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Letteratura scientifica selezionata sul tema "Bone resorption – Molecular aspects"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 1 febbraio 2022

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Articoli di riviste sul tema "Bone resorption – Molecular aspects"

Gao, Yongguang, Suryaji Patil e Jingxian Jia. "The Development of Molecular Biology of Osteoporosis". International Journal of Molecular Sciences 22, n. 15 (30 luglio 2021): 8182. http://dx.doi.org/10.3390/ijms22158182.

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Osteoporosis is one of the major bone disorders that affects both women and men, and causes bone deterioration and bone strength. Bone remodeling maintains bone mass and mineral homeostasis through the balanced action of osteoblasts and osteoclasts, which are responsible for bone formation and bone resorption, respectively. The imbalance in bone remodeling is known to be the main cause of osteoporosis. The imbalance can be the result of the action of various molecules produced by one bone cell that acts on other bone cells and influence cell activity. The understanding of the effect of these molecules on bone can help identify new targets and therapeutics to prevent and treat bone disorders. In this article, we have focused on molecules that are produced by osteoblasts, osteocytes, and osteoclasts and their mechanism of action on these cells. We have also summarized the different pharmacological osteoporosis treatments that target different molecular aspects of these bone cells to minimize osteoporosis.

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Asmah, Nur. "Molecular aspects of Enterococcus faecalis virulence". Journal of Syiah Kuala Dentistry Society 5, n. 2 (15 febbraio 2021): 89–94. http://dx.doi.org/10.24815/jds.v5i2.20020.

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The Enterococcus faecalis (E. Faecalis) virulence factor plays an essential role in the persistence of root canal infection. Virulence factors of Enterococcus faecalis such as lipoteichoic acid, extracellular superoxide, gelatinase, hyaluronidase, and cytolysin are known to increase the ability of Enterococcus faecalis to induce inflammatory processes, colonization formation, and increase resistance. The virulence factor of E. faecalis is mediated by LTA, which has pattern recognition receptors for cytokine release, bone resorption and triggers apoptosis of osteoblasts, osteoclasts, periodontal connective tissue, macrophages, and neutrophils, which have implications for the occurrence of periradicular lesions. Lipoteichoic acid is also involved in producing D-alanine, which stimulates signals to other bacteria to form biofilms. The E. faecalis will change the balance of oxygen radical production in the periapical lesion, fragment collagen. The fight host's defense mechanisms that cause periapical damage and worsening bone loss. Furthermore, cytolysin will respond to changes in oxygen conditions in the depleting root canals for the dominance of E. faecalis against other bacteria. The energy needs of E. faecalis that assisted by hyaluronidase, which degrades hyaluronan dentin. İt has to produce disaccharide degradation products that can be transported and metabolized intracellularly. These materials hydrolyzing the substrate to obtain essential carbon for its growth. This article aims to describe the molecular aspect of E. faecalis virulence that is involved in root canal infections.

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Marini, Francesca, Francesca Giusti, Teresa Iantomasi e Maria Luisa Brandi. "Congenital Metabolic Bone Disorders as a Cause of Bone Fragility". International Journal of Molecular Sciences 22, n. 19 (24 settembre 2021): 10281. http://dx.doi.org/10.3390/ijms221910281.

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Bone fragility is a pathological condition caused by altered homeostasis of the mineralized bone mass with deterioration of the microarchitecture of the bone tissue, which results in a reduction of bone strength and an increased risk of fracture, even in the absence of high-impact trauma. The most common cause of bone fragility is primary osteoporosis in the elderly. However, bone fragility can manifest at any age, within the context of a wide spectrum of congenital rare bone metabolic diseases in which the inherited genetic defect alters correct bone modeling and remodeling at different points and aspects of bone synthesis and/or bone resorption, leading to defective bone tissue highly prone to long bone bowing, stress fractures and pseudofractures, and/or fragility fractures. To date, over 100 different Mendelian-inherited metabolic bone disorders have been identified and included in the OMIM database, associated with germinal heterozygote, compound heterozygote, or homozygote mutations, affecting over 80 different genes involved in the regulation of bone and mineral metabolism. This manuscript reviews clinical bone phenotypes, and the associated bone fragility in rare congenital metabolic bone disorders, following a disease taxonomic classification based on deranged bone metabolic activity.

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Driessler, Frank, e Paul A. Baldock. "Hypothalamic regulation of bone". Journal of Molecular Endocrinology 45, n. 4 (26 luglio 2010): 175–81. http://dx.doi.org/10.1677/jme-10-0015.

