Lithium and bone healing

The study, led by Benjamin Alman from the Hospital For Sick Children, Toronto, investigated the role of the beta-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 beta-catenin-mediated gene transcription was activated in both bone and cartilage formation during fracture repair. In mice that lacked beta-catenin fracture healing was inhibited, whereas in mice expressing an activated form of beta-catenin bone healing was accelerated. Treating mice with lithium activated beta-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 beta-catenin functions differently at different stages of fracture repair. Although the relevance of this study to human fractures remains to be determined, activation of beta-catenin by lithium treatment has the potential to improve fracture healing, but probably only when given in later phases of fracture healing.

Citation: Chen Y, Whetstone HC, Lin AC, Nadesan P, Wei Q, et al. (2007) Beta-catenin signaling plays a disparate role in different phases of fracture repair: Implications for therapy to improve bone healing. PLoS Med 4(7): e249.

Source: Public Library of Science