalignment and

inflammation in articular tenderness in rheumatoid arthritis, psoriatic arthritis and osteoarthritis. Ann Rheum Dis 2021;128:annrheumdis-2020-218744.

2 van Steenbergen HW, van Nies JAB, Huizinga TWJ, et al. Characterising arthralgia in the preclinical phase of rheumatoid arthritis using MRI. Ann Rheum Dis 2015;74:1225–32.

3 van Steenbergen HW, Aletaha D, Beaart- van de Voorde LJJ, et al. EULAR definition of arthralgia suspicious for progression to rheumatoid arthritis. Ann Rheum Dis 2017;76:491–6.

4 Colebatch AN, Edwards CJ, Østergaard M, et al. EULAR recommendations for the use of imaging of the joints in the clinical management of rheumatoid arthritis. Ann Rheum Dis 2013;72:804–14.

5 Wakefield RJ, O’Connor PJ, Conaghan PG, et al. Finger tendon disease in untreated early rheumatoid arthritis: a comparison of ultrasound and magnetic resonance imaging. Arthritis Rheum 2007;57:1158–64.

6 Mangnus L, van Steenbergen HW, Reijnierse M, et al. Magnetic resonance Imaging- Detected features of inflammation and erosions in symptom- free persons from the general population. Arthritis Rheumatol 2016;68:2593–602.

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Supplementary file – Description of methods

Patients

Between April 2012 and February 2019, 645 patients were consecutively included in the Leiden CSA

cohort, of whom 602 met the inclusion criteria for this study (for flowchart see supplemental figure

1). CSA-patients had recent-onset (<1 year) arthralgia in the small joints, which was likely to progress

to RA based on the clinical expertise of the rheumatologist. Per definition, patients were excluded if

arthritis was detected upon physical examination or if a different explanation for the joint pain (e.g.

osteoarthritis, fibromyalgia) was more likely than imminent RA. Baseline visit consisted of physical

examination (including a 68-tender joint count), questionnaires (including assessment of patient-

reported joint pain on a mannequin), blood sampling and MRI. Follow-up visits were scheduled at 4,

12 and 24 months. When necessary, for instance in case of an increase of symptoms or when

patients experienced joint swelling, additional visits were planned. Follow-up ended when patients

developed arthritis (determined at physical examination of joints by the treating rheumatologist), or

else after 2 years. The cohort has been described in detail previously.[1]

During follow-up treatment with disease-modifying antirheumatic drugs (DMARDs, including

steroids) was not allowed. Since April 2015, CSA-patients with MRI-detected subclinical

inflammation could participate in a randomized double-blind placebo-controlled trial (RCT; Treat

Earlier, trial registration number: NTR4853), studying the effect of Methotrexate in preventing

progression to RA. This RCT is still ongoing; patients enrolled in this trial (n=97) were excluded from

longitudinal follow-up in the CSA cohort because of the 50% chance of DMARD-use.[2]

MRI scanning and scoring protocol

Within two weeks after inclusion, CSA-patients underwent contrast-enhanced MRI of 2nd-5th

metacarpophalangeal (MCP) joints of the most painful side (in case of equally severe symptoms on

BMJ Publishing Group Limited (BMJ) disclaims all liability and responsibility arising from any relianceSupplemental material placed on this supplemental material which has been supplied by the author(s) Ann Rheum Dis

doi: 10.1136/annrheumdis-2021-220511–2.:10 2021;Ann Rheum Dis, et al. Dumoulin QA

both sides, the dominant side was scanned). The protocol has been described previously.[3,4] MRI

was performed on a MSK-extreme 1.5T extremity MRI system (GE, Wisconsin, USA) using a 100mm

coil for the hand. The patient was positioned in a chair beside the scanner, with the hand fixed in the

coil with cushions. The following sequence was acquired before contrast administration: T1-

weighted fast spin-echo (FSE) sequence in the coronal plane (repetition time (TR) 575 ms, echo time

