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Bibliografias temáticas / Bones Pathophysiology

Literatura científica selecionada sobre o tema "Bones Pathophysiology"

Autor: Grafiati

Publicado: 4 de junho de 2021

Última modificação: 3 de fevereiro de 2022

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Artigos de revistas
Teses / dissertações
Livros
Capítulos de livros
Trabalhos de conferências
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Artigos de revistas sobre o assunto "Bones Pathophysiology":

1

Wiegerinck, R. F., R. Schreurs e F. W. Prinzen. "Pathophysiology of dyssynchrony: of squirrels and broken bones". Netherlands Heart Journal 24, n.º 1 (10 de dezembro de 2015): 4–10. http://dx.doi.org/10.1007/s12471-015-0765-7.

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2

Shapkin, Yu G., P. A. Seliverstov e E. A. Skripal. "THE PHENOMENON OF «SECOND HIT» AFTER OPERATIONS OF OSTEOSYNTHESIS IN CASE OF POLY-TRAUMA". Medical Journal of the Russian Federation 23, n.º 6 (15 de dezembro de 2017): 331–36. http://dx.doi.org/10.18821/0869-2106-2017-23-6-331-336.

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In case of poly-trauma the early operations of osteosynthesis under fractures of long bones, unstable fractures of pelvis and backbone bones being an operational trauma, can provoke progression of inflammatory reaction, development of systemic complications and poly-organ inadequacy i.e. causing a «second hit» effect. The pathophysiologic mechanisms of «second hit» phenomenon are complicated and they are implementing by means of modulation of immune response. The risk of development of the given phenomenon depends on period of implementation and method of osteosynthesis, severity of injuries and condition, age, concomitant pathology of patient, presence of chest trauma and craniocerebral trauma. The study of pathophysiology of «second hit» phenomenon is perspective for development and optimization of clinical concepts of treatment of patients with poly-trauma and skeletal damages.

3

Thévenin-Lemoine, C., J. Vial, J. L. Labbé, B. Lepage, B. Ilharreborde e F. Accadbled. "MRI of acute osteomyelitis in long bones of children: Pathophysiology study". Orthopaedics & Traumatology: Surgery & Research 102, n.º 7 (novembro de 2016): 831–37. http://dx.doi.org/10.1016/j.otsr.2016.06.014.

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4

Tasis, Nikolaos, Ioannis Tsouknidas, Argyrios Ioannidis, Konstantinos Nassiopoulos e Dimitrios Filippou. "Left Functional Pneumonectomy Caused by a Very Rare Giant Intrathoracic Cystic Lesion in a Patient with Gorham–Stout Syndrome: Case Report and Review of the Literature". Case Reports in Pulmonology 2018 (2018): 1–9. http://dx.doi.org/10.1155/2018/2406496.

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Gorham–Stout syndrome is an uncommon entity, with few cases reported in bibliography. It consists of osteolytic manifestations affecting various bones and replacing them with lymphangiomatous tissue. With pathophysiology unknown, Gorham–Stout disease affects also cardiorespiratory system usually causing lytic lesions to the bones of the thoracic cage or directly invading the thoracic duct. This is a case report of a unique respiratory manifestation of the disease and a review of its cardiorespiratory complications.

5

Kuhweide, R., V. Van de Steene, S. Vlaminck e J. W. Casselman. "Ramsay Hunt syndrome: pathophysiology of cochleovestibular symptoms". Journal of Laryngology & Otology 116, n.º 10 (outubro de 2002): 844–48. http://dx.doi.org/10.1258/00222150260293691.

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Ramsay Hunt’s hypothesis that herpes zoster oticus results from reactivation of the varicella zoster virus (VZV) in the geniculate ganglion is supported by the detection of viral genome in archival temporal bones of normals and Ramsay Hunt patients by the polymerase chain reaction. Ramsay Hunt syndrome is characterized by the presence of cochleovestibular symptoms in association with facial paralysis. VZV has also been demonstrated in the spiral and/or vestibular ganglion. Two cases are reported in which cochleovestibular symptoms outweighed the facial nerve symptoms, presumably representing VZV reactivation in the spiral and/or vestibular ganglion. From these observations and the known dormancy of VZV in non-neuronal satellite cells, it is argued that the cochleovestibular symptoms in Ramsay Hunt syndrome may result from VZV transmission across the nerves inside the internal auditory canal and that prompt treatment with an antiviral-corticosteroid combination might be justified in the management of any acute non-hydropic cochleovestibular syndrome.

