Abstract
Objective:
To evaluate the prevalence and clinical associations of ultrasound (US) findings of inflammatory arthritis and joint and soft tissue pathology in patients with systemic sclerosis (SSc).
Methods:
The hands and wrists of 43 SSc patients and 35 age-balanced controls were evaluated by clinical exam and musculoskeletal US. Synovial and tenosynovial pathology were assessed using semi-quantitative Gray Scale (GS) and Power Doppler (PD) scoring. US evaluation for osteophytes, erosions, ulnar artery occlusion, and median nerve cross-sectional areas was performed. Tender joints (TJ), swollen joints (SJ), modified Rodnan skin score (mRSS), digital ulcers, contractures, and calcinosis were evaluated. Concordance between US and physical exam findings at each joint region were assessed, and associations between their severity were analyzed.
Results:
TJs and SJs were present in 44.2% and 62.8% of SSc patients, respectively. Inflammatory arthritis, defined as having both GS>0 and PD>0, was observed in 18.6% of SSc patients and no controls. There was a high concordance by joint region between GS synovial hypertrophy and osteophytes (κ=0.88) as well as TJs (κ=0.72). SSc patients had more osteophytes compared to controls (48.8% vs 22.9%, p=0.018) as well as higher osteophyte severity (p=0.033).
Conclusions:
Despite a high percentage of tender and swollen joints, less than 20% of SSc patients met criteria for inflammatory arthritis on US. The high concordance of osteophytes with GS synovial hypertrophy and tender joints suggest that osteophytosis may be a significant contributor to joint pain in SSc patients.
Introduction
Hand and wrist pain are common complaints in patients with systemic sclerosis (SSc), yet the cause can be difficult to identify. SSc patients may present with any combination of peripheral disease manifestations including Raynaud’s phenomenon, digital ulceration, calcinosis, contractures, acroosteolysis, carpal tunnel syndrome, and articular and tendinous pathology, each with the potential to cause pain and dysfunction. Inflammatory arthritis is often cited as a contributing factor, and discriminating its presence or absence is important to guide immunosuppressive therapy1,2. Early clinical studies report a wide range of prevalence of inflammatory arthritis in SSc, between 16–88%, based on the presence of tender and swollen joints on exam3,4. Unfortunately, detection of true inflammatory arthritis on physical examination in SSc is complicated by overlying skin tightening and contractures, which may obscure palpation of the joints, tendons, and underlying synovitis.
In the past decade, musculoskeletal ultrasound has emerged as a valuable tool in rheumatology as a noninvasive means to detect articular and soft tissue pathology, including inflammatory arthritis, with a high degree of sensitivity and specificity. Typical ultrasound findings of inflammatory arthritis include: 1) B-mode imaging findings of synovial hypertrophy, effusions, and erosions, as well as 2) Power Doppler (PD) activity within the synovium denoting hyperemia5. Importantly, US findings of synovial hypertrophy and effusions are also seen in varying degrees in other conditions including tissue injury, crystalline arthropathies, and osteoarthritis. Furthermore, mild synovial hypertrophy on US is common in normal individuals and was detected in 48% of healthy participants in a large observational study (n=207).6 However, PD activity within the synovium is typically absent in non-pathological states. Therefore, clinical context, patient history, and the severity of US findings are all important factors in accurate interpretation.
Prior ultrasound studies suggest a high prevalence of synovitis (25–58%) and tenosynovitis (27%–45%) in several SSc cohorts1,7–9. Although these estimates are more precise than using clinical examination alone, these studies varied widely in terms of methodology and definitions for synovitis, with some defining any degree of B-mode synovial hypertrophy as synovitis, while others also requiring the presence of hyperemia on PD1,7–9. Additionally, most studies did not take into account the severity of synovial hypertrophy on ultrasound, and no studies evaluated associations between TJs, SJs, clinical findings, and ultrasound pathology by-joint and by-hand. Thus, the true prevalence of inflammatory arthritis and its contribution to pain in SSc remains uncertain.
