Готові списки джерел за темами / Bone resorption

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Добірка наукової літератури з теми "Bone resorption"

Автор: Grafiati
Опубліковано: 4 червня 2021
Оновлено: 1 серпня 2024

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Статті в журналах з теми "Bone resorption"

1

Carron, CP, DM Meyer, VW Engleman, JG Rico, PG Ruminski, RL Ornberg, WF Westlin, and GA Nickols. "Peptidomimetic antagonists of alphavbeta3 inhibit bone resorption by inhibiting osteoclast bone resorptive activity, not osteoclast adhesion to bone." Journal of Endocrinology 165, no. 3 (June 1, 2000): 587–98. http://dx.doi.org/10.1677/joe.0.1650587.

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Osteoclasts are actively motile on bone surfaces and undergo alternating cycles of migration and resorption. Osteoclast interaction with the extracellular matrix plays a key role in the osteoclast resorptive process and a substantial body of evidence suggests that integrin receptors are important in osteoclast function. These integrin receptors bind to the Arg-Gly-Asp (RGD) sequence found in a variety of extracellular matrix proteins and it is well established that the interaction of osteoclast alpha v beta 3 integrin with the RGD motif within bone matrix proteins is important in osteoclast-mediated bone resorption. In this study, we characterized the effects of two synthetic peptidomimetic antagonists of alpha v beta 3, SC-56631 and SC-65811, on rabbit osteoclast adhesion to purified matrix proteins and bone, and on bone resorption in vitro. SC-56631 and SC-65811 are potent inhibitors of vitronectin binding to purified alpha v beta 3. Both SC-56631 and SC-65811 inhibited osteoclast adhesion to osteopontin- and vitronectin-coated surfaces and time-lapse video microscopy showed that osteoclasts rapidly retract from osteopontin-coated surfaces when exposed to SC-56631 and SC-65811. SC-56631 and SC-65811 blocked osteoclast-mediated bone resorption in a dose-responsive manner. Further analysis showed that SC-65811 and SC-56631 reduced the number of resorption pits produced per osteoclast and the average pit size. SC-65811 was a more potent inhibitor of bone resorption and the combination of reduced pit number and size led to a 90% inhibition of bone resorption. Surprisingly, however, osteoclasts treated with SC-65811, SC-56631 or the disintegrin echistatin, at concentrations that inhibit bone resorption did not inhibit osteoclast adhesion to bone. These results suggest that alphavbeta3 antagonists inhibited bone resorption by decreasing osteoclast bone resorptive activity or efficiency but not by inhibiting osteoclast adhesion to bone per se.
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2

Chu, Pei-Wen, Yu-Hsu Chen, Chien-Hui Chen, and Shau-Kwaun Chen. "Inflammatory environments disrupt both bone formation and bone resorption." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 224.46. http://dx.doi.org/10.4049/jimmunol.204.supp.224.46.

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Abstract Inflammation has been associated with bone diseases such as osteoporosis and osteoarthritis. Bone loss were reported in the patients of several inflammatory diseases, such as rheumatoid arthritis, systemic lupus erythematosus, inflammatory bowel disease. However, how inflammation influence bone metabolism remains elusive. The bone loss in inflammatory environments are widely considered as the results of osteoclast overactivation which leads to excessive bone resorption. We previously discovered that osteoclasts induced from RAW macrophage treated with RANKL exhibited different cell properties and gene expression profile with undifferentiated macrophage. In this research we examined the excessive bone resorption hypothesis in in vitro systems. RANKL stimulated differentiation of RAW cells into bone-resorptive osteoclasts, and induction of pre-osteoblasts (MC-3T3 E1) into mature osteoblasts are utilized in this research. Inflammatory environments are mimic by treating cultured osteoclast or osteoblast with conditioned medium collected from bone marrow derived macrophage primed with LPS or interferon-γ. The pro-inflammatory cytokines inhibit the proliferation and disrupt the expression of genes that are needed for bone formation, such as osteocalcin and collagen. On the other hand, inflammatory environments did not activate osteoclast, nor promote bone resorption. Instead, pro-inflammatory cytokines inhibit osteoclastogenesis and bone resorption, induce mitochondrial dysfunctions and lead to apoptosis of osteoclast. These results indicated that the bone loss developed in the inflammatory environments might be due to the disruption of both bone formation and bone resorption.
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3

Slootweg, M. C., W. W. Most, E. van Beek, L. P. C. Schot, S. E. Papapoulos, and C. W. G. M. Löwik. "Osteoclast formation together with interleukin-6 production in mouse long bones is increased by insulin-like growth factor-I." Journal of Endocrinology 132, no. 3 (March 1992): 433–38. http://dx.doi.org/10.1677/joe.0.1320433.