6

Puntillo, Filomena, Mariateresa Giglio, Antonella Paladini, Gaetano Perchiazzi, Omar Viswanath, Ivan Urits, Carlo Sabbà, Giustino Varrassi e Nicola Brienza. "Pathophysiology of musculoskeletal pain: a narrative review". Therapeutic Advances in Musculoskeletal Disease 13 (janeiro de 2021): 1759720X2199506. http://dx.doi.org/10.1177/1759720x21995067.

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Musculoskeletal pain (excluding bone cancer pain) affects more than 30% of the global population and imposes an enormous burden on patients, families, and caregivers related to functional limitation, emotional distress, effects on mood, loss of independence, and reduced quality of life. The pathogenic mechanisms of musculoskeletal pain relate to the differential sensory innervation of bones, joints, and muscles as opposed to skin and involve a number of peripheral and central nervous system cells and mediators. The interplay of neurons and non-neural cells (e.g. glial, mesenchymal, and immune cells) amplifies and sensitizes pain signals in a manner that leads to cortical remodeling. Moreover, sex, age, mood, and social factors, together with beliefs, thoughts, and pain behaviors influence the way in which musculoskeletal pain manifests and is understood and assessed. The aim of this narrative review is to summarize the different pathogenic mechanisms underlying musculoskeletal pain and how these mechanisms interact to promote the transition from acute to chronic pain.

7

Shams, Ramsha, Kelsey P. Drasites, Vandana Zaman, Denise Matzelle, Donald C. Shields, Dena P. Garner, Christopher J. Sole, Azizul Haque e Narendra L. Banik. "The Pathophysiology of Osteoporosis after Spinal Cord Injury". International Journal of Molecular Sciences 22, n.º 6 (17 de março de 2021): 3057. http://dx.doi.org/10.3390/ijms22063057.

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Spinal cord injury (SCI) affects approximately 300,000 people in the United States. Most individuals who sustain severe SCI also develop subsequent osteoporosis. However, beyond immobilization-related lack of long bone loading, multiple mechanisms of SCI-related bone density loss are incompletely understood. Recent findings suggest neuronal impairment and disability may lead to an upregulation of receptor activator of nuclear factor-κB ligand (RANKL), which promotes bone resorption. Disruption of Wnt signaling and dysregulation of RANKL may also contribute to the pathogenesis of SCI-related osteoporosis. Estrogenic effects may protect bones from resorption by decreasing the upregulation of RANKL. This review will discuss the current proposed physiological and cellular mechanisms explaining osteoporosis associated with SCI. In addition, we will discuss emerging pharmacological and physiological treatment strategies, including the promising effects of estrogen on cellular protection.

8

Gore, Ashwini P., Soon Ho Kwon e Antine E. Stenbit. "A Roadmap to the Brittle Bones of Cystic Fibrosis". Journal of Osteoporosis 2011 (2011): 1–10. http://dx.doi.org/10.4061/2011/926045.

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Cystic fibrosis (CF) is an autosomal recessive disorder which despite advances in medical care continues to be a life-limiting and often fatal disease. With increase in life expectancy of the CF population, bone disease has emerged as a common complication. Unlike the osteoporosis seen in postmenopausal population, bone disease in CF begins at a young age and is associated with significant morbidity due to fractures, kyphosis, increased pain, and decreased lung function. The maintenance of bone health is essential for the CF population during their lives to prevent pain and fractures but also as they approach lung transplantation since severe bone disease can lead to exclusion from lung transplantation. Early recognition, prevention, and treatment are key to maintaining optimal bone health in CF patients and often require a multidisciplinary approach. This article will review the pathophysiology, current clinical practice guidelines, and potential future therapies for treating CF-related bone disease.

9

Assi, Tarek, Sarah Watson, Bachar Samra, Elie Rassy, Axel Le Cesne, Antoine Italiano e Olivier Mir. "Targeting the VEGF Pathway in Osteosarcoma". Cells 10, n.º 5 (18 de maio de 2021): 1240. http://dx.doi.org/10.3390/cells10051240.

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Osteosarcoma is the most common primary tumor of the bones affecting mainly young adults. Despite the advances in the field of systemic anticancer therapy, the prognosis of relapsed of metastatic osteosarcoma patients remain dismal with very short survival. However, the better understanding of the pathophysiology of this subtype of sarcoma has led to the identification of new targeted agents with significant activity. In fact, increased angiogenesis plays a major role in the tumor growth and survival of osteosarcoma patients. Several targeted agents have demonstrated a significant anti-tumor activity including multi-kinase inhibitors. In this review, we will discuss the pathophysiology, rationale, and role of targeting angiogenesis via the VEGF pathway in patients with osteosarcoma with emphasis on the published clinical trials and future directions.

