Bone Abstracts

Dysfunctions of Wnt/β-catenin and estrogen receptor signalling resulted in impaired mechanotransduction and bone loss as in osteoporosis. Previous studies demonstrated the interaction of these pathways in mechanotransduction in vitro and in vivo. In this study, the influence of the activation of estrogen receptor and β-catenin signalling on mechanically induced bone formation was investigated in ovariectomized mice. 12-week-old mice were ovariectomized. 4 weeks later, an estrogen pellet was implanted and the right ulna was loaded for 2 weeks on five consecutive days. For β-catenin activation, the Gsk-3β inhibitor SB415286 was injected daily during the loading period. Endocortical and periosteal bone formation rates (EcBFR, PsBFR) were calculated and bone structure was analysed. Each treatment group included six mice. Data were analysed for significance (value P<0.05) using the Mann–Whitney U test. All experimental procedures were approved by the National Ethics Committee. Loading induced bone formation. At the endocortical surface, estrogen induced bone formation and acted additively with loading. At the periosteal surface, both estrogen and SB415286 enhanced mechanically induced bone formation in ovariectomized mice. When estrogen and SB415286 were administered together, the sensitizing effect on mechanically induced bone formation of each activator alone was abolished in these mice.

The interaction of estrogen receptor and Wnt/β-catenin signalling might be one mechanism that is involved in regulating bone mass homeostasis in response to different loading conditions.