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ABSTRACT Insulin-like growth factor-I (IGF-I) is a potent stimulator of bone formation. Whether this growth factor also induces bone resorption has not been studied in detail. We used two organ culture systems to examine the direct effect of IGF-I on bone resorption. Fetal mouse radii/ulnae, containing mature osteoclasts, showed no response to IGF-I, indicating that osteoclastic activity is not influenced by IGF-I. Fetal mouse metacarpals/metatarsals, containing just osteoclast precursors and progenitors, showed an increase in resorption in response to IGF-I, indicating that IGF-I stimulates the formulation of osteoclast precursors/progenitors and thereby increases the number of osteoclasts. Interleukin-6 (IL-6) has been hypothesized to be a mediator of bone resorptive agents such as parathyroid hormone (PTH). Both radii/ulnae and metacarpals/metatarsals reacted to IGF-I with an increase in IL-6 production. IL-6 production by UMR-106 osteogenic osteosarcoma cells was positively modulated by IGF-I, indicating that osteoblasts are likely to be the cells responsible for increased IL-6 production by the bones, and that IL-6 might be a mediatory of IGF-I-stimulated bone resorption. Journal of Endocrinology (1992) 132, 433–438
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4

Chambers, T. J., and K. Fuller. "Bone cells predispose bone surfaces to resorption by exposure of mineral to osteoclastic contact." Journal of Cell Science 76, no. 1 (June 1, 1985): 155–65. http://dx.doi.org/10.1242/jcs.76.1.155.

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The cell-free endocranial surface of young adult rat parietal bones was used as a substrate for osteoclastic bone resorption, either without prior treatment, or after incubation of the parietal bones with collagenase or neonatal rat calvarial cells. Untreated, the endocranial surface consisted of unmineralized organic fibres; incubation with calvarial cells or collagenase caused disruption and removal of these fibres, with extensive exposure of bone mineral on the endocranial surface, without morphologically detectable mineral dissolution. Neonatal rabbit osteoclasts resorbed bone to a greater extent from parietal bones pre-incubated with calvarial cells or collagenase than from untreated bones; mineral exposure and subsequent osteoclastic resorption were both increased if calvarial cells were incubated with parathyroid hormone; removal of bone mineral after incubation with calvarial cells removed the predisposition to osteoclastic resorption. These experiments demonstrate that calvarial cells are capable of osteoid destruction, and indicate that one mechanism by which osteoblasts induce osteoclastic bone resorption may be through digestion of the unmineralized organic material that covers bone surfaces, to expose the underlying resorption-stimulating bone mineral to osteoclastic contact.
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5

Towhidul Alam, A. S. M., Christopher L. H. Huang, David R. Blake, and Mone Zaidi. "A hypothesis for the local control of osteoclast function by Ca2+, nitric oxide and free radicals." Bioscience Reports 12, no. 5 (October 1, 1992): 369–80. http://dx.doi.org/10.1007/bf01121500.

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Several important conclusions have recently emerged from in vitro studies on the resorptive cell of bone, the osteoclast. First, it has been established that osteoclast function is modulated locally, by changes in the local concentration of Ca2+ caused by hydroxyapatite dissolution. It is thought that activation by Ca2+ of a surface membrane Ca2+ receptor mediates these effects, hence providing a feedback control. Second, a number of molecules produced locally by the endothelial cell, with which the osteoclast is in intimate contact, have been found to affect bone resorption profoundly. For instance, the autocoid nitric oxide strongly inhibits bone resorption. Finally, reactive oxygen species have been found to aid bone resorption and enhance osteoclastic activity directly. Here, we will attempt to integrate these control mechanisms into a unified hypothesis for the local control of bone resorption.
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6

Borggaard, Xenia G., Dinisha C. Pirapaharan, Jean-Marie Delaissé, and Kent Søe. "Osteoclasts’ Ability to Generate Trenches Rather Than Pits Depends on High Levels of Active Cathepsin K and Efficient Clearance of Resorption Products." International Journal of Molecular Sciences 21, no. 16 (August 18, 2020): 5924. http://dx.doi.org/10.3390/ijms21165924.