10

Golovach, I. Yu. "Clinical significance of spondyloarthritis-attended enthesites: from pathophysiology to treatment (review)". PAIN, JOINTS, SPINE 11, n.º 1 (1 de abril de 2021): 17–27. http://dx.doi.org/10.22141/2224-1507.11.1.2021.226905.

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The article presents the latest views on enthesites’ anatomy and pathogenesis, clinical features, diagnostic and therapeutic options. The enthesis lesions are considered an outstanding pathologic and clinical manifestation of spondyloarthritis group; this symptom is included into the classification criteria by the Assessment of SpondyloArthritis International Society for the peripheral and axial forms. The typical spondyloarthritis-attended enthesites’ localizations are: the site of Achilles tendon and plantar aponeurosis’ attachment to the calcaneus, the lateral condyle of the humerus, the medial condyle of the femur, the upper edge of the patella, the upper edge of the iliac bones, trochanters of the femoral bones, spinous processes of the vertebrae. The structures focused in the entheses’ sites have anatomical, functional and physiological interactions and constitute a single synovial-entheseal complex. Unlike the rheumatoid arthritis with a key pathological process occurring in the synovial lining, the spondyloarthritis is mainly provoking the morphological modifications, namely enthesites, while the developing arthritis (synovitis) appears secondary to enthesites. The enthesitis is detected in 30–50 % of spondyloarthritis patients and associated with a higher activity, higher pain indices and a compromised life quality. The presence of enthesites in the psoriatic arthritis patients is associated with axial and peripheral joint lesions, a high chance of ankylosation, a high disease activity, pronounced pains, a compromised life quality and functional state, sleeping disorders. Furthermore, the enthesitis is considered a precursor of the negative disease outcome, and may forecast a lower probability of remission and a low activity. The entheseal inflammation occurs as a result of mechanical and/or infection-originating stress, resulting in the prostaglandin E2 and interleukin-23 activation with a further vasodilatation, and T-cell and Group 3 innate lymphoid cell (ILC3) activation. The innate immunity-generated inflammation is characterized by a release of tumor necrosis factor and interleukin-17, resulting in the immune cell influx, namely the polymorphonuclear neutrophils. Under the influence of interleukin-17 and interleukin-22, the mesenchymal proliferation is characterized by an activation and proliferation of resident mesenchymal stem cells in the periosteum. The enthesitis treatment strategies remain undefined; however, the ones most commonly used are the nonsteroidal anti-inflammatory drugs (NSAIDs), localized glucocorticoid injections, Apremilast, as well as targeted medications, namely the tumor necrosis factor, interleukin-17 and interleukin-23 inhibitors.

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Teses / dissertações sobre o assunto "Bones Pathophysiology":

1

Anderson, Paul Hamill. "The regulation of Vitamin D metabolism in the kidney and bone". Title page, contents and abstract only, 2002. http://web4.library.adelaide.edu.au/theses/09PH/09pha5486.pdf.

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Includes bibliographical references (leaves 226-273.) Investigates the regulation of the expression of CYP27B1, CYP24 and vitamin D receptor (VDR) mRNA, both in the bone and in the kidney, with the aim to determine whether the regulation of the vitamin D metabolism in the bone is independent from that in the kidney. The effects of age, dietary calcium and vitamin D status on the expression of these genes in both the kidney and the bone, as well as on a number of biochemical factors known to regulate the renal metabolism of 1,25D, such as PTH, calcium and 1,25D itself, were examined. CYP27B1 mRNA expression was also studied in histological sections of rat femoral bone.

2

Huang, C. C. "Pathophysiology of post-transplantation bone disease : mechanisms of bone loss after orthotopic liver transplantation". Thesis, University of Cambridge, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.604707.

