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.

image