Romosozumab Enhances Vertebral Bone Structure in Women With Low Bone Density.

Romosozumab monoclonal antibody treatment works by binding sclerostin and causing rapid stimulation of bone formation while decreasing bone resorption. The location and local magnitude of vertebral bone accrual by romosozumab and how it compares to teriparatide remains to be investigated. Here we analyzed the data from a study collecting lumbar computed tomography (CT) spine scans at enrollment and 12 months post-treatment with romosozumab (210 mg sc monthly, n = 17), open-label daily teriparatide (20 μg sc, n = 19), or placebo (sc monthly, n = 20).

Prevalence of Osteoporosis in Women in Buenos Aires Based on Bone Mineral Density at the Lumbar Spine and Femur.

The aim of the study was to report values for osteoporosis (OP) prevalence in Buenos Aires. Bone mineral density (BMD) at different skeletal sites was measured from November 2012 to July 2014. Participants were recruited through a newspaper advertisement inviting women at least 50 yr of age to receive free BMD measurement.

Effects of Romosozumab Compared With Teriparatide on Bone Density and Mass at the Spine and Hip in Postmenopausal Women With Low Bone Mass.

Romosozumab, a monoclonal antibody that binds sclerostin, has a dual effect on bone by increasing bone formation and reducing bone resorption, and thus has favorable effects in both aspects of bone volume regulation. In a phase 2 study, romosozumab increased areal BMD at the lumbar spine and total hip as measured by DXA compared with placebo, alendronate, and teriparatide in postmenopausal women with low bone mass. In additional analyses from this international, randomized study, we now describe the effect of romosozumab on lumbar spine and hip volumetric BMD (vBMD) and BMC at month 12 as assessed by QCT in the subset of participants receiving placebo, s.

Regression of an ossifying fibroma of the tibia after a fracture involving the lesion. Possible role of the periostina.

Ossifying fibroma (OF) of the long bones is a benign fibro-osseous lesion typically seen in the first decade of life. OF usually progresses until the age of 10 years, but is occasionally found to regress spontaneously after puberty. The pathogenesis of OF is unknown; however, it has been suggested that the basic defect is in the periosteum.