Abstract
Objective
To examine the association between radiographic structural damage and physical function (PF) in psoriatic arthritis (PsA).
Methods
Data were analyzed from a large longitudinal PsA cohort. PF was measured using the Health Assessment Questionnaire (HAQ, 0–3) and Short Form‐36 PF subscale (SF‐36, 0–100); radiographic joint damage was measured using the modified Steinbrocker score (mSS, 0–168). Associations between PF and mSS were analyzed using linear mixed models. We also evaluated the impact of the presence of any damaged joint (grade 2–4), joint damage by individual grades, and the number of damaged joints (grade 2–4) per patient on PF.
Results
Of 1,177 patients (mean ± SD age 44.61 ± 12.76 years; 55.8% men), baseline mSS was 2 (interquartile range [IQR] 0–8.5), HAQ was 0.62 (IQR 0.12–1.12), and SF‐36 PF was 60 (IQR 35–85). Higher mSS was significantly associated with worse SF‐36 PF (β = −0.10; 95% confidence interval [CI] −0.15 to −0.05) and HAQ (β = 0.003; 95% CI 0.002 to 0.004) after controlling for swollen joint count, sex, and disease duration. The number of damaged joints was associated with worse SF‐36 PF (β = −0.23; 95% CI −0.38 to −0.08) and HAQ (β = 0.005; 95% CI 0.002 to 0.009). The presence of a damaged joint (grade 2–4) alone did not impact PF. However, the presence of a joint with grade 4 destruction was associated with substantially worse SF‐36 PF (β = −3.04; 95% CI −5.93 to −0.15) and HAQ (β = 0.09; 95% CI 0.03 to 0.15). Increasing counts of grade 4 joints demonstrated a strong dose response with SF‐36 PF (β = −0.54; 95% CI −0.81 to −0.26) and HAQ (β = 0.01; 95% CI 0.01 to 0.02).
Conclusion
Radiographic structural damage, particularly severe joint destruction, is independently associated with impaired PF in PsA, highlighting the importance of early detection and prevention of damage.
INTRODUCTION
Persistent articular inflammation in psoriatic arthritis (PsA) disrupts the balance between destructive and reparative mechanisms in cartilage and bone. This results in classical radiographic findings including erosions, joint space narrowing (JSN), and new bone formation. 1 PsA significantly impacts quality of life, physical function (PF), and work disability, which are believed to reflect both disease activity and structural joint damage. 2 Structural damage can be observed as early as 2 years into the disease course 3 , 4 and is a predictor of future damage. 5
One of the primary therapeutic goals in PsA is to prevent or inhibit structural damage progression while optimizing functional status and quality of life. 6 Radiographic assessment provides an objective means to monitor structural damage over time and remains a standard approach in clinical trials of PsA. 7 , 8 , 9 , 10
Current research recommendations highlight the need to define prognostic factors, including the relationship between structural damage and functional outcomes. 11 Although it is widely accepted that structural damage is linked to poor functional outcomes, only one study to date has quantitatively evaluated this relationship using the modified Sharp‐van der Heijde (mSvdH) scoring system. 4 Importantly, that study was limited to a clinical trial database, which may not fully capture real‐world variability. The analyses adjusted only for disease activity, leaving other potential confounders, like demographics, unaccounted for. This gap complicates the interpretation of radiographic changes, as it remains unclear whether observed changes translate to clinically meaningful functional gains, especially in large, real‐world cohorts with long‐term follow‐up. 12 , 13 , 14
With the advent of biologic disease‐modifying antirheumatic drugs (bDMARDs) and targeted synthetic (ts) DMARDs, the prevalence of severe joint damage has declined. 15 This raises an important question of the precise contribution of radiographic progression to the PF impairment. Addressing this is crucial, as structural damage is generally irreversible and a major contributor to permanent disability.
Therefore, we hypothesized that structural damage is independently associated with PF. We aimed to study the impact of structural damage on PF in PsA in a large, real‐world cohort of PsA.
