Готові списки джерел за темами / Porphyromonas gingivalis

Добірка наукової літератури з теми "Porphyromonas gingivalis"

Автор: Grafiati
Опубліковано: 4 червня 2021
Оновлено: 20 лютого 2023

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  2. Дисертації
  3. Книги
  4. Частини книг
  5. Тези доповідей конференцій

Статті в журналах з теми "Porphyromonas gingivalis":

1

Britos, Maria Rosenda, Cynthya Solange Sin, Silvia Mercedes Ortega, and Olga Miriam Vasek. "Diseño y estandarización de la técnica de PCR para Porphyromonas gingivalis." Revista de la Facultad de Odontología 10, no. 1 (June 7, 2017): 25. http://dx.doi.org/10.30972/rfo.1012931.

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El objetivo del presente trabajo fue diseñar y estandarizar la técnica de PCR para detección en líquido gingival de Porphyromonas gingivalis, en pacientes con enfermedad periodontal. Material y métodos: Se utilizaron iniciadores específicos para el gen ARNr 16s de Porphyromonas gingivalis. La especificidad de los iniciadores se ensayó utilizando material genético extraído de la cepa de referencia Porphyromonas gingivalis ATCC 33277. Se ajustaron las condiciones de amplificación y concentraciones de la mezcla de reacción. Para validar la técnica se aplicó a diez muestras clínicas de líquido gingival de pacientes con enfermedad periodontal. Resultados: Se vizualizaron bandas nítidas a 197pb utilizando cebadores específicos en seis muestras clínicas, y se obtuvo sensibilidad hasta 15 ug/ml de ADN purificado de la cepa de referencia ATCC 33277.Conclusiones: Se validó y estandarizó una PCR sencilla para la detección de Porphyromonas gingivalis en líquido gingival
2

Griffen, Ann L., Mitzi R. Becker, Sharon R. Lyons, Melvin L. Moeschberger, and Eugene J. Leys. "Prevalence of Porphyromonas gingivalisand Periodontal Health Status." Journal of Clinical Microbiology 36, no. 11 (1998): 3239–42. http://dx.doi.org/10.1128/jcm.36.11.3239-3242.1998.

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Periodontitis is a common, progressive disease that eventually affects the majority of the population. The local destruction of periodontitis is believed to result from a bacterial infection of the gingival sulcus, and several clinical studies have provided evidence to implicate Porphyromonas gingivalis. If P. gingivalis is a periodontal pathogen, it would be expected to be present in most subjects with disease and rarely detected in subjects with good periodontal health. However, in most previous studies, P. gingivalis has not been detected in the majority of subjects with disease, and age-matched, periodontally healthy controls were not included for comparison. The purpose of the study reported here was to compare the prevalence of P. gingivalis in a group with periodontitis to that of a group that is periodontally healthy. A comprehensive sampling strategy and a sensitive PCR assay were used to maximize the likelihood of detection. The target sequence for P. gingivalis-specific amplification was the transcribed spacer region within the ribosomal operon. P. gingivalis was detected in only 25% (46 of 181) of the healthy subjects but was detected in 79% (103 of 130) of the periodontitis group (P < 0.0001). The odds ratio for being infected with P. gingivalis was 11.2 times greater in the periodontitis group than in the healthy group (95% confidence interval, 6.5 to 19.2). These data implicate P. gingivalisin the pathogenesis of periodontitis and suggest that P. gingivalis may not be a normal inhabitant of a periodontally healthy dentition.
3

Reyes, Leticia. "Porphyromonas gingivalis." Trends in Microbiology 29, no. 4 (April 2021): 376–77. http://dx.doi.org/10.1016/j.tim.2021.01.010.

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4

Belibasakis, Georgios, Thomas Thurnheer, and Nagihan Bostanci. "Porphyromonas gingivalis." Virulence 5, no. 4 (April 23, 2014): 463–64. http://dx.doi.org/10.4161/viru.28930.

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5

Zhou, Yun, Maryta Sztukowska, Qian Wang, Hiroaki Inaba, Jan Potempa, David A. Scott, Huizhi Wang та Richard J. Lamont. "Noncanonical Activation of β-Catenin by Porphyromonas gingivalis". Infection and Immunity 83, № 8 (1 червня 2015): 3195–203. http://dx.doi.org/10.1128/iai.00302-15.

