OBJECTIVES: Chronic inflammation in rheumatoid arthritis (RA) may interfere with bone remodelling. Small studies have suggested biologic DMARDs preserve bone mineral density at 6-12 months. Our objective was to determine the risk of non-vertebral osteoporotic fractures in RA subjects aged ≥50, comparing outcomes in patients who were exposed or unexposed to biologic DMARDs. METHODS: A nested case-control study from January 2002 to December 2008 was conducted using Quebec physician billing and hospital discharge data. RA subjects were identified from ICD-9/10 codes in billing and hospitalization data. Subjects were followed until the earliest of non-vertebral osteoporotic fracture (index date), death, or end of study period. A validated algorithm identified non-vertebral osteoporotic fractures from physician claims. Controls were matched to cases (4:1 ratio) on age, sex, and date of study entry. Biologic DMARD exposure was defined as being on treatment for ≥180 days pre-index. Conditional logistic regression was used, adjusting for indicators of RA severity, comorbidity, drugs influencing fracture risk, and measures of health care utilization. RESULTS: Over the study period, 1,803 cases were identified (7,175 controls). The most frequent fracture site was hip/femur (43.7%). In total, 190 subjects (53 cases, 137 controls) were exposed to biologic DMARDs. We were unable to demonstrate an association between biologic DMARDs and fracture risk (Odds Ratio, OR [95% Confidence Interval, CI]: 1.16 [0.51-2.62]). RA duration had the strongest impact on fracture risk; for subjects of RA duration ≥10 years (vs. <5), the OR was 6.40 (95% CI 3.57-11.46), while those with RA duration 5-10 years (vs. <5) had an OR of 3.05 (95%CI 1.90-4.89). The inability to detect an effect remained in sensitivity analyses. CONCLUSIONS: Despite the positive impact of biologic DMARDs on bone remodelling observed in small studies, we were unable to demonstrate a reduction in the risk of non-vertebral osteoporotic fractures in older adults with RA.