High-frequency ultrasound semi-quantitative assessment of cartilage damage in rheumatoid arthritis using the outcome measures in rheumatology scoring system

Introduction

Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease characterized by persistent synovitis and progressive structural damage, including cartilage damage and bone destruction (1). Cartilage damage contributes independently to irreversible functional impairment and long-term disability in RA (2,3). Cartilage loss also occurs in osteoarthritis (OA), the most common form of arthritis and a major cause of chronic pain and disability in older adults (4). Consequently, sensitive and reliable assessment of cartilage damage is important for characterizing structural joint involvement in these conditions.

Conventional radiography remains widely used to assess structural joint damage in clinical practice. However, it evaluates cartilage loss only indirectly through joint space narrowing and lacks sufficient sensitivity to detect early cartilage abnormalities (5). High-frequency ultrasound (US) is a non-invasive and radiation-free imaging modality that enables direct visualization of cartilage and has demonstrated sensitivity in detecting synovitis, cartilage damage, and bone erosion (6-8). Accordingly, it is recommended by the European Alliance of Associations for Rheumatology (EULAR) for the clinical assessment and management of inflammatory and degenerative joint diseases (9,10).

The Outcome Measures in Rheumatology (OMERACT) working group has proposed standardized semi-quantitative grading and quantitative measurement methods for US assessment of cartilage, particularly in metacarpophalangeal (MCP) joints, both of which have demonstrated good validity and reliability (8,11,12). However, although these methods are increasingly used, there remains limited evidence regarding the disease specificity and discriminatory value of US-detected cartilage damage for RA, particularly in comparison with OA and healthy controls (HCs) (5,13).

The aim of this study was to characterize the distribution and burden of US-detected cartilage damage in patients with RA using the OMERACT scoring system, and to compare these findings with those from OA patients and HCs, in order to better define RA-specific imaging patterns. We present this article in accordance with the STROBE reporting checklist (available at https://qims.amegroups.com/article/view/10.21037/qims-2026-0948/rc).

Methods

Study population

This single-center cross-sectional study enrolled adults (≥18 years old) from Peking University People’s Hospital between August 2023 and January 2026. A total of 129 patients fulfilled the 2010 American College of Rheumatology/EULAR classification criteria for RA (14) and 36 patients met the 2023 EULAR classification criteria for hand OA (15). Additionally, 59 HCs with no history of joint disease were included. The exclusion criteria included previous trauma or surgery involving the assessed hand joints, prior intra-articular injections, and pregnancy. The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the Ethics Committee of Peking University People’s Hospital (approval No. 2023PHB211-001). Written informed consent was provided by all participants. The study was registered in the Chinese Clinical Trial Registry (No. ChiCTR2500106342).

Baseline demographic characteristics, including age and sex, were recorded for all participants. For RA and OA patients, disease duration, laboratory findings, hand dominance, family history, and current treatments were recorded. Laboratory measurements included erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), rheumatoid factor (RF), and anti-cyclic citrullinated peptide (CCP) antibodies. Rheumatologists blinded to the US findings collected clinical information and conducted physical examinations. Disease activity of RA patients was evaluated using the disease activity score in 28 joints based on ESR (DAS28-ESR).

US assessment

All participants underwent US examinations by one of two experienced US specialists (W.L. and Y.X.), each with more than 5 years of experience in musculoskeletal ultrasonography. The examinations were performed using a Canon Aplio i800 (Canon Medical Systems, Otawara, Japan) with a 24-MHz linear probe in accordance with OMERACT guidelines (16). The ultrasonographers were blinded to clinical findings and laboratory results.

The second and third MCP and the second and third proximal interphalangeal (PIP) joints of both hands were selected for measurement, as these joints are frequently involved and commonly assessed in US studies of RA and hand OA (13,17). Participants were seated with their hands placed on the examination bed and their fingers flexed to approximately 60° during the examination. The probe was positioned perpendicular to the cartilage surface. The hyaline cartilage of each joint was scanned on the dorsal aspect in both longitudinal and transverse views. Each suspected abnormality was confirmed and documented in two orthogonal imaging planes.

Cartilage thickness was measured at the thickest point, including the cartilage-synovial interface but excluding the osteochondral junction. Cartilage in each joint was graded semi-quantitatively using the OMERACT 3-point grading of 0–2 scoring system (11) (Figure 1). The weighted score was calculated as (5 × total MCP grade + 3 × total PIP grade)/8 (18). Patient-level measures included the total cartilage grade, MCP and PIP subtotal grades, number of affected joints, and maximum cartilage grade. Cartilage location was evaluated by dividing each imaging plane into three anatomical zones. The transverse plane was divided into radial, middle, and ulnar zones, whereas the longitudinal plane was divided into distal, middle, and proximal zones. Cartilage involvement spanning all three zones was classified as widespread damage (Figure 2).

