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New Data May Explain the Role of Sclerostin in Bone Formation

Lara C. Pullen, PhD  |  October 9, 2017

“Our study is the first to examine the effect of mechanical loading on Wnt signaling under sclerostin ablation,” they note. These results suggest that Dkk1 plays a compensatory role in the absence of Sost.

In both Sost-knockout and littermate control mice, skeletal maturation led to increased cortical thickness, cortical area fraction and reduced bone formation in control bones. Although the authors note this change occurred with age, they did not investigate the mechanoresponsiveness of elderly Sost-knockout mice. Thus, the authors emphasize that this factor remains to be resolved, and therefore, any treatment strategy should consider the influence of age on ultimate bone mass gains.

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Lara C. Pullen, PhD, is a medical writer based in the Chicago area.

Reference

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  1. Pflanz D, Birkhold AI, Albiol L, et al. Sost deficiency led to a greater cortical bone formation response to mechanical loading and altered gene expression. Sci Rep. 2017 Aug 25;7(1):9435. doi: 10.1038/s41598-017-09653-9.

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Filed under:ConditionsOsteoarthritis and Bone Disorders Tagged with:bonebone formationOsteoporosissclerostin

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