Ocn⁺ cell–specific deletion in vivo without altering osteoclastogenesis and mesenchymal progenitors. (A) WT mice (Ctrl) Ocn⁺ osteolineage cell deletion mice (Mut) were monitored for body size and weight; n = 8–10 mice/group. Data show mean ± SEM. (B) Femurs and tibiae in the OcnCre^+/−;iDTR mutants or WT (Ctrl) mice were assessed histologically. Bottom images are at a higher magnification with arrows pointing to empty lacunae within the cortex and altered endosteal surface; images reflect comparable findings in all animals; n = 8/experiment. (C) Osteoblasts in the OcnCre^+/−;iDTR and WT mice were quantitated by histomorphometry; n = 7–8 mice/group. Data show mean ± SEM. (D and E) Ocn and DTR expression was examined in bone sections from untreated OcnCre^+/−;iDTR by immunohistochemistry using Ocn- and DTR-specific antibodies (D), or by immunofluorescence using Ocn-specific antibodies and TUNEL staining after DT treatment (E); n = 6 mice/group. (F) Osteoclast numbers were assessed by TRAP staining (n = 6 mice/group) and (G) osteoclast activity by collagen breakdown in sera using ELISA assay; n = 7–8 mice/group. Data show mean ± SEM. (H) Mesenchymal progenitor activity in the bone marrow of OcnCre^+/−;iDTR mutants or WT controls was assessed by CFU-Ob assay; n = 9 mice/group. Data show mean ± SEM. (I) CD31⁻CD45⁻Ter119⁻LepR⁺ cells in the bone marrow stroma of OcnCre^+/−;iDTR mutants and controls were quantified by flow cytometry; n = 6–7 mice/group. Data show mean ± SEM. (A–I) For each experiment, 3–6 independent repeats were performed.