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The Spontaneous Induction of Bone Formation by Intrinsically Osteoinductive Bioreactors for Human Patients
Published in Ugo Ripamonti, The Geometric Induction of Bone Formation, 2020
Prominently, activation is followed by osteoclastic activity at any given region of the trabeculae of bone; osteoclasts resorb mineralized bone and form resorption lacunae across the trabeculae; lacunae, pits, excavations along the trabeculae are simply concavities of different diameters and depths and variable radii of curvatures along the trabeculae of bone (blue arrows Figs. 7.5a,b). Osteoclastogenesis then ceases, and within the concavities, recruited osteoblastic cells are now laying newly formed osteoid, yet to be mineralized bone matrix (red arrows Figs. 7.5b,c).
Pathogenesis: Molecular mechanisms of osteoporosis
Published in Peter V. Giannoudis, Thomas A. Einhorn, Surgical and Medical Treatment of Osteoporosis, 2020
Anastasia E. Markatseli, Theodora E. Markatseli, Alexandros A. Drosos
The most important pathways in osteoclastogenesis are (a) IKK/NF-κB and (b) calcineurin/NFATc1. RANK's binding to TRAF 6 results in the activation of NF-κB and its transition to the nucleus. NF-κB induces the expression of the transcription factor c-Fos. NF-κB and c-Fos interact with NFATc1 and thus promote the transcription of genes implicated in osteoclastogenesis. NFATc1 plays a significant role in the modulation of osteoclastogenesis (170). The bisphosphorylation of calcineurin is calcium dependent and also leads to the activation of NFATc1. C-Fos and RNA polymerase II contribute to the increase of the NFATc1 activation (171) (Figure 2.2b).
Infection-driven periodontal disease
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
Thomas E. Van Dyke, Mike Curtis
Osteoclastogenesis is positively regulated by RANK–RANKL signaling and negatively regulated by osteoprotegerin (OPG), a soluble decoy receptor. OPG is produced by various cells, including dendritic cells and osteoblasts, and binds to RANKL, thus preventing RANKL from interactions with its biologically active receptor RANK. A main mechanism regulating bone resorption and formation is the relative concentration of RANKL and OPG. When RANKL expression is high relative to OPG, RANKL can bind RANK on osteoclast precursors, which tips the balance to favor activation of osteoclast formation and bone resorption; whereas when OPG levels are higher than RANKL expression, OPG binds free RANKL inhibiting it from binding to RANK, which leads to a reduction in osteoclast formation and apoptosis of osteoclasts. In vivo studies have shown that overexpression of OPG in transgenic mice resulted in severe osteopetrosis, while osteoporosis was seen in OPG-deficient mice due to an increase in the number of osteoclasts. Furthermore, analysis of RANKL and OPG levels in gingival tissue extracts or from gingival crevicular fluid has revealed a higher RANKL/OPG ratio from diseased sites than from healthy sites. During an inflammatory response, pro-inflammatory cytokines such as IL-1 or TNF-α can induce osteoclastogenesis by increasing the expression of RANKL by T cells and B cells as well, whereas the anti-inflammatory cytokine IL-10 inhibits RANKL but enhances OPG production.
RANK pathway in cancer: underlying resistance and therapeutic approaches
Published in Journal of Chemotherapy, 2023
The RANKL/RANK pathway has been linked to almost every stage of breast cancer progression, including early tumor growth and bone metastases. When BC cells, osteoblasts, osteoclasts, and the bone matrix come into contact, bone metastasis occurs. Metastasis of BC is due to the unique circumstances in bone tissue tumors. A nutrient-rich environment also promotes tumor cell migration and establishment in the bone. Cancer cells thrive in the bone matrix due to growth hormones and cytokines. RANKL can be produced in BC cells that migrate to the bone by the action of interleukin (IL)-6, IL-8, TGF-, prostaglandin E, or PTHrP. Growth factors and cytokines can be released when the bone matrix is broken down. This is known as osteoclastogenesis. As a result of this phenomenon, RANKL production rises. CXCR4/12, which is also activated by high levels of bone tissue RANKL, allows BC cells to migrate into and metastasize to bones, spreading throughout the body [8].
Enamel matrix derivative does not affect osteoclast formation or bone resorption in cultures of mouse bone marrow macrophages or human monocytes
Published in Acta Odontologica Scandinavica, 2022
Susanne Lindquist, Catrine Isehed, Anita Lie, Pernilla Lundberg
In conclusion, our present results show that the addition of EMD, with or without RANKL, to osteoclast precursor cells cultured on bone substrate did not affect osteoclastogenesis or bone resorption. However, previous studies have shown that EMD increases the RANKL/OPG ratio, and enhances osteoclast formation in crude BMC cultures [14,15]. Overall, the previous ex vivo [14,15] and clinical studies [2,16,17] indicate that EMD likely plays a dual function as a supplement in the surgical treatment of periodontitis and peri-implantitis – partly stimulating bone formation, but also increasing osteoclastogenesis and bone resorption [23]. Our present results neither confirm nor contradict this possible dual function, but rather contribute to our present understanding of the mechanism by excluding a direct interaction between EMD and osteoclast precursor cells.
Coexistence of Candida albicans and Enterococcus faecalis increases biofilm virulence and periapical lesions in rats
Published in Biofouling, 2021
Qian Du, Shasha Yuan, Shuangyuan Zhao, Di Fu, Yifei Chen, Yuan Zhou, Yangpei Cao, Yuan Gao, Xin Xu, Xuedong Zhou, Jinzhi He
Consistent with the in vitro microbiological findings, the current study further demonstrated that the co-infection of E. faecalis and C. albicans caused more severe local inflammation and bone resorption in the PTED rat model than the mono-infection model. It might be a result of the difference in the size of the bacterial population in these in vitro biofilm models. It has been reported that E. faecalis can promote TNF-α expression in macrophages at the gene and protein levels. TNF-α is an important pro-inflammatory cytokine and immunoregulatory factor, which causes bone destruction in the periapical region by promoting osteoclastogenesis and inhibiting osteoblast formation (Zhao 2017). IL-6 is major protein with osteoclast activating activity, leading to a high level of the bone resorption (Azuma et al. 2014). The elevated expression of TNF-α and IL-6 suggested that co-colonization of C. albicans and E. faecalis can promote the secretion of inflammation-related factors, and ultimately promote the development of PTED.