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On initial inspection, bone remodeling, the process whereby the skeleton adapts through time, appears to be relatively simple. Two cell types, the bone-forming osteoblasts and the bone-resorbing osteoclasts, interact to keep bone mass relatively stable throughout adult life. However, the complexity of the regulatory influences on these cells is continuing to expand our understanding of the intricacy of skeletal physiology and also the interactions between other organ systems and bone. One such example of the broadening of understanding in this field has occurred in the last decade with study of the central, neural regulation of bone mass. Initial studies of an adipose-derived hormone, leptin, helped define a direct, sympathetic pathway involving efferent neural signals from the hypothalamus to receptors on the osteoblast. Since the leptin-mediated pathway has been continuously modified to reveal a complex system involving neuromedin U, cocaine- and amphetamine-related transcript and serotonin interacting within the hypothalamus and brainstem to regulate both bone formation and resorption in cancellous bone, a number of other systems have also been identified. Neuropeptide Y, acting through hypothalamic Y2 receptors, is capable of skeleton-wide modulation of osteoblast activity, with important coordination between body weight and bone mass. Cannabinoids, acting through central cannabinoid receptor 1 and bone cell cannabinoid receptor 2 receptors, modulate osteoclast activity, thereby identifying pathways active on both aspects of the bone remodeling process. This review explores the key central pathways to bone and explores the complexity of the interactions being revealed by this emergent field of research.

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Leightner, Amanda C., Carina Mello Guimaraes Meyers, Michael D. Evans, Kim C. Mansky, Rajaram Gopalakrishnan e Eric D. Jensen. "Regulation of Osteoclast Differentiation at Multiple Stages by Protein Kinase D Family Kinases". International Journal of Molecular Sciences 21, n. 3 (5 febbraio 2020): 1056. http://dx.doi.org/10.3390/ijms21031056.

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Balanced osteoclast and osteoblast activity is necessary for skeletal health, whereas unbalanced osteoclast activity causes bone loss in many skeletal conditions. A better understanding of pathways that regulate osteoclast differentiation and activity is necessary for the development of new therapies to better manage bone resorption. The roles of Protein Kinase D (PKD) family of serine/threonine kinases in osteoclasts have not been well characterized. In this study we use immunofluorescence analysis to reveal that PKD2 and PKD3, the isoforms expressed in osteoclasts, are found in the nucleus and cytoplasm, the mitotic spindle and midbody, and in association with the actin belt. We show that PKD inhibitors CRT0066101 and CID755673 inhibit several distinct aspects of osteoclast formation. Treating bone marrow macrophages with lower doses of the PKD inhibitors had little effect on M-CSF + RANKL-dependent induction into committed osteoclast precursors, but inhibited their motility and subsequent differentiation into multinucleated mature osteoclasts, whereas higher doses of the PKD inhibitors induced apoptosis of the preosteoclasts. Treating post-fusion multinucleated osteoclasts with the inhibitors disrupted the osteoclast actin belts and impaired their resorptive activity. In conclusion, these data implicate PKD kinases as positive regulators of osteoclasts, which are essential for multiple distinct processes throughout their formation and function.

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Berardi, S., A. Corrado, N. Maruotti, D. Cici e F. P. Cantatore. "Osteoblast role in the pathogenesis of rheumatoid arthritis". Molecular Biology Reports 48, n. 3 (marzo 2021): 2843–52. http://dx.doi.org/10.1007/s11033-021-06288-y.

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AbstractIn the pathogenesis of several rheumatic diseases, such as rheumatoid arthritis, spondyloarthritis, osteoarthritis, osteoporosis, alterations in osteoblast growth, differentiation and activity play a role. In particular, in rheumatoid arthritis bone homeostasis is perturbed: in addition to stimulating the pathologic bone resorption process performed by osteoclasts in course of rheumatoid arthritis, proinflammatory cytokines (such as Tumor Necrosis factor-α, Interleukin-1) can also inhibit osteoblast differentiation and function, resulting in net bone loss. Mouse models of rheumatoid arthritis showed that complete resolution of inflammation (with maximal reduction in the expression of pro-inflammatory factors) is crucial for bone healing, performed by osteoblasts activity. In fact, abnormal activity of factors and systems involved in osteoblast function in these patients has been described. A better understanding of the pathogenic mechanisms involved in osteoblast dysregulation could contribute to explain the generalized and focal articular bone loss found in rheumatoid arthritis. Nevertheless, these aspects have not been frequently and directly evaluated in studies. This review article is focused on analysis of the current knowledge about the role of osteoblast dysregulation occurring in rheumatoid arthritis: a better knowledge of these mechanisms could contribute to the realization of new therapeutic strategies.