(TE) 11.2 ms, acquisition matrix 388×288, echo train length (ETL) 2). After intravenous injection of

gadolinium contrast (gadoteric acid, Guerbet, Paris, France, standard dose of 0.1 mmol/kg) the

following sequences were obtained: T1-weighted FSE sequence with frequency selective fat

saturation (fatsat) in the coronal plane (TR/TE 700/9.7ms, acquisition matrix 364×224, ETL 2), T1-

weighted FSE fatsat sequence in the axial plane (wrist: TR/TE 540/7.7 ms; acquisition matrix

320x192; ETL 2 and MCP-joints: TR/TE 570/7.7 ms; acquisition matrix 320x192; ETL 2). Field-of-view

was 100mm. Coronal sequences had 18 slices with a slice thickness of 2mm and a slice gap of

0.2mm. Axial sequences had a slice thickness of 3mm and a slice gap of 0.3mm with 16 slices for the

MCP-joints. We used the contrast enhanced T1-weighted fat suppressed sequence to assess

osteitis/bone marrow edema (BME). According to the RA MRI scoring system (RAMRIS)-method, T2-

weighted fat suppressed sequences, or when this sequence is not available a short tau inversion

recovery (STIR) sequence, should be used to assess BME. However, three previous studies have

demonstrated that a contrast enhanced T1-weigthed fat suppressed sequence has a strong

correlation with T2-weighted fat suppressed sequences.[5-7] Furthermore, the arthritis

subcommittee of the European Society of Musculoskeletal Radiology (ESSR) also recommends the

use of contrast enhanced T1-weighted fat suppressed sequences for depicting BME.[8] The T2-

weighted image shows increased water signal and a contrast-enhanced T1-weighted sequence

shows increased water content and the increased perfusion and interstitial leakage. A strong

correlation has been shown in arthritis patients and in patients without inflammatory diseases such

as bone bruises, intraosseous ganglions, bone infarcts and even nonspecific cases.[9,10] Based on

these results BME was assessed on contrast enhanced T1-weighted fat suppressed sequences as it



has a higher signal to noise ratio and allowed a shorter scan time for patients. All bones (with the

exception of metacarpal base 1 and the trapezium), joints and tendons were scored semi-

quantitatively according to the validated RAMRIS. Bones were scored separately for BME on a scale

0-3 based on the affected volume of the bone (no BME, >0-33%, >33-66%, >66%). Synovitis was

scored on a range 0-3 based on the volume of enhancing tissue in the synovial compartment (none,

mild, moderate, severe).[9] Similar to the scoring method described by Haavardsholm et al.,

tenosynovitis at the flexor side of MCP joints and MCP extensor peritendinitis were scored based on

the thickness of peritendinous effusion or synovial proliferation with contrast enhancement (normal,

<2mm, 2-5mm, >5mm (range 0-3)).[10] Scoring was performed independently by two trained

readers. Interreader and intrareader intraclass correlation coefficients were ≥0.90.

Definition of subclinical inflammation

Mean scores from both readers were used to determine the presence of subclinical inflammation

(synovitis, BME/osteitis, tenosynovitis) MCP-joints. As MRI-detected subclinical inflammation also

can be present in the general population, scores were dichotomized with MRI-data of symptom-free

controls as reference (n=193, as published previously).[11] Patients were considered positive for an

inflammatory feature if it is uncommon in symptom-free controls, i.e. present in <5% of symptom-

free controls at the same location and in the same age category (<40, 40-59, ≥60).

Statistical analyses

Logistic regression analysis was used to study the associations at baseline at patient level between

symptoms of the MCP-joints, subsequently MCP-tenderness by physical examination and patient-

reported MCP-joint pain, and different types of MRI-detected subclinical inflammation of the MCP-

joints. Considering patients with either MCP-tenderness by physical examination or patient-reported

pain, only the patients with an conducted MRI of the ipsilateral side were valued as ‘symptomatic’

(85%) whereas patients with an conducted MRI of the contralateral side were valued as ‘not



symptomatic’ (15%). Associations were studied univariable and multivariable for three types of MRI-

detected subclinical inflammation (synovitis, tenosynovitis, osteitis) since these features often occur

simultaneously. P-values <0.05 were considered statistically significant. IBM SPSS Statistics Version

25 was used.