Figure 1 Reference ultrasound images of metacarpophalangeal joint cartilage damage according to the OMERACT scoring system. The images illustrate the sonographic appearances of different cartilage grades. (A) Grade 0: normal appearance of the hyaline cartilage. (B) Grade 1: minimal changes, and localized thinning of the hyaline cartilage layer. (C) Grade 2: severe changes, and complete loss of cartilage. Arrows indicate cartilage damage sites. mh, metacarpal head; OMERACT, Outcome Measures in Rheumatology.

Figure 2 Two-dimensional ultrasound imaging of the right metacarpal head. Transverse sections (A-D): (A) damage at the radial portion; (B) damage at the ulnar portion; (C) damage at the middle portion; (D) widespread cartilage damage. Longitudinal sections (E-H): (E) damage at the distal portion; (F) damage at the proximal portion; (G) damage at the middle portion; (H) widespread cartilage damage. Arrows indicate cartilage damage sites. mh, metacarpal head; pp, proximal phalanx.

Synovial hypertrophy, power Doppler signal, and joint effusion were semi-quantitatively scored using a 4-point scale (0= absent, 1= mild, 2= moderate, 3= severe) (19). For each patient, the weighted score was calculated as (5 × total MCP score + 3 × total PIP score)/8. Bone erosion was recorded as present or absent at each joint and the total number of joints with bone erosion was calculated for each patient. Inter-observer reliability was assessed by having two ultrasonographers independently score a randomly selected subset of 50 participants (RA, OA, and HC). Intra-observer reliability was assessed by having one ultrasonographer re-score the same images after 2–4 weeks.

Data analysis

Continuous variables were summarized as the mean and standard deviation when approximately normally distributed and as the median and interquartile range (IQR) otherwise. Categorical variables were summarized as frequencies and percentages. Patients with RA were divided into two subgroups based on disease duration: less than 2 years (early RA) and 2 years or more (established RA). Joints with a semi-quantitative cartilage grade ≥1 were defined as having cartilage damage, whereas those with a grade of 0 were considered normal. Severe cartilage damage was defined as an OMERACT cartilage grade of 2.

Normally distributed continuous variables were compared using the independent-samples t-test for two groups and one-way analysis of variance (ANOVA) for three groups. Non-normally distributed variables were compared using the Kruskal-Wallis test, or Mann-Whitney U test, respectively. Categorical variables were compared using the Pearson χ² test or Fisher’s exact test. Multiple comparisons were adjusted using the Benjamini-Hochberg false discovery rate correction. Overdispersed patient-level integer count outcomes, including the total cartilage grade, MCP and PIP subtotal grades, and number of affected joints, were analyzed using negative binomial regression. Results are reported as incidence rate ratios (IRRs) with 95% confidence intervals (CIs). Maximum cartilage grade was treated as an ordinal outcome and analyzed using ordinal logistic regression, with results reported as common odds ratios (ORs) and 95% CIs. Joint-level cartilage damage was analyzed using logistic generalized estimating equations, with patient identifier specified as the clustering variable, an exchangeable working correlation structure, and robust standard errors. For RA versus OA comparisons, models were adjusted for age and disease duration; for RA versus HC comparisons, models were adjusted for age only. Weighted Cohen’s kappa coefficient was used to evaluate the consistency of the assessment results and was interpreted as follows: <0.4, poor agreement; 0.4–0.6, moderate agreement; 0.61–0.8, substantial agreement; and >0.8, almost perfect agreement.

Spearman correlation was used to evaluate the association between semi-quantitative cartilage grades and both clinical and US parameters in patients with hand OA and those with RA. Spearman correlation coefficients were interpreted as follows: 0.01–0.19, very weak to negligible correlation; 0.20–0.39, weak correlation; 0.40–0.69, moderate correlation; and ≥0.70, strong correlation.

All statistical analysis was conducted using R version 4.5.1 (R Foundation for Statistical Computing, Vienna, Austria). Unless otherwise specified, P<0.05 (two-tailed) was considered statistically significant.

