The Journal of Bone and Joint Surgery (American). 2008;90:3-8.
doi:10.2106/JBJS.G.01136
© 2008 The Journal of Bone and Joint Surgery, Inc.
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Beta-Catenin-Dependent Wnt Signaling in Mandibular Bone Regeneration

Philipp Leucht, MD, Jae-Beom Kim, PhD and Jill A. Helms, DDS, PhD

Corresponding author:
Jill A. Helms, DDS, PhD
Division of Plastic and Reconstructive Surgery, Department of Surgery, Stanford University Medical School, 257 Campus Drive, Stanford, CA 94305-5148.
E-mail address: jhelms{at}stanford.edu

Disclosure: In support of their research for or preparation of this work, one or more of the authors received, in any one year, outside funding or grants in excess of $10,000 from the National Institutes of Health (grant #R01 DE012462), the Northern California Arthritis Foundation, and the United States Air Force Office of Scientific Research. Neither they nor a member of their immediate families received payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity. No commercial entity paid or directed, or agreed to pay or direct, any benefits to any research fund, foundation, division, center, clinical practice, or other charitable or nonprofit organization with which the authors, or a member of their immediate families, are affiliated or associated.

Osteoblasts are derived from two distinct embryonic lineages: cranial neural crest, and mesoderm. Both populations of cells are capable of forming bone and cartilage during fetal development and during adult bone repair, but whether they use equivalent molecular pathways to achieve osteoblast differentiation is unknown. We addressed this question in the context of cranial repair and focused on the role of Wnt signaling in mandibular skeletal healing. Transgenic Wnt reporter mice were used to pinpoint Wnt-responsive cells in the injury callus, and in situ hybridization was used to identify some of the Wnt ligands expressed by cells during the repair process. A gene transfer technique was employed to abrogate Wnt signaling during mandibular healing, and we found that reparative intramembranous ossification requires a functional Wnt pathway. Finally, we evaluated how constitutive activation of the Wnt pathway, caused by mutation of the LRP5 receptor, affected bone repair in the mandible. Taken together, these data underscore the functional requirement for Wnt signaling in cranial skeletal healing.


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