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Kajarabille, Naroa, Javier Díaz-Castro, Silvia Hijano, Magdalena López-Frías, Inmaculada López-Aliaga e Julio J. Ochoa. "A New Insight to Bone Turnover: Role of -3 Polyunsaturated Fatty Acids". Scientific World Journal 2013 (2013): 1–16. http://dx.doi.org/10.1155/2013/589641.

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Background. Evidence has shown that long-chain polyunsaturated fatty acids (LCPUFA), especially theω-3 fatty acids such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are beneficial for bone health and turnover.Objectives. This review summarizes findings from bothin vivoandin vitrostudies and the effects of LC PUFA on bone metabolism, as well as the relationship with the oxidative stress, the inflammatory process, and obesity.Results. Some studies in humans indicate that LCPUFA can increase bone formation, affect peak bone mass in adolescents, and reduce bone loss. However, the cellular mechanisms of action of the LCPUFA are complex and involve modulation of fatty acid metabolites such as prostaglandins, resolvins and protectins, several signaling pathways, cytokines, and growth factors, although in certain aspects there is still some controversy. LCPUFA affect receptor activator of nuclear factorκβ(RANK), a receptor found on the osteoclast, causing bone resorption, which controls osteoclast formation.Conclusions. Since fatty acids are an endogenous source of reactive oxygen species, free radicals alter the process of bone turnover; however, although there are clinical evidences linking bone metabolism and dietary lipids, more clinical trials are necessary to prove whetherω-3 PUFA supplementation plays a major role in bone health.

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Lin, Peiya, Hiromi Niimi, Yujin Ohsugi, Yosuke Tsuchiya, Tsuyoshi Shimohira, Keiji Komatsu, Anhao Liu et al. "Application of Ligature-Induced Periodontitis in Mice to Explore the Molecular Mechanism of Periodontal Disease". International Journal of Molecular Sciences 22, n. 16 (18 agosto 2021): 8900. http://dx.doi.org/10.3390/ijms22168900.

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Periodontitis is an inflammatory disease characterized by the destruction of the periodontium. In the last decade, a new murine model of periodontitis has been widely used to simulate alveolar bone resorption and periodontal soft tissue destruction by ligation. Typically, 3-0 to 9-0 silks are selected for ligation around the molars in mice, and significant bone loss and inflammatory infiltration are observed within a week. The ligature-maintained period can vary according to specific aims. We reviewed the findings on the interaction of systemic diseases with periodontitis, periodontal tissue destruction, the immunological and bacteriological responses, and new treatments. In these studies, the activation of osteoclasts, upregulation of pro-inflammatory factors, and excessive immune response have been considered as major factors in periodontal disruption. Multiple genes identified in periodontal tissues partly reflect the complexity of the pathogenesis of periodontitis. The effects of novel treatment methods on periodontitis have also been evaluated in a ligature-induced periodontitis model in mice. This model cannot completely represent all aspects of periodontitis in humans but is considered an effective method for the exploration of its mechanisms. Through this review, we aimed to provide evidence and enlightenment for future studies planning to use this model.

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Kaur, Malkiet, Manju Nagpal e Manjinder Singh. "Osteoblast-n-Osteoclast: Making Headway to Osteoporosis Treatment". Current Drug Targets 21, n. 16 (14 dicembre 2020): 1640–51. http://dx.doi.org/10.2174/1389450121666200731173522.