PATIENTS AND METHODS
Setting
This was a longitudinal observational cohort study conducted at the Gladman Krembil PsA Program, Schroeder Arthritis Institute, Toronto, Ontario, Canada. 16 Since 1978, patients with PsA have been systematically observed at 6‐ to 12‐month intervals, with clinical, laboratory, and radiographic data collected using a standardized protocol. The assessments include detailed medical history, physical examination, evaluation of disease activity, patient‐reported outcomes, and laboratory tests. Radiographs of the hands, feet, pelvis, and cervical and lumbar spine are performed biennially. More than 99% of patients in the cohort meet the Classification Criteria for PsA. 1 All patients enrolled in the cohort up to May 15, 2025, with at least one PF assessment within 3 months of the radiographs were included.
Assessments
Demographic characteristics (age, sex, and disease duration), body weight, comorbidities (Charlson comorbidity index), smoking status (current smoker, ex‐smoker, or never smoker), clinical features (66 swollen joint count [SJC66], 68 tender joint count, enthesitis, dactylitis, and nail involvement), disease activity (Psoriasis Area and Severity Index and clinical Disease Activity index for PsA), 17 patient‐reported outcomes (Health Assessment Questionnaire [HAQ] and Medical Outcomes Survey Short Form‐36 [SF‐36]), laboratory values (erythrocyte sedimentation rate and C‐reactive protein), radiographic features (number of joints with erosions, sacroiliitis, syndesmophytes, and modified Steinbrocker score [mSS]), and treatment (nonsteroidal anti‐inflammatory drugs and conventional synthetic DMARDs, bDMARDs, and tsDMARDs) were retrieved from the database.
Structural damage in peripheral joints was evaluated on radiographs. All radiographs are reviewed in separate consensus reading sessions by at least two experienced readers (DDG, VC, and DP [Poddubnyy]) independent of clinical assessments. Radiographs were scored using the mSS system (range 0–168), 18 , 19 , 20 which is a radiographic scoring system that evaluates specific joints of the hands and feet. It includes 30 joints of the hands (bilateral wrists, metacarpophalangeal, proximal interphalangeal, and distal interphalangeal [DIP]) and 12 joints of the feet (metatarsophalangeal and first interphalangeal joints). Each joint is assigned a score from 0 to 4 based on the severity of damage:
0: Normal
1: Minimal damage (soft tissue swelling or juxta‐articular osteopenia)
2: Moderate damage (presence of erosion)
3: Severe damage (presence of erosion with JSN)
4: Total joint destruction (complete joint destruction with erosions all along the joint line, arthritis mutilans, subluxation, or ankylosis)
It has excellent interobserver and good intraobserver reliability. 18 PF was assessed using the HAQ (0–3) and the SF‐36 PF subscale (0–100). 21 , 22 Multiple visits per patient were assessed over the follow‐up.
Statistical analysis
Baseline characteristics at the time of study enrollment were described using descriptive statistics. Quantitative variables were described as mean ± SD or median (interquartile range [IQR]) if there was evidence for nonnormality. Qualitative variables were summarized in terms of frequencies and percentages.
We assessed the association between PF measures (SF‐36 PF and HAQ) and the mSS using univariable and multivariable linear mixed models (LMMs) with random intercepts with PF as the outcome. LMM were used to account for repeated measurements within the same patient over follow‐up by incorporating patient‐specific random intercepts, thereby allowing for studying association between observations from the same individual. The multivariable models were adjusted for covariates, including SJC66 at the time of the radiographs, sex, and disease duration of PsA, as visualized by a directed acyclic graph (Supplementary Figure 1). 23 , 24 Age was not included in the multivariable model because of collinearity with disease duration. We included SJC66 as an objective measure of articular disease activity.