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To enhance our understanding of the pathophysiology of bone disease associated with liver transplantation and of the mechanisms underlying bone loss in the three month period following transplantation, this prospective study was undertaken as follows: (1) bone pathophysiology was evaluated pre- and three months post-transplantation in transiliac biopsies using tetracycline-assisted histomorphometry; (2) cellular activities of bone formation and resorption pre- and post- transplantation were studied using quantitative enzyme cytochemistry in combination with histomorphometric methods; (3) cellular activities for markers of bone energy metabolism and biosynthesis and/or cell proliferation were investigated using quantitative enzyme cytochemistry; (4) plasma markers for bone metabolism were investigated at regular intervals in collaboration with other laboratories. It was concluded from this study that rapid bone loss early after transplantation is due both to increased bone turnover and a negative remodelling balance at the individual bone remodelling site. These changes were at least partially mediated by increased PTH levels secondary to a negative balance in plasma calcium. Cyclosporin A is known to increase intracellular calcium levels and inhibit calcium release from mitochondria. It also reduces glomerular filtration rate which could be sufficient to depress extracellular calcium levels and thereby cause the observed rise in PTH levels. The consequences of this for post transplant bone remodelling is a markedly enhanced risk of osteoporosis in these patients. Ensuring replete calcium and vitamin D levels pre-transplantation and supplementation of cyclosporin A treatment with vitamin D metabolites and calcium post-transplantation followed by careful monitoring of plasma calcium concentrations might offer a better overall outcome for preventing transplantation-associated osteoporosis at this early stage post transplantation.

3

Chapurlat, Roland, Deborah Gensburger, Juan Jimenez-Andrade, Joseph Ghilardi, Marilyn Kelly e Patrick Mantyh. "Pathophysiology and medical treatment of pain in fibrous dysplasia of bone". BioMed Central, 2012. http://hdl.handle.net/10150/610228.

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One of the most common complications of fibrous dysplasia of bone (FD) is bone pain. Usual pain killers are often of inadequate efficacy to control this bone pain. The mechanism of bone pain in FD remains uncertain, but by analogy with bone tumors one may consider that ectopic sprouting and formation of neuroma-like structures by sensory and sympathetic nerve fibers also occur in the dysplastic skeleton. Bone pain has been reported in up to 81% of adults and 49% of children. It affects predominantly the lower limbs and the spine. The degree of pain is highly variable and adults reports more pain than children. Bisphosphonates have been shown to reduce bone pain in uncontrolled studies. Their influence on bone strength remains unknown. In a randomized trial testing alendronate, bone pain was not significantly improved. Another trial assessing the effect of risedronate is ongoing. Possible future therapies include tocilizumab, denosumab and drugs targeting nerve growth factor and its receptor TrkA.

4

Borazjani, Ali. "Pathophysiology of Pelvic Organ Prolapse". Cleveland State University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=csu1432745397.

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5

Ismail, Medhat Mohamed. "Pathophysiology and therapy of bone marrow failure : studies of apoptosis and stem cell transplantation". Thesis, St George's, University of London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.269742.

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6

Elkin, Sarah Louise. "The pathogenesis and pathophysiology of low bone mineral density in adults with cystic fibrosis". Thesis, Imperial College London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.422707.

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7

Edwards, Sarah. "Investigating the role of a novel ER molecular chaperone : Creld2 in the physiology and pathophysiology of endochondral bone growth". Thesis, University of Manchester, 2015. https://www.research.manchester.ac.uk/portal/en/theses/investigating-the-role-of-a-novel-er-molecular-chaperone-creld2-in-the-physiology-and-pathophysiology-of-endochondral-bone-growth(6fd49909-beec-42d1-a546-8b2411616e59).html.

