General rights Copyright and moral rights for the publications made accessible in the public portal are retained by the authors and/or other copyright owners and it is a condition of accessing publications that users recognise and abide by the legal requirements associated with these rights.• Users may download and print one copy of any publication from the public portal for the purpose of private study or research.• You may not further distribute the material or use it for any profit-making activity or commercial gain • You may freely distribute the URL identifying the publication in the public portal Take down policy If you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediately and investigate your claim. backgroundBone loss increases after menopause. However, bone strength also depends on structural characteristics such as bone size. Whether bone size increases as a result of periosteal apposition and whether a strength index accounting for both bone density and bone size might predict the risk of fracture better than bone density alone are unclear. methodsBone mass and the skeletal structure of the distal radius were evaluated by single-photon absorptiometry every other year in 108 women, all of whom were followed from the time of menopause for a mean period of 15 years. Postmenopausal serum estradiol levels and fractures of the distal radius were noted. resultsThe mean ( ± SD) annual decrease in bone mineral density was 1.9 ± 0.7 percent. The medullary bone diameter increased annually by 1.1 ± 0.9 percent, and the periosteal diameter by 0.7 ± 0.3 percent; the strength index decreased by 0.7 ± 0.7 percent. The expansion of the medullary diameter and the expansion of the periosteal diameter were correlated with one another (r=0.54, P<0.001), and women in the highest quartile of medullary expansion had more loss of bone mineral density and greater periosteal apposition than women in the lowest quartile (P<0.001 for both comparisons). The postmenopausal serum estradiol level was correlated with changes in the periosteal diameter (r=¡0.25, P=0.009) and with changes in bone mineral density (r=0.34, P<0.001).A 1-SD decrement in the strength index at base line was associated with a risk ratio for fracture of the distal radius of 3.8 (95 percent confidence interval, 1.8 to 8.0). conclusionsIncreased bone loss after menopause is associated with increased periosteal apposition, which partially preserves bone strength. A strength index may be a helpful predictor of the risk of fracture.

In a sample of 1358 women and 858 men, ≥60 yr of age who have been followed-up for up to 15 yr, it was estimated that the mortality-adjusted residual lifetime risk of fracture was 44% for women and 25% for men. Among those with BMD T-scores ≤ −2.5, the risks increased to 65% in women and 42% in men.Introduction: Risk assessment of osteoporotic fracture is shifting from relative risk to an absolute risk approach. Whereas BMD is a primary predictor of fracture risk, there has been no estimate of mortality-adjusted lifetime risk of fracture by BMD level. The aim of the study was to estimate the residual lifetime risk of fracture (RLRF) in elderly men and women. Materials and Methods: Data from 1358 women and 858 men Ն60 yr of age as of 1989 of white background from the Dubbo Osteoporosis Epidemiology Study were analyzed. The participants have been followed for up to 15 yr. During the follow-up period, incidence of low-trauma, nonpathological fractures, confirmed by X-ray and personal interview, were recorded. Incidence of mortality was also recorded. BMD at the femoral neck was measured by DXA (GE-LUNAR) at baseline. Residual lifetime risk of fracture from the age of 60 was estimated by the survival analysis taking into account the competing risk of death. Results: After adjusting for competing risk of death, the RLRF for women and men from age 60 was 44% (95% CI, 40-48) and 25% (95% CI, 19-31), respectively. For individuals with osteoporosis (BMD T-scores Յ −2.5), the mortality-adjusted lifetime risk of any fracture was 65% (95% CI, 58-73) for women and 42% (95% CI, 24-71) for men. For the entire cohort, the lifetime risk of hip fracture was 8.5% (95% CI, 6-11%) for women and 4% (95% CI, 1.3-5.4%) for men; risk of symptomatic vertebral fracture was 18% (95% CI, 15-21%) for women and 11% (95% CI, 7-14%) for men. Conclusions: These estimates provide a means to communicate the absolute risk of fracture to an individual patient and can help promote the identification and targeting of high-risk individuals for intervention.