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Until recently, it was well-accepted that osteoclasts resorb bone according to the resorption cycle model. This model is based on the assumption that osteoclasts are immobile during bone erosion, allowing the actin ring to be firmly attached and thereby provide an effective seal encircling the resorptive compartment. However, through time-lapse, it was recently documented that osteoclasts making elongated resorption cavities and trenches move across the bone surface while efficiently resorbing bone. However, it was also shown that osteoclasts making rounded cavities and pits indeed resorb bone while they are immobile. Only little is known about what distinguishes these two different resorption modes. This is of both basic and clinical interest because these resorption modes are differently sensitive to drugs and are affected by the gender as well as age of the donor. In the present manuscript we show that: 1. levels of active cathepsin K determine the switch from pit to trench mode; 2. pit and trench mode depend on clathrin-mediated endocytosis; and 3. a mechanism integrating release of resorption products and membrane/integrin recycling is required for prolongation of trench mode. Our study therefore contributes to an improved understanding of the molecular and cellular determinants for the two osteoclastic bone resorption modes.
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7

Feng, Shi, Zhiyong Zhang, Lei Shi, Xiaojun Tang, Wei Liu, Lin Yin, and Bin Yang. "Temporal Bone Resorption." Journal of Craniofacial Surgery 26, no. 2 (March 2015): e185-e187. http://dx.doi.org/10.1097/scs.0000000000001452.

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8

Taguchi, Takafumi, and Yoshio Terada. "Subperiosteal Bone Resorption." New England Journal of Medicine 370, no. 21 (May 22, 2014): e32. http://dx.doi.org/10.1056/nejmicm1308814.

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9

Aspenberg, P., and P. Herbertsson. "PERIPROSTHETIC BONE RESORPTION." Journal of Bone and Joint Surgery. British volume 78-B, no. 4 (July 1996): 641–46. http://dx.doi.org/10.1302/0301-620x.78b4.0780641.

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10

Fuller, Karen, Barrie Kirstein, and Timothy J. Chambers. "Regulation and enzymatic basis of bone resorption by human osteoclasts." Clinical Science 112, no. 11 (May 1, 2007): 567–75. http://dx.doi.org/10.1042/cs20060274.

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Although much has been learned recently of the mechanisms that regulate osteoclastic differentiation, much less is known of the means through which their resorptive activity is controlled. This is especially so for human osteoclasts. We have recently developed an assay that allows us to measure resorptive activity while minimizing confounding effects on differentiation by optimizing osteoclastogenesis, so that measurable resorption occurs over a short period, and by relating resorption in each culture during the test period to the resorption that had occurred in the same culture in a prior control period. In the present study, we found that RANKL (receptor activator of nuclear factor κB ligand) strongly stimulated the release of CTX-I (C-terminal telopeptide degradation product of type I collagen) by osteoclasts over a similar range to that over which it induces osteoclastic differentiation, consistent with a distinct action on osteoclastic function. CT (calcitonin) dose-dependently inhibited bone resorption, whereas PTH (parathyroid hormone), IL (interleukin)-1, TNF-α (tumour necrosis factor-α), IL-6, IL-8, VEGF (vascular endothelial growth factor), MCP-1 (monocyte chemoattractant protein-1), MIP-1γ (macrophage inflammatory protein-1γ), IFN (interferon)-γ and dibutyryl cGMP had no significant effect. Ca2+, cyclosporin A, IFN-β and dibutyryl cAMP all strongly suppressed resorption. Bone resorption was also strongly suppressed by alendronate, the cysteine protease inhibitor E64 and the cathepsin K inhibitor MV061194. Inhibitors of MMPs (matrix metalloproteinases) had no effect on CTX-I release. Moreover, the release of the MMP-derived collagen fragment ICTP (C-terminal cross-linked telopeptide of type I collagen) represented less that 0.01% of the quantity of CTX-I released in our cultures. This suggests that MMPs make, at most, a very small contribution to the bone-resorptive activity of osteoclasts.
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Дисертації з теми "Bone resorption"

1

Pierce, Angela Mary. "Cellular mechanisms in bone and tooth resorption morphological studies in rats and monkeys /." Stockholm : Kongl. Carolinska Medico Chirurgiska Institutet, 1988. http://books.google.com/books?id=usBpAAAAMAAJ.

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2

Heath, J. K. "Studies on cellular interactions in bone resorption." Thesis, Anglia Ruskin University, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.354876.

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McCauley, Laurie Kay. "Cellular mechanisms of lymphocyte-mediated bone resorption /." The Ohio State University, 1991. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487759055156174.