We sought to address these shortcomings by evaluating for both inflammatory and noninflammatory pathology in consecutive SSc patients evaluated at our clinic, taking into account the severity of B-mode and PD findings for inflammatory arthritis, and assessing for by-joint and by-hand associations with clinical findings.
Methods
43 consecutive SSc patients meeting 2013 ACR/EULAR criteria and 35 age-balanced controls were prospectively examined by (RF) at Stanford University Medical Center, a practicing rheumatologist with 5 years US experience. SSc and control patients who were unable to tolerate a complete bilateral ultrasound examination were excluded. Additionally, control patients were excluded if they had a history of rheumatologic disease other than osteoarthritis.
The ultrasound examiner was blinded to the patients’ prior clinical, laboratory, and imaging findings at the time of examination. All scans were performed on the same GE Logiq E system equipped with a 5–12 MHz linear array probe in standard B-mode. PD evaluations were obtained using frequency of 7.7 MHz, with pulse repetition frequency in the range of 0.5–0.8 MHz, with low wall filter, and gain calibrated just below the threshold for artifactual signal underneath cortical bone. Rooms were kept at a comfortable temperature and maintained throughout all examinations.
Bilateral B-mode and PD examination included: 1st–5th dorsal metacarpophalangeal (MCP), the 2nd–5th volar MCP, proximal interphalangeal (PIP), and distal interphalangeal (DIP) joints, and associated flexor tendons. The radial aspect of the 2nd MCP and ulnar aspect of the 5th MCP were also evaluated for cortical irregularities. Selected views of the wrist in accordance with European League Against Rheumatism protocols were used to evaluate the radiocarpal, intercarpal, and radioulnar joints as well as the flexor and extensor tendon compartments10.
Median nerve cross sectional area, previously shown to be associated with median neuropathy, and Ulnar Artery Occlusion (UAO), previously shown to be associated with Raynaud’s phenomenon, calcinosis, and digital ulcers, were measured according to published methods11,12,21. All images were recorded, labelled, and stored for scoring at a later date.
Tender joints (TJ) and swollen joints (SJ) of the hands and wrists, modified Rodnan skin score (mRSS), contractures, nailfold capillary changes, and digital ulcerations were assessed clinically on the same day as the ultrasound examination by separate examiners trained in mRSS assessment and with extensive experience in SSc (MC and LC). Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels were obtained on the same day as the clinical and ultrasound examinations. Hand radiographs were obtained within 90 days of the examinations to assess for the presence of calcinosis and/or erosive arthropathy. Prior history of digital ulcers and/or digital gangrene was determined by review of the clinical record.
US images were reviewed in aggregate by three experienced ultrasonographers (RF, KS, and JH) several weeks after ultrasound evaluation. Two readers were completely blinded (KS and JH) to all patient data. The 3rd reader and US examiner (RF) was effectively blinded by reading the de-identified exams in aggregate several weeks after the ultrasound examination date. Images were reviewed and scored using a semiquantitative gray scale severity score (GS, 0–3) and PD score (0–3) for both joints and tendons as previously described by Szkudlarek and proposed by OMERACT5,13,14. Osteophytes were scored dichotomously and defined as cortical protrusions seen in two planes15. Erosions were scored dichotomously and defined as discontinuities in the bone surface on two perpendicular planes. A total of 19,968 scores were obtained, 256 per patient, the vast majority of which were zero or negative. Discordance between readers was rare (n=57) and was most commonly encountered in deciding between scoring of GS 0 vs GS 1. Discordant reads were discussed and if consensus could not be reached the final score was determined by RF. Inflammatory arthritis was defined as a combination of both GS > 0 and PD > 0 in at least one area (see discussion for details).
Statistical Analysis
For the purpose of statistical evaluations for concordance and correlations, the results from the consensus ultrasound reading were transformed into joint region scores to allow for direct by-joint analysis with TJs and SJs. To accomplish this for GS, PD, osteophytes, and erosions, the maximal observed value from all observations at each joint region was carried forward. As an example, the GS score for the 2nd MCP was derived by noting the maximum score from the MCP volar articular GS score, MCP dorsal articular GS score, and MCP flexor tendon GS score. Similar transformations were performed throughout the hand. As a result, the 45 images obtained for each hand per patient were reduced to 14 joint regions. This yielded a total of 28 joint region observations for GS and PD per patient with preserved laterality. In light of the difficulty assessing all of the cortical surfaces of the carpal bones by US, we did not attempt to quantify erosions or osteophytes in this area. Overall this approach yielded a total of 26 joint region observations per patient.
