- Design
- Multicentre observational cohort, up to 5 years
- Population
- 797 patients with active RA on biologic or targeted synthetic DMARDs
- Primary outcome
- Change in bone mineral density T score
- Effect
- Femoral neck and radius T scores fell (-0.11 to -0.33, P < .001) without osteoporosis treatment; 58% lost BMD
Advanced RA therapies are sometimes assumed to protect bone by damping inflammation. This multicentre observational study, published in April, followed bone density for up to five years in 797 patients starting biologic or targeted synthetic DMARDs for active RA; 152 were also on osteoporosis treatment.
Disease activity improved in both groups (CDAI about 26 to 7). Yet in those not on osteoporosis treatment, femoral neck and radius T scores fell significantly (mean change -0.11 to -0.33); in those on treatment, they did not change significantly. Overall, 58% lost bone density. Neither duration of advanced therapy nor average disease activity was associated with preserving bone, while longer osteoporosis treatment was.
This is observational, and patients on osteoporosis treatment may have differed in other ways. Fractures were not reported.
The clinical message is clear enough to act on: do not assume controlled RA means protected bone. Assess fracture risk and treat osteoporosis on its own merits.
- Assess fracture risk in every RA patient, including those in low disease activity.
- T scores fell over about three years in patients without osteoporosis treatment despite good RA control.
- Neither disease control nor duration of biologic therapy was linked to preserving bone.
- Start osteoporosis treatment on fracture risk, not on RA activity.
- Review glucocorticoid exposure, a major driver of bone loss in RA.
Why it matters
Osteoporosis treatment rates in RA are low, partly because good disease control is mistaken for bone protection.
Don't overread it
The study measured bone density, not fractures, and was observational.
The statistics, in plain English
A fall in T score of 0.1-0.3 over about three years is modest per patient but meaningful across a population at high fracture risk. Groups were not randomised, so the comparison with treated patients is indicative only.
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