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Porphyromonas gingivalisis an established pathogen in periodontal disease and an emerging pathogen in serious systemic conditions, including some forms of cancer. We investigated the effect ofP. gingivalison β-catenin signaling, a major pathway in the control of cell proliferation and tumorigenesis. Infection of gingival epithelial cells withP. gingivalisdid not influence the phosphorylation status of β-catenin but resulted in proteolytic processing. The use of mutants deficient in gingipain production, along with gingipain-specific inhibitors, revealed that gingipain proteolytic activity was required for β-catenin processing. The β-catenin destruction complex components Axin1, adenomatous polyposis coli (APC), and GSK3β were also proteolytically processed byP. gingivalisgingipains. Cell fractionation and Western blotting demonstrated that β-catenin fragments were translocated to the nucleus. The accumulation of β-catenin in the nucleus followingP. gingivalisinfection was confirmed by immunofluorescence microscopy. A luciferase reporter assay showed thatP. gingivalisincreased the activity of the β-catenin-dependent TCF/LEF promoter.P. gingivalisdid not increase Wnt3a mRNA levels, a finding consistent withP. gingivalis-induced proteolytic processing causing the increase in TCF/LEF promoter activity. Thus, our data indicate thatP. gingivaliscan induce the noncanonical activation of β-catenin and disassociation of the β-catenin destruction complex by gingipain-dependent proteolytic processing. β-Catenin activation in epithelial cells byP. gingivalismay contribute to a proliferative phenotype.
6

Andrian, E., D. Grenier, and M. Rouabhia. "Porphyromonas gingivalis-Epithelial Cell Interactions in Periodontitis." Journal of Dental Research 85, no. 5 (May 2006): 392–403. http://dx.doi.org/10.1177/154405910608500502.

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Emerging data on the consequences of the interactions between invasive oral bacteria and host cells have provided new insights into the pathogenesis of periodontal disease. Indeed, modulation of the mucosal epithelial barrier by pathogenic bacteria appears to be a critical step in the initiation and progression of periodontal disease. Periodontopathogens such as Porphyromonas gingivalis have developed different strategies to perturb the structural and functional integrity of the gingival epithelium. P. gingivalis adheres to, invades, and replicates within human epithelial cells. Adhesion of P. gingivalis to host cells is multimodal and involves the interaction of bacterial cell-surface adhesins with receptors expressed on the surfaces of epithelial cells. Internalization of P. gingivalis within host cells is rapid and requires both bacterial contact-dependent components and host-induced signaling pathways. P. gingivalis also subverts host responses to bacterial challenges by inactivating immune cells and molecules and by activating host processes leading to tissue destruction. The adaptive ability of these pathogens that allows them to survive within host cells and degrade periodontal tissue constituents may contribute to the initiation and progression of periodontitis. In this paper, we review current knowledge on the molecular cross-talk between P. gingivalis and gingival epithelial cells in the development of periodontitis.
7

Enersen, Morten, Kazuhiko Nakano, and Atsuo Amano. "Porphyromonas gingivalis fimbriae." Journal of Oral Microbiology 5, no. 1 (January 1, 2013): 20265. http://dx.doi.org/10.3402/jom.v5i0.20265.

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8

Darveau, Richard P., Carol M. Belton, Robert A. Reife, and Richard J. Lamont. "Local Chemokine Paralysis, a Novel Pathogenic Mechanism for Porphyromonas gingivalis." Infection and Immunity 66, no. 4 (April 1, 1998): 1660–65. http://dx.doi.org/10.1128/iai.66.4.1660-1665.1998.