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4

Stutzer, Andre. "Retinoid induced bone resorption, model and application /." [S.l.] : [s.n.], 1987. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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Ransjö, Maria. "Regulation of bone resorption by the adenylate cyclase-cyclic AMP system a biochemical study on mouse calvarial bones and isolated bone cells /." Umeå, Sweden : University of Umeå, 1988. http://catalog.hathitrust.org/api/volumes/oclc/18171035.html.

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Bernhold, Brechter Anna. "Kinins : important regulators in inflammation induced bone resorption." Doctoral thesis, Umeå : Univ, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-959.

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7

Moroz, Adam. "Reduced order modelling of bone resorption and formation." Thesis, De Montfort University, 2011. http://hdl.handle.net/2086/5409.

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The bone remodelling process, performed by the Bone Multicellular Unit (BMU) is a key multi-hierarchically regulated process, which provides and supports various functionality of bone tissue. It is also plays a critical role in bone disorders, as well as bone tissue healing following damage. Improved modelling of bone turnover processes could play a significant role in helping to understand the underlying cause of bone disorders and thus develop more effective treatment methods. Moreover, despite extensive research in the field of bone tissue engineering, bonescaffold development is still very empirical. The development of improved methods of modelling the bone remodelling process should help to develop new implant designs which encourage rapid osteointegration. There are a number of limitations with respect to previous research in the field of mathematical modelling of the bone remodelling process, including the absence of an osteocyte loop of regulation. It is within this context that this research presented in this thesis utilises a range of modelling methods to develop a framework for bone remodelling which can be used to improve treatment methods for bone disorders. The study concentrated on dynamic and steady state variables that in perspective can be used as constraints for optimisation problem considering bone remodelling or tissue remodelling with the help of the grafts/scaffolds.The cellular and combined allosteric-regulation approaches to modelling of bone turnover, based on the osteocyte loop of regulation, have been studied. Both approaches have been studied different within wide range of rate parameters. The approach to the model validation has been considered, including a statistical approach and parameter reduction approach. From a validation perspective the cellular class of modes is preferable since it has fewer parameters to validate. The optimal control framework for regulation of remodelling has been studied. Future work in to improve the models and their application to bone scaffold design applications have been considered. The study illustrates the complexity of formalisation of the metabolic processes and the relations between hierarchical subsystems in hard tissue where a relatively small number of cells are active. Different types/modes of behaviour have been found in the study: relaxational, periodical and chaotic modes. All of these types of behaviour can be found, in bone tissue. However, a chaotic or periodic modes are ones of the hardest to verify although a number of periodical phenomena have been observed empirically in bone and skeletal development. Implementation of the allosteric loop into cellular model damps other types of behaviour/modes. In this sense it improves the robustness, predictability and control of the system. The developed models represent a first step in a hierarchical model of bone tissue (system versus local effects). The limited autonomy of any organ or tissue implies differentiation on a regulatory level as well as physiological functions and metabolic differences. Implementation into the cellular phenomenological model of allosteric-like loop of regulation has been performed. The results show that the robustness of regulation can be inherited from the phenomenological model. An attempt to correlate the main bone disorders with different modes of behaviour has been undertaken using Paget’s disorder in bone, osteoporosis and some more general skeleton disorders which lead to periodical changes in bone mass, reported by some authors. However, additional studies are needed to make this hypothesis significant. The study has revealed a few interesting techniques. When studying a multidimensional phenomenon, as a bone tissue is, the visualisation and data reduction is important for analysis and interpretation of results. In the study two novel technical methods have been proposed. The first is the graphical matrix method to visualise/project the multidimensional phase space of variables into diagonal matrix of regular combination of two-dimensional graphs. This significantly simplifies the analysis and, in principle, makes it possible to visualise the phase space higher than three-dimensional. The second important technical development is the application of the Monte-Carlo method in combination with the regression method to study the character and stability of the equilibrium points of a dynamic system. The advantage of this method is that it enables the most influential parameters that affect the character and stability of the equilibrium point to be identified from a large number of the rate parameters/constants of the dynamic system. This makes the interpretation of parameters and conceptual verification of the model much easier.
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Ljunggren, Östen. "Involvement of bradykinin in inflammation induced bone resorption." Umeå : University of Umeå, 1991. http://catalog.hathitrust.org/api/volumes/oclc/24493228.html.

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9

Korhonen, T. (Tommi). "Bone flap survival and resorption after autologous cranioplasty." Doctoral thesis, Oulun yliopisto, 2019. http://urn.fi/urn:isbn:9789526222530.

