caa a22 4500 605520879 CHVBK 20210128100737.0 cr unu---uuuuu 210128e20151101xx s 000 0 eng 10.1007/s00223-015-0034-1 doi (NATIONALLICENCE)springer-10.1007/s00223-015-0034-1 Identifying the Cellular Mechanisms Leading to Heterotopic Ossification [Elektronische Daten] [O. Davies, L. Grover, N. Eisenstein, M. Lewis, Y. Liu] Heterotopic ossification (HO) is a debilitating condition defined by the de novo development of bone within non-osseous soft tissues, and can be either hereditary or acquired. The hereditary condition, fibrodysplasia ossificans progressiva is rare but life threatening. Acquired HO is more common and results from a severe trauma that produces an environment conducive for the formation of ectopic endochondral bone. Despite continued efforts to identify the cellular and molecular events that lead to HO, the mechanisms of pathogenesis remain elusive. It has been proposed that the formation of ectopic bone requires an osteochondrogenic cell type, the presence of inductive agent(s) and a permissive local environment. To date several lineage-tracing studies have identified potential contributory populations. However, difficulties identifying cells in vivo based on the limitations of phenotypic markers, along with the absence of established in vitro HO models have made the results difficult to interpret. The purpose of this review is to critically evaluate current literature within the field in an attempt identify the cellular mechanisms required for ectopic bone formation. The major aim is to collate all current data on cell populations that have been shown to possess an osteochondrogenic potential and identify environmental conditions that may contribute to a permissive local environment. This review outlines the pathology of endochondral ossification, which is important for the development of potential HO therapies and to further our understanding of the mechanisms governing bone formation. Springer Science+Business Media New York, 2015 Ossification nationallicence Myoblast nationallicence Endothelium nationallicence Epithelium nationallicence Mesenchyme nationallicence Stem cell nationallicence Chondrogenic nationallicence Osteogenic nationallicence Pericyte nationallicence Davies O. School of Mechanical and Manufacturing Engineering, Loughborough University, Ashby Road, LE11 3TU, Loughborough, UK aut Grover L. School of Chemical Engineering, University of Birmingham, Edgbaston, B15 2TT, Birmingham, UK aut Eisenstein N. School of Chemical Engineering, University of Birmingham, Edgbaston, B15 2TT, Birmingham, UK aut Lewis M. School of Sport, Exercise and Health Sciences, Loughborough University, Epinal Way, LE11 3TU, Loughborough, UK aut Liu Y. School of Mechanical and Manufacturing Engineering, Loughborough University, Ashby Road, LE11 3TU, Loughborough, UK aut Calcified Tissue International Springer US; http://www.springer-ny.com 97/5(2015-11-01), 432-444 0171-967X 97:5<432 2015 97 223 https://doi.org/10.1007/s00223-015-0034-1 text/html Onlinezugriff via DOI BK010053 XK010053 XK010000 Metadata rights reserved Springer special CC-BY-NC licence nationallicence 1 review-article jats NATIONALLICENCE NATIONALLICENCE NL-springer NATIONALLICENCE 856 40 https://doi.org/10.1007/s00223-015-0034-1 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Davies O. School of Mechanical and Manufacturing Engineering, Loughborough University, Ashby Road, LE11 3TU, Loughborough, UK aut NATIONALLICENCE 700 1- Grover L. School of Chemical Engineering, University of Birmingham, Edgbaston, B15 2TT, Birmingham, UK aut NATIONALLICENCE 700 1- Eisenstein N. School of Chemical Engineering, University of Birmingham, Edgbaston, B15 2TT, Birmingham, UK aut NATIONALLICENCE 700 1- Lewis M. School of Sport, Exercise and Health Sciences, Loughborough University, Epinal Way, LE11 3TU, Loughborough, UK aut NATIONALLICENCE 700 1- Liu Y. School of Mechanical and Manufacturing Engineering, Loughborough University, Ashby Road, LE11 3TU, Loughborough, UK aut NATIONALLICENCE 773 0- Calcified Tissue International Springer US; http://www.springer-ny.com 97/5(2015-11-01), 432-444 0171-967X 97:5<432 2015 97 223