Fig. 6

Ccr5-deficient male mice are resistant to RANKL-induced bone loss. a, b Micro-computed tomography (μCT) images (scale bars, 100 μm) and the analysis of the femurs of 7-week-old Ccr5 ^−/− and their wild-type littermates (Ccr5 ^+/+) (n = 4–6 mice per group). The BMD, BV/TV, Tb.N, and Conn-Dens were scored and statistically compared. c The levels of serum mouse RANKL, OPG, TRAP, and CTX were measured by an ELISA, and statistically compared. d Representative images of histological sections of the distal femurs obtained from wild-type and Ccr5 ^−/− mice are shown. The sections were stained to show the activity level of TRAP (shown in red), and Villanueva staining was performed to reveal the osteoid and osteoblasts (in pale purple); the nuclei were revealed by toluidine blue staining (in blue). The stained sections were observed by differential interference contrast (DIC) microscopy. Magnification (objective lens): ×10 (upper panel), ×20 (middle panel), and ×40 (lower panel), respectively. Scale bars, 100 μm, n = 4–6. e Quantitative bone histomorphometric analyses were conducted of the trabecular bones in the distal femurs of Ccr5 ^+/+ and Ccr5 ^−/− mice. The osteoclast number (N.Oc), osteoclast surface per bone surface (Oc.S/BS), osteoclast number per bone perimeter (N.Oc/B.Pm) and osteoclast number per osteoclast perimeter (N.Oc./Oc.Pm.) were scored and statistically compared. Each sample was duplicated. *P < 0.05 (by one-way analysis of variance (ANOVA)) in comparison to WT or RANKL-injected WT. All values are shown as the mean ± SD, n = 4–6