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ABSTRACT Periodontitis, which is widespread in the adult population, is a persistent bacterial infection associated with Porphyromonas gingivalis. Gingival epithelial cells are among the first cells encountered by both P. gingivalis and commensal oral bacteria. The chemokine interleukin 8 (IL-8), a potent chemoattractant and activator of polymorphonuclear leukocytes, was secreted by gingival epithelial cells in response to components of the normal oral flora. In contrast, P. gingivalis was found to strongly inhibit IL-8 accumulation from gingival epithelial cells. Inhibition was associated with a decrease in mRNA for IL-8. Antagonism of IL-8 accumulation did not occur in KB cells, an epithelial cell line that does not support high levels of intracellular invasion by P. gingivalis. Furthermore, a noninvasive mutant of P. gingivalis was unable to antagonize IL-8 accumulation. Invasion-dependent destruction of the gingival IL-8 chemokine gradient at sites of P. gingivaliscolonization (local chemokine paralysis) will severely impair mucosal defense and represents a novel mechanism for bacterial colonization of host tissue.
9

Jauregui, Catherine E., Qian Wang, Christopher J. Wright, Hiroki Takeuchi, Silvia M. Uriarte, and Richard J. Lamont. "Suppression of T-Cell Chemokines by Porphyromonas gingivalis." Infection and Immunity 81, no. 7 (April 15, 2013): 2288–95. http://dx.doi.org/10.1128/iai.00264-13.

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ABSTRACTPorphyromonas gingivalisis a major pathogen in periodontal disease and is associated with immune dysbiosis. In this study, we found thatP. gingivalisdid not induce the expression of the T-cell chemokine IP-10 (CXCL10) from neutrophils, peripheral blood mononuclear cells (PBMCs), or gingival epithelial cells. Furthermore,P. gingivalissuppressed gamma interferon (IFN-γ)-stimulated release of IP-10, ITAC (CXCL11), and Mig (CXCL9) from epithelial cells and inhibited IP-10 secretion in a mixed infection with the otherwise stimulatoryFusobacterium nucleatum. Inhibition of chemokine expression occurred at the level of gene transcription and was associated with downregulation of interferon regulatory factor 1 (IRF-1) and decreased levels of Stat1. Ectopic expression of IRF-1 in epithelial cells relievedP. gingivalis-induced inhibition of IP-10 release. Direct contact betweenP. gingivalisand epithelial cells was not required for IP-10 inhibition. These results highlight the immune-disruptive potential ofP. gingivalis. Suppression of IP-10 and other Th1-biasing chemokines byP. gingivalismay perturb the balance of protective and destructive immunity in the periodontal tissues and facilitate the pathogenicity of oral microbial communities.
10

Waller, Tobias, Laura Kesper, Josefine Hirschfeld, Henrik Dommisch, Johanna Kölpin, Johannes Oldenburg, Julia Uebele, et al. "Porphyromonas gingivalis Outer Membrane Vesicles Induce Selective Tumor Necrosis Factor Tolerance in a Toll-Like Receptor 4- and mTOR-Dependent Manner." Infection and Immunity 84, no. 4 (February 8, 2016): 1194–204. http://dx.doi.org/10.1128/iai.01390-15.

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Porphyromonas gingivalisis an important member of the anaerobic oral flora. Its presence fosters growth of periodontal biofilm and development of periodontitis. In this study, we demonstrated that lipophilic outer membrane vesicles (OMV) shed fromP. gingivalispromote monocyte unresponsiveness to liveP. gingivalisbut retain reactivity to stimulation with bacterial DNA isolated fromP. gingivalisor AIM2 ligand poly(dA·dT). OMV-mediated tolerance ofP. gingivalisis characterized by selective abrogation of tumor necrosis factor (TNF). Neutralization of interleukin-10 (IL-10) during OMV challenge partially restores monocyte responsiveness toP. gingivalis; full reactivity toP. gingivaliscan be restored by inhibition of mTOR signaling, which we previously identified as the major signaling pathway promoting Toll-like receptor 2 and Toll-like receptor 4 (TLR2/4)-mediated tolerance in monocytes. However, despite previous reports emphasizing a central role of TLR2 in innate immune recognition ofP. gingivalis, our current findings highlight a selective role of TLR4 in the promotion of OMV-mediated TNF tolerance: only blockade of TLR4—and not of TLR2—restores responsiveness toP. gingivalis. Of further note, OMV-mediated tolerance is preserved in the presence of cytochalasin B and chloroquine, indicating that triggering of surface TLR4 is sufficient for this effect. Taking the results together, we propose thatP. gingivalisOMV contribute to local immune evasion ofP. gingivalisby hampering the host response.
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Статті в журналах Дисертації

Дисертації з теми "Porphyromonas gingivalis":

1

Loomer, Peter Michael. "The direct effects of Porphyromonas gingivalis 2561 on bone formation and mineral resorption in vitro." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ27685.pdf.

