The validity of the WHO 10-yr probability of major osteoporotic fracture model (FRAX) for prediction of vertebral fracture has not been tested. The authors of a recent study [1] analyzed how well FRAX for major osteoporotic fractures (with and without femoral neck BMD) predicted the risk of vertebral fracture. They also compared the predictive validity of FRAX, femoral neck BMD, and prevalent vertebral fracture detected by radiographs at baseline alone or in combination to predict future vertebral fracture. They analyzed data from the Fracture Intervention Trial placebo groups (3.8-y follow-up, n = 3221).
The objective of this study [1] was to test the efficacy of supplemental vitamin D and active forms of vitamin D with or without calcium in preventing falls among older individuals. This meta-analysis was performed by searching Medline, the Cochrane central register of controlled trials, BIOSIS, and Embase up to August 2008 for relevant articles. Further studies were identified by consulting clinical experts, bibliographies, and abstracts. Only double blind randomised controlled trials of older individuals (mean age 65 years or older) receiving a defined oral dose of supplemental vitamin D (vitamin D3 (cholecalciferol) or vitamin D2 (ergocalciferol)) or an active form of vitamin D (1α-hydroxyvitamin D3 or 1,25-dihydroxyvitamin D3) and with sufficiently specified fall assessment were considered for inclusion.
Increased bone resorption is associated with increased risk of cardiovascular events in men: the MINOS study
08/06/2010 in Clinical dataBetter assessment of the association between cardiovascular disease and osteoporosis in older men may help identify shared etiologies for bone and heart health in this population. The authors of this study [1] assessed the association of BMD and bone turnover markers (BTMs) with risk of cardiovascular events (myocardial infarction or stroke) in 744 men > 50 yr of age.
Although quantitative ultrasound (QUS) is known to be correlated with BMD and bone structure, its long-term predictive power for fractures in comparison with DXA is unclear. The authors of a recent study [1] examined this in a sample of men and women in the European Prospective Investigation into Cancer (EPIC)-Norfolk who had both heel QUS and hip DXA between 1995 and 1997.
There are surprisingly few data on long-term mortality following osteoporotic fracture and even fewer following subsequent fracture. This study [1] examined long-term mortality risk in women and men following all osteoporotic fractures and assessed the association of subsequent fracture with that risk. This was achieved through a prospective cohort from the Dubbo Osteoporosis Epidemiology Study of community-dwelling women and men aged 60 years and older from Dubbo, Australia, who sustained a fracture between April 1989 and May 2007. Main outcome measures were age- and sex-specific standardized mortality ratios (SMRs) compared with the overall Dubbo population for hip, vertebral, major, and minor fractures.
Antifracture efficacy with supplemental vitamin D has been questioned by recent trials. For that reason, the authors of a recent study [1] performed a meta-analysis on the efficacy of oral supplemental vitamin D in preventing nonvertebral and hip fractures among older individuals (> 65 years). They included 12 double-blind randomized controlled trials (RCTs) for nonvertebral fractures (n=42 279) and 8 RCTs for hip fractures (n=40 886) comparing oral vitamin D, with or without calcium, with calcium or placebo. To incorporate adherence to treatment, they multiplied the dose by the percentage of adherence to estimate the mean received dose (dose x adherence) for each trial.
MEPE (Matrix Extracellular PhosphoglycoprotEin) is a protein secreted by osteoblasts and osteocytes. Its synthesis is increased in several phosphate and bone-mineral metabolic disorders such as hypophosphatemic rickets and oncogenic hypophosphatemic osteomalacia. Under normal circumstances, MEPE is cleaved to release a peptide which acts as an inhibitor of bone mineralization. MEPE may be a substrate for an enzyme called PHEX, and PHEX may prevent proteolysis of MEPE and release of the peptide which inhibits bone mineralization. In patients with X-linked hypophosphatemic rickets (XLH) and in mice with the Hyp mutation, PHEX is mutated and therefore cannot bind to MEPE. This results in the release of MEPE into the circulation, thereby causing hypophosphatemia and renal Pi wasting. To elucidate the causative role of MEPE in these disorders, the authors of a recent study [1] created a murine model overexpressing MEPE protein in bone.
In the course of attempting to define the bone “secretome,” a gene encoding a small membrane protein novel to osteoblasts was identified. Although previously identified in silico as ifitm5, no functional studies had been undertaken on this gene. A recent study [1] characterized the expression patterns and localization of this gene in vitro and in vivo and assessed its role in matrix mineralization in vitro.
The absence of significant changes in bone mineral density caused by decline or overproduction of calcitonin (CT) in humans has raised the question of whether the pharmacological action of CT as an inhibitor of bone resorption is also of physiological relevance.
Low bone mass in adults is a major risk factor for low-impact fractures, and is considered to be of complex origin because of interaction of environmental and genetic factors, each with modest effect. The objective of this study [1] was to assess the relative impact of genetics and environment, and quantify the risk in relatives of osteopenic individuals. The authors studied 440 Icelandic nuclear families with 869 first-degree relatives of both sexes. Index cases (male or female) had BMD in the lumbar spine or hip >1.5 SD less than sex-matched controls. Heritability of BMD was estimated by maximum likelihood method, and variance component analysis was used to partition the genetic and environmental effects. Relative risk of low BMD (< −1 SD) in first-degree relatives was estimated, and heritable decrement in BMD was calculated compared with controls.
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