Posts Tagged ‘bone mineral density’

Glucocorticoid-induced osteoporosis (OP) is better treated with Teriparatide, synthetic form of the human parathyroid hormone, than alendronate.

This finding was disclosed by a recent study in which researchers suggested that glucocorticoid-induced OP patients who are administered with teriparatide for 36 months had a greater increase in bone mineral density (BMD) and fewer new vertebral fractures than those treated with alendronate.

From Sciencedaily.com:

Glucocorticoids are steroid hormones that are naturally produced in the body or synthetically created compounds (drugs) used to reduce inflammation. These steroid drugs are used to control inflammation in patients with such autoimmune diseases as rheumatoid arthritis, systemic lupus erythematosus, and Crohn’s disease as well as inflammatory conditions such as asthma. Glucocorticoid-induced osteoporosis occurs when patients taking steroid medications such as prednisone, prednisolone, dexamethasone, and cortisone exhibit reduced bone mass and bone strength.

This 36-month, randomized, double-blind, controlled trial, led by Kenneth Saag, M.D., from the University of Alabama, was conducted at 76 centers located in 13 countries. A total of 428 patients between the ages of 22-89 with confirmed OP who had received greater than 5 mg/day of prednisone or equivalent for more than 3 months preceding screening were included. Research measures included changes in lumbar spine and hip bone, BMD, changes in bone biomarkers, fracture incidence, and safety.

The findings of this study are published in the November issue of Arthritis & Rheumatism, a journal of the American College of Rheumatology (ACR).

A protein secreted from adipocytes, Adiponectin, has been found to be the metabolic link between obesity and both bone mineral density (BMD) and reduced susceptibility to fractures.

The finding was revealed during a study by researchers at the University of Toronto, Faculty of Medicine, Toronto, Canada, which appeared in an issue of Experimental Biology and Medicine.

From News-Medical.Net:

Female mice overexpressing adiponectin had weaker vertebra at 8 weeks of age than control mice and this delay in bone development persisted through to the end of the study period, representing early adulthood. The weaker vertebra model compression fractures of the lumbar spine in humans, among the most common type of fragility fracture associated with low bone mass and osteoporosis. The strength of the femur neck, representing the hip, was also weaker in both females and males overexpressing adiponectin. Serum adiponectin levels were inversely correlated with femur bone mineral content, further emphasizing that a high level of adiponectin impedes bone development at not only the lumbar spine but also the hip. Whether or not the delay in bone development resolves in later life or is sustained and leads to an increased risk of fragility fracture, particularly during aging when bone loss rapidly occurs due to declining levels of sex steroids, requires further investigation.

The research team, Dr. Michael C. Archer, Earle W. McHenry Professor and Chair, Dr. Wendy E. Ward, Associate Professor, Dr. Kafi Ealey, Postdoctoral Fellow and predoctoral student Jovana Kaludjerovic, in the Department of Nutritional Sciences, evaluated whether or not the diponectin modulates bone development using transgenic mice that overexpress this protein.