Additionally, we assessed the presence of joint damage (at least one joint graded as 2, 3, or 4) and the number of damaged joints per patient (graded as 2, 3, or 4 to include erosion, JSN, and total joint destruction) for their association with SF‐36 PF and HAQ using univariable and multivariable LMMs with random effects. These were adjusted for SJC66, sex, and disease duration of PsA at the time of radiographs. These models were also repeated to determine associations between presence of different grades of joint damage (at least one joint graded as 2 [erosion], 2 and 3 [erosion and JSN], or 4 [total joint destruction]) and number of joints per patient with different grades of damage (grade 2 [erosion], grades 2 and 3 [erosion and JSN], and grade 4 [complete destruction]) and SF‐36 and HAQ. Statistical analyses were conducted using SAS version 9.3 (SAS Institute, Cary, NC, USA) and R version 4.2.3. P values of <0.05 were deemed statistically significant, and results were expressed as β estimate with 95% confidence intervals (CIs).
Consent and ethics
We obtained ethics approval from the University Health Network Research Ethics Board (08‐0630). All patients provided informed consent at enrollment. The data underlying this article will be shared upon reasonable request to the corresponding author.
RESULTS
A total of 1,177 patients were included in the study with a median of 2 (IQR 1–3) visits per patient over follow‐up. The mean ± SD age at enrollment was 44.6 ± 12.8 years, and 657 (55.8%) were male. The mean ± SD age at PsA onset was 38.8 ± 13.5 years. At baseline, the median SJC66 was 2 (IQR 0–5), with dactylitis present in 316 patients (26.9%), enthesitis in 253 (23.7%), and axial disease in 326 (28%). The mean ± SD mSS was 9.7 ± 21.2, with a median of 2 (IQR 0–8.5). The median HAQ score was 0.6 (IQR 0.1–1.1), and the median SF‐36 PF score was 60 (IQR 35–85) (Table 1).
Table 1.
Baseline characteristics of patients at enrollment*
| Characteristics (N = 1,177) | Data |
|---|---|
| Demographics | |
| Age, mean (SD), y | 44.61 (12.76) |
| Male sex, n (%) | 657 (55.8) |
| Age at onset of PsA, mean (SD), y | 38.84 (13.50) |
| Age at onset of psoriasis, mean (SD), y | 28.82 (14.76) |
| Duration of PsA, median [IQR], y | 2.69 [0.71–8.19] |
| Ever smoking, n (%) | 490 (42.3) |
| Body mass index, mean (SD) | 28.90 (6.25) |
| Charlson comorbidity index, median [IQR] | 1.00 [1.00–1.00] |
| Clinical features | |
| 66‐Swollen joint count, median [IQR] | 2.00 [0.00–5.00] |
| 68‐Tender joint count, median [IQR] | 4.00 [1.00–10.00] |
| Dactylitis, n (%) | 316 (26.9) |
| Enthesitis, n (%) | 253 (21.7) |
| Nail disease, n (%) | 663 (56.4) |
| Axial disease, n (%) | 326 (28.0) |
| Disease activity, median [IQR] | |
| PASI score | 1.70 [0.00–4.50] |
| DAPSA | 17.00 [9.80–29.22] |
| Patient‐reported outcomes, median [IQR] | |
| HAQ | 0.62 [0.12–1.12] |
| SF‐36 PF | 60.00 [35.00–85.00] |
| SF‐36 PCS | 37.06 [28.72–47.79] |
| SF‐36 MCS | 48.48 [37.55–56.37] |
| Radiographic features | |
| Erosions, n (%) | 591 (51.3) |
| Radiographic damaged joint count, median [IQR] | 1.00 [0.00–4.00] |
| Modified Steinbrocker score, median [IQR] | 2.00 [0.00–8.50] |
| Syndesmophytes, n (%) | 137 (11.8) |
| Sacroiliitis, n (%) | 253 (21.8) |
| Laboratory variables, n (%) | |
| Abnormal ESR a | 492 (42.4) |
| Abnormal CRPb | 493 (49.3) |
| HLA B*27 | 157 (16.0) |
| HLA C*06 | 261 (26.7) |
| Treatment, n (%) | |
| Conventional synthetic DMARDs | 451 (38.3) |
| NSAIDs | 773 (65.7) |
| Biologic DMARDs | 115 (9.8) |
| Targeted synthetic DMARDs | 6 (0.5) |
CRP, C‐reactive protein; DAPSA, Disease Activity in Psoriatic Arthritis; DMARD, disease‐modifying antirheumatic drug; ESR, erythrocyte sedimentation rate; HAQ, Health Assessment Questionnaire; IQR, interquartile range; MCS, mental component score; NSAID, nonsteroidal anti‐inflammatory drug; PASI, Psoriasis Area and Severity Index; PCS, physical component score; PF, physical function; PsA, psoriatic arthritis; SF, Short Form.
