Smoking is associated with lower areal bone mineral density and higher fracture risk, although most evidence has been derived from studies in elderly subjects. This study [1] investigates smoking habits in relation to areal and volumetric bone parameters and fracture prevalence in young, healthy males at peak bone mass. Healthy male siblings (n=677) at the age of peak bone mass (25 to 45 years) were recruited in a cross-sectional population-based study. Trabecular and cortical bone parameters of the radius and cortical bone parameters of the tibia were assessed using peripheral quantitative computed tomography (pQCT). Areal bone mass was determined using dual energy X-ray absorptiometry (DXA). Sex steroids and bone markers were determined using immunoassays. Prevalent fractures and smoking habits were assessed using questionnaires.

Self-reported fractures were more prevalent in the current and early smokers than in the never smokers (P<.05), with a fracture prevalence odds ratio for early smokers of 1.96 after adjustment for age, weight, educational level, and alcohol use and exclusion of childhood fractures. Current smoking was associated with a significantly larger endosteal circumference and a decreased cortical thickness at the tibia.
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Fragility fractures cause significant morbidity and mortality. Effective osteoporosis treatment can reduce fracture incidence, but it is not clear whether it reduces mortality. The aim of this meta-analysis study [1] was to determine whether effective osteoporosis treatment reduces mortality. The authors searched Medline and the Cochrane Central Register of Trials prior to September 2008, as well as 2000–2008 American Society for Bone and Mineral Research conference abstracts. Eligible studies were randomized placebo-controlled trials of approved doses of medications with proven efficacy in preventing both vertebral and nonvertebral fractures, in which the study duration was longer than 12 months and there were more than 10 deaths. Trials of estrogen and selective estrogen receptor modulators were specifically excluded. Data were extracted from the text of the retrieved articles, published meta-analyses, or the Food and Drug Administration web site.

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Poor vitamin D status is common in the elderly and is associated with bone loss and fractures. The aim of this study [1] was to assess worldwide vitamin D status in postmenopausal women with osteoporosis according to latitude and economic status, in relation to parathyroid function, bone turnover markers, and BMD. The study was performed in 7441 postmenopausal women from 29 countries participating in a clinical trial, with BMD T-score at the femoral neck or lumbar spine < -2.5 or one to five mild or moderate vertebral fractures. Serum 25(OH)D, PTH, alkaline phosphatase (ALP), bone turnover markers osteocalcin (OC) and C-terminal cross-linked telopeptides of type I collagen (CTX), and BMD of the lumbar spine, total hip, femoral neck, and trochanter were measured.

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Childhood fractures are common. Their clinical relevance to osteoporosis and fractures in later life is unclear. The aim of this study [1] was to determine the predictive risk of childhood fracture on the risk of fracture in later life. Men and women >50 y of age were recruited from population registers for participation in the European Prospective Osteoporosis Study (EPOS). Subjects completed an interviewer-administered questionnaire that included questions about previous fractures and the age at which the first of these fractures occurred. Lateral spine radiographs were performed to ascertain prevalent vertebral deformities. Subjects were followed prospectively by postal questionnaire to determine the occurrence of clinical fractures. A subsample of subjects had BMD measurements performed. A cox proportional hazards model was used to determine the predictive risk of childhood fracture between the ages of 8 and 18 y on the risk of future limb fracture and logistic regression was used to determine the association between reported childhood fractures and prevalent vertebral deformity.

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Bone mineral density is known to decrease rapidly after the menopause. There is limited evidence about the separate contributions of a woman’s age, menopausal status and age at menopause to the incidence of hip fracture. Over one million middle-aged women joined the UK Million Women Study in 1996–2001 providing information on their menopausal status, age at menopause, and other factors, which was updated, where possible, 3 y later. All women were registered with the UK National Health Service (NHS) and were routinely linked to information on cause-specific admissions to NHS hospitals. 561,609 women who had never used hormone replacement therapy and who provided complete information on menopausal variables (at baseline 25% were pre/perimenopausal and 75% postmenopausal) were followed up for a total of 3.4 million woman-years (an average 6.2 y per woman).

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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.

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Better 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.

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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.

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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.

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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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