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. 2022 Apr 6;8(14):eabl8054. doi: 10.1126/sciadv.abl8054

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Fig. 6. — (A and B) μCT images and quantitative analysis of pathological new bone formation in hind paw of DBA/1;CXCL12^Col2 mice at the age of 20 weeks with or without EHT1864 administration. Scale bars, 500 μm. n = 6 per group. ANOVA (F_2,15 = 34.40). (C) H&E staining, SOFG staining, immunohistochemical staining, and immunofluorescence staining of Prx1 in plantar surface of hind paw of DBA/1;CXCL12^Col2 mice at the age of 20 weeks with or without EHT1864 administration. Scale bars, 200 μm. n = 6 per group. (D and E) Quantitative analysis of Prx1 in (C). ANOVA (F_2,15 = 17.62; F_2,15 = 71.39). (F) Photo of CXCL12^Col2 mice at the age of 20 weeks with or without EHT1864 administration. Scale bar, 5 mm. (G and H) μCT images and quantitative analysis of pathological new bone formation in the spine of CXCL12^Col2 PGIS mice at the age of 20 weeks with or without EHT1864 administration. Scale bars, 200 μm. n = 6 per group. ANOVA (F_2,15 = 34.74). (I) H&E staining, TB staining, immunohistochemical staining, and immunofluorescence staining of Sca1 in spine of CXCL12^Col2 PGIS mice at the age of 20 weeks with or without EHT1864 administration. Scale bars, 200 μm. n = 6 per group. (J and K) Quantitative analysis of Sca1 in (I). ANOVA (F_2,15 = 29.55; F_2,15 = 18.36). (L) Schematic diagram illustrating CXCL12-induced pathological new bone formation and recruitment of OPCs. Data are shown as means ± SEM. One-way ANOVA with Levene’s test, followed by the Tukey’s post hoc test was used.