Data from case-control studies as well as from a cross-sectional study suggest an independent association between Parkinson’s disease (PD) and prevalent lower bone mineral density. Among older PD patients in randomized trials, control group participants experienced bone mineral density (BMD) loss exceeding 4% per year, suggesting that PD is associated with rapid incident bone loss. Retrospective and case-control studies have suggested that PD increases risk for fractures. However, prospective data are limited. The objective of this study [1] was to examine the association of PD with bone loss and fractures in older men. This prospective cohort study analyzed data from 5937 community dwelling men aged >65 years at six clinical centers of the Osteoporotic Fractures in Men (MrOS) study. At baseline and visit two (mean interval 4.6 years), community-diagnosed PD was ascertained by self-report and hip BMD was measured using dual energy x-ray absorptiometry (DXA). Incident fractures were self-reported. Fractures and deaths were centrally adjudicated.
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Despite the sexual dimorphism of bone, hip fracture risk is very similar in men and women at the same absolute bone mineral density (BMD). A recent study was conducted with the objective of elucidating the main structural properties of bone that underlie the measured BMD and that ultimately determine the risk of hip fracture in elderly men and women [1]. This study is part of the Rotterdam Study (a large prospective population-based cohort) and included 147 incident hip fracture cases in 4806 participants with DXA-derived hip structural analysis (mean follow-up, 8.6 y).
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Calcineurin is a protein phosphatase that regulates several physiological processes and is the target for cyclosporine A. Pharmacological inhibition of calcineurin by low concentrations of cyclosporin A increases osteoblast differentiation in vitro and bone mass in vivo. To determine whether calcineurin exerts direct actions on osteoblasts, the authors of a recent study [1] generated mice lacking a calcineurin regulatory subunit selectively in osteoblasts.
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Cardiovascular disease and osteoporotic fractures are two major public health problems. Cardiovascular disease and osteoporosis coexist in women: progression of aortic calcifications has been associated with faster bone loss. Low BMD has been shown to predict cardiovascular events and cardiovascular mortality, whereas the association between the extension of aortic calcifications and hip fracture risk is controversial. In contrast to these findings in women, few studies concern the relationship between osteoporosis and cardiovascular disease in men.
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Some studies have reported associations between cardiovascular diseases (CVD) and bone mineral loss. Osteoclast regulatory factors can affect vascular calcifications, and a high blood pressure can induce abnormalities in calcium metabolism and increase bone mineral loss in women. Low bone mineral density is not only an important predictor of osteoporotic fracture, but is also a risk factor for mortality.
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The differentiation of multipotent stemcells of mesodermal origin results in the formation of adipocytes, chondrocytes, osteoblasts, and myoblasts. In humans, osteoporosis and age-related osteopenia are associated with an increase in marrow fat tissue and osteoblast numbers correlated negatively with the number of adipocytes. Osteoblastic differentiation is driven by runx2, and then characterized by the expression of alkaline phosphatase, osteocalcin, and eventually by the mineralization of the extracellular matrix.
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