Trabecular and cortical bone involvement in rheumatoid arthritis by DXA and DXA-based 3D modelling.

Rheumatoid arthritis (RA) patients had a higher risk of developing low bone mineral density (BMD) or osteoporosis. RA patients on classic disease-modifying antirheumatic drug (c-DMARD) therapy showed significantly lower BMD than controls, while no significant differences in most parameters were found between RA patients receiving biological disease-modifying antirheumatic drugs (b-DMARDs) and controls. The 3D analysis allowed us to find changes in the trabecular and cortical compartments. INTRODUCTION: To evaluate cortical and trabecular bone involvement of the hip in RA patients by dual-energy X-ray absorptiometry (DXA) and 3D analysis. The secondary end-point was to evaluate bone involvement in patients treated with classic (c-DMARD) or biological (b-DMARD) disease-modifying antirheumatic drug therapies and the effect of the duration of the disease and corticosteroid therapy on 3D parameters. METHODS: A cross-sectional study of 105 RA patients and 100 subjects as a control group (CG) matched by age, sex, and BMI was carried out. BMD was measured by DXA of the bilateral femoral neck (FN) and total hip (TH). The 3D analyses including trabecular and cortical BMD were performed on hip scans with the 3D-Shaper software. RESULTS: FN and TH BMD and trabecular and cortical vBMD were significantly lower in RA patients. The c-DMARD (n = 75) group showed significantly lower trabecular and cortical vBMD than the CG. Despite the lower values, the b-DMARD group (n = 30) showed no significant differences in most parameters compared with the CG. The trabecular and cortical 3D parameters were significantly lower in the group with an RA disease duration of 1 to 5 years than in the CG, and the trabecular vBMD was significantly lower in the group with a duration of corticosteroid therapy of 1 to 5 years than in the CG, while no significant differences were found by standard DXA in the same period. CONCLUSIONS: RA patients had a higher risk of developing low BMD or osteoporosis than controls. RA patients receiving c-DMARD therapy showed significantly lower BMD than controls, while no significant differences in most parameters were found between RA patients receiving b-DMARDs and controls. 3D-DXA allowed us to find changes in trabecular and cortical bone compartments in RA patients.

Effect of Denosumab on Bone Mineral Density and Markers of Bone Turnover among Postmenopausal Women with Osteoporosis.

The aim of this study was to evaluate the effect of denosumab (Dmab) on bone mineral density (BMD) and bone turnover markers after 1 year of treatment. Additionally, the effect of Dmab in bisphosphonate-naïve patients (BP-naïve) compared to patients previously treated with bisphosphonates (BP-prior) was analyzed. This retrospective study included 425 postmenopausal women treated with Dmab for 1 year in clinical practice conditions in specialized centers from Argentina. Participants were also divided according to previous bisphosphonate treatment into BP-naïve and BP-prior. A control group of patients treated with BP not switched to Dmab matched by sex, age, and body mass index was used. Data are expressed as mean ± SEM. After 1 year of treatment with Dmab the bone formation markers total alkaline phosphatase and osteocalcin were significantly decreased (23.36% and 43.97%, resp.), as was the bone resorption marker s-CTX (69.61%). Significant increases in BMD were observed at the lumbar spine, femoral neck, and total hip without differences between BP-naïve and BP-prior. A better BMD response was found in BP-prior group compared with BP treated patients not switched to Dmab. Conclusion. Dmab treatment increased BMD and decreased bone turnover markers in the whole group, with similar response in BP-naïve and BP-prior patients. A better BMD response in BP-prior patients versus BP treated patients not switched to Dmab was observed.

Bone morphometry and differences in bone fluorine containing compounds in rats treated with NaF and MFP.

Sodium fluoride (NaF) and sodium monofluorophosphate (MFP) are drugs used to increase bone mass. They have been considered equivalent but the results of the treatments were not always coincident. Most studies have been carried out in osteoporotic women or ovariectomized rats pointing to the result in bone mass rather than at the mechanism of action. Convincing evidence indicates that pharmacokinetic of NaF is different from MFP. While only fluoride is found in bones and plasma of rats treated with NaF, in MFP-treated rats, there are also fluorine (F) bound to plasma alpha-macroglobulin and bone covalently bound F. A significant increase in bone mass of rats was observed after 30 days of treatment with NaF and MFP in young rats. This increase in bone mass correlates with the increase in number and thickness of trabeculas in cancellous bone. In the femur of MFP-treated rats, there was an increase in the inertia momentum of the diaphysis without changes in bone width. In addition, bone F content of MFP-treated animals is twice of the content of NaF-treated rats. This difference is the consequence of bone covalently bound F, which is absent in NaF-treated rats. In addition, alpha-macroglobulin was detected in noncollagenous bone matrix of MFP-treated rats. Although F in feces and plasma did not differ among treatments, the urinary excretion of F was lower in MFP than in NaF-treated rats, which is consistent with the higher bone F content.