Skip to main content
. 2018 Jun 7;3(11):e98673. doi: 10.1172/jci.insight.98673

Figure 6. Dkk1 neutralizing antibody has negligible skeletal effects in WT mice but has potent anabolic effects in Sost–/– mice.

Figure 6

Percent change in (A) whole-body bone mineral content (BMC) and (B) proximal tibia BMC, calculated from just prior to the start of treatment (at 8 weeks of age) to sacrifice at 16 weeks of age, capturing 8 weeks of Dkk1 mAb (αDkk1-mAb) or vehicle injection in WT (red bars) and Sost–/– (purple bars) mice. (C–E) Femoral μCT properties in the distal metaphyseal spongiosa (bone volume fraction [BV/TV]) and midshaft cortex (cortical thickness [Ct.Th]) measured in 16-week-old mice, after 8 weeks of vehicle or Dkk1 antibody treatment. Note the increase in bone mass induced by Dkk1 inhibition in Sost–/– but not WT mice. (G–I) Quantification of (G) ultimate force from 3-point bending tests of the femoral diaphysis and (I) bone formation rates from the same region, revealing increased bone strength and formation rates induced by Dkk1 inhibition in Sost–/– but not WT mice. Representative fluorochrome-labeled sections (H) illustrate the increase in bone formation over the experimental period (from yellow to red label). All panels are based on data/images from female mice. *P < 0.05 compared with genotype-matched vehicle-treated mice. For all experiments, n = 9–12 mice/group. Data in A, B, C, E, G, and I were analyzed using unpaired t tests within each Sost background.