ESR > 20 mm; bCRP > 6 mg/L.
Association of mSS with PF
In univariable analysis, mSS was significantly associated with SF‐36 PF (β = −0.12; 95% CI −0.17 to −0.07) (Table 2). In multivariable analysis, the mSS was significantly associated with SF‐36 PF (β = −0.10; 95% CI −0.15 to −0.05), SJC66 (β = −1.51; 95% CI −1.75 to 1.28), male sex (β = 12.50; 95% CI 9.53 to 15.46), and disease duration (β = −0.14; 95% CI −0.25 to −0.04). Similarly, mSS was significantly associated with HAQ (β = 0.003; 95% CI 0.002–0.005) in univariable analysis (Table 2). In multivariable analysis, HAQ was associated with mSS (β = 0.003; 95% CI 0.002 to 0.004), SJC66 (β = 0.04; 95% CI 0.03–0.04), male sex (β = −0.30; 95% CI −0.37 to −0.24), and disease duration (β = 0.005; 95% CI 0.003 to 0.007) (Figure 1).
Table 2.
Results of the association between SF‐36 PF and HAQ and with physical function using univariable linear mixed models*
| SF‐36 PF | HAQ | |||||
|---|---|---|---|---|---|---|
| Estimate | 95% CI | P value | Estimate | P value 95% CI | P value | |
| Modified Steinbrocker score (0–168) | −0.12 | −0.17 to −0.07 | <0.001 | 0.003 | 0.002 to 0.005 | <0.001 |
| Presence of a damaged joint (grade 2,3, or 4 vs 1 or 0) | −0.58 | −2.87 to 1.71 | 0.620 | 0.016 | −0.03 to 0.06 | 0.529 |
| Number of damaged joints (grade 2, 3, or 4) | −0.32 | −0.47 to −0.18 | <0.001 | 0.008 | 0.005 to 0.012 | <0.001 |
| Presence of a severely damaged joint (grade 4 vs 0, 1, 2, or 3) | −5.16 | −8.07 to −2.25 | <0.001 | 0.15 | 0.01 to 0.22 | <0.001 |
| Number of severely damaged joints (grade 4) | −0.63 | −0.91 to −0.35 | <0.001 | 0.017 | 0.01 to 0.02 | <0.001 |
| SJC (0–66) | −1.59 | −1.83 to −1.36 | <0.001 | 0.04 | 0.03 to 0.04 | <0.001 |
| Sex, male | 12.64 | 9.61 to 15.67 | <0.001 | −0.31 | −0.38 to −0.24 | <0.001 |
| Duration of PsA, y | −0.09 | −0.19 to 0.01 | 0.07 | 0.004 | 0.002 to 0.006 | <0.001 |
| Age, y | −0.13 | −0.25 to −0.02 | 0.03 | 0.003 | −0.31 to −0.08 | 0.06 |
CI, confidence interval; HAQ, Health Assessment Questionnaire; PF, physical function; PsA, psoriatic arthritis; SF‐36, Short Form‐36; SJC, swollen joint count.
Figure 1.
Results of the association between modified Steinbrocker score and physical function using multivariable linear mixed models. CI, confidence interval; HAQ, Health Assessment Questionnaire; PsA, psoriatic arthritis; SF‐36, Short Form‐36; SJC, swollen joint count.