References

[1] van Steenbergen HW, van Nies JAB, Huizinga TWJ, et al. Characterising arthralgia in the

preclinical phase of rheumatoid arthritis using MRI. Annals of the Rheumatic Diseases 2015;74:1225-

1232.

[2] Niemantsverdriet E, Dakkak YJ, Burgers LE, Bonte-Mineur F, Steup-Beekman GM, van der

Kooij SM, Boom HD, Allaart CF, de Jong PHP, van der Helm-van Mil AHM. TREAT Early Arthralgia to

Reverse or Limit Impending Exacerbation to Rheumatoid arthritis (TREAT EARLIER): a randomized,

double-blind, placebo-controlled clinical trial protocol. Trials. 2020 Oct 16;21(1):862.

[3] van Steenbergen HW, van Nies JAB, Huizinga TWJ, et al. Characterising arthralgia in the

preclinical phase of rheumatoid arthritis using MRI. Annals of the Rheumatic Diseases 2015;74:1225-

1232.

[4] Leonie E Burgers, Robin M ten Brinck, Annette H M van der Helm-van Mil, Is joint pain in

patients with arthralgia suspicious for progression to rheumatoid arthritis explained by subclinical

inflammation? A cross-sectional MRI study – Supplementary file. Rheumatology, Volume 58, Issue 1,

January 2019, Pages 86–93.

[5] Stomp W, Krabben A, van der Heijde D et al. Aiming for a shorter rheumatoid arthritis MRI

protocol: can contrast-enhanced MRI replace T2 for the detection of bone marrow oedema? Eur

Radiol 2014;24:2614-22.

[6] Schmid MR, Hodler J, Vienne P et al. Bone marrow abnormalities of foot and ankle: STIR

versus T1-weighted contrast-enhanced fat-suppressed spin-echo MR imaging. Radiology

2002;224:463-9.

[7] Mayerhoefer ME, Breitenseher MJ, Kramer J et al. STIR vs. T1-weighted fat-suppressed

gadolinium-enhanced MRI of bone marrow edema of the knee: computer-assisted quantitative 6

comparison and influence of injected contrast media volume and acquisition parameters. J Magn

Reson Imaging 2005;22:788-93.



[8] Sudol-Szopinska I, Jurik AG, Eshed I et al. Recommendations of the ESSR Arthritis

Subcommittee for the Use of Magnetic Resonance Imaging in Musculoskeletal Rheumatic Diseases.

Semin Musculoskelet Radiol 2015;19:396-411.

[9] Ostergaard M, Peterfy C, Conaghan P et al. OMERACT Rheumatoid Arthritis Magnetic

Resonance Imaging Studies. Core set of MRI acquisitions, joint pathology definitions, and the

OMERACT RA-MRI scoring system. J Rheumatol 2003;30:1385-6.

[10] Haavardsholm EA, Ostergaard M, Ejbjerg BJ et al. Introduction of a novel magnetic

resonance imaging tenosynovitis score for rheumatoid arthritis: reliability in a multireader

longitudinal study. Ann Rheum Dis 2007;66:1216-20.

[11] Mangnus L, van Steenbergen HW, Reijnierse M et al. Magnetic Resonance Imaging-Detected

Features of Inflammation and Erosions in Symptom-Free Persons From the General Population.

Arthritis Rheumatol 2016;68:2593-602.





Supplementary Table 1 Baseline characteristics of study population

Abbreviations: MCP (metacarpophalangeal), ACPA (Anti-citrullinated protein autoantibodies), RF

(rheumatoid factor), CRP (C-reactive protein), ESR (erythrocyte sedimentation rate), TJC (tender joint

count), VAS (visual analog scale), IA (inflammatory arthritis).

