canonical wnt signaling in differentiated osteoblasts controls osteoclast differentiation inactivation of betacatenin in mesenchymal progenitors prevents osteoblast differentiation inactivation of lrp5 a gene encoding a likely wnt coreceptor results in low bone mass osteopenia by decreasing bone formation these observations indicate that wnt signaling controls osteoblast differentiation and suggest that it may regulate bone formation in differentiated osteoblasts here we study later events and find that stabilization of betacatenin in differentiated osteoblasts results in high bone mass while its deletion from differentiated osteoblasts leads to osteopenia surprisingly histological analysis showed that these mutations primarily affect bone resorption rather than bone formation cellular and molecular studies showed that betacatenin together with tcf proteins regulates osteoblast expression of osteoprotegerin a major inhibitor of osteoclast differentiation these findings demonstrate that betacatenin and presumably wnt signaling promote the ability of differentiated osteoblasts to inhibit osteoclast differentiation thus they broaden our knowledge of the functions wnt proteins have at various stages of skeletogenesis