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The skeleton and muscles
Published in Frank J. Dye, Human Life Before Birth, 2019
Endochondral ossification occurs when mesenchymal cells called chondrocytes aggregate and begin to secrete proteins. Cartilage is a type of connective tissue composed of these chondrocytes, their secreted extracellular matrix, and the surrounding layer of perichondrium (the fibrous connective tissue covering cartilage). This cartilage has the general shape of the bone that is to be formed (Figure 14.2).
Articular Cartilage
Published in Manoj Ramachandran, Tom Nunn, Basic Orthopaedic Sciences, 2018
Tim S. Waters, Nima Heidari, George Bentley
Type X collagen similarly forms a meshwork and is present in the calcified cartilage layer. It is associated with cartilage calcification and is produced by hypertrophied chondrocytes during endochondral ossification. It is therefore found in the physis, fracture callus, heterotopic ossification, calcifying cartilaginous tumours and osteoarthritis.
Cartilage and Craniofacial Growth
Published in D. Dixon Andrew, A.N. Hoyte David, Ronning Olli, Fundamentals of Craniofacial Growth, 2017
Olli Ronning, Heli Vinkka-Puhakka
The chondrocytes in the central part of the nasal septum of the young rat are spherical with no particular orientation, and are surrounded by a seemingly faint matrix. The cells are flattened at the peripheries and oriented perpendicular to the cartilage margin. The chondrocytes grow larger with age and the matrix becomes more dense. The peripheral orientation of the chondrocytes becomes less distinct, except rostrally where the cells assume an almost columnar distribution. Posteriorly the cells are involved in endochondral ossification (Ronning, 1971). Quantitative autoradiographic scrutiny of the cartilaginous nasal septum in the rabbit revealed that cell proliferation is most active posteriorly, in the area of endochondral ossification, and anteroinferiorly, while there was less activity in the anterosuperior and central areas. Thus, despite local differences in proliferative activity, it is the increase in the whole cellular mass that contributes to the growth of the septum (Long et al., 1968).
Epidermal growth factor signalling pathway in endochondral ossification: an evidence-based narrative review
Published in Annals of Medicine, 2022
L. Mangiavini, G. M. Peretti, B. Canciani, N. Maffulli
Bones form through two complex processes: intramembranous or endochondral ossification. During the former, mesenchymal cells directly differentiate in osteoblasts by activating the RUNX-2 pathway. This process occurs in most of the calvarial bones and in the clavicle [1]. Endochondral ossification is more complex, and it involves an initial cartilage anlage, which is then replaced by bone [1]. Mesenchymal progenitors first condensate and then start differentiating into chondrocytes. These latter cells pile up in columns, exit the cell cycle, and secrete an osteogenic matrix and pro-angiogenic factors, such as Vascular Endothelial Growth Factor (VEGF) [2,3]. Subsequently, perichondrial cells surrounding the primary cartilage anlage invade the template together with blood vessels, and they differentiate into osteoblasts, forming the primary ossification centre. Subsequently, chondrocytes form the growth plate at both ends of the primary ossification centre [4].
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].
Controlled release of celecoxib inhibits inflammation, bone cysts and osteophyte formation in a preclinical model of osteoarthritis
Published in Drug Delivery, 2018
A. R. Tellegen, I. Rudnik-Jansen, B. Pouran, H. M. de Visser, H. H. Weinans, R. E. Thomas, M. J. L. Kik, G. C. M. Grinwis, J. C. Thies, N. Woike, G. Mihov, P. J. Emans, B. P. Meij, L. B. Creemers, M. A. Tryfonidou
Prolonged local exposure to celecoxib inhibited subchondral bone changes and osteophyte formation, characteristic for OA. An increasing body of evidence points to an interplay between bone and cartilage in OA (Karsdal et al., 2008), even suggesting a key role for subchondral bone in OA development (Botter et al., 2011). Targeting bone changes may be an effective strategy to reduce symptoms and disease progression in OA, as bone marrow lesions, bone cysts, osteophytes and bone shape were associated with structural progression and pain in patients with knee OA (Tanamas et al., 2010; Barr et al., 2015). The mechanism by which CXB inhibits OA bone changes may at least partially be related to its inhibitory effect on hypertrophic differentiation (Welting et al., 2011). The process of OA at least partially recapitulates chondrocyte hypertrophic differentiation during endochondral ossification (Dreier 2010), which was also observed in the present OA model where significantly more collagen X in the degenerating cartilage was found. Notably, local delivery of CXB-PEAMs partially counteracted cartilage collagen type X deposition, while it was even more effective in slowing progression of OA-related subchondral bone changes and osteophyte formation. This is in accordance with previous reports exploring the disease-modifying effects of oral celecoxib administration (Panahifar et al., 2014).