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Cysteine rich with EGF-like domains 2 (Creld2) is a novel endoplasmic reticulum (ER) resident molecular chaperone that has been recently implicated in the ER stress signalling response (ERSS) and the unfolded protein response (UPR). Global transcriptomic data derived from in vivo mouse models of rare chondrodysplasias; Multiple Epiphyseal Dysplasia (MED Matn3 p.V194D) and Metaphyseal chondrodysplasia type Schmid (MCDS Col10a1 p.N617K), identified a significant upregulation in Creld2 expression in mutant chondrocytes. These chondrodysplasias share a common disease signature consisting of aberrant folding of a matrix component often as a result of inappropriate alignment of intramolecular disulphide bonds. This in turn culminates in toxic protein aggregation, intracellular retention mutant polypeptides and a classical ER stress response. The aim of this study was to further analyse the function of Creld2 in cartilage development and chondrodysplasias in which endochondral bone growth is perturbed. Protein disulphide isomerases (PDIAs) were amongst the most up-regulated genes in the MED and MCDS mouse models, consistent with the prolonged exposure of normally 'buried' cysteine residues. This led to the hypothesis that Creld2 was functioning as a novel PDI-like oxidoreductase to assist in the correct folding and maturation of aggregated misfolded polypeptide chains through REDOX regulated thiol disulphide exchange. A series of Creld2-CXXA substrate trapping mutants were generated in order to determine whether Creld2 possessed inherent isomerase activity. Here potential substrates interacting with Creld2 were 'trapped' as mixed disulphide intermediates, then isolated by immunoprecipitation and identified by mass spectrometry analysis. It was demonstrated that Creld2 possessed a catalytic active CXXC motif in its N-terminus that enabled the molecular chaperone to participate in REDOX regulated thiol disulphide exchange with at least 20 potential substrates including; laminin (alpha3,β3,γ2), thrombospondin 1, integrin alpha3 and type VI collagen. There was also numerous co-chaperones and foldases thought to be part of a specialised protein-protein interactome (PPI) for folding nascent polypeptides translocating the ER lumen. Moreover, co-immunoprecipitation experiments supported a protein-protein interaction between Creld2 and mutant matrilin-3, thereby inferring a potential chondro-protective role in resolving non-native disulphide bonded aggregates in MED. An established biochemical approach was employed to test the hypothesis that all MATN3-MED disease causing mutations have a generic cellular response to the β-sheet V194D mutation, consisting of intracellular retention, protein aggregation and ER stress induction. Several missense mutations were selected for analyses which encompassed a spectrum of disease severity and included examples of both β-sheet and alpha helical mutations. It was possible to define a reliable and reproducible assay for categorising MATN3 missense mutations into pathological or benign based on these basic parameters. This study was extended further to determine whether there were common pathological mechanisms behind MED and Bethlem myopathy (BM) caused by missense mutations in von Willebrand Factor A domain (vWF-A) containing proteins (matrilin-3 and type VI collagen respectively). We chose to compare and contrast the effects of an archetypal MATN3-MED causing mutation (R121W) with the equivalent COL6A2-BM causing mutation (R876H). These mutations compromised protein folding and maturation, resulting in the familiar disease profile of intracellular retention, protein aggregation and an ER stress response in an artificial overexpression system. However, the mutant C2 domain was efficiently targeted for degradation whilst mutant matrilin-3 vWF-A domain appeared to be resistant to these molecular processes.Molecular genetics was employed to study the role of Creld2 in vivo. Creld2-/- null mice (both global and conditional) were generated to directly examine the role of Creld2 in endochondral bone growth. Global knock-out mice were viable with no overt phenotype at birth. However, female Creld2-/- null mice showed a significant reduction in body weight and tibia bone length at 3 weeks of age. A cartilage specific knock-out was generated to determine whether these skeletal abnormalities were attributed to a systemic or a direct effect on cartilage development. [Creld2Flox/Flox Col2Cre (+)] demonstrated a severe chondrodysplasia with significantly reduced body weight and long bone growth compared to control littermates. Morphological and histochemical analysis of mutant growth plates revealed gross disorganisation of the chondrocyte columns with extensive regions of hypocellularity. These pathological features were confirmed to be the result of reduced chondrocyte proliferation and increased/spatially dysregulated apoptosis throughout all zones of differentiation. Taken together, these data provide evidence that Creld2 possesses isomerase activity and exhibits distinct substrate specificity. Furthermore, Creld2 has a fundamental role in post-natal cartilage development and chondrocyte differentiation in the growth plate.

8

Davies, Matthew Rhys. "The role of bone morphogenetic protein 7 in the pathophysiology and treatment of vascular calcification associated with chronic renal failure". Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1444711/.

