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BookmarkScienceDaily (Aug. 1, 2007) — Researchers have described a novel molecular pathway that may have a critical role in bone healing and have suggested that lithium, which affects this pathway, has the potential to improve fracture healing.
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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.
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. http://medicine.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pmed.0040249
