Effectiveness of denosumab, teriparatide and romosozumab for glucocorticoid-induced osteoporosis: a propensity score-matched cohort study
Authors' conclusion
BTM levels reflected expected pharmacological actions of each drug. ROMO showed greater LS BMD gains than DMAb, while TPTD demonstrated a similar response, whereas DMAb may provide earlier benefits at cortical-rich sites.
Study context
- Population
- Patients with glucocorticoid-induced osteoporosis (GIOP) (92.1% female, mean age 73.5 years, 35.7% osteoporosis treatment naive, oral GC 5.4 mg/day prednisolone equivalent, baseline lumbar spine (LS) bone mineral density (BMD) T-score −2.5)42 per group
- Participants
- 42 / 42 / 42
- Exposure
- Denosumab vs teriparatide vs romosozumab
- Denosumab (DMAb)n = 42reference
- TPTDn = 42
- Romosozumab (ROMO)n = 42
- Outcome
- BTMs and BMD
- Follow-up
- 12 months
Methodological detailsmulticentre, propensity-score matched
- Multicentre
- Propensity-score matched
Main finding
As reported in the abstract
LS BMD increase
P = 0.008 for ROMO vs DMAb
Observational data: associations, not effects.
Further findings
Total hip BMD change · 12 months
| Outcome | DMAb | TPTD | ROMO | P value |
|---|---|---|---|---|
| Total hip BMD change · 6 monthsDMAb vs TPTD | 2.6% | −0.6% | 1.8% | P = 0.01 for DMAb vs TPTD |
| Total hip BMD change · 6 monthsROMO vs TPTD | P = 0.042 for ROMO vs TPTD |
- Femoral neck BMD increase from baseline, DMAb · 6 and 12 months
- 2.2%
- Femoral neck BMD increase from baseline, DMAb: 2.2% at 6 months
Bone turnover markers (BTMs)
- DMAb suppressed BTM levels, whereas TPTD increased them
- ROMO: increased formation and decreased resorption markers
Total hip BMD change · 12 months
- No significant differences
Femoral neck BMD increase from baseline, DMAb · 6 and 12 months
- Significant increases with DMAb
Original publication
Effectiveness of denosumab, teriparatide and romosozumab for glucocorticoid-induced osteoporosis: a propensity score-matched cohort study. Rheumatology (Oxford). Published 12 February 2026. doi:10. 1093/ rheumatology/ keag082
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