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2

Meuric, Vincent. "Virulence de Porphyromonas gingivalis." Rennes 1, 2008. http://www.theses.fr/2008REN1B197.

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"Porphyromonas gingivalis est une bactérie anaérobie stricte responsable des maladies parodontales. La respiration et la régulation des gènes de virulence restent inconnues. Ce travail explore la chaîne respiratoire et montre l'aérotolérance de la bactérie. Les résultats affirment la capacité de transmission aéroportée et inter individus par des mécanismes activant des gènes de résistance au stress oxydatif tel que "tpx" sous la dépendance d'OsyR régulateur transcriptionnel. Après une analyse de la littérature sur les principaux gènes de virulence, hémagglutinines et gingipaïnes, les études expérimentales ont montré que l'oxygène atmosphérique n'influence pas leur expression. Par contre, la coagrégation "in vitro" avec "T. Denticola", autre parodontopathogène, entraîne la surespression de "hagA", "rgpA" et "kgp" et par ce phénomène favorise le développement de la maladie parodontale. "
3

Hoppe, Tatjana [Verfasser]. "Maligne Transformation gingivaler Epithelzellen durch Porphyromonas gingivalis / Tatjana Hoppe." Bonn : Universitäts- und Landesbibliothek Bonn, 2017. http://d-nb.info/1140525883/34.

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4

Lobos, Matthei Ignacio Felipe. "Regulación de survivina en células epiteliales gingivales infectadas por Porphyromonas gingivalis." Tesis, Universidad de Chile, 2014. http://www.repositorio.uchile.cl/handle/2250/117229.

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Memoria para optar el título de Bioquímico
La periodontitis crónica es una enfermedad de etiología infecciosa, caracterizada por la respuesta inflamatoria e inmune exacerbada por parte del hospedero que produce la destrucción de tejidos de soporte del diente. Actualmente, se postula que para el establecimiento de esta patología se produce una sucesión ecológica desde una comunidad microbiana asociada a salud hacia una asociada a enfermedad periodontal. En esta sucesión es imprescindible la presencia de ciertos patógenos que faciliten el remodelamiento de la microbiota oral y la progresión hacia enfermedad, siendo Porphyromonas gingivalis un patógeno clave en este proceso. P. gingivalis es una bacteria anaerobia estricta capaz de invadir y permanecer al interior de células epiteliales gingivales. Interesantemente, la infección por P. gingivalis produce una mayor viabilidad celular, mediante la modulación de proteínas relacionadas con apoptosis. Se ha sugerido que la proteína inhibidora de la apoptosis, survivina, podría contribuir a la inhibición de la apoptosis mediada por P. gingivalis; sin embargo, su participación en este proceso no está completamente dilucidada. En esta memoria de título se estudió si P. gingivalis es capaz de modular los niveles de survivina en la línea celular de epitelio gingival OKF6/TERT2 y si esta modulación está relacionada con el grado de virulencia de la bacteria. Para ello, se infectaron células OKF6/TERT2 utilizando dos cepas de referencia y un aislado clínico, cada una con diferente virulencia. Luego, se determinaron los niveles de proteína y transcrito de survivina a tiempos tempranos y tardíos post-invasión, mediante Western blot y RT-PCR. Los resultados obtenidos indican que P. gingivalis es capaz de disminuir los niveles de survivina y que esta modulación podría estar relacionada con la virulencia de la bacteria. Sin embargo, la disminución de survivina no estaría relacionada directamente con la inhibición de apoptosis que genera la infección por P. gingivalis
Chronic periodontitis is an infectious disease characterized by an exacerbated inflammatory and immune response by the host, which causes the destruction of the tooth supporting tissues. Nowadays, it is assumed that for the onset of this pathology an ecological succession from a bacterial community associated to health, to one associated with periodontal disease is produced. In this succession, the presence of certain pathogens facilitate the remodeling of the oral microbiota and the consequent progression to disease, being Porphyromonas gingivalis a key pathogen in this process. P. gingivalis is a strict anaerobic bacterium capable of invading and persisting within gingival epithelial cells. Interestingly, infection by P. gingivalis produce an increase in the viability of these cells by modulation of apoptosis related proteins. It has been suggested that the apoptosis inhibitory protein, survivin, could contribute to the inhibition of apoptosis mediated by P. gingivalis; however, its participation in this process is still unknown. In this work, we studied whether P. gingivalis is capable of modulate survivin levels in gingival epithelial cells OKF6/TERT2 and if this modulation is related to bacterial virulence. To achieve this goals we infected OKF6/TERT2 cells with two reference strains and one clinical isolate, each with different virulence. Survivin protein and transcript levels were determined at early and late post-infection times by Western blot and RT-PCR. The results of this work indicated that P. gingivalis is capable of decreasing survivin levels and this modulation could be related to virulence features of the bacterium. Nevertheless, survivin decrease would not be directly related to the inhibition of apoptosis induced by P. gingivalis
5

