The study, led by Benjamin Alman from the Hospital For Sick Children, Toronto, investigated the role of the â-catenin signaling pathway, which activates T cell factor -dependent gene transcription, and which is known to have a key regulatory role in embryonic skeletal development.
By studying mice with fractures the researchers were able to show that â-catenin-mediated gene transcription was activated in both bone and cartilage formation during fracture repair.
In mice that lacked â-catenin fracture healing was inhibited, whereas in mice expressing an activated form of â-catenin bone healing was accelerated. Treating mice with lithium activated â-catenin in the healing fracture, but healing was enhanced only when treatment was given after the fracture occurred, rather than before.
These results show that that â-catenin functions differently at different stages of fracture repair. Although the relevance of this study to human fractures remains to be determined, activation of â-catenin by lithium treatment has the potential to improve fracture healing, but probably only when given in later phases of fracture healing.