Results

This study included 224 participants, including 129 patients with RA, 36 patients with OA, and 59 HCs. Of the RA patients, 89 (69.0%) were classified as having early RA (disease duration of less than 2 years), whereas 40 (31.0%) had established RA (disease duration of 2 years or more). A total of 1,792 finger joints were analyzed, including 1,032 from the RA group, 288 from the OA group, and 472 from HCs. Baseline demographic and clinical characteristics are reported in Table 1. Significant differences were observed in age across the three groups. Patients with RA were significantly younger than those with OA but older than HCs (P<0.05). Among OA patients, 13 (36.1%) had a disease duration exceeding 12 months. Hand deformities were observed in 6 patients with hand OA (16.7%). Osteophytes were documented in 22 of 36 patients (61.1%), predominantly involving the distal interphalangeal (DIP) and PIP joints. Regarding treatment, 116 patients with RA (89.9%) received conventional synthetic disease-modifying antirheumatic drugs, 25 (19.4%) received non-steroidal anti-inflammatory drugs, 18 (14.0%) received glucocorticoids, 9 (7.0%) received targeted synthetic disease-modifying antirheumatic drugs, and 7 (5.4%) received biological disease-modifying antirheumatic drugs. Among OA patients, 20 (55.6%) received glucosamine, 18 (50.0%) received non-steroidal anti-inflammatory drugs, and 11 (30.6%) received no treatment. Compared with the OA group, patients with RA exhibited significantly higher levels of CRP (P=0.006), ESR (P<0.001), RF (P<0.001), and anti-CCP (P<0.001).

The intra-observer reliability demonstrated substantial to almost perfect agreement, with weighted kappa values ranging from 0.76 to 0.88. The inter-observer reliability was substantial, with weighted kappa values ranging from 0.62 to 0.78.

US characteristics of cartilage in patients with RA

The prevalence of cartilage damage was 46.5% in RA patients, 38.9% in OA patients, and 11.9% in HCs. Severe cartilage damage was observed in 10.1% of RA patients and 11.1% of OA patients, whereas no severe cartilage damage was detected in HCs. After adjustment for age and disease duration, MCP total cartilage grading scores (IRR =2.17; 95% CI: 1.12–4.20; P=0.021), the number of affected joints per patient (IRR =1.92; 95% CI: 1.08–3.43; P=0.027) and the overall cartilage grading scores (IRR =1.76; 95% CI: 1.01–3.06; P=0.046) remained significantly higher in RA patients than in OA patients. After adjustment for age, RA patients showed a consistently higher cartilage damage burden than HCs. MCP total cartilage grading scores demonstrated the strongest association (IRR =3.56; 95% CI: 1.39–9.16; P=0.008), followed by the maximum cartilage grade (OR =3.31; 95% CI: 1.30–8.40; P=0.012), the overall cartilage grading scores (IRR =2.20; 95% CI: 1.12–4.33; P=0.023), and the number of affected joints (IRR =2.07; 95% CI: 1.05–4.10; P=0.036) (Table 2).

At the joint level, the distribution of cartilage damage grades differed significantly between RA, OA, and HC groups (Table 3). Compared with OA, RA showed a lower proportion of grade 0 joints and a higher proportion of joints with cartilage damage, particularly in MCP joints. After adjustment and accounting for within-patient clustering, RA joints had higher odds of cartilage damage than OA joints (OR =1.91; 95% CI: 1.03–3.57; P=0.041). This difference was mainly attributable to MCP joints, in which cartilage damage was more frequent in RA than in OA (OR =2.85; 95% CI: 1.27–6.39; P=0.011). When compared with HCs, cartilage damage was more frequent in RA joints across all examined joints (13.8% vs. 3.2%). After adjustment for age and accounting for within-patient clustering, RA was associated with higher overall odds of cartilage damage than HC (OR =2.62; 95% CI: 1.002–6.87; P=0.049). However, the joint-category analyses did not reach statistical significance for either MCP joints (OR =3.72; 95% CI: 0.75–18.31; P=0.107) or PIP joints (OR =1.50; 95% CI: 0.52–4.31; P=0.455).

In patients with RA, cartilage damage was most frequently observed at the right MCP2 and MCP3 joints. In contrast, cartilage damage in patients with OA showed a more uniform distribution across joints, with relatively greater involvement of the PIP3 joints (Figure 3A). Regarding the distribution of the most severely affected joint, RA patients demonstrated a predominance in the right MCP2 and MCP3, whereas no distinct distribution pattern was observed in OA patients or HCs (Figure 3B).

