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Physiological aspects of blastema formation in mice
Published in David M. Gardiner, Regenerative Engineering and Developmental Biology, 2017
A second remarkable effect of HBO treatment on digit regeneration is an enhancement of bone degradation during the pre-blastema phase of regeneration (Sammarco et al. 2014, 2015). Bone degradation is an extreme example of tissue histolysis that remodels the amputation wound before blastema formation. It is reasonable to assume that all tissues involved in the regenerative response undergo some form of histolysis to establish a functional interface between the mature tissues of the stump and the newly developing tissues of the regenerate. Bone degradation involves the activity of highly specialized multinucleated cells called osteoclasts, which are derived from monocytes and attack mineralized bone. Osteoclasts attach to bone and create a focal resorptive compartment that establishes an acidic microenvironment that releases bone minerals and exposes the organic matrix of the bone for proteolytic digestion by cathepsin K, an acid protease secreted by osteoclasts. The activity of osteoclasts has been studied in the context of normal and abnormal bone turnovers, particularly in the context of bone diseases such as osteoporosis and osteopetrosis (Charles and Aliprantis 2014). During normal bone turnover, osteoclast degradation of bone is coupled with the formation of new bone tissue by osteoblasts; thus, these two cell types interact to coordinate the progressive resorption and laying down of new bone tissue in adults. Osteoclastogenesis is regulated in part by the activation of the RANK cell surface receptor (receptor activator of nuclear factor κβ) expressed by osteoclasts and its ligand, RANKL. RANK/RANKL signaling is negatively regulated by a secreted RANK decoy receptor called osteoprotegerin (OPG), which competitively binds RANKL (Honma et al. 2014).
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
The bone-cell interaction model can best be utilised to explain bone biochemistry. Osteoblasts secrete osteoprotegerin (OPG), which acts in an inhibitory capacity upon osteoclasts and ultimately prevents resorption of bone. Gradually, the osteoblast matures to become entrapped in the mineralised matrix to form an osteocyte and in the process loses its OPG secreting capacity, thereby becoming vulnerable to osteoclast-mediated resorption. It is for this reason that injured, dead or old bones undergo resorption.
Polymers for Artificial Joints
Published in Severian Dumitriu, Valentin Popa, Polymeric Biomaterials, 2020
Masayuki Kyomoto, Toru Moro, Kazuhiko Ishihara
A second important mechanism relevant to the role of macrophages in implant loosening is revealed by data demonstrating that wear particle-associated macrophages are capable of differentiating into multinucleated cells that exhibit all the phenotypic features of osteoclasts. Osteoclasts are highly specialized multinucleated cells that are uniquely capable of carrying out lacunar resorption. Osteoclasts are formed by fusion of bone marrow-derived mononuclear precursors that circulate in the monocyte fraction. A number of cellular and humoral factors are known to influence RANKL and osteoprotegerin (OPG) expression. Osteoclast formation in periprosthetic tissues can effectively be viewed as a balance between the productions of these two factors. Various cytokines and growth factors (apart from macrophage CSF) abundant in periprosthetic tissues in aseptic loosening, such as IL-1 and TNF-α, increase the OPG mRNA expression by osteoblasts, suggesting that these factors that stimulate osteoclastic bone-resorbing activity appear to act conversely to downregulate osteoclast formation. Prostaglandins such as PGE2 have also been shown to increase RANKL production and to decrease OPG release, thus stimulating osteoclast formation and bone resorption. Inflammatory cells, such as T-cells, are present in the arthroplasty membrane and may influence osteoclast differentiation and periprosthetic osteolysis by modulating RANKL expression and OPG production. Recent studies have also highlighted the role of certain cytokines (e.g., TNF-α, IL-1β, and IL-1) in inducing osteoclast formation both in the presence and absence of RANKL.
Diagnosis and management of implant debris-associated inflammation
Published in Expert Review of Medical Devices, 2020
Stuart B. Goodman, Jiri Gallo, Emmanuel Gibon, Michiaki Takagi
Osteoprotegerin (OPG) is a natural soluble decoy protein that has the ability to inhibit the Receptor Activator of NF-κB Ligand (RANKL). In a mouse calvarial model of osteolysis, Ulrich-Vinther et al. investigated a gene therapy drug using a recombinant adeno-associated virus (rAAV) to induce production of OPG in myocytes [113]. Titanium-implanted mice treated with the rAAV showed high levels of OPG and significantly decreased numbers of osteoclasts and bone resorption. Yang et al. [114] exposed implanted bone tissue, within established pouches in BALB/c mice, with UHMWPE particles. AAV encoding the human OPG gene (rAAV-hOPG) or the β galactosidase marker gene (rAAV-LacZ) was then injected into the air pouches. This resulted in significantly less mRNA expression of osteoclast markers in OPG-transduced pouches, compared with rAAV-LacZ-transduced pouches. The transduction and expression of OPG also considerably decreased the gene copies of the biologic RANK. Similar results were obtained by Kim et al. [115].
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
Osteoprotegerin (OPG) is synthesized from osteoblast and regulates remodeling of bone by inhibiting RANKL-RANK binding and osteoclast differentiation [25]. US was reported to increase osteoblasts bone-forming proteins including OPG [17]. This effect was revealed in six studies demonstrating positive outcomes.