Bugueño, Valdebenito Isaac Maximiliano. "Caracterización de aislados clínicos de Porphyromonas gingivalis y su efecto en la viabilidad de células epiteliales gingivales." Tesis, Universidad de Chile, 2014. http://www.repositorio.uchile.cl/handle/2250/130110.

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Trabajo de Investigación Requisito para optar al Título de Cirujano Dentista
La periodontitis es una enfermedad infecciosa multifactorial, caracterizada por una respuesta inflamatoria exacerbada que produce la destrucción de las estructuras que dan soporte al diente, incluyendo la encía, el ligamento periodontal, el cemento radicular y el hueso alveolar. Para la iniciación de las periodontitis, se requiere la presencia de una comunidad bacteriana subgingival compleja en la cual coexisten diversos géneros y especies microbianas. Dentro de las especies del complejo rojo de Socransky que contribuyen a la etiología de la enfermedad periodontal, está Porphyromonas gingivalis (P. gingivalis). P. gingivalis es una bacteria Gram negativo que tendría especial relevancia en la progresión de la periodontitis. Entre los factores de virulencia de P. gingivalis se encuentran el lipopolisacárido (LPS), las fimbrias y el antígeno K o cápsula, los cuales están involucrados en el proceso de infección. La expresión de estos factores de virulencia por parte de la bacteria, puede variar de manera importante entre individuos, generando una respuesta distinta en los tejidos infectados, como en células epiteliales gingivales. Se ha descrito que P. gingivalis puede invadir las células epiteliales de la encía y modular diferentes vías de señalización que generen inhibición de la activación del sistema inmune e inhibición de la apoptosis celular. En este trabajo, se evaluaron características de la envoltura celular, y propiedades macro y microscópicas de aislados clínicos de P. gingivalis y cepas de referencia, y se evaluó su efecto sobre la viabilidad de células epiteliales gingivales. De esta manera, se analizaron parámetros macromorfológicos de las cepas en medios sólido y líquido. Se evaluó la capacidad de formación de biopelículas, la carga superficial (mediante ensayos de unión a citocromo C y ensayos de hidrofobicidad), se estudió la presencia de cápsula (tinción con tinta china) y caracterizó los perfiles electroforéticos del LPS. Finalmente, se estudió la viabilidad y el nivel de apoptosis de células epiteliales gingivales infectadas por 9 dos cepas virulentas de referencia y 7 aislados clínicos de P. gingivalis, utilizando la línea celular OKF6/TERT2. Estos ensayos fueron realizados en tiempos tempranos, intermedios y tardíos de infección. Nuestros resultados mostraron diferencias en el crecimiento entre aislados clínicos de individuos sanos comparados con enfermos, tanto en medio sólido como en medio líquido. En la mayoría de los aislados clínicos se observó presencia de cápsula. Además, todos formaron más biopelículas que las cepas de referencia, y no se encontraron diferencias significativas entre las muestras de pacientes sanos y enfermos. Adicionalmente, la mayoría de los aislados clínicos presentó una mayor carga superficial que las cepas de referencias. Nuestros resultados también mostraron que todos los aislados clínicos y cepas de referencia de P. gingivalis fueron capaces de invadir células OKF6/TERT2. Adicionalmente, observamos que algunos aislados clínicos aumentaron significativamente la viabilidad celular a tiempos tempranos y tardíos de infección, incluso más que la cepa W50 descrita como una cepa muy virulenta y altamente invasiva. En síntesis, nuestros resultados indican que existen diferencias macromorfológicas y de envoltura celular entre aislados clínicos de P. gingivalis provenientes de individuos sanos y enfermos y que la infección por P. gingivalis mantiene o aumenta la viabilidad en la línea celular derivada de epitelio gingival OKF6/TERT2, como consecuencia de la modulación de la apoptosis. También, observamos que éste fenómeno es dependiente de la virulencia de la cepa. La virulencia se relaciona con características de la envoltura celular y con la presencia de ciertos componentes específicos. Estos aislados clínicos más virulentos podrían estar asociados a cuadros clínicos más agresivos.
6