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Background: Bone is a dynamic tissue that continuously undergoes the modeling and remodeling process to maintain its strength and firmness. Bone remodeling is determined by the functioning of osteoblast and osteoclast cells. The imbalance between the functioning of osteoclast and osteoblast cells leads to osteoporosis. Osteoporosis is divided into primary and secondary osteoporosis. Generally, osteoporosis is diagnosed by measuring bone mineral density (BMD) and various osteoblast and osteoclast cell markers. Methods: Relevant literature reports have been studied and data has been collected using various search engines like google scholar, scihub, sciencedirect, pubmed, etc. A thorough understanding of the mechanism of bone targeting strategies has been discussed and related literature has been studied and compiled. Results: Bone remodeling process has been described in detail including various approaches for targeting bone. Several bone targeting moieties have been stated in detail along with their mechanisms. Targeting of osteoclasts and osteoblasts using various nanocarriers has been discussed in separate sections. The toxicity issues or Biosafety related to the use of nanomaterials have been covered. Conclusion: The treatment of osteoporosis targets the inhibition of bone resorption and the use of agents that promote bone mineralization to slow disease progression. Current osteoporosis therapy involves the use of targeting moieties such as bisphosphonates and tetracyclines for targeting various drugs. Nanotechnology has been used for targeting various drug molecules such as RANKLinhibitors, parathyroid hormone analogues, estrogen agonists and antagonists, Wnt signaling enhancer and calcitonin specifically to bone tissue (osteoclast and osteoblasts). So, a multicomponent treatment strategy targeting both the bone cells will be more effective rather than targeting only osteoclasts and it will be a potential area of research in bone targeting used to treat osteoporosis. The first section of the review article covers various aspects of bone targeting. Another section comprises details of various targeting moieties such as bisphosphonates, tetracyclines; and various nanocarriers developed to target osteoclast and osteoblast cells and summarized data on in vivo models has been used for assessment of bone targeting, drawbacks of current strategies and future perspectives.

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Gatti, Martina, Francesca Beretti, Manuela Zavatti, Emma Bertucci, Soraia Ribeiro Luz, Carla Palumbo e Tullia Maraldi. "Amniotic Fluid Stem Cell-Derived Extracellular Vesicles Counteract Steroid-Induced Osteoporosis In Vitro". International Journal of Molecular Sciences 22, n. 1 (22 dicembre 2020): 38. http://dx.doi.org/10.3390/ijms22010038.

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Background—Osteoporosis is characterized by defects in both quality and quantity of bone tissue, which imply high susceptibility to fractures with limitations of autonomy. Current therapies for osteoporosis are mostly concentrated on how to inhibit bone resorption but give serious adverse effects. Therefore, more effective and safer therapies are needed that even encourage bone formation. Here we examined the effect of extracellular vesicles secreted by human amniotic fluid stem cells (AFSC) (AFSC-EV) on a model of osteoporosis in vitro. Methods—human AFSC-EV were added to the culture medium of a human pre-osteoblast cell line (HOB) induced to differentiate, and then treated with dexamethasone as osteoporosis inducer. Aspects of differentiation and viability were assessed by immunofluorescence, Western blot, mass spectrometry, and histological assays. Since steroids induce oxidative stress, the levels of reactive oxygen species and of redox related proteins were evaluated. Results—AFSC-EV were able to ameliorate the differentiation ability of HOB both in the case of pre-osteoblasts and when the differentiation process was affected by dexamethasone. Moreover, the viability was increased and parallelly apoptotic markers were reduced. The presence of EV positively modulated the redox unbalance due to dexamethasone. Conclusion—these findings demonstrated that EV from hAFSC have the ability to recover precursor cell potential and delay local bone loss in steroid-related osteoporosis.

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Tesi sul tema "Bone resorption – Molecular aspects"

Cheng, Tak Sum. "Molecular identification and characterization of novel osteoclast V-ATPase subunits". University of Western Australia. School of Surgery and Pathology, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0068.

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[Truncated abstract] Osteoclasts are multinucleated giant cells responsible for the resorption of the mineralized bone matrix during the process of bone remodelling. During activation towards bone resorption, polarization of the osteoclast results in the formation of a unique plasma membrane, the ruffled border, the actual resorptive organelle of the osteoclast. Through this domain protons are actively pumped into the resorption lacuna creating an acidic microenvironment that favours the dissolution of the mineralized bone matrix. The polarised secretion of protons is carried out by the action of the vacuolar-type (H+)-ATPase (V-ATPase), composed of functionally and structurally distinct subunits of the V1 and V0 domains. The general structure of the V-ATPase complex is highly conserved from yeast to mammals, however, multiple isoforms for specific V-ATPase subunits do exist exhibiting differential subcellular, cellular and tissue-specific localizations. This study focuses on the molecular identification and characterization of V-ATPase accessory subunit Ac45 and the d2 isoform of the V0 domain d subunit in osteoclasts. Using the techniques of cDNA Subtractive Hybridization and DNA Micro-Array analyses respectively, the accessory subunit Ac45 and the d2 isoform of the V0 domain d subunit were identified in RAW264.7-cells derived OcLs. ... Using web-based computational predictions, two possible transmembrane domains, an N-terminus 'signal anchor' sequence and a C-terminus dilysine- like endoplasmic reticulum (ER) retention signal were identified. By confocal microscopy, EYFP-tagged e was found to localize to the perinuclear region of transfected COS-7 cells in compartments representing the ER and Golgi apparatus with some localization in late endosomal/lysosomal-like vesicles. ER truncation of e did not alter its subcellular localization but exhibited significantly weaker association with Ac45 compared to the wild-type as depicted by BRET analyses. Association with the other V0 subunits remain unaffected. This may hint at a possibility that Ac45 may play a role in the masking of the ER signal of e following it's incorporation into the V0 domain. Although no solid evidence for a role in the assembly of the mammalian VATPase have been established, subunit e still represents a potential candidate whose role in the V-ATPase complex requires further investigation. Collectively, the data presented in this thesis has provided further insight into the composition of the osteoclast V-ATPase proton pump by: 1) identifying an accessory subunit, Ac45 which shows promise as a potential candidate for the regulation and/or targeting of the V-ATPase complex in osteoclasts and truncation of its targeting signal impairs osteoclastic bone resorption; 2) identification and preliminary characterization of the d2 isoform of the V0 domain d subunit whose exact role in the V-ATPase complex and in osteoclasts remains to be determined, although its has been implicated to be essential for osteoclastic function; and 3) Preliminary characterization of subunit-e, a potential assembly factor candidate for the mammalian V-ATPase V0 domain.