Association between the presence of joint damage with PF
The presence of at least one joint with grades 2, 3, or 4 damage was not associated with SF‐36 PF in both univariable (β = −0.58; 95% CI −2.87 to 1.71) and multivariable analysis (β = 1.00, 95% CI −1.25 to 3.25). Similarly, the presence of a joint with grades 2, 3, or 4 damage was not significantly associated with HAQ in both univariable (β = 0.016; 95% CI −0.03 to 0.06) and multivariable analysis (β = −0.03, 95% CI −0.08 to 0.02) (Figure 2).
Figure 2.
Results of the association between the presence of a damaged joint (grade 2, 3, or 4 vs 0 or 1) with physical function using multivariable linear mixed models. CI, confidence interval; HAQ, Health Assessment Questionnaire; PsA, psoriatic arthritis; SF‐36, Short Form‐36; SJC, swollen joint count. Color figure can be viewed in the online issue, which is available at http://onlinelibrary.wiley.com/doi/10.1002/art.70145/abstract.
The presence of at least one joint exhibiting total joint destruction was associated with poorer SF‐36 PF scores on univariable analysis (β = −5.16; 95% CI −8.07 to −2.25) and multivariable analysis (β = −3.04; 95% CI −5.93 to −0.15). Similarly, it was significantly associated with HAQ in both univariable (β = 0.15; 95% CI 0.09–0.22) and multivariable analysis (β = 0.09; 95% CI 0.03–0.15). Separate analyses of the presence of grade 2 and grades 2 and 3 damage were not associated with PF (Supplementary Tables 1–3).
Association of the number of damaged joints with PF
The number of damaged joints (graded 2, 3, or 4) per patient was significantly associated with SF‐36 PF in univariable analysis (β = −0.3; 95% CI −0.47 to −0.18) and multivariable analysis (β = −0.23; 95% CI −0.38 to −0.08). Similarly, the number of damaged joints (graded 2, 3, or 4) was significantly associated with HAQ in univariable (β = 0.008; 95% CI 0.005–0.012) and multivariable analysis (β = 0.005; 95% CI 0.002–0.009) (Figure 3).
Figure 3.
Results of the association between the number of damaged joints (grade 2, 3, or 4) per patient with physical function using multivariable linear mixed models. CI, confidence interval; HAQ, Health Assessment Questionnaire; PsA, psoriatic arthritis; SF‐36, Short Form‐36; SJC, swollen joint count. Color figure can be viewed in the online issue, which is available at http://onlinelibrary.wiley.com/doi/10.1002/art.70145/abstract.
This association was stronger when the number of totally damaged joints (grade 4) per patient was studied with SF‐36 PF in both univariable (β = −0.63; 95% CI −0.91 to −0.35) and multivariable analysis (β = −0.54; 95% CI −0.81 to −0.26). Similarly, the number of totally damaged joints (grade 4) was associated with HAQ in both univariable (β = 0.017; 95% CI 0.01–0.02) and multivariable analysis (β = 0.01; 95% CI 0.01–0.02). Separate analyses of the number of grades 2 and 3 joints per patient were not associated with PF (Supplementary Tables 4–6).
DISCUSSION
In this study, we could demonstrate an association between mSS and PF. After adjusting for disease activity, sex, and disease duration, we noted a small but statistically significant decrease in PF with increasing mSS. However, disease activity and sex emerged as the most prominent contributors to functional impairment. Importantly, both the presence of a single severely damaged joint and the cumulative number of severely damaged joints were significantly associated with poorer PF in individuals with PsA, highlighting novel quantitative insights into structural damage burden in real‐world cohorts.
Our analysis showed that a 1‐unit increase in the mSS was associated with a 0.10‐point worsening in the SF‐36 PF score and a 0.003‐point deterioration in HAQ scores. Although these changes are modest, they were statistically significant and independent of disease activity. To contextualize this, increases of 10, 50, and 100 units in mSS would correspond to worsening of SF‐36 PF by 1, 5, and 10 points, respectively, and worsening of HAQ by 0.03, 0.15, and 0.3 points. A similar relationship was previously observed in a post hoc analysis of a phase 3 trial of golimumab in PsA, in which a 1‐unit increase in the modified mSvdH score was linked to a 0.002‐point increase in HAQ. Thus, mSvdH scores of 10, 50, and 100 would correspond to predicted HAQ scores of 0.02, 0.1, and 0.2, respectively. 13 It is important to note that such high radiographic scores are rarely encountered in clinical practice.
