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Usage of Additive Manufacturing in Customised Bone Tissue-Engineering Scaffold
Published in Harish Kumar Banga, Rajesh Kumar, Parveen Kalra, Rajendra M. Belokar, Additive Manufacturing with Medical Applications, 2023
Macrophages present in the bone marrow are responsible for giving rise to osteoclasts from their mononuclear precursor cell lineage (Figure 11.3). Upon formation, they undergo rapid maturation upon receiving stimulation from interleukin-1 & 6 along with macrophage colony-stimulating factor. After completion of the maturation process, these osteoclasts enter the circulation in a resting i.e. non-resorbing state owing to the inhibitory effects exerted by calcitonin. The signal to override this inhibitory effect is provided systemically by parathormone and by RANKL (receptor activator nuclear Rankl kappa-beta ligand) locally. Not only is RANKL secreted by cancers to form pathological bone cavities, it is also a feature of normal osteoblast secretion to upregulate bone resorption. RANKL undergoes binding to osteoclast membrane RANK receptors to facilitate resorption. To maintain a check on this process in terms of physiology, normal osteoblasts also secrete OPG which plays the role of a false ligand that acts as a competitor with RANKL to bind with the RANK receptor on the osteoclast membrane (Feng, 2005; Kostenuik, 2005; Wada, Nakashima, Hiroshi & Penninger, 2006; Xing, Schwarz & Boyce, 2005).
Bone remodeling mathematical models using advanced discretization techniques: A review
Published in J. Belinha, R.M. Natal Jorge, J.C. Reis Campos, Mário A.P. Vaz, João Manuel, R.S. Tavares, Biodental Engineering V, 2019
M.M.A. Peyroteo, J. Belinha, L.M.J.S. Dinis, R.M. Natal Jorge
Ruling both types of remodeling are a set of bone regulatory factors, such as insulin-like growth factors (IGF) I and II, transforming growth factor-β (TGF-β) superfamily, matrix metalloproteinases (MMPs), receptor activator of nuclear factor-Kb (RANK) and its cognate partner RANK ligand (RANKL), osteoprotegerin (OPG), fibroblast growth factor-2 (FGF-2) and bone morphogenetic proteins (BMPs). Among these, the RANKL/RANK/OPG system plays a key role in the control of bone resorption. When activated by RANKL, RANK causes differentiation of osteoclasts and promotes their function and survival (Cohen Jr., 2006; Teitelbaum and Ross, 2003; Xiao et al., 2016). However, OPG can bind to RANKL, preventing it from binding to RANK, which leads to an inhibition of osteoclastogenesis (Graves et al., 2011; Simonet et al., 1997). Thus, RANKL/OPG ratio expression ratio is a relevant indication of bone resorption. Regarding bone tissue formation, TGF-β is an important stimulator involved in osteoblastic differentiation and production of bone matrix (Bonewald and Dallas, 1994), as well as FGF-2 (Downey et al., 2009). Moreover, IGF I and II are responsible for controlling the number and function of osteoblasts (Cohick and Clemmons, 1993), as well as mediating the interaction between osteoblasts and osteoclasts (Mohamed, 2008).
Mechanical Control of Bone Remodeling
Published in Jiro Nagatomi, Eno Essien Ebong, Mechanobiology Handbook, 2018
Our laboratory has shown that biophysical factors generated during loading, including electrical fields, pressure, and mechanical deformation, inhibit osteoclastogenesis in vitro.44–46 In these experiments, primary murine marrow cultures were grown in the presence of 1α25-Dihydroxyvitamin D3 to stimulate osteoclast formation. Mechanical loading was applied continuously and osteoclasts, identified as multinuclear, tartrate-resistant acid phosphatase positive cells, were counted after 1 week in culture. Loading was effective when dosed during the early stages of osteoclast recruitment, essentially during the initial entry of monoblastic precursors into the osteoclast lineage.46 We found further that the mechanical inhibitory effect was not transferable via a soluble factor secreted into the medium, suggesting that either direct effects on osteoclast precursors, or on a fixed molecule necessary to osteoclast recruitment, was critical to inhibition. This fixed factor, as will be described below, was identified as Receptor activator of nuclear factor kappaB ligand (RANKL), a molecule that is displayed on the surface of bone stromal cells and osteoblasts and is necessary for osteoclastogenesis.47
Impact of occupational cadmium exposure on bone in sewage workers
Published in International Journal of Occupational and Environmental Health, 2018
Mona M Taha, Heba Mahdy-Abdallah, Eman M Shahy, Khadiga S Ibrahim, Safaa Elserougy
Osteoprotegerin (OPG) is a secreted glycoprotein that represents one of the members of the tumor necrosis factor family. It prevents receptor activator of the nuclear factor kappa B ligand (RANKL) from binding to receptor activator of the nuclear factor kappa B (RANK), thereby resulting in inhibition of osteoclast differentiation and activation [13]. It is produced by osteoblasts and plays a critical role in numerous physiological processes, especially osteoclastogenesis [14].
Prevention and repair of orthodontically induced root resorption using ultrasound: a scoping review
Published in Expert Review of Medical Devices, 2023
Mahmoud Sedky Adly, Afnan Sedky Adly, Richard Younes, Marwan El Helou, Ivan Panayotov, Frederic Cuisinier, Delphine Carayon, Elias Estephan
US was found to regulate RANK/RANKL pathway and it is well identified that RANKL is an essential factor in osteoclastogenesis. Therefore, our findings were contradictory about whether US can upregulate or down-regulate RANKL expression in relation to its effect on osteoclasts numbers and activity as it is strongly related to the required goals of each study [17,24,28,30].