Osteopathy and resistance to vitamin D toxicity in mice null for vitamin D binding protein
J. Clin. Invest. Fayez F. Safadi, et al. 103:239 doi:10.1172/JCI5244 [Go to this article.]

Figure 4
Bone mineralization defect after mild dietary vitamin D deficiency in DBP^–/– mice. Sections of femurs from age- and sex-matched groups of vitamin D–deficient (vitamin D⁻) DBP^+/+ and DBP^–/– mice were stained with Masson's trichrome. Representative photomicrographs from a DBP^+/+ (a) and a DBP^–/– (b) mouse are shown. Osteoid seams were characteristically thicker in the DBP^–/– group (arrowhead). This difference was not observed in mice fed vitamin D–sufficient chow. (c–f) Quantitative histomorphometric analyses of mice on vitamin D–deficient diets demonstrated significant abnormalities in OS/BS (male animals, n = 5; trend similar among females, but not significant; c) and osteoid thickness (both sexes compared, n = 10; d) in DBP^–/– mice. The bones of mice from both groups were labeled by two injections of the fluorochrome (calcein) at a 7-day interval, and bone sections were subjected to quantitative histomorphometric analyses to determine the amount of mineralization during this period. The MAR (both sexes compared, n = 7, 8; e) and the MS/BS (both sexes compared, n = 6; f) were indicative of a quantitative mineralization defect in DBP^–/– mice. DBP^+/+ and DBP^–/– mice maintained on normal diets showed no significant differences in any of these parameters (not shown). MAR, mineral apposition rate; MS/BS, mineralizing surface/bone surface; OS/BS, osteoid surface/bone surface.