This 2-year prospective controlled exercise intervention trial in 99 girls at Tanner stage 1, evaluating a school curriculum-based training program on a population-based level, showed that the annual gain in BMC, aBMD, and bone size was greater in the intervention group than in the controls.

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This non-randomized prospective controlled study evaluates a daily school-based exercise intervention program of 40 min/school day for 1 year in a population-based cohort of 81 boys aged 7-9 years. Controls were 57 age-matched boys assigned to the general school curriculum of 60 min/week. Bone mineral content (BMC; g) and areal bone mineral density (aBMD; g/cm(2)) were measured with dual X-ray absorptiometry (DXA) of the total body, the third lumbar vertebra (L3) and the femoral neck (FN). Bone width for L3 and FN was calculated from the lumbar spine and hip scan. No differences between the groups were found at baseline in age, anthropometrics or bone parameters. The mean annual gain in L3 BMC was 5.9 percentage points higher (P<0.001), L3 aBMD a mean 2.1 percentage points higher (P=0.01) and L3 width a mean 2.3 percentage points higher (P=0.001) in the cases than in the controls. When all individuals were included in one cohort, the total duration of exercise including both school-based and spare-time training correlated with L3 BMC (r=0.26, P=0.003), L3 aBMD (r=0.18, P=0.04) and L3 width (r=0.24, P=0.006). The study suggests that exercise in pre-pubertal boys influences the accrual of bone mineral and bone width and that a 1-year school-based exercise program confers skeletal benefits, at least in the lumbar spine.

Objective A prospective evaluation of the long-term effects of early menopause on mortality, risk of fragility fracture and osteoporosis.Design Prospective population-based observational study.Setting Malmö, Sweden.Population A total of 390 white north European women aged 48 years at the start of the study.Methods At baseline, bone mineral density (BMD) was measured by single-photon absorptiometry (SPA) in the distal forearm and menopausal status was noted. Menopause was determined according to the World Health Organization criterion of a minimum of 12 months of continuous amenorrhoea. Women were divided into early menopause (occurring before age 47 years) and late menopause (occurring at age 47 years or later). At age 77, forearm BMD was re-measured by SPA and proximal femur and lumbar spine BMD were measured by dual-energy X-ray absorptiometry (DXA). The prevalence of osteoporosis was determined using the DXA data. Mortality rate and the incidence of fractures were registered up until age 82. Data are presented as means with 95% confidence intervals (95% CI).Main outcome measures Incidence of fragility fractures, mortality, prevalence of osteoporosis at age 77.Results Women with early menopause had a risk ratio of 1.83 (95% CI 1.22-2.74) for osteoporosis at age 77, a risk ratio of 1.68 (95% CI 1.05-2.57) for fragility fracture and a mortality risk of 1.59 (95% CI 1.04-2.36).Conclusions Menopause before age 47 is associated with increased mortality risk and increased risk of sustaining fragility fractures and of osteoporosis at age 77.

During pregnancy and lactation, changes occur in a variety of factors which have great potential to influence bone mineral density (BMD). Smoking habits, the level of alcohol consumption, the level of physical activity, body weight, soft tissue composition and hormone levels are all factors that change during the course of these conditions. Some of these factors are capable of increasing BMD, and some can reduce it. Due to these various changes, it is virtually impossible to predict the development in BMD that will occur during a pregnancy and lactation. However, longitudinal studies have suggested that both pregnancy and lactation are associated with a BMD loss of up to 5%, albeit that the BMD recovers after weaning. Cross-sectional studies have indicated that women with many children and a long total period of lactation have similar or higher BMD and similar or lower fracture risk than their peers who have not given birth. As the studies showing this trend have been observational and cross sectional case-control studies, the conclusions can only be regarded as being suggestive, and no causality can be proven.

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