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Tamoxifen-Inducible CreER-Mediated Gene Targeting in Periosteum via Bone-Graft Transplantation
Chao Xie, MD; Ming Xue, MS; Qun Wang, PhD; Edward M. Schwarz, PhD; Regis J. O'Keefe, MD, PhD; Xinping Zhang, PhD
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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 (NIH) and the Musculoskeletal Transplant Foundation (MTF). 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.

The Journal of Bone and Joint Surgery, Incorporated
J Bone Joint Surg Am, 2008 Feb 01;90(Supplement 1):9-13. doi: 10.2106/JBJS.G.01212
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Periosteum plays a key role in bone repair through activation of residing stem and/or progenitor cells. The molecular signals regulating differentiation and expansion of periosteal stem cells during early repair are poorly understood. Understanding the molecular basis for initiation and completion of bone healing is vital for the success of bone-tissue engineering and regeneration therapy for impaired bone healing. We established a live-bone-graft transplantation model that allows us to quantitatively evaluate the fate of the periosteal cells and cell-initiated endochondral bone healing with use of a transgenic and knockout mouse model. By combining this live-bone-graft transplantation method with a tamoxifen-inducible CreER-mediated gene recombination model (R26CreER), we developed a novel approach to efficiently delete genes in periosteal cells during the initiation of skeletal repair. This approach allows us to use floxed mice to examine the function of genes whose germline deletion results in lethality during development. Successful bone repair and regeneration therapies require a deeper understanding of the signals and signaling pathways that are critical for the morphogenesis of the repair tissues. Early lethality in genetically manipulated mice prohibits an understanding of the function of genes in the adult repair process. Our current approach overcomes this encumbrance and enables examination of gene function in a time-dependent and repair-tissue-specific manner.

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    These activities have been planned and implemented in accordance with the Essential Areas and policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint sponsorship of the American Academy of Orthopaedic Surgeons and The Journal of Bone and Joint Surgery, Inc. The American Academy of Orthopaedic Surgeons is accredited by the ACCME to provide continuing medical education for physicians.
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