Figure 3 Prevalence and distribution of ultrasound-detected cartilage damage across hand joints. (A) Prevalence of cartilage damage (grade ≥1) in RA, OA, and HCs across individual joints. (B) Within-group distribution of the joints with the maximum cartilage grade. HC, healthy control; OA, osteoarthritis; RA, rheumatoid arthritis.

Distribution of cartilage damage

Ultrasonography demonstrated a higher prevalence of cartilage damage in MCP joints compared with PIP joints in patients with RA, reaching statistical significance (17.3% vs. 10.5%, P<0.001) (Figure 4A). In the OA group, cartilage damage was more frequently observed in PIP joints than in MCP joints (11.1% vs. 9.0%), though the difference did not reach statistical significance. No significant differences were observed between dominant and non-dominant hands in either group (RA: 14.7% vs. 13.0%, P=0.365; OA: 11.4% vs. 9.0%, P=0.525) (Figure 4B). In RA patients, transverse-plane lesions showed no clear preferential pattern, with slightly more widespread involvement, whereas longitudinal-plane lesions were more frequently observed in distal regions (P<0.05). In OA patients, transverse-plane lesions showed a tendency to be located on the ulnar side, whereas longitudinal-plane lesions were more frequently observed in distal regions (Figure 4C,4D).

Figure 4 Distribution patterns of ultrasound-detected cartilage damage in patients with RA and OA. (A) Joint-level prevalence of cartilage damage across MCP and PIP joints. (B) Comparison of cartilage damage between dominant and non-dominant hands. (C) Transverse-plane distribution of cartilage damage, categorized as U, R, M, and W. (D) Longitudinal-plane distribution of cartilage damage, categorized as D, P, M, and W. Statistical significance is indicated as follows: ns, not significant; **, P<0.01. D, distal; M, middle; MCP, metacarpophalangeal; OA, osteoarthritis; P, proximal; PIP, proximal interphalangeal; RA, rheumatoid arthritis; R, radial; U, ulnar; W, widespread.

Other US characteristics in patients with RA

Semi-quantitative scores for synovial hypertrophy and power Doppler signal in the RA group were significantly higher than those in the OA and HC groups (Table 4). However, no significant differences were observed between RA and OA regarding joint effusion semi-quantitative scores, or the number of tenosynovitis cases. Bone erosions were detected in 25 of 129 RA patients (19.4%) at the patient level and in 69 of 1,032 joints (6.7%) at the joint level. In contrast, only 1 of 36 OA patients (2.8%) had bone erosion, and no erosions were found in HCs. Regarding cartilage thickness, mean MCP cartilage thickness in RA patients (0.46±0.09 mm) was significantly lower than that in HCs (0.58±0.13 mm, P<0.001), but did not differ from OA patients (0.45±0.09 mm, P=0.327). Similarly, PIP cartilage thickness in RA patients (0.32±0.07 mm) was significantly lower than that in HCs (0.42±0.13 mm, P<0.001), whereas no difference was found between RA and OA (0.32±0.06 mm, P=0.861).

Differences between early and established RA

After adjustment for age, patients with early RA showed a lower burden of cartilage damage compared with those with established RA, as reflected by a smaller number of affected joints, a lower maximum cartilage grade, and lower total cartilage scores. The proportion of patients with at least one affected joint was significantly higher in established RA than it was in early RA (62.5% vs. 39.3%, P=0.024) (Table 5).

Relationship between US-detected cartilage damage and clinical factors

To investigate the correlation between semi-quantitative cartilage grades and clinical characteristics, Spearman correlation analyses were conducted. In patients with RA, age, disease duration, CRP, ESR, DAS28-ESR, synovial hypertrophy semi-quantitative score, power Doppler signal score, and bone erosion score were weakly correlated with cartilage grading scores (Table S1). In patients with OA, age, joint effusion semi-quantitative score and power Doppler signal score demonstrated moderate correlations.

Discussion

High-frequency US enables direct assessment of cartilage damage in the small joints of the hand. In the present study, RA was characterized by a higher overall cartilage damage burden and a distinct anatomical distribution pattern, rather than greater maximum single-joint severity. At the patient level, RA was associated with higher MCP cartilage scores and a greater number of affected joints, indicating a characteristic structural pattern compared with OA and HC. This study further supports the usefulness of the OMERACT three-grade cartilage scoring system for structural assessment in RA.