An earlier study from our cohort reported that HAQ scores remained relatively stable over time in patients with increasing joint damage but no ongoing inflammation, up to a damaged joint count of 21. 25 , 26 This pattern may be because of the different ways in which inflammation and structural damage affect PF. Inflammation impacts PF through pain, joint stiffness, and systemic symptoms such as fatigue, often resulting in rapid and noticeable declines in function. In contrast, joint damage typically leads to mechanical limitations that develop gradually, allowing time for patients to adapt and compensate. As a result, the perceived effect on PF may be less immediate. Nonetheless, in our analysis, the impact of structural damage on PF persisted even after adjusting for disease activity, underscoring its independent contribution to disability. Given that radiographic damage can occur as early as 6 months after PsA onset, early and aggressive disease control is essential to prevent long‐term functional decline. 3 , 27
In addition to structural damage, we found that longer disease duration and female sex were significantly associated with reduced PF. Among these, female sex had the strongest association, consistent with prior studies identifying it as a key determinant of disability. 28 This association persisted even after adjusting for disease activity, suggesting potential sex‐based differences in pain perception. Experimental data in spondyloarthritis support the influence of hormonal and immune response differences on pain processing. 29 Sociocultural factors may also contribute; for example, women often perform fine‐motor tasks that place greater strain on the hands and joints and men typically have greater muscle mass, which may confer some physical resilience.
We found that the presence of any damaged joint (grades 2, 3, or 4) was not associated with impaired PF, whereas the presence of a severely damaged joint (grade 4) showed a clear meaningful effect. This may reflect the functional importance of the specific joint involved; for instance, low‐grade damage to DIP joints may have less impact on PF than similar damage to the wrist. Alternatively, it is possible that only complete joint destruction, rather than milder forms of damage, has substantial functional consequences. The presence of even a single grade‐4 joint was associated with significantly worse PF. The reduction in SF‐36 PF (−3.04 points) approaches the established minimum clinically important difference of 5 points, and the HAQ worsening of 0.09 is similarly meaningful. 30 , 31 Moreover, increasing counts of grade‐4 joints demonstrated a strong dose response relationship, with each additional destroyed joint associated with further functional decline (SF‐36 PF = −0.63; HAQ = +0.02). These results align with prior studies showing that cumulative structural damage drives impairments in PF. 25
PF is a core domain in PsA clinical trials and is incorporated into most composite indices and response criteria. 32 The significant association we observed between radiographic damage and PF reinforces the need to include patient‐reported outcomes when assessing treatment efficacy. Unlike disease activity, the disability related to structural damage is irreversible, highlighting the importance of its prevention.
A major strength of our study is the use of data from a well‐characterized, prospectively observed, real‐world PsA cohort. We used two complementary measures of PF (SF‐36 PF and HAQ) to robustly examine the relationship with radiographic damage. Long‐term follow‐up data enabled meaningful assessment of structural progression and its impact.
However, this study has limitations. We focused on peripheral joint damage, without accounting for axial involvement. Additionally, the mSS does not include evaluation of larger joints such as the shoulders, elbows, hips, and knees, which are not routinely imaged because of potential confounding by conditions such as osteoarthritis. Nevertheless, we believe the mSS is a useful surrogate for global joint damage in PsA. Although PF was measured through patient‐reported outcomes that may be influenced by unmeasured variables, our use of two distinct tools and multivariable adjustment aimed to mitigate this issue. Sex and disease activity were strongly associated with PF, which may obscure the independent impact of mSS on minimal clinically important difference for SF‐36 PF and HAQ.