To evaluate concordance between semi-quantitative scoring of GS, PD, TJs, SJs, and osteophytes at each joint region, Chance-Corrected Gwet’s agreement coefficients were calculated. Subsequently, overall severity scores for each variable (GS, PD, osteophytes, ER, TJs and SJs) were obtained for each patient by summing scores across all joint regions and correlations between these scores were assessed by Spearman’s rank correlation. Wilcoxon rank-sum test was applied to compare the osteophyte severity between SSc patients and controls. To evaluate whether osteophytes are more common in SSc patients, the osteophyte severity score was dichotomized as absent when 0 and present otherwise, and chi-square test was used. Associations between RF or CCP and US findings of GS severity > 0, PD severity > 0, or GS and PD scores > 0 were evaluated by chi-square test. All tests were two-sided with p < 0.05 considered significant. All statistical analyses were done by statistical software SAS version 9.4 (SAS Institute Inc., Cary, NC).
Results
Study population
43 SSc patients were enrolled and underwent ultrasound examination, 93% of which were female with mean age 58 (±14) years and mean disease duration from first non-Raynaud’s symptom 10.4 (±9.3) years (Table 1). 39.5% of patients were classified as diffuse cutaneous SSc and the mean mRSS was 10.2 (±8.2). Raynaud’s phenomenon was present in 97.7% of patients, and 44.2% reported a history of digital ulcers with 16.2% having active digital ulcers at the time of exam. Over half of participants had contractures and 34.9% had calcinosis. SSc-associated antibodies were observed in 76.7% of patients with no SSc-associated auto-antibodies in 23.2%. Inflammatory markers in the SSc cohort showed a median ESR 15.0 mm/hour [interquartile range (IQR) 8.0–36.3] and median C-reactive protein 0.3 mg/L [IQR 0.2–0.8]. Rheumatoid factor (RF) and anti-cyclic citrullinated peptide (CCP) antibodies were found in 18.6% and 7.0% of SSc participants, respectively. Treatment regimens at the time of enrollment consisted of non-biologic DMARDs in 53.5% (mycophenolate 27.9%; azathioprine 2.3%; methotrexate 7.0%; hydroxychloroquine 25.6%), with a lesser degree of NSAID (14.0%), prednisone (9.3%), and biologic DMARDs or JAK inhibitors (7.0%). We also enrolled 35 age-balanced control patients, of which 77% were female with a mean age of 57 (±13) years, and two patients had a previously diagnosed history of osteoarthritis in the fingers.
Table 1.
Characteristics of SSc cohort and controls
| Controls | n = 35 |
|---|---|
| Age, mean (± SD) | 57 (13) |
| Female, n (%) | 27 (77.1) |
| SSc Cohort | n = 43 |
| Age, mean (± SD) | 58 (14) |
| Female, n (%) | 40 (93.0) |
| Diffuse disease, n (%) | 17 (39.5) |
| MRSS, total, mean (± SD) | 10.2 (8.2) |
| Years since first non-Raynaud’s symptom, mean (± SD) | 10.4 (9.3) |
| Baseline ESR, median (IQR) mm/h | 15.0 (8.0–36.3) |
| Baseline CRP, median (IQR) mg/L | 0.3 (0.2–0.8) |
| Antibodies, n (%) | |
| Anticentromere | 17 (39.5) |
| Anti-topoisomerase | 10 (23.3) |
| RNA-polymerase-3 | 6 (14.0) |
| U1/U3 RNP or anti-PM/Scl | 6 (14.0) |
| No SSc-associated antibodies | 10 (23.2) |
| Rheumatoid Factor | 8 (18.6) |
| CCP | 3 (7.0) |
| Disease Features, n (%) | |
| Raynaud’s | 42 (97.7) |
| History of digital ulcers | 19 (44.2) |
| Active digital ulcers | 7 (16.2) |
| Digital Gangrene or Ischemia | 2 (4.7) |
| Nailfold Capillary Changes | 31 (72.1) |
| Contractures | 22 (51.2) |
| Calcinosis | 15 (34.9) |
| Medications, n (%) | |
| Prednisone | 4 (9.3) |
| NSAIDS | 6 (14.0) |
| Non-biologic DMARD | 23 (53.8) |
| Biologic DMARD or JAK Inhibitor | 3 (7.0) |