Maley, Janette. "Genetic studies on Porphyromonas gingivalis W83." Thesis, University of Leicester, 1994. http://hdl.handle.net/2381/35395.

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Until recently molecular biological approaches to the study of putative virulence factors of the oral pathogen Porphyromonas gingivalis were limited. This was due to the absence of a genetic system which could facilitate the production of isogenic mutant derivatives. Among the many components produced, the capsule is believed to be of particular importance in the pathogenicity of P. gingivalis. In order to identify mutants lacking capsular polysaccharide, purified capsular material from P. gingivalis W83 was used to generate capsule-specific antisera. However, these antisera contained antibodies which recognised lipopolysaccharide. The use of polymyxin B-agarose was found to be useful in the removal of LPS-reactive material. Capsular polysaccharide was purified further and shown to be free of detectable LPS. A system for conjugal transfer of plasmid DNA from Escherichia coli to P. gingivalis was developed. This method was then used for the introduction of the suicide-vector R751::Tn4351?4 into P. gingivalis. Examination of a number of P. gingivalis Tn4351 mutants demonstrated the presence of multiple copies of Tn4351 in the chromosome of the mutants. Recovery of plasmid pNJR12 from P. gingivalis transconjugants led to the isolation of IS 1126. This insertion sequence was present in the chromosome of all strains of P. gingivalis examined but absent from other members of the genus. The amino acid sequence of the major open reading frame (ORF1) was derived from the nucleotide sequence of IS 1126. ORF1 contained the conserved motifs displayed by the transposase proteins of IS-elements belonging to the IS4 family.
7

Xie, Hua. "Regulation of fimbrillin expression in Porphyromonas gingivalis." Thesis, Connect to this title online; UW restricted, 1998. http://hdl.handle.net/1773/6392.

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8

Rodrigues, Richelle Soares. "PrevalÃncia de Porphyromonas gingivalis, genÃtipo fima II de Porphyromonas gingivalis e Aggregatibacter actinomycetemcomitans em indivÃduos com periodontite agressiva generalizada." Universidade Federal do CearÃ, 2014. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=11486.