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Wang, Cathy Ting-Peng. "Molecular dissection of RANKL signaling pathways in osteoclasts". University of Western Australia. School of Surgery and Pathology, 2007. http://theses.library.uwa.edu.au/adt-WU2008.0037.

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[Truncated abstract] Bone remodeling is intricately regulated by osteoclast-mediated bone resorption and osteoblast-mediated bone formation. The elevation in osteoclast number and/or activity is a major hallmark of several common pathological bone disorders including post-menopausal osteoporosis, osteoarthritis, Paget's disease, and tumour-mediated osteolysis. Receptor activator of nuclear factor kappa B ligand (RANKL) is a key cytokine for osteoclast differentiation and activation. The association of RANKL to its cognate receptor, RANK, which is expressed on osteoclast precursors and mature osteoclasts, is essential for osteoclast formation and activation. The intimate interaction between RANKL and RANK triggers the activation of a cascade of signal transduction pathways including NF-κB, NFAT, MAPK and PI3 kinase. Although osteoclast signaling pathways have been intensively studied, the precise molecules and signaling events which underlie osteoclast differentiation and function remain unclear. In order to dissect the molecular mechanism(s) regulating osteoclast differentiation and activity, this thesis herein explores the key RANKL/RANK-mediated signaling pathways. Four truncation mutants within the TNF-like domain of RANKL [(aa160-302), (aa160-268), (aa239-318) and (aa246-318)] were generated to investigate their potential binding to RANK and the activation to RANK-signal transduction pathways. All were found to differentially impair osteoclastogenesis and bone resorption as compared to the wild-type RANKL. The impaired function of the truncation mutants of RANKL on osteoclast formation and function correlates with their reduced ability to activate crucial RANK signaling including NF-κB, IκBα, ERK and JNK. Further analysis revealed that the truncation mutants of RANKL exhibited differentially affinity to RANK as observed by in vitro pull-down assays. ... It is possible that Bryostatin 1 acts via upregulation of a fusion mechanism as the RANKL-induced OCLs are morphologically enlarged, exhibiting increased nuclei number expressing high level of DC-Stamp. Furthermore, Rottlerin was shown to inhibit NF-κB activity, whereas Bryostatin 1 showed the opposing effects. Both inhibitor and activator were also found to modulate other key osteoclastic signaling pathways including NFAT and total c-SRC. These findings implicate, for the first time, Protein Kinase C delta signaling pathways in the modulation of RANKL-induced osteoclast differentiation and activity. Taken together, the studies presented in this thesis provide compelling molecular, biochemical and morphological evidence to suggest that: (1) RANKL mutants might potentially serve as peptide mimic to inhibit RANKL-induced signaling, osteoclastogenesis and bone resorption. (2) A cross talk mechanism between extracellular Ca2+ and RANKL exist to regulate on osteoclast survival. (3) TPA suppressed RANKL-induced osteoclastogenesis predominantly during the early stage of osteoclast differentiation via modulation of NF-κB. (4) Selective inhibition of Protein Kinase C signaling pathways involved in osteoclastogenesis might be a potential treatment method for osteoclast-related bone diseases. (5) Protein Kinase C delta signaling pathways play a key role in regulating osteoclast formation and function.

