b/ts-DMARDs Do Not Arrest Bone Loss in RA Save

In rheumatoid arthritis (RA), the goal is to control or arrest inflammation such that articular and bony damage is halted. While we have many effective therapies, it is not clear that biologic or targeted synthetic disease-modifying antirheumatic drugs (b/tsDMARDs) can prevent or improve osteoporosis outcomes in RA. A current real-world study showed that 1 year of b/tsDMARDs use did not arrest osteoporosis progression. 

This study assessed BMD for up to 5 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.

From a total of 797 RA patients, some were not on anti-osteoporosis (–) drugs (n = 645) while others received anti-osteoporosis (+) therapy (n=152). After a a median 3.1-year follow-up disease activity (CDAI) improved in both groups (26.0/24.4 → 6.6/6.8). 

However, bone (BMD) outcomes differed.  T-scores (femoral neck and radius) decreased significantly in the in the anti-osteoporosis (-) group but not in the anti-osteoporosis (+) group [anti-osteoporosis (–). 

Overall, 460 patients (58%) experienced a decrease in T-score. A high baseline T-score correlated with a subsequent decrease, while 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.

This study demonstrated thta even when RA activity was b/tsDMARDs controlled, BMD still decreased.  Thus bony outcomes, and osteoporosis is not as amenable to anti-inflammatory control in RA, and should be viewed as independent of RA specific therapies.