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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The recent identification of the genes responsible for several human genetic diseases affecting bone homeostasis and the characterization of mouse models for these diseases indicated that canonical Wnt signaling plays a critical role in the control of bone mass [1]. A recent study [2] reports that the osteoblast-specific transcription factor Osterix (Osx), which is required for osteoblast differentiation, inhibits Wnt pathway activity. In calvarial cells of Osx-null embryos, expression of the Wnt antagonist Dkk1 was abolished, and that of Wnt target genes c-Myc and cyclin D1 was increased. Moreover, these studies demonstrated that Osx bound to and activated the Dkk1 promoter. In addition, Osx inhibited β-catenin-induced reporter activity and β-catenin-induced secondary axis formation in Xenopus embryos. Importantly, data from calvaria of Osx-null embryos indicate that Osx inhibited the Wnt pathway in osteoblasts in vivo. This study further shows that Osx disrupts binding of transcription factor TCF to DNA. This provides a likely mechanism for the inhibition by Osx of β-catenin transcriptional activity.
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Quantitative ultrasound has been shown to predict risk of fracture in various populations. However, this ability may be modified by the presence of previous fracture in very frail older people. The authors of a recent study [1] assessed bone strength by quantitative ultrasound (QUS) and clinical risk factors at baseline for 1 982 institutionalised older people. Fractures were ascertained for 2 years from baseline and validated by X-ray reports.

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