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Irani, Dilshad Minocher. "Role of the surface associated material of Eikenella corrodens in bone resorption associated with periodontal disease : a research thesis submitted in fulfilment of the requirements for the degree of Master of Science in Dentistry". Title page, contents and summary only, 1998. http://web4.library.adelaide.edu.au/theses/09DSM/09dsmi65.pdf.

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Tan, Jamie We-Yin. "The investigation of RANKL TNF-like core domain by truncation mutation". University of Western Australia. School of Surgery and Pathology, 2003. http://theses.library.uwa.edu.au/adt-WU2004.0032.

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Osteoclasts are multinucleated cells found exclusively in bone and are derived from the haematopoietic cells of monocytes/macrophage lineage. The cell-to-cell interaction between osteoblastic/stromal cells and osteoclast precursor cells is necessary for osteoclastogenesis. Receptor Activator of NF-κB ligand (RANKL) was identified as a membrane-bound TNF ligand family member that is the ‘master’ cytokine expressed on osteoblastic/stromal cells, which stimulate osteoclastogenesis through cell-to-cell contact with osteoclast precursors. RANKL is considered to be a factor that is necessary and sufficient for the induction of osteoclastogenesis (Lacey, et al., 1998). RANKL is a type II transmembrane cytokine of the TNF ligand superfamily and has an active TNF-like core domain at the extracellular domain. This active TNF-like core domain is thought to be the region through which it binds to it’s active receptor, RANK, for the activation of signal transduction pathways for the initiation of processes leading to osteoclastogenesis (Lacey, et al., 1998; Li, et al., 1999). It was hypothesized that any change in the active TNF-like core domain might affect the ability of RANKL binding to RANK and consequently affect the activation of signal transduction pathways and osteoclastogenesis. Hence, this thesis sought to investigate the effects of changes in the active TNF-like core domain by truncation mutation on the ability of RANKL binding to RANK and consequently affect the activation of signal transduction pathways and osteoclastogenesis. A cDNA fragment encoding the full-length TNF-like core domain of rat RANKL (rRANKL) (aa160-318) was cloned into the bacterial expression pGEX vectors and stably expressed in Eschechia coli as a fusion protein with the C-terminus of glutathione S-transferase (GST). Four mutants (aa160-302, aa160-268, aa239-318 and aa246-318) were also generated by truncation mutation in the TNF-like core domain, and cloned into the pGEX vector to produce GST-rRANKL mutants. The proteins were over-expressed and affinity purified to 95% in purity. GST-rRANKL (160-318) containing the full length TNF-like core domain was able to induced osteoclastogenesis in spleen cells in the presence of M-CSF and in RAW264.7 cells in the absence of M-CSF. It was also found to activate mature osteoclast activity in vitro, ex vivo and in vivo. It has the highest binding affinity to RANK and the greatest potency for NF-κB activation as well as the induction of osteoclastogenesis compared to the truncated mutants. Mutants generated by truncation of the TNF-like core domain revealed that the TNF-like core domain is important for the interaction with the RANK, for high binding affinity, NF-κB activation and induction of osteoclastogenesis. In general, the truncated mutants not only displayed a reduction in the binding affinity to RANK, but also a reduction in NF-κB activation, and significantly reduced potency in the induction of osteoclastogenesis. Interestingly, mutant GST-rRANKL (160-268) showed a higher affectivity than the other mutants did, in that it had greater binding affinity to RANK, and in NF-κB activation than the rest of the truncated mutants. Mutants GST-rRANKL (239-318) and GST-rRANKL (246-318) on the other hand, showed little potency in the induction of osteoclast formation, however, might have an inhibitory effect through competition with full length GST-rRANKL (160-318) as well as inducing a response in vivo resulting in an increase in the serum calcium level. In conclusion, this thesis demonstrated that the TNF-like core domain of RANKL is active, and imperative in the binding to RANK, activating signal transduction pathways and induction of osteoclastogenesis. Changes in the active TNF-like core domain affected the ability, affinity and efficiency of RANKL binding to the receptor, RANK and consequently affected the activation of signal transduction pathways and osteoclastogenesis.

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Hou, Peng. "Matrix metalloproteinases in the osteoclast, with special emphasis on the molecular cloning and the functional role of matrix metalloproteinase-12". Thesis, University of Sheffield, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287350.

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Peng, Songlin, e 彭松林. "Investigation of the cellular and molecular mechanisms for the dual effect of strontium on bone". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B45585167.

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Tkachenko, Evgeniy. "Measures of Individual Resorption Cavities in Three-Dimensional Images in Cancellous Bone". Case Western Reserve University School of Graduate Studies / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=case1301413780.

