It is anticipated that

It is anticipated that the vast amount of data generated using this approach can be used to build, feed and validate computational models of bone which incorporate all of the different length scales, from the organ-level to the cellular level [64] and [72]. By combining computational and experimental approaches in this way it is hoped that the move towards a more complete understanding of the osteocyte and bone biology in general will be expedited. The current state of our knowledge regarding the molecular mechanisms which underpin the mechanical response of bone is at best fragmented. The Wnt/β-catenin signaling pathway [73] and [74] has received much attention

and is now recognized as an important regulator of bone mass and bone cell function, however it still remains to be determined how this pathway interacts with other key molecular components, which include RANKL, sclerostin [75], [76] and [77], nitric oxide [78], prostaglandin this website [79] and the many others identified in the in vivo loading studies presented here. Whilst

in vivo models exploiting comprehensive gene expression tools may have identified a number of candidate genes/proteins how these different elements interact remains a probabilistic construct. If definitive answers are to be found synergistic approaches will be required using the technologies discussed here. In summary, advanced techniques for imaging osteocytes ex vivo, in situ, and in vivo combined Gefitinib molecular weight with localized quantification of gene expression will be key to unraveling the function of these fascinating cells. Factor into this the emerging field of multiscale computational modeling and it becomes clear that the tools are now at our disposal to significantly enhance our understanding of osteocytes in bone biology. The authors declare no conflicts of interest. Authors

gratefully acknowledge funding from (2010_071, DJW/RM), the Swiss National Science Foundation (SNF 205321_132779, PS/RM) and the National Institutes of Health (R21-AR054449, RO1-AR051517 and PO1-AR46798, SLD). “
“Osteogenesis imperfecta (OI or brittle bone disease) is a hereditary disease which results in extreme bone fragility. Mutation of the genes coding for collagen type 1 (col-1) is the main cause of OI, resulting in a quantitative or qualitative alteration of col-1 production. This leads to extremely active bone remodelling, disorganized woven bone tissue, reduced trabecular and cortical bone mass and degraded bone mechanical properties [1]. There is currently no direct cure for OI and only symptomatic treatments are available, such as physiotherapy to increase postural strength, surgery to correct bone deformation and bisphosphonate treatment.

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