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Biologic and Targeted Synthetic Disease-Modifying Antirheumatic Drugs Do Not Arrest Bone Loss in Patients With
Takafumi Aritomi1,2, Koshiro Sonomoto1,3,4, Shingo Nakayamada1,5
1First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health Japan, Kitakyushu, Japan.
Objective:
Osteoporosis causes fractures that further increase the disease burden of rheumatoid arthritis (RA); however, osteoporosis treatment rates remain low. Although several studies have reported that biologic or targeted synthetic disease-modifying antirheumatic drugs (b/tsDMARDs) can prevent or improve osteoporosis in RA, our large-scale, real-world study showed that one-year b/tsDMARDs use did not arrest osteoporosis progression. This study aimed to examine longer-term changes in bone mineral density (BMD).
Methods:
BMD was observed for up to five years in patients receiving b/tsDMARDs for active RA. The primary endpoint was change in BMD (T score), and the secondary endpoint was change in T score-related factors.
Results:
In total, 797 patients (antiosteoporosis-, n = 645; antiosteoporosis+, n = 152) were included, with a median 3.1-year follow-up (2,489 patient-years). Clinical Disease Activity Index (CDAI) improved in both groups (antiosteoporosis- 26.0 to 6.6; antiosteoporosis+ 24.4 to 6.8). T scores decreased significantly in the femoral neck and radius in the antiosteoporosis- group but not in the antiosteoporosis+ group (antiosteoporosis-: mean change -0.11 to -0.33, both P < 0.001; antiosteoporosis+ -0.01 to -0.10, P = 0.830 and 0.071, respectively). Overall, 460 patients (58%) experienced a decrease in T score. A high baseline T score correlated with a subsequent decrease, whereas longer osteoporosis treatment duration correlated with an increase. Unexpectedly, the duration of b/tsDMARD use and mean CDAI during observation were not associated with BMD maintenance.
Conclusion:
Even when RA activity was controlled with b/tsDMARDs, BMD still decreased. This study emphasizes the importance of considering osteoporosis as an independent aspect of RA, beyond inflammation control.
Insights
Biologic or targeted synthetic disease-modifying antirheumatic drugs (b/tsDMARDs) did not prevent bone mineral density (BMD) loss in rheumatoid arthritis (RA) patients over 5 years. Osteoporosis management in RA requires addressing factors beyond inflammation control.
Area of Science:
- Rheumatology
- Endocrinology
- Bone Metabolism
Background:
- Rheumatoid arthritis (RA) significantly increases fracture risk, yet osteoporosis treatment rates are low.
- Biologic or targeted synthetic disease-modifying antirheumatic drugs (b/tsDMARDs) are used to manage RA, with some evidence suggesting potential benefits for osteoporosis.
- Previous studies indicated that 1-year b/tsDMARDs use did not halt osteoporosis progression in RA patients.
Purpose of the Study:
- To investigate the longer-term effects of b/tsDMARDs on bone mineral density (BMD) in patients with active rheumatoid arthritis (RA).
- To determine if sustained control of RA disease activity with b/tsDMARDs influences BMD changes over time.
- To identify factors associated with BMD changes in RA patients undergoing b/tsDMARD therapy.
Main Methods:
- A real-world, observational study followed 797 RA patients treated with b/tsDMARDs for up to 5 years.
- Bone mineral density (BMD) T-scores were assessed as the primary endpoint, with changes in related factors as secondary endpoints.
- Patients were categorized based on concurrent anti-osteoporosis treatment (anti-osteoporosis (-) vs. anti-osteoporosis (+)).
Main Results:
- Despite significant improvement in Clinical Disease Activity Index (CDAI) scores, BMD (T-scores) decreased significantly in the femoral neck and radius for patients not receiving anti-osteoporosis treatment.
- BMD T-scores remained relatively stable in patients receiving concurrent anti-osteoporosis treatment.
- 58% of all patients experienced a decrease in T-score; baseline T-score and duration of osteoporosis treatment were associated with BMD changes, while b/tsDMARDs duration and mean CDAI were not.
Conclusions:
- Rheumatoid arthritis (RA) patients treated with b/tsDMARDs can still experience bone mineral density (BMD) loss, even with controlled disease activity.
- Osteoporosis should be considered an independent comorbidity in RA management, requiring specific interventions beyond inflammation control.
- Concurrent anti-osteoporosis treatment appears crucial for maintaining BMD in RA patients on b/tsDMARDs.
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