In conclusion, structural joint damage, as quantified by the mSS, is independently associated with impaired PF in PsA, even after adjusting for disease activity and other confounders. A 1‐unit increase in mSS is associated with a 0.10‐point decline in SF‐36 PF and a 0.003‐point increase in HAQ. Both the presence of even a single severely damaged joint and the cumulative damage burden significantly contribute to reduced function. These findings emphasize the need for early diagnosis and effective intervention to prevent irreversible disability in PsA.
AUTHOR CONTRIBUTIONS
All authors contributed to at least one of the following manuscript preparation roles: conceptualization AND/OR methodology, software, investigation, formal analysis, data curation, visualization, and validation AND drafting or reviewing/editing the final draft. As corresponding author, Dr Poddubnyy confirms that all authors have provided the final approval of the version to be published and takes responsibility for the affirmations regarding article submission (eg, not under consideration by another journal), the integrity of the data presented, and the statements regarding compliance with institutional review board/Declaration of Helsinki requirements.
Supporting information
Disclosure form.
Supplementary Table 1: Results of the analyses of the association between the presence of a severely damaged joint (grade 4 vs 1/2/3 on the modified Steinbrocker score) with physical function
Supplementary Table 2: Results of the analyses of the association between the presence of a damaged joint (grade 2 vs 0/1 on the modified Steinbrocker score) with physical function
Supplementary Table 3: Results of the analyses of the association between the presence of a damaged joint (grade 2/3 vs 0/1 on the modified Steinbrocker score) and physical function
Supplementary Table 4. Results of the analyses of the association between the number of damaged joints (grade 4 on the modified Steinbrocker score) per patient with physical function
Supplementary Table 5. Results of the analyses of the association between the number of damaged joints (grade 3 on the modified Steinbrocker score) per patient with physical function
Supplementary Table 6. Results of the analyses of the association between the number of damaged joints (grade 2 on the modified Steinbrocker score) per patient and physical function
Supplementary Figure 1: Directed Acyclic Graph (DAG) used to represent the role of potential confounders.
ACKNOWLEDGMENTS
The Gladman Krembil PsA Program is funded by a grant from the Krembil Foundation and the Schroeder Arthritis Institute.
1Gladman Krembil Psoriatic Arthritis Program, Centre for Prognosis Studies in the Rheumatic Diseases, Schroeder Arthritis Institute, Krembil Research Institute, University Health Network, Toronto, Ontario, Canada; 2Division of Rheumatology, Department of Medicine, University of Toronto, Toronto, Ontario, Canada; 3Institute of Medical Science, University of Toronto, Toronto, Ontario, Canada; 4Rheumatology Unit, Department of Medicine, Hadassah Medical Center and Faculty of Medicine, Hebrew University of Jerusalem, Israel; 5Department of Statistics and Actuarial Science, University of Waterloo, Waterloo, Ontario, Canada; 6Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada.
Additional supplementary information cited in this article can be found online in the Supporting Information section (https://acrjournals.onlinelibrary.wiley.com/doi/10.1002/art.70145).
Author disclosures and graphical abstract are available at https://onlinelibrary.wiley.com/doi/10.1002/art.70145.
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Supplementary Materials
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Supplementary Table 1: Results of the analyses of the association between the presence of a severely damaged joint (grade 4 vs 1/2/3 on the modified Steinbrocker score) with physical function
Supplementary Table 2: Results of the analyses of the association between the presence of a damaged joint (grade 2 vs 0/1 on the modified Steinbrocker score) with physical function
Supplementary Table 3: Results of the analyses of the association between the presence of a damaged joint (grade 2/3 vs 0/1 on the modified Steinbrocker score) and physical function
Supplementary Table 4. Results of the analyses of the association between the number of damaged joints (grade 4 on the modified Steinbrocker score) per patient with physical function
Supplementary Table 5. Results of the analyses of the association between the number of damaged joints (grade 3 on the modified Steinbrocker score) per patient with physical function
Supplementary Table 6. Results of the analyses of the association between the number of damaged joints (grade 2 on the modified Steinbrocker score) per patient and physical function
Supplementary Figure 1: Directed Acyclic Graph (DAG) used to represent the role of potential confounders.