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. 2020 Aug 6;5(15):e137062. doi: 10.1172/jci.insight.137062

Figure 2. Neutralization of FGF 23 improves bone microarchitecture and mineralization in NHD13 mice.

Figure 2

After treatment of 2-month-old WT (WT) and NUP98/HOXD13 (NHD13) mice with FGF‑23 Ab over 8 weeks, bone phenotype of femora, bone histology of femora/vertebrae, and serum were analyzed. (A–D) Using μCT, quantitative data of bone volume over total volume (n = 9) (A), trabecular number (n = 9) (B), trabecular separation (n = 9) (C), and trabecular thickness (n = 9) (D) were assessed. (E and F) Vertebrae were stained with von Kossa/van Gieson to analyze the osteoid and define the osteoid surface per bone surface (n = 7–9) and mineralization lag time (n = 6–8). (G) P1NP serum levels were measured by ELISA (n = 13–16). (H) Five and 2 days before sacrifice, mice received i.p. calcein injections. Based on this double labeling, the bone formation rate in vertebrae was determined (n = 6–8). (I and J) TRAP‑stained femora were used to determine osteoblast (n = 6–9) and osteoclast number (n = 8–9). Data are shown as mean ± SD of 5 independent experiments. Statistical analysis was performed by 2-way ANOVA for the effect of MDS, FGF‑23 Ab treatment, and the interaction of both. Statistical significance of Bonferroni’s multiple comparisons is denoted. *P < 0.05; **P < 0.01; ***P < 0.001 vs. control. #P < 0.05; ##P < 0.01; ###P < 0.001 vs. WT control.