BoneKEy Reports

Journal Information
ISSN / EISSN : 2047-6396 / 2047-6396
Current Publisher: Springer Science and Business Media LLC (10.1038)
Total articles ≅ 536
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Latest articles in this journal

BoneKEy Reports, Volume 6; doi:10.1038/bonekey.2016.82

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Sandra M Sacco, Caitlin Saint, Amanda B Longo, Charles B Wakefield, Phil L Salmon, Paul J Leblanc,
BoneKEy Reports, Volume 6; doi:10.1038/bonekey.2016.87

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, Greg D Gamble, Ian R Reid
BoneKEy Reports, Volume 5; doi:10.1038/bonekey.2016.85

Hyperparathyroidism may be associated with skeletal and cardiovascular abnormalities, but it is unclear whether these associations exist for high-normal levels of parathyroid hormone (PTH). We assessed relationships between PTH and anthropometric, skeletal and cardiometabolic indices in normal men. Body composition, blood pressure, biochemistry and bone mineral density (BMD) were evaluated in 151 healthy men. BMD was reassessed at 2 years, and coronary artery calcium (CAC) was measured at 3.5 years. Relationships between PTH and other baseline characteristics, CAC scores and change in BMD were evaluated. PTH correlated positively with baseline body mass index, fat mass, diastolic blood pressure, triglycerides, total and low-density lipoprotein (LDL) cholesterol, (r=0.19–0.25, P=0.02–0.002), and with category of CAC score. Relationships between PTH and cardiometabolic indices remained significant after adjustment for age, 25-hydroxyvitamin D and estimated glomerular filteration rate. Men in the top PTH tertile (⩾4.4 pmol l−1, n=51) were more likely to have LDL cholesterol ⩾3.5 mmol l−1, diastolic blood pressure ⩾85 mm Hg, and CAC score >0 than men in lower tertiles. PTH was not associated with history of fracture, baseline BMD, or change in BMD over 2 years. In summary, in this cohort of healthy men, PTH levels are linearly related to adiposity and to cardiometabolic indices, but not to BMD or bone loss. These findings suggest that adiposity should be considered as an independent cause of secondary hyperparathyroidism, and they may be relevant to patients with normocalcemic hyperparathyroidism, in whom high PTH levels may be a marker of adiposity and cardiometabolic risk rather than always indicating parathyroid autonomy.
, , Michael Blauth, Markus Windolf
BoneKEy Reports, Volume 5; doi:10.1038/bonekey.2016.86

The high incidence of secondary hip fractures and the associated markedly increased mortality call for preventive actions that could help to avoid these injuries. By providing immediate strengthening and not relying on patient compliance, internal prophylactic augmentation of the osteoporotic proximal femur may overcome the main limitations of systemic bone drugs and wearable protective pads. However, such a method would have to provide sufficient and reliable strengthening effect with minimal risks and side effects to justify the need of an invasive treatment. The requirements for an internal reinforcement approach are thus strict and include mechanical, biological, clinical, ethical and financial criteria. Here we first attempt to describe the properties of an ideal augmentation method. Previously published methodologies and techniques developed at our research institute, including approaches using cements, metals, other materials or combined approaches, are then reviewed and evaluated according to these aspects. We conclude that none of the discussed methodologies appears to be able to deliver a sufficiently high gain-versus-risk ratio that could justify the clinical application and thus augmentation of the osteoporotic proximal femur remains a challenge. Finally, we provide suggestions for the development and evaluation of future strategies.
Gloria Allocca, Anjali P Kusumbe, ,
BoneKEy Reports, Volume 5; doi:10.1038/bonekey.2016.84

Confocal and two-photon microscopy has been widely used in bone research to not only produce high quality, three-dimensional images but also to provide valuable structural and quantitative information. In this article, we describe step-by-step protocols for confocal and two-photon microscopy to investigate earlier cellular events during colonisation of cancer cells in bone using xenograft mouse models. This includes confocal/two-photon microscopy imaging of paraformaldehyde fixed thick bone sections and frozen bone samples.
Melissa L Knothe Tate, Nicole Y C Yu, Iman Jalilian, André F Pereira, Ulf R Knothe
BoneKEy Reports, Volume 5; doi:10.1038/bonekey.2016.70

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, Jeffrey L Price
BoneKEy Reports, Volume 5; doi:10.1038/bonekey.2016.80

Deletion of proprotein convertase Mbtps1 in bone osteocytes leads to a significant postnatal increase in skeletal muscle size and contractile function, while causing only a 25% increase in stiffness in long bones. Concerns about leakiness in skeletal muscle were discounted since Cre recombinase expression does not account for our findings, and, Mbtps1 protein and mRNA is not deleted. Interestingly, the response of normal skeletal muscle to exercise and the regenerative response of skeletal muscle to the deletion of Mbtps1 in bone share some key regulatory features including a preference for slow twitch muscle fibers. In addition, transcriptional regulators PPAR, PGC-1α, LXR, and repressors DEC1 and DEC2 all occupy central positions within these two pathways. We hypothesize that the age-dependent muscle phenotype in Dmp1-Cre Mbtps1 cKO mice is due to bone→muscle crosstalk. Many of the myogenic genes altered in this larger and functionally improved muscle are regulated by circadian core transcriptional repressors DEC1 and DEC2, and furthermore, display a temporal coordination with Dec1 and Dec2 expression consistent with a regulatory co-dependency. These considerations lead us to propose that Dmp1-Cre Mbtps1 cKO osteocytes activate myogenesis by increased release of an activator of muscle PPAR-gamma, for example, PGE2 or sphingosine-1-P, or, by diminished release of an inhibitor of LXR, for example, long-chain polyunsaturated fatty acids. We hope that further investigation of these interacting pathways in the Dmp1-Cre Mbtps1 cKO model will lead to clinically translatable findings applicable to age-related sarcopenia and other muscle wasting syndromes.
Sandeep Paul,
BoneKEy Reports, Volume 5; doi:10.1038/bonekey.2016.81

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Elizabeth Rendina-Ruedy,
BoneKEy Reports, Volume 5; doi:10.1038/bonekey.2016.71

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