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Burger, Nicolaas Daniel Lombard. "Failure analysis of ultra-high molecular weight polyethyelene acetabular cups". Pretoria : [s.n.], 2005. http://upetd.up.ac.za/thesis/available/etd-12142006-134036.

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Mbimba, Thomas S. Jr. "TRAFICKING PROTEIN PARTICLE COMPLEX (TRAPPC) -9:A NOVEL PROTEIN REGULATOR OF NF-kB MEDIATED BONE FORMATION AND RESORPTION". Kent State University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=kent1448841594.

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Cheng, Yin-wo, e 鄭燕和. "Molecular basis for the increased osteoblast activity in a mouse modelwith hyperostosis". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B34612981.

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Libri sul tema "Bone resorption – Molecular aspects"

Wackym, Phillip A. Molecular temporal bone pathology, parts III and IV. Philadelphia, PA: Lippincott-Raven, 1998.

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Raisz, Lawrence G. (Lawrence Gideon), 1925-, Martin T. John e ScienceDirect (Online service), a cura di. Principles of bone biology. 3^a ed. Amsterdam: Elsevier, 2008.

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Rosen, Vicki. The cellular and molecular basis of bone formation and repair. New York: Springer, 1995.

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1957-, Thies Robert Scott, a cura di. The cellular and molecular basis of bone formation and repair. Austin: R.G. Landes, 1995.

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Dietz, Georg. Calcium hydroxide and bone regeneration: Odontological aspects of induced osteogenesis in experiment and clinical practice. München: G. Dietz, 1998.

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Cardew, Gail. The molecular basis of skeletogenesis. Chichester: Wiley, 2001.

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(Foreword), G. A. Rodan, Felix Bronner (Editor) e Mary C. Farach-Carson (Editor), a cura di. Bone Formation (Topics in Bone Biology). Springer, 2003.

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Gurmit, Singh, e Orr F. William, a cura di. Bone metastasis and molecular mechanisms: Pathophysiology. Dordrecht: Kluwer Academic, 2004.

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Orr, William, e Gurmit Singh. Bone Metastasis and Molecular Mechanisms: Pathophysiology. Springer-Verlag New York Inc., 2004.

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Singh, Gurmit. Bone Metastasis and Molecular Mechanisms: Pathophysiology. Springer, 2010.

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Capitoli di libri sul tema "Bone resorption – Molecular aspects"

Woo, Je-Tae, Yasuo Ohba, Kahori Tagami, Koji Sumitani, Kohji Yamaguchi, Tomoko Tsuji, Takao Kataoka e Kazuo Nagai. "Low Molecular Weight Microbial Metabolites that Suppress Bone Resorption by Inhibiting Vacuolar Type Proton Pump Activity of Osteoclasts". In Animal Cell Technology: Basic & Applied Aspects, 627–32. Dordrecht: Springer Netherlands, 1997. http://dx.doi.org/10.1007/978-94-011-5746-9_102.

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Russell, Graham, Gabrielle Mueller, Claire Shipman e Peter Croucher. "Clinical Disorders of Bone Resorption". In The Molecular Basis of Skeletogenesis, 251–71. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/0470846658.ch17.

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Kiyoi, Takeshi. "Bone Resorption Activity in Mature Osteoclasts". In Methods in Molecular Biology, 215–22. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8802-0_22.

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Bab, Itai A., e Jona J. Sela. "Cellular and Molecular Aspects of Bone Repair". In Principles of Bone Regeneration, 11–41. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-2059-0_2.

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Biosse-Duplan, Martin, William C. Horne e Roland Baron. "Cell and Molecular Biology of the Osteoclast and Bone Resorption". In Mineralized Tissues in Oral and Craniofacial Science, 17–27. West Sussex, UK: John Wiley & Sons, Inc.,, 2013. http://dx.doi.org/10.1002/9781118704868.ch3.

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Winston, Drew J. "Cytomegalovirus Infection in Bone Marrow Transplantation". In Molecular Aspects of Human Cytomegalovirus Diseases, 183–204. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-84850-6_11.

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Brunetti, Giacomina, Angela Oranger, Silvia Colucci e Maria Grano. "Experimental Model for Studying the Involvement of Regulatory Cytotoxic T Cells in Bone Resorption". In Methods in Molecular Biology, 269–81. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1158-5_15.