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Abstract This thesis evaluated the factors affecting bone flap survival and bone flap resorption after primary cranial reparation surgery, cranioplasty, conducted to repair a cranial bone defect with an autologous cryopreserved bone flap. Emphasis is put on the predictors, progression, and definition of an important yet poorly understood postoperative complication, bone flap resorption. Study I assessed the rates and predictors of bone flap removal and bone flap resorption in a Finnish retrospective multicentre setting. 40% of patients developed complications of whom half required bone flap removal. Bone flap resorption and surgical site infections were the underlying cause in 90% of bone flap removal surgeries. The prevalence of both surgical site infections and bone flap resorption was 9%. In summary, young age was found to predict bone flap resorption and smoking predisposed patients to infections requiring bone flap removal. Study II applied computed tomography-based volumetry to evaluate the prevalence of subclinical bone flap resorption and to monitor its progression. In the follow-up, 90% of patients were found to have decreased bone flap volumes indicating varying degrees of resorption. However, the progression of bone flap resorption as a function of follow-up time was non-linear on the cohort level, and thus routine radiological follow-up seems unjustified. Most bone flaps do not appear to resorb enough to require removal even in the long-term follow-up. Study III addressed the unclarity in the definition of bone flap resorption. The computed tomography-based Oulu Resorption Score was developed to standardise the interpretation of radiological bone flap resorption and to guide follow-up interventions. The score values range from 0 to 9 with increasing values implying more severe bone flap resorption. Coupled with radiological evaluation conducted by independent neurosurgeons, an Oulu Resorption Score of ≥5 was defined to be clinically relevant. Further, the scores were divided into four grades based on the recommended follow-up procedures. Grades 0 (score 0) and I (scores 1 to 4) require no additional follow-up, but those with a grade II (score 5 to 8) or III (score 9) should be referred to neurosurgical consultation with reoperation considered at least in cases of grade III bone flap resorption
Tiivistelmä Tässä väitöstyössä selvitettiin potilaan omalla kylmäsäilytetyllä luuistutteella tehtyjen kallon luupuutosten ensikertaisten korjausleikkausten tuloksiin vaikuttavia tekijöitä. Erityisesti tarkasteltiin luuistutteen liukenemisen, erään tärkeän, joskin heikosti ymmärretyn komplikaation ennustavia tekijöitä, etenemistä ja määritelmää. Tutkimuksessa I selvitettiin luuistutteen poiston ja liukenemisen yleisyyttä ja näihin vaikuttavia tekijöitä suomalaisessa takautuvassa monikeskusaineistossa. Potilaista 40 %:lle kehittyi komplikaatio. Komplikaatioista puolet johti istutteen poistoon. Luuistutteen liukeneminen ja leikkausalueinfektiot muodostivat 90 % poistoon johtaneista komplikaatioista. Sekä infektioiden että istutteen liukenemi¬sen esiintyvyys oli 9 %. Nuori ikä altisti istutteen liukenemiselle ja tupakointi leikkausalueinfektiolle. Tutkimuksessa II sovellettiin tietokonetomografiaan perustuvaa tilavuusmittausta luuistutteen oireettoman liukenemisen esiintyvyyden ja etenemistaipumuksen selvittämiseksi. Seurannassa 90 %:lla potilaista todettiin alentunut luuistutteen tilavuus viitaten asteeltaan vaihtelevaan istutteen liukenemiseen. Koko tutkimusjoukon tasolla istutteiden liukeneminen ei kuitenkaan edennyt lineaarisesti seuranta-ajan funktiona, joten rutiininomainen seuranta kuvantamistutkimuksin ei vaikuta perustellulta. Suurin osa luuistutteista liukeni niin vähän, ettei uutta leikkausta tarvittu pitkässäkään seurannassa. Tutkimuksessa III käsiteltiin luuistutteen liukenemisen nykyisellään epäselvää määritelmää ja kehitettiin uusi tietokonetomografiaan perustuva pisteytysjärjestelmä (Oulu resorption score) tarkoituksena vakioida radiologisten luuistutteen liukenemislöydösten tulkinta ja ohjata hoitolinjan valintaa. Pisteytysarvot vaihtelevat välillä 0-9. Kasvava arvo kuvaa luuistutteen liukenemisen vaikeusasteen kasvua. Luokitus yhdistettiin riippumattomien neurokirurgien radiologisiin arvioihin, joiden perusteella pistemäärä ≥5 määriteltiin kliinisesti merkitykselliseksi. Pistemäärät jaettiin neljään luokkaan suositeltujen jatkotoimenpiteiden mukaisesti. Luokkia 0 (0 pistettä) ja I (1–4 pistettä) vastaava luuistutteen liukeneminen ei vaadi jatkotoimenpiteitä. Luokkia II (5–8 pistettä) ja III (9 pistettä) vastaavasta luuistutteen liukenemisesta suositellaan konsultoitavan neurokirurgia. Uusintaleikkausta suositellaan harkittavan ainakin luokan III tapauksissa
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10

Neale, Susan Dorothy. "The role of macrophages in pathological bone resorption /." Title page, table of contents and abstract only, 1998. http://web4.library.adelaide.edu.au/theses/09MSM/09msmn348.pdf.