*Summed inflammation scores of al joints scanned through CSA protocol (MCP-joints,

metatarsophalangeal (MTP)-joints and the wrist)

Patients Total cohort N=602 Patients with MCP

tenderness N= 226

Patients without MCP

tenderness N= 376

P-value

Female gender, n (%) 454 (75) 171 (76) 283 (75) 0.91

Age, mean (SD) 44 (13) 44 (13) 45 (13) 0.32

Symptom duration weeks,

median (IQR)

19 (9-43) 19 (8-39) 18 (9-48) 0.19

ACPA-positive, n (%) 81 (14) 18 (8) 63 (17) 0.003

RF-positive, n (%) 121 (20) 31 (14) 90 (24) 0.003

CRP, median (IQR) 3 (3-4.7) 3 (3-4.4) 3 (3-4.8) 0.77

ESR, median (IQR) 6 (2-14) 6 (2-14) 6 (2-14) 0.23

68-TJC by health care

professional, median (IQR)

5 (2-10) 9 (5-15) 3 (1-7) <0.001

68-TJC patient-reported,

median (IQR)

16 (8-29) 22 (10-32) 14 (7-26) 0.001

No. of tender MCPs (2-5),

median (IQR)

0 (0-2) 2 (1-5) 0 (0-0) <0.001

No. of patient-reported

painful MCPs (2-5), median

(IQR)

3 (0-8) 6 (2-8) 1 (0-8) <0.001

VAS, mean (SD) 4.7 (2.3) 5.5 (2.0) 4.3 (2.4) <0.001

Progression to IA, n (%) 98 (16) 39 (17) 59 (16) 0.61

Follow up duration months,

median (IQR)

25 (14-28) 25 (14-28) 25 (14-28) 0.95

MRI-detected subclinical inflammation scores*, median (IQR)

Total synovitis score 1 (0-3) 1.25 (0-3) 1 (0-2.5) 0.42

Total osteitis score 1 (0-2) 1 (0-1.5) 1 (0-2) 0.38

Total tenosynovitis score 0 (0-1.5) 0 (0-1.5) 0 (0-1.5) 0.47

Total inflammation score 2.5 (1-5.9) 2.75 (1-6) 2.5 (1-5.5) 0.20





Supplementary Table 2 Associations between subclinical inflammation features and MCP-

tenderness by physical examination (A) or patient-reported MCP-pain (B)

A MCP-tenderness by physical

examination B Patient-reported MCP-pain

UNIVARIABLE MULTIVARIABLE* UNIVARIABLE MULTIVARIABLE*

OR (95% CI) OR (95% CI) OR (95% CI) OR (95% CI)

Total cohort

Synovitis 1.76 (1.10-2.81) 1.61 (0.98-2.65) 2.87 (1.29-6.39) 2.54 (1.12-5.77)

Osteitis 0.82 (0.41-1.63) 0.70 (0.35-1.42) 2.49 (0.91-6.81) 2.20 (0.79-6.11)

Tenosynovitis 1.69 (1.12-2.55) 1.54 (1.00-2.36) 1.51 (0.83-2.74) 1.27 (0.68-2.35)

Any subclinical

inflammation

1.84 (1.29-2.63) - 2.00 (1.21-3.30) -

Patients who progressed to inflammatory arthritis

Synovitis 1.65 (0.59-4.62) 1.49 (0.47-4.71) 4.33 (0.48-39.36) 5.67 (0.44-73.26)

Osteitis 0.80 (0.19-3.44) 0.69 (0.15-3.11) 1.56 (0.15-16.53) 0.95 (0.08-12.04)

Tenosynovitis 1.55 (0.65-3.70) 1.37 (0.52-3.58) 1.35 (0.36-5.08) 0.70 (0.15-3.34)

Any subclinical

inflammation

1.79 (0.74-4.30) - 1.80 (0.48-6.74) -

*Multivariable analyses contain the variables synovitis, osteitis and tenosynovitis



Documents

Correspondence on Role of joint damage, malalignment and