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Tsuji, Tomoko, Kohji Yamaguchi, Mika Yada, Kaoru Yamada e Daisuke Uemura. "Norzoanthamine Suppresses PTH-Stimulated IL-6 Production in Vitro and Bone Resorption in Vivo". In Animal Cell Technology: Basic & Applied Aspects, 137–41. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-011-5161-0_24.

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Dawidowska, Małgorzata. "Isolation of Mononuclear Cells from Human Blood and Bone Marrow by Density Gradient Centrifugation". In Molecular Aspects of Hematologic Malignancies, 305–8. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-29467-9_19.

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Wiren, Kristine M. "Androgen Action in Bone: Basic Cellular and Molecular Aspects". In Osteoporosis, 359–83. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-459-9_16.

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Atti di convegni sul tema "Bone resorption – Molecular aspects"

Ungur, Petru, Elisabeta Patcas, Petru A. Pop, Silviu Corbu e Florin M. Marcu. "Theoretical and Practical Aspects About Bio-Lubrication of Synovial Joints by Radioactive Molecular Treatment". In ASME 2008 9th Biennial Conference on Engineering Systems Design and Analysis. ASMEDC, 2008. http://dx.doi.org/10.1115/esda2008-59160.

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Abstract (sommario):

The paper has presented the result of tests and researches realized at our university and Oncology Clinical Hospital from Oradea, Radiotherapy Section, about improving of biolubrication between cartilages in relative moving of synovial joints with osteoarthritis, having slow evolution under non-conventional treatment of irradiation with gamma ray. By radioactive molecular treatment of synovial joints with gamma ray, type hinge of knee and spheres of disorder hip (gon-arthrosis and cox-arthrosis), changed molecular structures of porous cartilages and of synovial fluid in contact. All these due to partial recovering of mechanical-elastic and damper system that was spoiling, with a great reducer of pains, altering some orthopedic and non-conventional treatments at overweight patients, which are been impossible by surgery. This paper has presented a theoretical model of human body subjected the applied and conjunction forces, which explained the damping of vibrations and shocks inside of synovial joints by elastic modulus-E of bone cartilages in contact and variation of dynamic viscosity-η of synovial fluid. This work had proposed to promoted osteoarthritis therapy by using irradiation with gamma ray, being ones of the most modern active molecular treatments by using irradiation with particles in radiotherapy from neurological field.

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Hauert, R. "A Review of DLC Coatings for Biological Applications". In World Tribology Congress III. ASMEDC, 2005. http://dx.doi.org/10.1115/wtc2005-63879.

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Diamond-like carbon (DLC) is a class of materials with outstanding mechanical, tribological and biological properties. From in-vitro experiments, it is known that by incorporating other elements into the DLC film, the ratios of the different proteins adsorbed on the surface can be changed. These proteins will then subsequently control cell attachment, cell proliferation and cell differentiation. In a total hip joint replacement, the metallic femoral head, which slides against a polyethylene pan, causes polymeric wear debris. These wear particles may then trigger inflammatory reactions, resulting in osteolysis (bone resorption) and subsequent implant loosening. DLC has proven its outstanding tribological properties in many technical applications, mainly due to the build up of a transfer layer on the counterpart. DLC coated load bearing implants sliding against ultra high molecular weight polyethylene (UHMWPE) have been investigated. The different in-vitro experiments apparently showed contradicting results, mainly due to the different experimental setups and especially the different liquids used as lubricants. The synovial fluid present in a biological joint, contains large organic molecules which function as a boundary lubricants. Phospholipids, proteoglycans or proteins can be chemisorbed on the joint surfaces and trap water molecules, resulting in water acting as a viscose lubricant. When a DLC coated femoral head is tested against a polyethylene pan in a hip joint simulator, using synovial fluid as a lubricant, the build up of a transfer layer, protecting the softer counterpart (i.e. the polymer) does not seem to take place and the UHMWPE counterpart still shows wear. However, when DLC slides against DLC in medical applications, the build up of a transfer layer may not be a critical issue or is not drastically altered by the presence of proteins, and very low wear rates could be obtained in different in-vitro tests. Additionally, DLC coatings have an excellent haemocompatibility, which is expressed in a decreased thrombus formation. When exposed to blood, an increased ratio of albumin to fibrinogen adsorption, as well as decreased blood platelet activation is observed on coated surfaces. A few DLC coated cardiovascular implants such as artificial heart valves, blood pumps and stents are already commercially available. When coating a metal with DLC, good adhesion is obtained due to the about one nanometer thick metal-carbide reaction layer at the DLC/substrate interface. Upon implantation, it has to be guaranteed that this reaction layer is also chemically long-term stable under in-vivo conditions.

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