China
Africa
Explore chapters and articles related to this topic
Craniofacial Regeneration—Bone
Published in Vincenzo Guarino, Marco Antonio Alvarez-Pérez, Current Advances in Oral and Craniofacial Tissue Engineering, 2020
Laura Guadalupe Hernandez, Lucia Pérez Sánchez, Rafael Hernández González, Janeth Serrano-Bello
Bone is a richly vascularized connective tissue, the process of neovascularization plays a significant role in the process of bone development (endochondral and intramembranous ossification), regeneration and remodeling, which involves both angiogenesis and vasculogenesis (Fishero et al. 2014; Filipowska et al. 2017).
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.
The skeleton and muscles
Published in Frank J. Dye, Human Life Before Birth, 2019
The initiation of intramembranous ossification occurs when specific mesenchymal cells called osteoblasts begin to secrete a specific extracellular matrix. This matrix, together with an enzyme, alkaline phosphatase, causes deposits of calcium phosphate crystals to form, resulting in the formation of bone.
Comparison of the Bone Regenerative Capacity of Three-Dimensional Uncalcined and Unsintered Hydroxyapatite/Poly-d /l -Lactide and Beta-Tricalcium Phosphate Used as Bone Graft Substitutes
Published in Journal of Investigative Surgery, 2021
Yunpeng Bai, Jingjing Sha, Takahiro Kanno, Kenichi Miyamoto, Katsumi Hideshima, Yumi Matsuzaki
The human OCN gene encodes bone γ-carboxyglutamic acid protein, a secreted protein produced primarily by osteoblasts [39]. Consequently, OCN is routinely used as a serum marker of well-differentiated osteoblastic bone formation and is thought to regulate mineralization within the bone matrix. During the bone-defect healing period, calcium granules first expand into the fracture containing callus chondrocytes and are then transported into the extracellular matrix (ECM), where they form the initial mineral deposits with phosphate [40]. During this process, soft callus is transformed into hard callus; generally, the peak of hard callus formation is reached by 14 days in animal models. This change can be defined not only by the histomorphometry of mineralized tissue but also by the detection of ECM markers such as OCN, type I procollagen, alkaline phosphatase, and osteonectin [30]. OCN is also considered an osteoblast-specific gene that is expressed during ossification, along with master transcriptional factors such as Runx2 and Osterix [41, 42]. During embryonic and postnatal bone development and fracture healing, intramembranous ossification consists mainly of osteogenic mesenchymal condensation and direct differentiation into osteoblasts, eventually producing bone [43, 44]. By contrast, the process of endochondral ossification is characterized not only by the differentiation of chondrocytes by mesenchymal condensation to form a cartilaginous template that is eventually replaced with bone but also by osteoblast cells that sometimes participate to form the bone collar, which subsequently becomes cortical bone [43].
In vivo characterization of carbon dots–bone interactions: toward the development of bone-specific nanocarriers for drug delivery
Published in Drug Delivery, 2021
Rachel DuMez, Esmail H. Miyanji, Lesly Corado-Santiago, Bryle Barrameda, Yiqun Zhou, Sajini D. Hettiarachchi, Roger M. Leblanc, Isaac Skromne
Zebrafish provides a robust, in vivo model to test C-dots’ interaction with biological tissues, as their transparency allows direct observation of C-dots’ photoluminescence. Importantly, bone formation and maintenance in zebrafish are remarkably similar to that of other vertebrates (Witten et al., 2017; Busse et al., 2020; Tonelli et al., 2020). During embryogenesis in fish, birds, and mammals, bones develop either through the direct aggregation of bone-forming cells (intramembranous ossification; e.g. cranial bones) or through the deposition of a mineral matrix on a collagen scaffold (endochondral ossification; e.g. long bones) (Salhotra et al., 2020). Once formed, adult bones undergo homeostatic turnover and can continue to increase in diameter through the process of appositional growth, whereby new mineralized tissue is added to the bone’s surface (Rauch, 2005; Suniaga et al., 2018; Salhotra et al., 2020). These appositional growth and remodeling processes are carried out in zebrafish by similar skeletal cells and ossification mechanisms that have been observed in mammals (Busse et al., 2020; Tonelli et al., 2020). In addition, zebrafish can rapidly regenerate caudal fin tissue, including bony fin-rays, in less than 6 days (Busse et al., 2020; Tonelli et al., 2020). This remarkable regenerative capacity, together with transparency and thinness, makes the caudal fin of the adult zebrafish an excellent model to study bone homeostasis, repair, and regeneration.
The Efficacy of Recombinant Platelet-Derived Growth Factor on Beta-Tricalcium Phosphate to Regenerate Femoral Critical Sized Segmental Defects: Longitudinal In Vivo Micro-CT Study in a Rat Model
Published in Journal of Investigative Surgery, 2020
Mohammed Badwelan, Mohammed Alkindi, Sundar Ramalingam, Nasser Nooh, Khalid Al Hezaimi
Platelet derived growth factor (PDGF) is a potent mitogen and chemoattractant for mesenchymal and osteogenic cells and stimulates angiogenic molecules which play an essential role in bone regeneration [11]. Although several isoforms of recombinant PDGF (AA, AB, BB, CC, and DD) have been reported to be released from platelets following tissue injury, PDGF-BB is considered capable of binding with all known receptor isotypes and possesses profound physiological functions [12, 13]. Preclinical studies in animals have reported the ability of PDGF, when used alone, to increase the rate of fracture repair [14] and induce new bone formation when injected subperiosteally [15]. Similarly, PDGF used in combination with mineralized bone allografts and xenografts, within calvarial and dental alveolar ridge bone defects, has been reported to form significant volumes of new bone both in animal and clinical studies [16, 17]. Based on a clinical study, Nevins and Reynolds [18] reported better bone augmentation around dental implant sites when using a combination of PDGF with beta-TCP. Nevertheless, new bone formation around dental implant sites at best mimics intramembranous ossification and is not comparable to bone regeneration within segmental defects, which occurs through endochondral ossification [19, 20].