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Книги з теми "Bone resorption"

1

Bronner, Felix, Mary C. Farach-Carson, and Janet Rubin, eds. Bone Resorption. London: Springer-Verlag, 2005. http://dx.doi.org/10.1007/b136184.

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2

Felix, Bronner, Farach-Carson Mary C. 1958-, and Rubin Janet, eds. Bone resorption. London: Springer, 2005.

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3

Harvey, Wilson. Prostaglandins in bone resorption. Boca Raton, Fla: CRC Press, 1988.

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4

Pierce, Angela Mary. Cellular mechanisms in bone and tooth resorption: Morphological studies in rats and monkeys. Stockholm: Kongl. Carolinska Medico Chirurgiska Institutet, 1988.

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5

Brown, R. James. Histological and compositional responses of bone to immobilization and other experimental conditions: Semi-annual report. San Francisco, Calif: Institute of Chemical Biology, University of San Francisco, 1985.

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6

Thamsborg, Gorm. Effect of nasal salmon calcitonin on calcium and bone metabolism. København [Denmark]: Lægeforeningens Forlag, 1999.

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7

Maria, Bijvoet Olav Leonardus, ed. Bisphosphonate on bones. Amsterdam: Elsevier, 1995.

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8

Arun, Shanbhag, Rubash Harry E, and Jacobs Joshua J. 1956-, eds. Joint replacement and bone resorption: Pathology, biomaterials, and clinical practice. New York: Taylor & Francis, 2005.

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9

Åkesson, Louise. Panoramic radiography in the assessment of the marginal bone level. Malmö: Department of Oral Radiology, Faculty of Odontology, Lund University, 1991.

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10

Ljunggren, Östen. Experimental studies on bone resorption: Effects of parathyroid hormone and vitamin D. Uppsala: Univ., 1993.

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Частини книг з теми "Bone resorption"

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Griffon, Dominique. "Bone Resorption." In Complications in Small Animal Surgery, 658–64. Chichester, UK: John Wiley & Sons, Ltd, 2017. http://dx.doi.org/10.1002/9781119421344.ch97.

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Kumar, Vinay V., Supriya Ebenezer, and Andreas Thor. "Bone Augmentation Procedures in Implantology." In Oral and Maxillofacial Surgery for the Clinician, 407–26. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-15-1346-6_19.

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AbstractSuccessful implant dentistry mandates implants to be placed in an appropriate three-dimensional manner that supports the prosthesis adequately. Due to the resorption patterns of edentulous jaws, the ideal position of implants required varying amounts of bone augmentation. Commonly carried out bone-augmentation procedures are Guided Bone Regeneration, onlay bone grafting and sinus floor elevation. This chapter discusses the resorption pattern of edentulous jaws, the biology of alveolar bone of relevance to the maxillofacial surgeon, the biomaterials used for augmentation and the commonly carried out augmentation procedures.
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Zambonin Zallone, A., and G. Zambonin. "Cellular Basis of Bone Resorption." In Bone Densitometry and Osteoporosis, 83–93. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-80440-3_5.

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Caniggia, Angelo. "Pathophysiology of Bone Formation and Resorption." In Bone Regulatory Factors, 235–52. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4757-1508-8_14.

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Ross, F. Patrick. "Osteoclast Biology and Bone Resorption." In Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, 25–33. Ames, USA: John Wiley & Sons, Inc., 2013. http://dx.doi.org/10.1002/9781118453926.ch3.

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Gowen, M., B. R. MacDonald, D. E. Hughes, H. Skjodt, and R. G. G. Russell. "Immune Cells and Bone Resorption." In Phosphate and Mineral Homeostasis, 261–73. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5206-8_33.