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Vascular calcification (VC) is an important complication of chronic renal failure (CRF), and a risk factor for reduced survival. Osteoblast-like cells in the vessel wall derived from resident vascular smooth muscle cells (VSMC) are considered central to the pathogenesis of VC, which is exacerbated by mineral ion abnormalities inherent in renal osteodystrophy (ROD). Nevertheless, its aetiology is incompletely understood, and no effective therapies exist. Recently, CRF has been characterised as a state of Bone Morphogenetic Protein 7 (BMP7) deficiency, and animal studies have shown that administration of this renal morphogen is efficacious in treating several aspects of renal failure, including progressive renal fibrosis and ROD. The hypothesis of this thesis is that BMP7 deficiency contributes to the pathogenesis of VC, by facilitating the emergence of the osteoblast-like cell, and that exogenous BMP7 administration abrogates it by normalising VSMC behaviour. This hypothesis was tested in atherosclerotic Low Density Lipoprotein Receptor Null (ldlf/j) mice. Uraemia was superimposed surgically to generate VC. Animals received BMP7 or vehicle over 15 weeks. Untreated uraemic animals had increased VC on histological and chemical grounds, and demonstrated increased expression of the characteristic osteoblast protein osteocalcin was demonstrated in vascular tissues. Both changes were reversed by BMP7 administration. Uraemic animals were shown to have an adynamic form of ROD, also reversed by BMP7 administration, suggesting that normalisation of mineral ion abnormalities may underlie the benefits of BMP7 on VC in CRF. In addition, in vitro studies showed that BMP7 can act directly on vascular cells to reduce extracellular calcification under conducive conditions. Finally, in an appendix, preliminary data is presented showing that expression of LRP5, a protein involved in the control of normal bone mineralization, may be increased in Idlf1 animals, suggesting that consequences of this genotype may be important to VC pathogenesis in this model.

9

Ho, Ken Choong Khoon School of Medicine UNSW. "Characterization of critical size sheep cranial defect model for study of bone graft substitute". 2007. http://handle.unsw.edu.au/1959.4/40499.

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This is an original study to quantify and grade defect healing in a large animal cranial bone substitute model. The study of various therapies to heal cranial defects requires an appropriate ?critical? animal model. An experimental animal model should be analogous and recognizable as an appropriate challenge to human physiology. In addition, the defect must fail to heal unless treated with the tissue engineering therapy under study. Sheep as a large animal model was chosen because of its ability to tolerate creation of large skull defects analogous to clinical scenario, and its biology of healing as a high order mammal would be closer human beings. There is no agreement on the critical size limits for cranial defects. Various sizes have been termed "critical" in publications utilizing sheep. These ranged from 20-22mm. This study will investigate whether a 20mm defect is adequate. Bilateral circular cranial defects of 10, 20 and 25mm diameters were created in 12 adult sheep. Based on guided tissue engineering principles, defect protection was utilized to prevent in-growth of fibroblasts and other connective tissue cells from the surroundings. As bone tissue regeneration strategies usually involve osteoconduction element, an animal model that considered the defect protection role of osteoconduction would be more appropriate. Repopulation and regeneration of the defect was maximized as an added challenge Bioresorbable polylactic acid co-polymer mesh (MacroPoreTM) and Titanium mesh (TiMeshTM) was used as defect protection. The cranial defects were harvested at 8 and 16 weeks. The end-point analysis included Faxitron X-ray images, DEXA (Dual Energy X-ray Absorptiometry), and histology. The defects were graded to assess their ability to eventually heal. 10mm defects fully healed at 16 weeks. There was new bone formation spanning the entire defect seen on histology. 25mm defects were spanned by thin fibrous tissue only. There was variability in the healing potential of 20mm defect. Based on presence of bone islands within the defect, half of the 20mm defects demonstrated ability to heal while the other half actually had new bone spanning the defects on histology. Critical size cranial defect in sheep for the study of bone graft substitute has to be larger than 25mm diameter. The model is then utilized to study the use of Pro Osteon and AGF compared with the gold standard of autologous bone graft.

10

Dodge, Todd Randall. "Experimental and Computational Analysis of Dynamic Loading for Bone Formation". Thesis, 2013. http://hdl.handle.net/1805/3670.

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Indiana University-Purdue University Indianapolis (IUPUI)
Bone is a dynamic tissue that is constantly remodeling to repair damage and strengthen regions exposed to loads during everyday activities. However, certain conditions, including long-term unloading of the skeleton, hormonal imbalances, and aging can disrupt the normal bone remodeling cycle and lead to low bone mass and osteoporosis, increasing risk of fracture. While numerous treatments for low bone mass have been devised, dynamic mechanical loading modalities, such as axial loading of long bones and lateral loading of joints, have recently been examined as potential methods of stimulating bone formation. The effectiveness of mechanical loading in strengthening bone is dependent both on the structural and geometric characteristics of the bone and the properties of the applied load. For instance, curvature in the structure of a bone causes bending and increased strain in response to an axial load, which may contribute to increased bone formation. In addition, frequency of the applied load has been determined to impact the degree of new bone formation; however, the mechanism behind this relationship remains unknown. In this thesis, the application of mechanical loading to treat osteoporotic conditions is examined and two questions are addressed: What role does the structural geometry of bone play in the mechanical damping of forces applied during loading? Does mechanical resonance enhance geometric effects, leading to localized areas of elevated bone formation dependent on loading frequency? Curvature in the structure of bone was hypothesized to enhance its damping ability and lead to increased bone formation through bending. In addition, loading at frequencies near the resonant frequencies of bone was predicted to cause increased bone formation, specifically in areas that experienced high principal strains due to localized displacements during resonant vibration. To test the hypothesis, mechanical loading experiments and simulations using finite element (FE) analysis were conducted to characterize the dynamic properties of bone. Results demonstrate that while surrounding joints contribute to the greatest portion of the damping capacity of the lower limb, bone absorbs a significant amount of energy through curvature-driven bending. In addition, results show that enhanced mechanical responses at loading frequencies near the resonant frequencies of bone may lead to increased bone formation in areas that experience the greatest principal strain during vibration. These findings demonstrate the potential therapeutic effects of mechanical loading in preventing costly osteoporotic fractures, and explore characteristics of bone that may lead to optimization of mechanical loading techniques. Further investigation of biomechanical properties of bone may lead to the prescribing of personalized mechanical loading treatments to treat osteoporotic diseases.