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Анотація:
CoordenaÃÃo de AperfeiÃoamento de Pessoal de NÃvel Superior
Conselho Nacional de Desenvolvimento CientÃfico e TecnolÃgico
Porphyromonas gingivalis e Aggregatibacter actinomycetemcomitans sÃo periodontopatÃgenos associados à periodontite agressiva. A fÃmbria, uma estrutura relacionada à adesÃo e à invasÃo de cÃlulas, à um dos principais fatores de virulÃncia de P. gingivalis. Baseado na sequÃncia de nucleotÃdeos, seis genÃtipos(fimA) que codificam a fÃmbria principal dessas bactÃrias foram identificados, sendo o fimA II mais comumente relacionado à destruiÃÃo periodontal. O objetivo deste trabalho foi avaliar, por meio de reaÃÃo em cadeia da polimerase em amostras de placa subgengival dos sÃtios com maior profundidade de sondagem de pacientes com periodontite agressiva, a prevalÃncia de P. gingivalis, do genÃtipo fimA II de P. gingivalis e de A. actinomycetemcomitans, assim como relacionar a presenÃa desses patÃgenos ou genÃtipo à idade e aos parÃmetros clÃnicos periodontais (Ãndice de placa, Ãndice de sangramento gengival, profundidade de sondagem e nÃvel de inserÃÃo) encontrados nesses pacientes. Foram selecionados 45 pacientes com periodontite agressiva generalizada, com idade entre 15 e 40 anos. Nessa populaÃÃo, 64,4% apresentaram P. gingivalis e 28,8% apresentaram A. actinomycetemcomitans em sua microbiota subgengival. Dos pacientes positivos para P. gingivalis, 82,6% apresentaram o genÃtipo fimA II. Ao se relacionar a presenÃa ou ausÃncia das bactÃrias ou genÃtipo aos dados clÃnicos e idade, foi observada diferenÃa estatisticamente significante entre o nÃvel clÃnico de inserÃÃo do sÃtio coletado de pacientes com presenÃa de P. gingivalis e seu genÃtipo fimA II quando comparados aos pacientes negativos para essa bactÃria e genÃtipo, sendo a perda de inserÃÃo significativamente maior em pacientes que apresentaram P. gingivalis e em paciente com seu genÃtipo fimA II. AlÃm disso, foi encontrada mÃdia de idade significativamente mais elevada em pacientes positivos para P. gingivalis que em pacientes negativos para essa bactÃria. Concluiu-se, assim, que P. gingivalis e seu genÃtipo fimA tipo II estÃo presentes em alta prevalÃncia em pacientes com periodontite agressiva, que A. actinomycetemcomitans està presente em menor proporÃÃo de indivÃduos na populaÃÃo estudada e que P. gingivalis parece ser mais comumente encontrada em bolsas mais profundas e em indivÃduos mais velhos.
Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans are periodontal pathogens associated with aggressive periodontitis. The fimbriae, a structure related to adhesion and invasion of cells, is one of the major virulence factors of P. gingivalis. Based on the nucleotide sequence, six genotypes(fimA) encoding the major fimbriae of these bacteria were identified, and the fimA II is the most commonly associated with periodontal destruction. The objective of this study was to evaluate, by polymerase chain reaction in subgingival plaque samples from sites with highest probing depth in patients with aggressive periodontitis, the prevalence of P. gingivalis, P. gingivalis genotype fimA II and A. actinomycetemcomitans, and relate the presence of these pathogens or genotype to age and clinical periodontal parameters (plaque index, gingival bleeding index, probing depth and clinical attachment level) in these patients. We selected 45 patients with generalized aggressive periodontitis, aged from 15 to 40 years. 64.4% of these patients harbored P. gingivalis and 28.8% harbored A. actinomycetemcomitans in their subgingival microbiota. In patients positive for P. gingivalis, 82.6 % presented the genotype fimA II. In relation to the presence or absence of bacteria or gene to clinical data and age, a statistically significant difference between clinical attachment level was observed in the selected sites of patients with the presence of P. gingivalis and its genotype fimA II when compared to patients negative for these bacteria and genotype, with periodontal loss significantly higher in patients harboring P. gingivalis and in patients harboring genotype fimA II. In addition, the average age in patients positives for P. gingivalis was significantly higher than in negative ones. It is therefore concluded that P. gingivalis and its genotype fimA II are present in high prevalence in patients with aggressive periodontitis, A. actinomycetemcomitans is present in a smaller proportion of individuals in the studied population and P. gingivalis seems to be more commonly found in deeper sites and older individuals.
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Rodrigues, Richelle Soares. "Prevalência de Porphyromonas gingivalis, genótipo fima II de Porphyromonas gingivalis e Aggregatibacter actinomycetemcomitans em indivíduos com periodontite agressiva generalizada." reponame:Repositório Institucional da UFC, 2014. http://www.repositorio.ufc.br/handle/riufc/7904.

