04May 2014

Bone 2014; 62:22-28

Notch1 and Notch2 inactivation increased porosity and reduced thickness of cortical bone. These effects were modest and more evident in 3 and 6 month old female than in male mice of the same age. In conclusion, Notch1 and Notch2 expression in osteoblast precursors regulates cancellous bone volume and microarchitecture.

Autor: Zanotti S, Canali E.
04May 2014
bone logo

Bone. 2015 May 24;79:37-42. doi: 10.1016/j.bone.2015.05.022. [Epub ahead of print]

The maintenance of bone homeostasis is largely dependent upon cellular communication between osteoclasts and osteoblasts. Microvesicles (MVs) have received a good deal of attention and are increasingly considered as mediators of intercellular communication due to their capacity to merge with and transfer a repertoire of bioactive molecular content (cargo) to recipient cells, triggering a variety of biologic responses. Here, we demonstrated that MVs shed from osteoblasts contain RANKL protein and can transfer it to osteoclast precursors through receptor ligand (RANKL-RANK), leading to stimulation of RANKL-RANK signaling to facilitate osteoclast formation. Such MV-mediated intercellular communication between osteoblasts and osteoclasts may represent a novel mechanism of bone modeling and remodeling. It may be worthwhile to further explore MVs as tools to modify the biological responses of bone cells or develop an alternative drug to treat bone diseases.

Autor: Deng L, Wang Y, Peng Y, Wu Y, Ding Y, Jiang Y, Shen Z, Fu Q.
04Abr 2014

Calcif Tissue Int. 2014 Jun;94(6):597-607. doi: 10.1007/s00223-014-9855-6. Epub 2014 Apr 6.

These results provide further evidence that PPI use may increase fracture risk in the elderly and highlight the need for clinicians to periodically reassess elderly patients’ individualized needs for ongoing PPI therapy, while weighing potential risks and benefits

Autor: Ding J, Heller DA, Ahern FM, Brown TV
04Abr 2014
bone logo

Bone 61 (2014) 138–148.

This review examines recent developments in the understanding of why the elderly hip becomes fragile. This growing understanding is suggesting novel testable approaches for reducing risk of hip fracture that might translate into control of the growing worldwide impact of hip fractures on our ageing populations.

Autor: Reeve J, Loveridge N.
05Mar 2014
endocrine society

Mol Endocrinol. 2014 Jul;28(7):1150-65

We conclude that osteocytogenesis is accompanied by changes in gene expression that may be driven by both genetic and epigenetic components. These changes are likely responsible for the osteocyte phenotype and may contribute to reduced sensitivity to 1,25(OH)(2)D(3).

Autor: St John HC, Bishop KA, Meyer MB, Benkusky NA, Leng N, Kendziorski C, Bonewald LF, Pike JW.
05Feb 2014

Nature. 2014 Feb 13;506(7487):240-4. doi: 10.1038/nature12883. Epub 2014 Jan 15

These findings demonstrate that genetic alterations in osteoblasts can induce acute myeloid leukaemia, identify molecular signals leading to this transformation and suggest a potential novel pharmacotherapeutic approach to acute myeloid leukaemia.

Autor: Kode A, Manavalan JS, Mosialou I, Bhagat G, Rathinam CV, Luo N, Khiabanian H, Lee A, Murty VV
04Feb 2014

In conclusion, our study does not support the hypothesis that calcium supplementation increases either carotid artery intimal medial thickness or carotid atherosclerosis.

In addition, calcium supplementation and high total calcium intake may indeed reduce carotid atherosclerosis.

Autor: Joshua R Lewis, Kun Zhu, Peter L Thompson and Richard L Prince
04Ene 2014

J Clin Invest. 2014 Apr 1;124(4):1-13. doi: 10.1172/JCI72323. Epub 2014 Mar 18.

Together, these results underscore the involvement of bone, among other tissues, in the disruption of whole-body glucose homeostasis resulting from a HFD and the involvement of insulin and osteocalcin cross-talk in glucose intolerance. Furthermore, our data indicate that insulin resistance develops in bone as the result of lipotoxicity-associated loss of insulin receptors.

Autor: Wei J, Ferron M, Clarke CJ, Hannun YA, Jiang H, Blaner WS, Karsenty G.