Mais fontes

Livros sobre o assunto "Bones Pathophysiology":

1

Medicine, Conference on Skeletal Biology and. Skeletal biology and medicine. Boston, Mass: Published by Blackwell Pub. on behalf of the New York Academy of Sciences, 2007.

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2

NATO Advanced Study Institute on Advances in Bone Regulatory Factors: Morphology, Biochemistry, Physiology, and Pharmacology (1989 Erice, Italy). Bone regulatory factors: Morphology, biochemistry, physiology, and pharmacology. New York: Plenum Press, 1990.

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3

International Symposium on Bone Circulation (4th 1987 Toulouse, France). Bone circulation and bone necrosis: Proceedings of the IVth International Symposium on Bone Circulation, Toulouse (France), 17th-19th September 1987. Berlin: Springer-Verlag, 1990.

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4

Conference on Skeletal Biology and Medicine (2nd 2007 New York, N.Y.). Skeletal biology and medicine. Boston, Mass: Blackwell Pub., on behalf of the New York Academy of Sciences, 2007.

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5

Conference on Skeletal Biology and Medicine (4th 2011 New York, N.Y.). Skeletal biology and medicine II: Bone and cartilage homeostasis and bone disease. Editado por Zaidi Mone. Boston, Mass: Published by Blackwell Pub. on behalf of the New York Academy of Sciences, 2011.

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6

Behari, Jitendra. Biophysical bone behavior. Singapore: John Wiley, 2009.

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7

N.Y.) Conference on Skeletal Biology and Medicine (3rd 2010 New York. Skeletal biology and medicine. Editado por Zaidi Mone e New York Academy of Sciences. Boston, Mass: Published by Blackwell Pub. on behalf of the New York Academy of Sciences, 2010.

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8

NATO Advanced Study Institute on Advances in Bone Regulatory Factors: Morphology, Biochemistry, Physiology, and Pharmacology (1989 Erice, Italy). Bone regulatory factors: Morphology, biochemistry, physiology, and pharmacology. New York: Plenum Press, 1990.

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9

Lee, Diane. The pelvic girdle: An integration of clinical expertise and research. 4^a ed. Edinburgh: Elsevier/Churchill Livingstone, 2011.

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10

Lundon, Katie. Orthopedic rehabilitation science: Principles for clinical management of nonmineralized connective tissue. Amsterdam: Butterworth-Heinemann, 2003.

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Mais fontes

Capítulos de livros sobre o assunto "Bones Pathophysiology":

1

Mori, Satoshi. "Bone Microdamage and Its Repair: Pathophysiology of Bone Fatigue". In Mechanical Loading of Bones and Joints, 139–45. Tokyo: Springer Japan, 1999. http://dx.doi.org/10.1007/978-4-431-65892-4_14.

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Roodman, G. David. "Pathophysiology of Bone Metastases". In Bone Metastases, 31–50. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-1-4020-9819-2_2.

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3

Chirgwin, John M., e G. David Roodman. "Pathophysiology of Bone Metastases". In Bone Metastases, 3–17. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-7569-5_1.

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4

Van der Wall, Hans, Barry Elison, Clayton Frater, Warwick Bruce e Stephen Clarke. "Pathophysiology of Bone Metastases". In Radionuclide and Hybrid Bone Imaging, 59–84. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-02400-9_3.