SSc = systemic sclerosis; RNP = anti-ribonucleoprotein antibodies; CCP = anti-citrullinated protein antibodies, MRSS = modified Rodnan skin score; ESR = estimated sedimentation rate; CRP = C-reactive protein; IQR = interquartile range; NSAIDS = non-steroidal anti-inflammatory drugs; DMARD = disease modifying anti-rheumatic drugs; JAK = janus kinase
Clinical and US findings in SSc and control patients
Figure 1 depicts the distribution and grade of clinical and ultrasound findings for each patient. TJs and SJs were observed in 44.2% and 62.8% of SSc patients, respectively. GS scores of one or higher in at least one joint region were found in 37 (86.0%) of SSc patients compared to 22 (62.9%) of controls. Patients with highest GS scores of 1, 2, or 3 in any joint region were seen in 48.8%, 30.2%, and 7.0% of SSc patients, respectively, compared to 57.1%, 5.7%, and 0% of controls (p=0.003). PD scores > 0 were seen in 8 (18.6%) of SSc patients (maximum grade 1 and 2, 4.7% and 14.0% respectively) and no controls. In light of these findings, inflammatory arthritis, defined by a combination of GS > 0 and PD > 0 was observed in 8 (18.6%) of SSc patients and no controls (Table 2). Only one patient with inflammatory arthritis was RF positive and none demonstrated CCP positivity. Of the 17 diffuse SSc patients, 4 (23.5%) had inflammatory arthritis compared to 4 (15.4%) of the 26 SSc patients with limited disease. There were 12 patients in our cohort with early disease (less than 5 years), of which only 1 patient (8.3%) demonstrated findings of inflammatory arthritis. PD findings were observed in 5 wrists, 8 MCP joints, and 4 DIP joints.
Figure 1. Heat map of ultrasound and clinical examination findings.

Each row corresponds to unique systemic sclerosis (SSc) patients or healthy controls. Rows 1–17 = limited SSc; rows 18–43 = diffuse SSc; rows C01–C35 = healthy controls. For gray scale score and power doppler score: white = 0, yellow =1, orange =2, and red =3. For tender joints, swollen joints, erosions, and osteophytes: white = absent, black = present. Left and right laterality for each consolidated joint region were combined for visualization in this figure but were preserved for all statistical analyses.
Table 2.
Comparison of ultrasound findings between systemic sclerosis (SSc) patients and controls
| SSc n = 43 |
Controls n = 35 |
p | |
|---|---|---|---|
| Highest GS Score | 0.003 | ||
| GS0 | 6 (14.0) | 13 (37.2) | |
| GS1 | 21 (48.8) | 20 (57.1) | |
| GS2 | 13 (30.2) | 2 (5.7) | |
| GS3 | 3 (7.0) | 0 | |
| Highest PD Score | 0.018 | ||
| PD0 | 35 (81.3) | 35 (100) | |
| PD1 | 2 (4.7) | 0 | |
| PD2 | 6 (14.0) | 0 | |
| Inflammatory Arthritis (GS>0 and PD>0) | 8 (18.6) | 0 | <0.001 |
| Tenosynovial hypertrophy (GS > 0) | 13 (30.2) | 3 (8.5) | 0.0241 |
| Erosions | 8 (18.6) | 0 | <0.007 |
| Osteophytes | 21 (48.8) | 8 (22.9) | 0.018 |
| Ulnar Artery Occlusion (UAO) | 16 (37.2) | 0 | <0.001 |
| Median nerve area | 12.1 (±3.3) mm2 | 10.0 (±2.1) | 0.001 |
SSc = systemic sclerosis, GS = gray scale, PD = power doppler
Osteophytes on US were more common (48.8% vs 22.9%, p=0.018, Table 2) and more severe (p=0.005, Figure 2) in SSc patients compared to controls. Osteophytes were seen in 74% of SSc patients with TJs and 56.8% of those with GS. The distribution of osteophytes on US included 35 MCPs, 9 PIPs and 21 DIP joints. Overlap between PD and osteophytes were observed in 3 MCP and 4 DIP joints. Erosions in the digits were seen in 8 (18.6%) of SSc patients on US and no controls (p=0.007, Table 2). In contrast, X-ray findings in the fingers revealed osteophytes in 10 (23.3%) SSc patients and erosions in 6 (14.0%). Of patients with erosions, 4 (66.7%) had findings consistent with erosive osteoarthritis on X-ray. Two patients with erosive osteoarthritis on X-ray had corresponding power doppler activity and carried the highest GS severity scores of the cohort.
