Hypertension and osteoporosis are two major age-related disorders; however, the underlying molecular mechanism for this comorbidity is not known. The renin–angiotensin system (RAS) plays a central role in the control of blood pressure and has been an important target of antihypertensive drugs. Using a chimeric RAS model of transgenic THM (Tsukuba hypertensive mouse) expressing both the human renin and human angiotensinogen genes, the authors of a recent study [1] showed that activation of RAS induces high turnover osteoporosis with accelerated bone resorption.

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Although patients with type 2 diabetes have an increased risk of hip fracture, risk of vertebral fracture (VF) and its association with BMD are still unclear. A recent study [1] examined Japanese type 2 diabetic patients (161 men >50 y and 137 postmenopausal women) and nondiabetic controls (76 and 622, respectively) by lateral spine radiography and DXA at the lumbar spine (L), femoral neck (FN), and radius (R).

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The use of proton pump inhibitors has been associated with an increased risk of hip fracture. The authors of a recent study [1] sought to further explore the relation between duration of exposure to proton pump inhibitors and osteoporosis-related fractures. They used administrative claims data to identify patients with a fracture of the hip, vertebra, or wrist between April 1996 and March 2004. Cases were each matched with 3 controls based on age, sex, and comorbidities. They calculated adjusted odds ratios (OR) for the risk of hip fracture and all osteoporosis-related fractures for durations of proton pump inhibitor exposure ranging from 1 or more years to more than 7 years.

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Few studies have analyzed the geographical variations in the relationship between age and hip fracture incidence. The goal of this study [1] was to assess these variations among women under 85 within the same country. The study population included women aged 50 to 85 who were living in France in 2004. Hip fracture cases were identified in the French Diagnosis Related Groups (DRG)-like database using the diagnosis code for closed hip fractures and procedural codes for treatment. The Moran index and a spatial model using latitude and longitude were used to assess the geographical heterogeneities of cumulative incidence risk (CIR) and age effect.

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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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Previous studies have shown increased bone density and reduced risk of fracture in patients taking thiazide diuretics. In vitro, a direct effect of thiazides on osteoblasts has been reported. However, the long-term effects of low-dose thiazides on mineral metabolism have not been reported in normal subjects. The authors of this study [1] conducted a randomized, double-blinded trial in normal subjects aged 60 to 79 years, using hydrochlorothiazide 12.5 or 25 mg/d or placebo for 3 years. Subjects were encouraged to maintain calcium intake of 1 to 1.5 g/day. Measurements of serum and urine calcium metabolism were done at baseline, 6 months, and yearly. Data were analyzed in 88 men and 177 women who had taken study medication. Adjusted changes in the measurements from baseline to 1 and 3 years were compared among groups.

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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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Clinical studies have shown that total body fat mass is related to both bone density and fracture risk and that fat ingestion reduces bone turnover. These effects are at least partially mediated by endocrine mechanisms, but it is possible that lipids might act directly on bone. This study [1] assessed the effects of broad fractions of milk lipids in osteoblasts, bone marrow, and neonatal mouse calvariae.
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