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      Biology of Bone Formation, Fracture Healing, and Distraction Osteogenesis :

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          The biology of fracture healing.

          The biology of fracture healing is a complex biological process that follows specific regenerative patterns and involves changes in the expression of several thousand genes. Although there is still much to be learned to fully comprehend the pathways of bone regeneration, the over-all pathways of both the anatomical and biochemical events have been thoroughly investigated. These efforts have provided a general understanding of how fracture healing occurs. Following the initial trauma, bone heals by either direct intramembranous or indirect fracture healing, which consists of both intramembranous and endochondral bone formation. The most common pathway is indirect healing, since direct bone healing requires an anatomical reduction and rigidly stable conditions, commonly only obtained by open reduction and internal fixation. However, when such conditions are achieved, the direct healing cascade allows the bone structure to immediately regenerate anatomical lamellar bone and the Haversian systems without any remodelling steps necessary. In all other non-stable conditions, bone healing follows a specific biological pathway. It involves an acute inflammatory response including the production and release of several important molecules, and the recruitment of mesenchymal stem cells in order to generate a primary cartilaginous callus. This primary callus later undergoes revascularisation and calcification, and is finally remodelled to fully restore a normal bone structure. In this article we summarise the basic biology of fracture healing. Copyright © 2011 Elsevier Ltd. All rights reserved.
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            Vascular endothelial growth factor stimulates bone repair by promoting angiogenesis and bone turnover.

            Several growth factors are expressed in distinct temporal and spatial patterns during fracture repair. Of these, vascular endothelial growth factor, VEGF, is of particular interest because of its ability to induce neovascularization (angiogenesis). To determine whether VEGF is required for bone repair, we inhibited VEGF activity during secondary bone healing via a cartilage intermediate (endochondral ossification) and during direct bone repair (intramembranous ossification) in a novel mouse model. Treatment of mice with a soluble, neutralizing VEGF receptor decreased angiogenesis, bone formation, and callus mineralization in femoral fractures. Inhibition of VEGF also dramatically inhibited healing of a tibial cortical bone defect, consistent with our discovery of a direct autocrine role for VEGF in osteoblast differentiation. In separate experiments, exogenous VEGF enhanced blood vessel formation, ossification, and new bone (callus) maturation in mouse femur fractures, and promoted bony bridging of a rabbit radius segmental gap defect. Our results at specific time points during the course of healing underscore the role of VEGF in endochondral vs. intramembranous ossification, as well as skeletal development vs. bone repair. The responses to exogenous VEGF observed in two distinct model systems and species indicate that a slow-release formulation of VEGF, applied locally at the site of bone damage, may prove to be an effective therapy to promote human bone repair.
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              Current concepts of molecular aspects of bone healing.

              Fracture healing is a complex physiological process. It involves the coordinated participation of haematopoietic and immune cells within the bone marrow in conjunction with vascular and skeletal cell precursors, including mesenchymal stem cells (MSCs) that are recruited from the surrounding tissues and the circulation. Multiple factors regulate this cascade of molecular events by affecting different sites in the osteoblast and chondroblast lineage through various processes such as migration, proliferation, chemotaxis, differentiation, inhibition, and extracellular protein synthesis. An understanding of the fracture healing cellular and molecular pathways is not only critical for the future advancement of fracture treatment, but it may also be informative to our further understanding of the mechanisms of skeletal growth and repair as well as the mechanisms of aging.
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                Author and article information

                Journal
                Journal of Craniofacial Surgery
                Journal of Craniofacial Surgery
                Ovid Technologies (Wolters Kluwer Health)
                1049-2275
                2017
                July 2017
                : 28
                : 5
                : 1380-1389
                Article
                10.1097/SCS.0000000000003625
                d49d647f-99d2-4f74-86c8-da756ac80060
                © 2017

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