Hip fracture is associated with high early mortality. Little is known about long-term survival and subsequent fracture risk. The aim of this study [1] was to evaluate survival and fracture risk after hip fracture in women at different ages. All women suffering a hip fracture during 1984–1985 in Malmö, Sweden, were identified (n = 766) and followed up to 22 y or death. All new radiographic examinations related to musculoskeletal trauma with or without fracture were registered. Survival (mortality) and fracture was evaluated in 5-y age bands and in age groups (<75, 75–84, and >85 y).

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Recent studies have indicated a link between bone metabolism and cardiovascular events in patients with chronic kidney disease (CKD). CKD is a major health problem worldwide. This study [1] evaluates the role of noninvasive markers of bone metabolism in predicting cardiovascular morbidity (coronary artery disease, peripheral vascular disease, stroke) and mortality in patients with mild to severe forms of CKD. In a prospective cohort study, 627 patients with CKD were screened. To focus on bone metabolism, traditional risk factors for cardiovascular events were excluded, and 135 patients with CKD stages 1–5 were followed for 4 yrs. Glomerular filtration rate was calculated by the Modification of Diet in Renal Disease (MDRD) formula. PTH (measured by four different assays), vitamin D 25 and 1,25, bone-specific alkaline phosphatase (BSALP), TRACP-5b, osteocalcin, serum collagen cross-link molecules, RANKL, and osteoprotegerin were determined. Predictors of cardiovascular events were evaluated by multivariable logistic regression, Kaplan-Meier survival, and Cox regression analysis.
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Calorie restriction is promoted to increase longevity, yet this regimen could lead to bone loss and fracture, and therefore affect quality of life. In a recent study [1], 46 individuals were randomized to 4 groups for 6 months: (1) healthy diet (control group); (2) 25% calorie restriction from baseline energy requirements (CR group); (3) 25% energy deficit by a combination of CR and increased aerobic exercise (CR+EX group); and (4) low-calorie diet (890 kcal/d; goal, 15% weight loss) followed by weight maintenance (LCD group). Bone mineral density (total body and hip by dual-energy x-ray absorptiometry) and serum bone markers (bone specific alkaline phosphatase, osteocalcin, cross-linked C-telopeptide of type I collagen, and cross-linked N-telopeptide of type I collagen) were measured at baseline and after 6 months.
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Bone mineral density (BMD) is a dynamic variable and is known to decline with advancing age. Although it has been shown that either low BMD or the greater the difference between two measurements in BMD is associated with all-cause mortality in women, it is not known whether the rate of BMD loss contributes to mortality risk independent of baseline BMD. Furthermore, the associations between BMD and bone loss and mortality in men have not been studied. Body weight is strongly related to BMD, such that higher weight is associated with higher BMD and reduced fracture risk. Although it was suggested that weight loss and weight fluctuation are associated with an increased risk of mortality, it is unknown whether the effect of weight loss or weight fluctuation on mortality is independent of baseline BMD and rate of bone loss. To answer these questions, a recent study [1] collected data from 1059 women and 644 men, older than 60 (as of 1989), of white background. All-cause mortality was recorded annually between 1989 and 2004. BMD at the femoral neck was measured by DXA at baseline and at approximately every 2 yr afterward. Data on incident osteoporotic fractures and concomitant diseases, including cardiovascular diseases, all types of cancer, and type I/II diabetes mellitus, was also recorded.
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X-linked hypophosphatemia (XLH) is the archetypal vitamin D–resistant disease in humans, and the most common form of inherited rickets, with an incidence of approximately 1 in 20 000 live births. The disease is characterized by renal phosphate (Pi) wasting with resulting hypophosphatemia, abnormal vitamin D metabolism, defective bone and cartilage mineralization, dentine defects, and stunted growth. Recently, the gene involved in the pathogenesis of XLH was identified and designated as PHEX (the phosphate-regulating gene with homologies to endopeptidases on the X chromosome). The murine homolog of the human disease, the hyp-mouse, has a phenotype identical to that evident in patients with XLH, and is due to a large deletion in the 3′ region of the Phex gene. These findings suggest that a mutation in the PHEX/Phex gene is responsible for the phenotypic changes in patients with XLH and the hyp-mouse. Although PHEX/Phex expression occurs primarily in osteoblast lineage cells, transgenic Phex expression in hyp-mouse osteoblasts fails to rescue the phenotype, suggesting that Phex expression at other sites underlies XLH.
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