In clinical trials, antifracture

efficacy has been proven

In clinical trials, antifracture

efficacy has been proven at vertebral, nonvertebral, and hip sites. This issue commences with a special guest article focusing on microarchitecture and the importance of advances in bone quality assessment. In an attempt to identify more patients at risk of osteoporosis, the issue follows up with an article outlining the background and development of the FRAX tool. The subsequent articles selleck chemical outline how to address the main risks identified in FRAX with strontium ranelate. These are age, disease severity, which includes BMD and previous fracture history, gender, glucocorticoid use, and lifestyle habits. It is important S3I-201 purchase to note that physicians should recommend bone KPT-8602 mouse mineral density testing for younger women at risk and for postmenopausal women under 65 years who have risk factors for osteoporosis other than being postmenopausal, in order to identify more patients who may require treatment. The issue concludes with an important comparative analysis of different ways of evaluating treatments for osteoporosis.

It is hoped that this will help clinicians in their own identification of patients at risk of osteoporosis and provide information regarding options for treatment. Conflicts of interest J.-Y. Reginster (on behalf of the Department of Public Health, Epidemiology and Health Economics of the University of Liège, Liège, Belgium): consulting fees or paid advisory boards: Servier, Novartis, Negma, Lilly, Wyeth, Amgen, GlaxoSmithKline, Roche, Merckle, Nycomed, NPS, Theramex, UCB; lecture fees when speaking at the invitation of a commercial sponsor: Merck Sharp and Dohme, Lilly, Rottapharm, IBSA, Genevrier, Novartis, Servier, Roche, check GlaxoSmithKline, Teijin, Teva, Ebewee Pharma, Zodiac, Analis, Theramex, Nycomed, Novo-Nordisk; grant support

from industry: Bristol Myers Squibb, Merck Sharp & Dohme, Rottapharm, Teva, Lilly, Novartis, Roche, GlaxoSmithKline, Amgen, Servier. M.L. Brandi is a consultant for and has received honoraria and grant/research support from MSD, Procter & Gamble, Servier, Nycomed, Glaxo, NPS and Amgen.”
“Introduction Osteoporosis is a complex disease characterized by low bone mass and microarchitectural deterioration of bone tissue, leading to enhanced bone fragility and a consequent increase in fracture risk [1]. Assessment of bone mineral density (BMD) is a common approach to evaluate the risk of osteoporosis. BMD is under strong genetic control with heritability ranging from 0.63 to 0.75 at the femoral neck, 0.61 to 0.83 at the lumbar spine, and 0.66 to 0.79 at total hip [2–4]. Recently published genome-wide association studies have revealed a few well-known candidate genes, such as low-density lipoprotein receptor-related protein 5, receptor activator of nuclear factor kappa B ligand (RANKL), osteoprotegerin, estrogen receptor 1, and sclerostin as the causal genes that contribute to BMD variation [5–7].

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