Figure 2. Osteophyte severity among SSc patients and controls with osteophytes.

Osteophyte severity score calculated by summing individual joint region scores per patient. Median with interquartile range shown. Comparison of osteophyte severity by Wilcox rank-sum test. SSc = systemic sclerosis.
Tenosynovial hypertrophy noted on gray scale scoring > 0 was more frequent in SSc than controls (30.2% vs 8.6%, p=0.024) and was nearly exclusively observed in the wrist in both cohorts (Table 2). Several prior studies have noted fibrotic appearing hyperechoic tendon sheaths in SSc, most notable in the wrist extensor region.7,24,25 We observed this finding in the wrist extensor tendons in 60.5% of individuals without preference for diffuse or limited disease. Ulnar artery occlusion (UAO) was found in 16 (37.2%) SSc patients and no controls. The mean median nerve area was 12.1 (±3.3) mm2 compared to 10.0 (±2.1) for controls (p=0.001) (Table 2).
Associations between clinical, laboratory, and US findings
GS findings showed stronger concordance with TJs than SJs (κ = 0.72 [0.69, 0.76] vs 0.52 [0.47, 0.57]). The severity of GS findings also showed greater correlation with the severity of TJs than the severity of SJs (ρ = 0.47 vs 0.32). Osteophytes were highly concordant with both GS (κ = 0.88 [0.86, 0.90]) and TJs (κ = 0.80 [0.77, 0.83]), and osteophyte severity correlated with both GS severity (ρ = 0.59, p < 0.001) and TJ severity (ρ = 0.49, p < 0.001). TJs and SJs did not correlate with median nerve cross sectional area, UAO, calcinosis, digital ulcers, mRSS, or contractures (Table 3). Neither RF nor CCP were associated with GS severity > 0, PD severity > 0, or US identified inflammatory arthritis (Table 3).
Table 3.
Concordance (κ), correlations (ρ), and associations between clinical, laboratory, and ultrasound findings
| Concordance and Correlations | κ (CI) | ρ (p) |
|---|---|---|
| Tender Joints (TJs) and Gray Scale Score (GS) | 0.72 (0.69, 0.76) | 0.47 (0.001) |
| Tender Joints (TJs) and Osteophytes (OS) | 0.80 (0.77, 0.83) | 0.49 (< 0.001) |
| Osteophytes (OS) and Gray Scale Score (GS) | 0.88 (0.86, 0.90) | 0.59 (<0.001) |
| Swollen Joints (SJs) and Gray Scale Score (GS) | 0.52 (0.47, 0.57) | 0.32 (0.04) |
| Swollen Joints (SJs) and Osteophytes (OS) | 0.61 (0.56, 0.66) | 0.20 (0.2) |
| TJs | SJs | |
| Correlations | ρ (p) | ρ (p) |
| Median nerve | 0.08 (0.6) | 0.07 (0.6) |
| Ulnar artery occlusion (UAO) | 0.13 (0.4) | −0.14 (0.4) |
| Calcinosis | 0.01 (0.9) | −0.26 (0.09) |
| Digital ulcers | −0.02 (0.8) | −0.32 (0.3) |
| Contractures | −0.17 (0.3) | 0.02 (0.9) |
| Modified Rodnan skin score (mRSS) | −0.28 (0.3) | 0.08 (0.6) |
| Associations | RF | CCP |
| GS > 0 and PD > 0 (inflammatory arthritis) | p = 1.0 | p = 1.0 |
| GS severity score > 0 | p = 1.0 | p = 0.37 |
| PD severity score > 0 | p = 1.0 | p = 1.0 |
Since multiple GS and OS measurements were obtained per joint region, single scores corresponding to the highest values observed in the joint region were recorded. κ value = chance-corrected Cohen’s Kappa statistic (GS and PD scores were transformed into binary variables 0 versus 1–3). CI = 95% confidence interval. ρ =Spearman correlation coefficients using severity scores calculated by summing individual joint region scores per patient. Associations between ultrasound, RF, CCP determined by chi-squared test. RF =rheumatoid factor; CCP =anti-cyclic citrullinated peptide antibodies.
