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. 2009 Jul 15;136(16):2747–2756. doi: 10.1242/dev.033571

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Fig. 5. — Quantitative analysis of the osteoblast defect in Gpr48^-/- mice. (A) Both trabecular bone mineral density (BMD) and cortical BMD dramatically decreased in Gpr48^-/- mice as assessed on microCT sections. (B) Deletion of Gpr48 leads to a reduction in bone volume/tissue volume (BV/TV), trabecular thickness, trabecular number, and increased trabecular separation as assessed by histomorphometric analysis. (C) Gpr48 regulates the kinetic indices of mineral apposition (MAR), bone formation rates (BFR/BS) and mineralizing surface (MS/BS). (D) Deletion of Gpr48 causes significant defects in osteoid characteristics, including decreased osteoid thickness (O.Th), osteoid surface (OS/BS) and osteoid volume (OV/BV). In each case, results show mean±s.d., n=3, age and sex matched; ^**P<0.01 in A-D.