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Kerschan-Schindl, Katharina, Ursula Föger-Samwald e Peter Pietschmann. "Pathophysiology of Bone Fragility". In Principles of Bone and Joint Research, 83–97. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-58955-8_6.

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Bartl, Reiner, e Christoph Bartl. "Classifying Bone Disorders According to Pathophysiology". In Bone Disorders, 55–59. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-29182-6_9.

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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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Jones, John Paul. "Pathophysiology of Osteonecrosis". In Bone Circulation and Vascularization in Normal and Pathological Conditions, 249–61. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2838-8_28.

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Pietschmann, P., R. Gruber e M. Peterlik. "Pathophysiology and Aging of Bone". In Radiology of Osteoporosis, 3–24. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-662-05235-8_1.

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Thürlimann, Beat. "Physiology and Pathophysiology of Bone". In Recent Results in Cancer Research, 1–20. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-59845-6_1.

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Trabalhos de conferências sobre o assunto "Bones Pathophysiology":

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Hedrich, Christian. "SP0187 PATHOPHYSIOLOGY AND THERAPEUTIC CONSEQUENCES AUTO-INFLAMMATORY BONE DISORDERS". In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.8494.

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Slichter, Sherrill J. "PATHOPHYSIOLOGY OF THROMBOCYTOPENIA AND RESULTANT CLINICAL INDICATIONS FOR PLATELET TRANSFUSION". In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643996.

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Resumo:

Careful evaluation of platelet survival data in normal individuals and patients with thrombocytopeniasecondary to marrow aplasia has demonstrated that platelets are lost from circulation by two mechanisms a fixed fraction of platelets, amounting to approxi mately 7,100 platelets/ul/day, are lost randomly while the remaining platelets are removed by senescent mechanisms. At platelet counts of <100,000/ul, platelet survival becomes progressively shorter as the fixed platelet loss becomes a proportionately greater fraction of the circulating platelets. Thus, there is a direct relationship between platelet count and platelet survival in thrombocytopenic patients. Therefore, when judging the effectiveness of platelet therapy in thrombocytopenic patients, the influence of platelet count on platelet survival must be considered. As yet, there have been no studies to determine if there are ways to interrupt this fixed platelet loss? whether such therapy might improve platelet support in thrombocyotpenic patients by prolonging platelet survival? or, alternatively, whether such therapy might enhance the bleeding risk if random platelet removal is related to physiologic platelet-endothelial cell interactions.Besides taking into account the effect of thrombocytopenia on the expected response to platelet transfusions, the risk of alloimmunization with platelet transfusion therapy requires a careful assessment of the indications for platelet transfusions for each patient.Based on 51Cr-labeled stool blood loss measurements, we have determined that the bleeding risk is minimal at platelet counts above 10,000 platelets/ul.Only when the platelet count falls to a lower level of 5,000/ul is GI bleeding significantly increased. However, there are certain medications that may enhance the bleeding risk and require platelet transfusions to be given at higher platelet counts.In those patients who are thrombocytopenic, not because of failure of marrow platelet production, but rather because of accelerated platelet removal, indications for platelet transfusions must be adjusted to meet the particular problem. For example, for patients with autoimmune thrombocytopenic purpura, platelet transfusions are rarely indicated (one exception being intracerebral bleeding) because of the rapid rate of platelet removal and because the patients are usually releasing young hyperfunctional platelets from the bone marrow reducing the hemorrhagic risk at any given platelet count. In some patients with consumptive coagulopathies, even though platelet removal is rapid, platelets may have to be provided until specific therapy resolves the underlying disease process causing the platelet consumption. For these patients, increased levels of fibrinogen/fibrin degregation products, as well as various medications they maybe receiving, may produce platelet dysfunction necessitating platelet transfusions at higher platelet levels. Finally, massive transfusion patients may develop a dilution thrombocytopenia requiring platelet transfusions.

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de la Puente, Pilar, Rebecca Gilson, Barbara Muz, Feda Azab, Justin King, Samuel Achilefu, Ravi Vij e Abdel Kareem Azab. "Abstract 5356: 3D tissue-engineered bone marrow niche as novel method to study pathophysiology and drug resistance in multiple myeloma". In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-5356.

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Relatórios de organizações sobre o assunto "Bones Pathophysiology":

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Zhang, Jiwang. The Role of Necroptosis in the Pathophysiology of Bone Marrow Failure. Fort Belvoir, VA: Defense Technical Information Center, março de 2014. http://dx.doi.org/10.21236/ada604192.

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