Discussion
This study offers valuable insight into the etiology of hand and wrist pain in patients with SSc and examines the relationship between physical exam findings and ultrasound-identified pathology. This is also the first study to analyze concordance and correlation between clinical exam and ultrasound findings on a by-joint level in SSc patients. We observed a high percentage of tender joints (44.2%) and swollen joints (62.8%), demonstrating the pervasiveness of articular symptoms in this population. However, swollen joints were less concordant with GS synovial changes compared to tender joints (κ = 0.52 [0.47, 0.57] vs. 0.72 [0.69, 0.76]) which exemplifies the challenges in physical exam of SSc patients. It also suggests that swollen joint counts may be of less clinical utility in assessment for inflammatory arthritis in SSc. Using a more stringent cutoff for pathologic synovial hypertrophy of GS ≥ 2, ultrasound examination revealed pathologic synovial hypertrophy in 37.2% of SSc patients.
OMERACT recently defined synovitis on ultrasound as GS ≥ 1 and PD ≥ 0, making GS alone sufficient to identify synovitis5,14. The group’s rationale for this decision was due to concerns over heterogeneity between ultrasound equipment with poorer PD sensitivity. Subsequently, a large study identified synovitis based on this definition in 48% of healthy individuals, highlighting the challenges of identifying inflammatory arthritis using these ultrasound GS and PD criteria6. In line with several prior publications, we chose to define inflammatory arthritis using a more stringent cutoff of both GS > 0 and PD > 0, with careful calibration of our PD settings to maximize sensitivity16. Using this definition, we found a relatively low prevalence of active inflammatory arthritis (18.6%) in our cohort of SSc patients and no controls.
Conversely, we found a high prevalence of osteophytosis in SSc patients compared to controls (48.8% vs 22.9%, p=0.018). Similar findings were noted by Cuomo et. al. who reported osteophytes in 58% of 45 SSc patients as detected by ultrasound1. This study also noted synovitis (defined as effusion and/or synovial proliferation) in 58%, but did not comment on the overlap of osteophytosis with these findings. Our analyses showed that osteophytes were strongly concordant with both GS score and TJs at each joint region, and that overall osteophyte severity was correlated with both overall GS score severity and TJ severity.
Prior studies have shown GS changes in patients with isolated osteoarthritis and degenerative joint disease17,18. Keen et. al found GS synovitis (defined as a composite of synovial hypertrophy and effusion per OMERACT) in 46% of OA patients18. Furthermore, patients with erosive osteoarthritis (EOA), a subset of OA characterized by proliferative osteophytes and subchondral erosions of the interphalangeal joints, are even more likely to have inflammatory signs on ultrasound (synovial hypertrophy, effusion, PD) compared to non-erosive OA19.
