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. 2014 May 13;2:14005. doi: 10.1038/boneres.2014.5

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Copyright © 2014 Sichuan University

This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/3.0/

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Bone formation after PTH administration is increased in mice lacking Hif-1α in osteoblasts and osteocytes. Ten-week-old female control and Hif-1α mutant (ΔHif-1α) mice were treated with vehicle or PTH for 6 weeks by daily s.c. injection. (a) Representative microCT images illustrate trabecular bone structure in the distal femur of control and ΔHif-1α mice after treatment with PTH at the indicated doses. (b–d) Bone volume per tissue volume (BV/TV) (b), trabecular number (Tb. N) (c) and trabecular thickness (Tb. Th) (d) were quantified by microCT. (e–g) The mineralizing surface per bone surface (MS/BS) (e), mineral apposition rate (MAR) (f) and bone formation rate per bone surface (BFR/BS) (g) were assessed by dynamic histomorphometry. (h and i) Levels of P1NP (h) and CTx (i) were measured in serum collected from control and ΔHif-1α mice. Results from e through i are presented as % change from baseline levels in saline-treated animals, which were equivalent in control and ΔHif-1α mice. *P≤0.05 vs. control mice with matched treatment. P1NP, amino pro-peptide of type 1 collagen; CTx, C-terminal telopeptide; s.c., subcutaneous.