Animal models determined the mechanism of action of LRP5 mutations in the osteoblast spectrum (Kato et al., 2002; Babij et al., 2003; Yadav et al., 2008), generating LRP5−/− mice that exhibit early-onset osteoporosis and sustained embryonic ocular angiogenesis, the former associated with reduced bone formation and mineralization due to reduced osteoblast proliferation in postnatal mice (Kato et al., 2002). This evidence concerns the gene LRP5 and osteoporosis.