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Current therapy for rheumatoid arthritis (RA) should not only suppress inflammation, but should also prevent local and generalized bone mineral density (BMD) loss. The drug of choice to treat secondary osteoporosis (OP) is denosumab, a monoclonal antibody, which binds RANKL, inhibiting the interaction with its receptor, which tends to reduce osteoclast activity and bone resorption.Objective: to evaluate the effect of denosumab on BMD in the axial and peripheral skeleton of RA patients with OP. Subjects and methods. 52 postmenopausal women with RA and OP received subcutaneous denosumab 60 mg at baseline and after 6 months. BMD was measured at baseline and after 12 months, by dual-energy X-ray absorptiometry at three sites: lumbar spine, femoral neck, and distal forearm.Results. The patients’ mean age was 58.4±6.4 years; the mean RA duration was 19.0±10.9 years. All the patients received anti-inflammatory therapy, including 30 (57.7%) patients who took glucocorticoids (GC). Preandpost-treatment BMD in the lumbar spine was 0.814±0.101 and 0.848±0.103 g/cm2 (р < 0.001), in the femoral neck – 0.629±0.089 and 0.641±0.090 g/cm2 (p = 0.02), in the distal forearm – 0.497±0.094 and 0.502±0.091 g/cm2 (р = 0.34) respectively. Regardless of the administration of GC, stabilization or significant positive changes were noted in all the skeletal regions under studyConclusion. Therapy with subcutaneous denosumab 60 mg twice a year at an injection interval of 6 months could significantly increase BMD in the lumbar spine and femoral neck and stabilize it in the distal forearm in RA patients with OP irrespective of the use of GC.DOI: http://dx.doi.org/10.14412/1995-4484-2015-134-138