Background/Purpose: The Western population is getting older; consequently the proportion of elderly persons presenting with Rheumatoid Arthritis (RA) is increasing. We studied whether age is associated to the severity of RA at presentation and during the disease course, measured using radiographic joint damage.

Methods: Relationship between age and structural damage was studied in 7,232 radiographs of hands and feet of 1,879 RA-patients included in five European and North-American cohorts (Leiden EAC, Groningen, Lund, Umeå, Wichita). Within 702 early RA-patients included in the Leiden EAC between 1993-2006 associations between age and joint space narrowing (JSN) and erosions were evaluated separately; secondly mediation analyses were performed to explore whether the association of age with joint damage was mediated by symptom duration at diagnosis, swollen joint count (SJC), tender joint count (TJC), CRP or ACPA. Finally, 56 RA-patients included in the Leiden EAC between 2010-2012 underwent 1.5 Tesla MRI of the most symptomatic hand and foot at baseline and radiographs at baseline and after 1 year. The MRI-inflammation score (RAMRIS-synovitis plus bone marrow edema) was evaluated.

Results: In all cohorts, age at diagnosis was positively associated with more severe joint damage at baseline and during follow-up. A meta-analysis of these cohorts revealed that per year increase in age, patients had 2.6% (ß1.026 p<0.001) more joint damage. Both JSN and erosion-scores correlated with age; pearson correlation coefficients were significantly stronger for erosion-scores than for JSN-scores (r 0.38 versus 0.29, p=0.006). Structural damage in PIP , CMC-1 and MTP-1 joints increased with age, however a similar increase was observed in wrist, MCP and MTP(2-5)-joints. Together this suggests that the association of joint damage with age cannot be totally explained by osteoarthritis. Age at diagnosis was associated with a shorter symptom duration (ß0.99, p= 0.011), a lower odds on ACPA-positivity (OR 0.98 p<0.001) and was not associated with the SJC or TJC. Older age was positively associated with CRP (ß1.016, p<0.001) but in a multivariate analysis including age and CRP, CRP was not associated with radiographic damage (ß1.00, p=0.14). Therefore, symptom duration, ACPA and regular measures of inflammation did not mediate the association between age and joint damage. Finally, we questioned whether subclinical inflammation was a mediator. Age was significantly associated with the severity of MRI-detected inflammation when adjusted for CRP and SJC (ß1.018, p=0.027). The effect size of the association between age and joint damage reduced after including MRI-inflammation in the analysis (from ß1.032, p=0.004 to ß1.025, p=0.021, adjusted for CRP and SJC), suggesting partial mediation.

Conclusion: RA-patients with a higher age at diagnosis had more severe joint damage at the time of diagnosis and during the disease course. This effect was partially explained by more severe subclinical joint inflammation at higher age. To what extend the remaining part of the effect is caused by disease-specific processes or is related to ‘normal ageing’ needs to be explored in further studies.

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ACR Meeting Abstracts - https://acrabstracts.org/abstract/studies-on-ageing-and-the-severity-of-radiographic-joint-damage-in-rheumatoid-arthritis/