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Russell, Graham, Gabrielle Mueller, Claire Shipman, and 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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Délaissé, J. M., P. Ledent, Y. Eeckhout, and G. Vaes. "Cysteine proteinases and bone resorption." In Cysteine Proteinases and their Inhibitors, edited by Vito Turk, 259–68. Berlin, Boston: De Gruyter, 1986. http://dx.doi.org/10.1515/9783110846836-029.

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Schett, Georg. "Bone Formation Versus Bone Resorption in Ankylosing Spondylitis." In Advances in Experimental Medicine and Biology, 114–21. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0298-6_8.

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Mundy, G. R. "Hormonal Factors Which Regulate Bone Resorption." In Physiology and Pharmacology of Bone, 215–47. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77991-6_6.

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Тези доповідей конференцій з теми "Bone resorption"

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Johansson, Lars, Ulf Edlund, Anna Fahlgren, and Per Aspenberg. "A Model for Bone Resorption." In ASME 8th Biennial Conference on Engineering Systems Design and Analysis. ASMEDC, 2006. http://dx.doi.org/10.1115/esda2006-95401.

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In the present paper a model for the resorption of bone, such as that observed at the interface between surgical implants and bone tissue, is developed. While there are many previous studies where models for bone remodelling calculations are proposed, these have been based on the stress or strain state of the bone tissue itself as the driving force for bone remodelling. We, instead, develop a constitutive model based on observations in recent experiments where it seems that fluid pressure, or possibly fluid flow velocity, is a major factor in the bone resorption process.
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Deguchi, Takahiro, Sami V. Koho, Tuomas Näreoja, Juha Peltonen, and Pekka Hänninen. "Tomographic STED microscopy to study bone resorption." In SPIE BiOS, edited by Thomas G. Brown, Carol J. Cogswell, and Tony Wilson. SPIE, 2015. http://dx.doi.org/10.1117/12.2079157.

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Altman, Allison R., Beom Kang Huh, Abhishek Chandra, Wei-Ju Tseng, Ling Qin, and X. Sherry Liu. "3D In Vivo Bone Dynamic Imaging of PTH’s Anabolic Action." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14671.

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Aging shifts bone remodeling toward a negative balance between bone formation and resorption, causing bone loss and increased fracture risk. Anti-resorptive agents are commonly used to inhibit bone resorption and stabilize bone mass. While they are effective to prevent further bone loss, there is also a great need for anabolic agents which can reverse bone deterioration and regain lost skeletal integrity. Intermittent parathyroid hormone (PTH) treatment is the only FDA-approved anabolic treatment for osteoporosis, which greatly stimulates bone formation. Combined therapy of anti-resorptive drugs, such as alendronate (ALN), and PTH have been proposed and are expected to further stimulate bone formation. However, studies show conflicting results regarding the effectiveness of combined treatments: some have reported the addition of ALN to impair PTH function [1, 2], while others suggest an improvement over PTH monotherapy [3, 4]. The first objective of this study is to document the immediate changes of individual trabecular structures due to PTH and combined therapy within 12 days using in vivo micro computed tomography (μCT). As PTH is typically prescribed for 1 to 3 years to osteoporotic patients, a treatment of 12 days for rats (approximately equivalent to one year of human life) may be more clinically relevant than long-term treatment studies on rats. The secondary purpose of this study was to gain insight into the mechanism of combined versus PTH treatments through a bone dynamic imaging strategy to track events over an individual remodeling site. We hypothesized that PTH and combined treatments would immediately enhance bone formation on the trabecular surface.
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Fujita, Hiroshi, Kazuhiro Ido, Weam Farid Mousa, Kazuyasu Ushio, Hirokazu Iida, Keiichi Kawanabe, Shigeto Yura, Masanori Oka, and Takashi Nakamura. "FEMORAL BONE RESORPTION OBSERVED IN CANINE THA USING BIOACTIVE BONE CEMENT." In Proceedings of the 12th International Symposium on Ceramics in Medicine. WORLD SCIENTIFIC, 1999. http://dx.doi.org/10.1142/9789814291064_0124.

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Chong, Desmond Y. R., Ulrich N. Hansen, and Andrew A. Amis. "Computational Biomechanical Analysis of Fixation Performance and Bone Resorption of Tibial Prosthesis Implantation." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-205205.

