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The Potential of FGF-2 in Craniofacial Bone Tissue Engineering: a Review

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The Potential of FGF-2 in Craniofacial Bone Tissue Engineering: a Review cells Review The Potential of FGF-2 in Craniofacial Bone Tissue Engineering: A Review Anita Novais 1,2, Eirini Chatzopoulou 1,2,3, Catherine Chaussain 1,2 and Caroline Gorin 1,2,* 1 Pathologies, Imagerie et Biothérapies Orofaciales, Université de Paris, URP2496, 1 rue Maurice Arnoux, 92120 Montrouge, France; [email protected] (A.N.); [email protected] (E.C.); [email protected] (C.C.) 2 AP-HP Département d’Odontologie, Services d’odontologie, GH Pitié Salpêtrière, Henri Mondor, Paris Nord, Hôpital Rothschild, Paris, France 3 Département de Parodontologie, Université de Paris, UFR Odontologie-Garancière, 75006 Paris, France * Correspondence: [email protected]; Tel./Fax: +33-(0)1-5807-6724 Abstract: Bone is a hard-vascularized tissue, which renews itself continuously to adapt to the mechanical and metabolic demands of the body. The craniofacial area is prone to trauma and pathologies that often result in large bone damage, these leading to both aesthetic and functional complications for patients. The “gold standard” for treating these large defects is autologous bone grafting, which has some drawbacks including the requirement for a second surgical site with quantity of bone limitations, pain and other surgical complications. Indeed, tissue engineering combining a biomaterial with the appropriate cells and molecules of interest would allow a new therapeutic approach to treat large bone defects while avoiding complications associated with a second surgical site. This review first outlines the current knowledge of bone remodeling and the different signaling pathways involved seeking to improve our understanding of the roles of each to be able to stimulate or inhibit them. Secondly, it highlights the interesting characteristics of one growth factor in particular, FGF-2, and its role in bone homeostasis, before then analyzing its potential Citation: Novais, A.; Chatzopoulou, usefulness in craniofacial bone tissue engineering because of its proliferative, pro-angiogenic and E.; Chaussain, C.; Gorin, C. The Potential of FGF-2 in Craniofacial pro-osteogenic effects depending on its spatial-temporal use, dose and mode of administration. Bone Tissue Engineering: A Review. Cells 2021, 10, 932. https://doi.org/ Keywords: FGF-2; bone tissue engineering; angiogenesis; mineralization; signaling pathways 10.3390/cells10040932 Academic Editor: Barbara Kaltschmid 1. Introduction Received: 5 March 2021 The skeletal system is dynamic, metabolically active and functionally diverse. As Accepted: 15 April 2021 well as a structural function, it has a metabolic role. It supports and protects the vital Published: 17 April 2021 internal organs and is the site of synthesis of the hematopoietic marrow and provides sites of muscle attachment for locomotion. Bone is involved in both mineral metabolism, via Publisher’s Note: MDPI stays neutral calcium and phosphate homeostasis, and acid–base balance, via the buffering of hydrogen with regard to jurisdictional claims in ions [1]. Moreover, it has been suggested that bone has other important endocrine functions published maps and institutional affil- in fertility, glucose metabolism, appetite regulation and muscle function [2,3]. The craniofa- iations. cial area is prone to trauma and pathologies that often result in large bone damage, these leading to both aesthetic and functional complications for patients. Throughout life, the craniofacial area is at risk of complex injuries that require bone grafting to restore function. The etiology of such injuries may be accidental (e.g., acute trauma), congenital (e.g., birth Copyright: © 2021 by the authors. defects or deformities), pathological (e.g., maxillofacial tumors, such as ameloblastoma, or Licensee MDPI, Basel, Switzerland. infection) or surgical. Whenever the lesions are extensive, they cause large bone defects that This article is an open access article cannot self-repair because they exceed the body’s natural regenerative capacity. The “gold distributed under the terms and standard” for treating these large defects is autologous bone grafting. Since the defects are conditions of the Creative Commons extensive, harvesting of the necessary bone at the donor site can cause major morbidity, Attribution (CC BY) license (https:// including bone deformity, as well as pain and occasionally continuous progressive resorp- creativecommons.org/licenses/by/ tion. Tissue engineering has made it possible to approach these issues from another angle. 