We encountered four SSc patients in our cohort with severe osteophytes in the fingers with prominent enveloping synovium, with and without hyperemia on PD with an overall appearance suggestive of erosive osteoarthritis (Figure 3). All four of these patients’ X-rays had a combination of findings of non-marginal, central subchondral erosions with a “gull-winging” appearance, along with severe osteophytosis and ankylosis consistent with erosive osteoarthritis radiographically20. Similar findings were not observed in any of the age-balanced controls. In a prior population-based study of individuals aged 55 and greater, the prevalence of radiographic EOA was estimated to be 2.8% in the general population (mean age without EOA of 66.1 ± 7.0 years; with EOA of 68.5 ± 6.5 years)22. Although our study was not designed to determine the prevalence of EOA, the increased prevalence of 9.3% in our SSc population is intriguing, particularly in light of the younger age of our cohort (mean age 58 ± 14 years), and warrants further investigation.
Figure 3. Degrees of osteophytosis on ultrasound imaging of the distal interphalangeal joint in patients with systemic sclerosis.

Ultrasound imaging of the volar aspect of the distal interphalangeal joint (DIP) in systemic sclerosis in A) a normal joint, B) moderate osteophytosis, and C) severe osteophytosis and synovitis with the appearance of inflammatory osteoarthritis with doppler activity. FT = flexor tendon, MP = middle phalanx, DP = distal phalanx, OS = osteophytes, green arrowheads = synovial border.
Taken as a whole, our findings raise the question of whether a significant proportion of the synovial hypertrophy previously reported on US studies in SSc patients may be due to osteophytosis as opposed to traditional inflammatory arthritis. While it is possible that the SSc patients in this and prior studies have coexisting OA separate from their rheumatologic disease, the higher prevalence and severity of osteophytosis in SSc patients compared to age-balanced controls suggests that there is a link between these processes. We postulate that there is likely a spectrum of joint disease in SSc spanning from degenerative osteoarthritis, to erosive osteoarthritis, to a more typical inflammatory arthritis overlap. Distinguishing these entities is clinically important as the treatment paradigms vary greatly ranging from conservative measures to escalation of immunosuppression.
We found an increased median nerve cross sectional area in SSc patients compared to controls; however, this finding was not correlated with tender or swollen joints of the same hand. Similarly, UAO, mRSS, calcinosis, digital ulcers, and contractures did not correlate with tender or swollen joints in the same hand. While increased median nerve cross sectional area is often associated with carpal tunnel syndrome, and UAO with Raynaud’s phenomena, calcinosis, and digital ulcers, they do not appear to have a significant impact on articular pain.
Potential limitations of this study include the cross-sectional study design which does not take into account disease duration or evolution over time. Additionally, all images were obtained by a single ultrasonographer; however, the scans were saved and read in aggregate at a later date by a panel of three ultrasonographers, effectively blinding the readers. Although TJ, SJ, GS and PD were assessed in the wrist, we did not quantify erosions and osteophytes in this location due to the complex 3-dimensional nature of the wrist and inability to view all of the cortical surfaces which are better assessed by other imaging modalities. However, we believe our exhaustive evaluation of the erosions and osteophytes in the joints of the fingers yielded unique insights into how these features are related to synovial hypertrophy, PD, tender, and swollen joints. We did not collect patient reported pain and functional outcomes in this cohort, and in future studies, addition of these outcomes may further elucidate the clinical significance of ultrasound findings. Lastly, 55.8% of our SSc patients were also on DMARDS (34.9% excluding mycophenolate), which can reduce PD activity in inflammatory arthritis23 and may have resulted in a reduced prevalence of inflammatory arthritis in our study. In addition, our cohort’s average disease duration was 10 years, compared to a range of averages of 5 to 11 years in prior studies.7–9 Although patients with shorter disease duration may be more likely to have inflammatory arthritis, we did not observe this in our cohort.
In conclusion, our results reinforce prior studies showing a high degree of articular symptoms and pathology in SSc patients, but also challenge the idea that these symptoms are predominately due to inflammatory arthritis. SSc patients carry a higher burden of osteophytosis compared to age-balanced controls. Moreover, the high concordance between osteophyte presence and severity with TJs that have associated synovial hypertrophy suggests that osteophytosis and associated reactive synovitis may be a significant contributor to joint pain. Given the challenges of physical exam, musculoskeletal ultrasound is a powerful tool to evaluate the spectrum of articular disease in patients with SSc and should be incorporated into future studies.
Footnotes
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