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Long-term survivorship of total knee replacement (TKR) relies on the periprosthetic bone strength and its initial fixation stability. Aseptic loosening caused by mechanical factors is a recognised failure mode for knee prostheses. Bone resorption due to “stress-shielding” of the stiff stemmed implants will potentially lead to weakened bone strength, and also presents a challenge for revision surgery. While the bone cement is commonly used to provide mechanical attachment of the prosthesis to the bone, cement fatigue and bone-cement interface failures would eventually lead to component migration and aseptic loosening of the tibial components. The cementless fixation relies on bony ingrowth into the porous surfaces of the prosthesis thereby providing a biological attachment. Its fixation strength would depend largely on the initial stability of the fixation, where excessive bone-prosthesis relative motion (>50μm) would inhibit the osseointegration process [1]. The above are caused partly by a lack of knowledge of the optimum implant design and fixation technique factors.
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Chen, George, Joachim Loo, Margasanti Wijaya, and Yik Thai Hoe. "Determination of Resorption in Bone using Phase Shifting Interferometry." In Bio-Optics: Design and Application. Washington, D.C.: OSA, 2011. http://dx.doi.org/10.1364/boda.2011.jtua2.

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Dong, X. Neil, Y. Young Huang, and X. Edward Guo. "Transversely Isotropic Model of Osteonal Cortical Bone: Contribution of Haversian and Resorptive Porosity." In ASME 1999 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1999. http://dx.doi.org/10.1115/imece1999-0438.

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Abstract Age related changes in porosity of cortical bone have been previously reported. The cortical porosity increases with age in both men and women, from 4.6% in men and 4% in women at age 40 to 10% and more at age 80 (Laval-Jeantet et al., 1983). The porosity is defined as the percentage of cortical bone occupied by vascular and resorption cavities. There are a few quantitative data regarding the influences of Haversian canal and resorption space on porosity. Age related increases in Haversian canal size and Haversian canal number contribute to the increasing porosity of cortical bone for the elderly men and women (Thompson, 1980; Nyssen-behets et al., 1997). The number of osteoclastic resorption space is also greater in the old men than in the young men (Nyssen-Behets et al., 1997).
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Timchenko, Elena V., Pavel E. Timchenko, Elena V. Pisareva, Michael Y. Vlasov, Larisa T. Volova, Oleg O. Frolov, Yana V. Fedorova, et al. "Optical analysis of cortical bone tissue in modelling bone resorption in microgravity environment." In XLIV ACADEMIC SPACE CONFERENCE: dedicated to the memory of academician S.P. Korolev and other outstanding Russian scientists – Pioneers of space exploration. AIP Publishing, 2021. http://dx.doi.org/10.1063/5.0036909.

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Penninger, Charles L., Andre´s Tovar, Glen L. Niebur, and John E. Renaud. "Signaling Pathways for Bone Resorption Predicted as a Hybrid Cellular Automaton Process." In ASME 2010 International Mechanical Engineering Congress and Exposition. ASMEDC, 2010. http://dx.doi.org/10.1115/imece2010-39358.

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Анотація:
The bone remodeling process provides for various functions such as mineral homeostasis, damage repair, and adaptation to mechanical loading. At present, a clear link between the mechanical stimulation of bones and the biochemical response is not fully understood. Computational simulations can provide a means to test hypotheses and gain insight into processes that are difficult to examine experimentally. The objective of this work is to predict the effect of damage and strain as the stimulus for regulating the cellular signaling activity of remodeling. In this study, potential signaling pathways that mediate this cellular activity were incorporated in a hybrid cellular automaton (HCA) algorithm. Biological rules were implemented in this model to control recruitment, differentiation, and activation of osteoclasts. Prominent processes for describing recruitment and inhibition of the bone cells, as reported from experimental studies, are utilized. This work focuses on the resorption of a damaged site on a trabecular strut.
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Kolb, Alexus D., and Karen M. Bussard. "Abstract 3993: 'Educated' osteoblasts suppress osteoclastogenesis and bone resorption in a bone mimetic microenvironment." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-3993.

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Звіти організацій з теми "Bone resorption"

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Guan, Junwen, and J. Guan. Risk factors for bone flap resorption after autologous bone cranioplasty: protocol for a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2020. http://dx.doi.org/10.37766/inplasy2020.5.0063.

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M, Gilbert. Case Report: An Extreme Case of Alveolar Bone Resorption in an Edentulous Mandible. Science Repository, May 2019. http://dx.doi.org/10.31487/j.dobcr.2019.02.03.

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Aleksandrov, V. A., A. V. Aleksandrov, L. N. Shilova, and N. V. Aleksandrova. Diagnostic role of angiopoietin-like protein type 3 in assessing the activity of resorptive processes in bone tissue in women with rheumatoid arthritis. Ljournal, 2020. http://dx.doi.org/10.18411/wco-iof-esceo-2020-309.

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