4.0/). Cells 2021, 10, 932. https://doi.org/10.3390/cells10040932 https://www.mdpi.com/journal/cells Cells 2021, 10, 932 2 of 28 Cells 2021, 10, 932 2 of 28 progressive resorption. Tissue engineering has made it possible to approach these issues from another angle. Before talking about tissue engineering; however, it is necessary to Beforedescribe talking the tissue about of tissue interest. engineering; This review however, is, therefore, it is necessary organized to into describe three thesections, tissue the of interest.first describing This review general is, therefore,bone physiology organized (e.g., into its three composition, sections, the functioning first describing and signaling general bonepathways), physiology the second (e.g., itsthe composition, implication functioningof FGF-2 in andbone signaling physiology pathways),, and the thethird second high- thelighting implication the interesting of FGF-2 characteristics in bone physiology, of FGF- and2 for thecraniofacial third highlighting bone engineering the interesting and its characteristicsvarious current of potential FGF-2 for uses craniofacial for promot boneing engineering bone repair. and its various current potential uses for promoting bone repair. 2. Background on Bone Physiology 2. Background on Bone Physiology In the skeleton, there are two types of bone differentiated by their structure—cortical In the skeleton, there are two types of bone differentiated by their structure—cortical and trabecular. Although both types have an identical chemical composition, they differ and trabecular. Although both types have an identical chemical composition, they differ both macroscopically and microscopically [4] (Appendix Figure A1). both macroscopically and microscopically [4] (AppendixA Figure A1). 2.1.2.1. BoneBone CompositionComposition BoneBone is a mineralized mineralized connective connective tissue tissue composed composed of of bone bone cells, cells, vessels, vessels, and and an anex- extracellulartracellular matrix matrix (ECM), (ECM), which which is produced is produced by th bye thebone bone cells. cells. The proportion The proportion of these of thesecomponents components varies varies with bone with type bone (long type or (long flat orbone) flat bone)and anatomical and anatomical site [5] site. The [5 miner-]. The mineralizedalized component component of bone of bonetissue tissue gives gives rigidity rigidity and andhardness hardness to the to thematerial, material, while while the theorganic organic components components of the of theECM ECM provide provide flexib flexibilityility [6].[ 6]. 2.1.1.2.1.1. Bone CellsCells TheThe osteoblast,osteoblast, aa specialized specialized bone-forming bone-forming cell, cell, mostly mostly differentiated differentiated from from mesenchy- mesen- malchymal stem stem cells cells (MSCs) (MSCs) [7,8], [7,8 produces], produce ands secretesand secrete the majors the major bone matrixbone matrix protein protein essential es- forsential matrix for mineralization,matrix mineralization, namely, typenamely, I collagen type I [collagen9,10]. These [9,10 cells]. These work cells in clusters work in on clus- the boneters on surface the bone [5], becomingsurface [5] committed, becoming tocommitted one of various to one possible of various fates, possible thanks fates, to some thanks key proteinsto some andkey pathwayproteins and signaling, pathway such signaling, as runt-related such as transcription runt-related factortranscription 2 (Runx-2) factor and 2 Osterix(Runx-2) (Figure and Os1).terix (Figure 1). FigureFigure 1.1. BoneBone remodeling regulation can be paracrine or endocrine. endocrine. Several Several factors factors participate participate in in paracrineparacrine regulationregulation includingincluding cytokinescytokines (IL-1,(IL-1, IL-6,IL-6,TNF-alpha, TNF-alpha, IL-4 IL-4 and and interferon-gamma), interferon-gamma), PGE2, PGE2, VEGF, and hypoxia, as well as bone cells. There are three main cell types involved: osteo- VEGF, and hypoxia, as well as bone cells. There are three main cell types involved: osteoblasts, blasts, osteocytes and osteoclasts. Osteoblasts, which differentiate from mesenchymal progenitors osteocytes and osteoclasts. Osteoblasts, which differentiate from mesenchymal progenitors thanks thanks to certain proteins (Runx2, Osx and Wnt) and FGF signaling pathways, are responsible for tobone certain formation. proteins They (Runx2, can also Osx become and Wnt) oste andocytes FGF able signaling to regulate pathways, osteoblastogenesis are responsible through for bonepro- formation.duction of Theyinhibitors can also(DKK become-1 and osteocytesSOST), that able inhibit to regulate Wnt signaling. osteoblastogenesis Lastly, osteoclasts, through involved production in ofbone inhibitors resorption (DKK-1 are activated and SOST), through that inhibitRANK- WntRANKL signaling.-OPG signaling Lastly, osteoclasts, pathway cross involved-talk. When- in bone resorption are activated through RANK-RANKL-OPG signaling pathway cross-talk. Whenever there Cells 2021, 10, 932 3 of
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