Microenvironmental Regulation of Chondrocyte Plasticity in Endochondral Repair-A New Frontier for Developmental Engineering.

Autor:	Wong SA; Department of Orthopaedic Surgery, Orthopaedic Trauma Institute, University of California, San Francisco, San Francisco, CA, United States.; School of Dentistry, University of California, San Francisco, San Francisco, CA, United States., Rivera KO; Department of Orthopaedic Surgery, Orthopaedic Trauma Institute, University of California, San Francisco, San Francisco, CA, United States.; School of Dentistry, University of California, San Francisco, San Francisco, CA, United States., Miclau T 3rd; Department of Orthopaedic Surgery, Orthopaedic Trauma Institute, University of California, San Francisco, San Francisco, CA, United States., Alsberg E; Department of Orthopaedic Surgery and Biomedical Engineering, Case Western Reserve University, Cleveland, OH, United States., Marcucio RS; Department of Orthopaedic Surgery, Orthopaedic Trauma Institute, University of California, San Francisco, San Francisco, CA, United States.; School of Dentistry, University of California, San Francisco, San Francisco, CA, United States., Bahney CS; Department of Orthopaedic Surgery, Orthopaedic Trauma Institute, University of California, San Francisco, San Francisco, CA, United States.
Jazyk:	angličtina
Zdroj:	Frontiers in bioengineering and biotechnology [Front Bioeng Biotechnol] 2018 May 15; Vol. 6, pp. 58. Date of Electronic Publication: 2018 May 15 (Print Publication: 2018).
DOI:	10.3389/fbioe.2018.00058
Abstrakt:	The majority of fractures heal through the process of endochondral ossification, in which a cartilage intermediate forms between the fractured bone ends and is gradually replaced with bone. Recent studies have provided genetic evidence demonstrating that a significant portion of callus chondrocytes transform into osteoblasts that derive the new bone. This evidence has opened a new field of research aimed at identifying the regulatory mechanisms that govern chondrocyte transformation in the hope of developing improved fracture therapies. In this article, we review known and candidate molecular pathways that may stimulate chondrocyte-to-osteoblast transformation during endochondral fracture repair. We also examine additional extrinsic factors that may play a role in modulating chondrocyte and osteoblast fate during fracture healing such as angiogenesis and mineralization of the extracellular matrix. Taken together the mechanisms reviewed here demonstrate the promising potential of using developmental engineering to design therapeutic approaches that activate endogenous healing pathways to stimulate fracture repair.
Databáze:	MEDLINE
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