Effects of conditional deletion of <i>Fgfr1</i> in <i>Hyp</i> osteocytes on bone histology in 6-week-old mice.

<p>Representative images of (A) the distal femoral growth plate, (B) the femoral cortical bone by Goldner staining, and (C) femoral segital section by Alizarin Red double labeling in four genotypes of mice. Compared with control mice, <i>Fgfr1</i>^Dmp1-cKO-null mice had normal growth plate, no osteomalacia in cortical bone, and normal mineral apposition rate. However, <i>Hyp</i> mice showed a unorganized growth plate, an apparent increase of un-mineralized osteoid in both trabecular and cortical bone areas, and significant reduction in mineral apposition rate, compound <i>Hyp</i>;<i>Fgfr1</i>^Dmp1-cKO-null mice exhibited a recovery of organized growth plate, only fewer un-mineralized osteoid in cortical bone, and increased mineral apposition rate between control and <i>Hyp</i> mice, suggesting a partial rescue of the hypophosphatemic rickets phenotype in the compound <i>Hyp</i>;<i>Fgfr1</i>^Dmp1-cKO-null mice. Data are mean ± S.D. from 5–6 individual mice. Values sharing the same superscript in C are not significantly different at <i>P</i><0.05.