These results are broadly consistent with previous US studies of cartilage damage in RA. Zheng et al. reported good reliability of the OMERACT threegrade cartilage scoring system (20). Hurnakova et al. using the Disler 0–4 scoring system, found that cartilage damage in RA was concentrated at the second and third metacarpal heads, whereas OA showed a more uniform distribution (13), and Navalho et al. similarly observed a predilection of inflammatory arthritis for radial MCP joints (21). The distinct distribution may be explained by anatomical and pathophysiological factors (17,22). MCP joints contain a larger synovial volume and richer vascular supply than PIP joints, rendering them particularly vulnerable to pannus-mediated destruction (23,24). In contrast, the more uniform distribution in hand OA is mainly associated with mechanical stress-induced cartilage wear (24), accompanied by cartilage matrix degradation imbalance and osteophyte formation at the joint margins, with synovial inflammation playing a contributing role (25,26). The stronger inflammatory process in RA may contribute to the greater structural burden observed in this group. These explanations should be considered cautiously because local biomechanics and pathological mechanisms were not directly evaluated.

Semi-quantitative cartilage grading provided clearer group-level differentiation than quantitative cartilage thickness measurement. In this study, mean cartilage thickness did not differ significantly between RA and OA at either MCP or PIP joints, whereas both were significantly thinner than those of HCs. This may be because quantitative measurements are affected by age, body size, individual anatomy, joint position, transducer orientation, and the definition of cartilage boundaries (5,25). Furthermore, the morphological overlap between RA and hand OA indicates that cartilage grade alone has limited disease specificity. In this cohort, RA was also associated with greater synovial hypertrophy, increased power Doppler signal, higher rates of bone erosion, and markedly elevated inflammatory biomarker levels. In contrast, patients with OA exhibited increased osteophytes. Cartilage assessment may therefore provide complementary information when interpreted together with inflammatory, erosive, serological, and clinical features.

Patients with established RA demonstrated a significantly higher cartilage damage burden than those with early RA, with a higher proportion showing at least one affected joint (62.5% vs. 39.3%, P=0.024). Of note, early RA patients already exhibited detectable cartilage abnormalities above the HC baseline, suggesting that cartilage damage may occur early in the disease course. However, the cross-sectional design did not allow the time of cartilage damage onset or the rate of progression to be determined.

In patients with RA, cartilage damage was significantly associated with clinical factors (age, disease duration, CRP, ESR, and DAS28-ESR) and US parameters (synovial hypertrophy, power Doppler signal, and bone erosion), consistent with a review by Ogura et al. (5). These associations may reflect a link between persistent synovial inflammation and cartilage matrix degradation but do not establish causality or temporal sequence. In OA patients, cartilage grades correlated most strongly with age, joint effusion, and power Doppler signal, consistent with the role of aging, mechanical loading, and low-grade synovial inflammation as co-drivers of structural damage (26).

This study has several limitations. First, the cross-sectional design cannot establish a definitive causal relationship between US findings and disease outcomes. Second, the HC group was significantly younger than the RA group, which may limit the generalizability of age-adjusted comparisons. Third, only MCP2/3 and PIP2/3 joints were examined and inclusion of additional joints (e.g., MCP4/5, DIP joints, and wrists) may provide a more complete assessment of disease distribution. Finally, the OA sample size was relatively limited, likely contributing to the wide confidence intervals observed in some regression models. Future studies with larger samples and longitudinal follow-up are needed to evaluate changes in US-detected cartilage damage over time and to clarify its prognostic value.

Conclusions

US-based semi-quantitative cartilage grading using the OMERACT system revealed a distinct pattern of cartilage involvement in RA, characterized by a higher overall burden, MCP-predominant distribution, and specific anatomical patterns, rather than maximum single-joint severity. OMERACT semi-quantitative US grading may support comparative research characterization of cartilage involvement, but longitudinal studies are required to establish its prognostic or monitoring value.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://qims.amegroups.com/article/view/10.21037/qims-2026-0948/rc

Data Sharing Statement: Available at https://qims.amegroups.com/article/view/10.21037/qims-2026-0948/dss

Funding: This work was supported by Canon Medical Systems (China) Co., Ltd. (No. 2023-Z-65) and the Beijing Natural Science Foundation (No. L241071 to W.L.).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://qims.amegroups.com/article/view/10.21037/qims-2026-0948/coif). All authors report that this work was supported by Canon Medical Systems (China) Co., Ltd. (No. 2023-Z-65). The funder provided financial support but had no involvement in the study design, execution, analysis, data interpretation, or manuscript preparation. W.L. reports funding from Beijing Natural Science Foundation (No. L241071). The authors have no other conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the Ethics Committee of Peking University People’s Hospital (No. 2023PHB211-001) and informed consent was taken from all individual participants.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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