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Pediatric Imaging in General Radiography
Published in Christopher M. Hayre, William A. S. Cox, General Radiography, 2020
Allen Corrall, Joanna Fairhurst
Intramembranous ossification starts early in fetal life and is the process particularly responsible for plates of bone such as the bones of the skull. Endochondral ossification (replacement of cartilage ‘chondro’ by bone ‘ossify’) also usually starts in the fetus by development of the cartilaginous template from mesenchymal cells (cells that can differentiate into osteoblasts and chondrocytes). Invasion of chondroblasts helps the template grow in length and width and by the end of the process the beginnings of the medullary cavity develop. A nutrient artery forms and pierces the perichondrium (the perichondrium becomes the periosteum), and the increased blood supply stimulates perichondrium to specialize into bone cells to form a collar of bone (the periosteum). The spongy bone of the diaphysis starts to form and is eventually replaced by compact bone.
Drugs as Novel Biomaterials for Scaffolds
Published in Gilson Khang, Handbook of Intelligent Scaffolds for Tissue Engineering and Regenerative Medicine, 2017
Judee Grace E. Nemeño, Soojung Lee, Jeewon Yoon, Hun-Young Yoon, Jeong Ik Leea
Furthermore, Avastin has also been repositioned for cartilage and osteochondral regeneration in osteoarthritis as well as in rheumatoid arthritis. This repurposing strategy is grounded on the principle of endochondral ossification. In terms of the developmental process, long bones and cartilages originate from the mesenchyme that eventually forms the cartilage tissue. It is through the invasion of blood vessels (that deliver growth factors that stimulate the proliferating, hypertrophic chondrocytes) that induce the development of bone via endochondral ossification. The avascular nature of the terminal parts of the bone induced the maintenance of the cartilages which is achieved via inhibition of blood vessel formation by certain growth factors or cytokines. In this developmental process, Chondromodulin I is an antiangiogenic protein in healthy naïve cartilage which functions in maintaining the avascular nature of this tissue and Avastin as a monoclonal antibody against VEGF is believed to work like chondromodulin. Hence, this paved the way to the application of Avastin as a biomaterial in tissue engineering for further studies related to developmental biology and even its clinical application as treatment for cartilage defects.39
Principles and Biological Pathways to Tissue Regeneration: The Tissue Regenerative Niche
Published in Claudio Migliaresi, Antonella Motta, Scaffolds for Tissue Engineering, 2014
Ranieri Cancedda, Claudia Lo Sicco
Many of the molecular mechanisms and tissue differentiation profiles observed during embryonic development are repeated during the bone fracture repair. Similar to bone development, bone repair occurs through a combination of intra-membraneous and endochondral ossification. Intra-membraneous ossification involves direct formation of the bone without previous formation of the cartilage by committed osteoprogenitors and undifferentiated mesenchymal cells that reside in the periosteum. This process results in the formation of a callus within a few millimeters from the fracture site, described histologically as "hard callus." Endochondral ossification consists of recruitment, proliferation, and differentiation of undifferentiated mesenchymal cells into cartilage, which becomes calcified and eventually replaced by bone [Tsiridis et al., 2007].
The opportunity of using alloplastic bone augmentation materials in the maxillofacial region– Literature review
Published in Particulate Science and Technology, 2019
Simion Bran, Grigore Baciut, Mihaela Baciut, Ileana Mitre, Florin Onisor, Mihaela Hedesiu, Avram Manea
Endochondral ossification involves previously formed cartilage tissue which is subsequently transformed into bone. This process unfolds in five steps. At first, the mesenchymal cells are commited to become cartilage cells. A second phase contains the transformation of mesenchyme cells into chondrocytes. The third step includes the formation of a bone model by the condrocytes, which secrete a cartilage-specific extracellular matrix. Then, the chondrocytes stop dividing and increase their volume dramatically, becoming hypertrophic chondrocytes which alter the matrix they produced (by adding collagen X and more fibronectin) to enable it to become mineralized by calcium carbonate. In the last phase, the cartilage model is invaded by blood vessels and the hypertrophic chondrocytes undergo apoptosis. This previously occupied space will become bone marrow. The cartilage cells are replaced by osteoblasts that begin forming bone matrix on the partially degraded cartilage. In the end, all the cartilage is replaced by bone. The replacement of chondrocytes by bone cells takes places simultaneously with the mineralization of the extracellular matrix. Hypertrophic chondrocytes secrete numerous small vesicles into the extracellular matrix that contain enzymes that are active in the generation of calcium and phosphate ions and initiate the mineralization process within the cartilaginous matrix.(Gilbert 2000) Both intramembranous and endochondral ossification processes are guided by specific growth factors, but seem to be influenced by the cyclic tensile strain applied onto them. This might be why the bone remodels and reaches complete maturity only after functional loads are applied. (Carroll, Buckley, and Kelly 2017)
Effect of fluoride on bone and growth plate cartilage
Published in Journal of Environmental Science and Health, Part C, 2021
Mercedes Lombarte, Brenda L. Fina, Lucas R. Brun, Stella Maris Roma, Alfredo Rigalli, Di Loreto V E
Bone is a dynamic tissue that grows in length and width, and it is modeled and remodeled throughout life. These actions are important for bone mass acquisition and for the definitive morphology of the bone. The longitudinal bone growth occurs by endochondral ossification on the epiphyseal growth plate cartilage (GPC). This highly specialized dynamic structure is responsible for the bone growth, where the cartilage mineralizes and is replaced by primary trabecular bone. Subsequently, the primary bone is resorbed and replaced by secondary trabecular bone.1