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RODRIGUES, Richelle Soares. Prevalência de Porphyromonas gingivalis, genótipo fima II de Porphyromonas gingivalis e Aggregatibacter actinomycetemcomitans em indivíduos com periodontite agressiva generalizada. 2014. 44 f. Dissertação (Mestrado em Odontologia) - Universidade Federal do Ceará. Faculdade de Farmácia, Odontologia e Enfermagem, Fortaleza, 2014.
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Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans are periodontal pathogens associated with aggressive periodontitis. The fimbriae, a structure related to adhesion and invasion of cells, is one of the major virulence factors of P. gingivalis. Based on the nucleotide sequence, six genotypes(fimA) encoding the major fimbriae of these bacteria were identified, and the fimA II is the most commonly associated with periodontal destruction. The objective of this study was to evaluate, by polymerase chain reaction in subgingival plaque samples from sites with highest probing depth in patients with aggressive periodontitis, the prevalence of P. gingivalis, P. gingivalis genotype fimA II and A. actinomycetemcomitans, and relate the presence of these pathogens or genotype to age and clinical periodontal parameters (plaque index, gingival bleeding index, probing depth and clinical attachment level) in these patients. We selected 45 patients with generalized aggressive periodontitis, aged from 15 to 40 years. 64.4% of these patients harbored P. gingivalis and 28.8% harbored A. actinomycetemcomitans in their subgingival microbiota. In patients positive for P. gingivalis, 82.6 % presented the genotype fimA II. In relation to the presence or absence of bacteria or gene to clinical data and age, a statistically significant difference between clinical attachment level was observed in the selected sites of patients with the presence of P. gingivalis and its genotype fimA II when compared to patients negative for these bacteria and genotype, with periodontal loss significantly higher in patients harboring P. gingivalis and in patients harboring genotype fimA II. In addition, the average age in patients positives for P. gingivalis was significantly higher than in negative ones. It is therefore concluded that P. gingivalis and its genotype fimA II are present in high prevalence in patients with aggressive periodontitis, A. actinomycetemcomitans is present in a smaller proportion of individuals in the studied population and P. gingivalis seems to be more commonly found in deeper sites and older individuals.
Porphyromonas gingivalis e Aggregatibacter actinomycetemcomitans são periodontopatógenos associados à periodontite agressiva. A fímbria, uma estrutura relacionada à adesão e à invasão de células, é um dos principais fatores de virulência de P. gingivalis. Baseado na sequência de nucleotídeos, seis genótipos(fimA) que codificam a fímbria principal dessas bactérias foram identificados, sendo o fimA II mais comumente relacionado à destruição periodontal. O objetivo deste trabalho foi avaliar, por meio de reação em cadeia da polimerase em amostras de placa subgengival dos sítios com maior profundidade de sondagem de pacientes com periodontite agressiva, a prevalência de P. gingivalis, do genótipo fimA II de P. gingivalis e de A. actinomycetemcomitans, assim como relacionar a presença desses patógenos ou genótipo à idade e aos parâmetros clínicos periodontais (índice de placa, índice de sangramento gengival, profundidade de sondagem e nível de inserção) encontrados nesses pacientes. Foram selecionados 45 pacientes com periodontite agressiva generalizada, com idade entre 15 e 40 anos. Nessa população, 64,4% apresentaram P. gingivalis e 28,8% apresentaram A. actinomycetemcomitans em sua microbiota subgengival. Dos pacientes positivos para P. gingivalis, 82,6% apresentaram o genótipo fimA II. Ao se relacionar a presença ou ausência das bactérias ou genótipo aos dados clínicos e idade, foi observada diferença estatisticamente significante entre o nível clínico de inserção do sítio coletado de pacientes com presença de P. gingivalis e seu genótipo fimA II quando comparados aos pacientes negativos para essa bactéria e genótipo, sendo a perda de inserção significativamente maior em pacientes que apresentaram P. gingivalis e em paciente com seu genótipo fimA II. Além disso, foi encontrada média de idade significativamente mais elevada em pacientes positivos para P. gingivalis que em pacientes negativos para essa bactéria. Concluiu-se, assim, que P. gingivalis e seu genótipo fimA tipo II estão presentes em alta prevalência em pacientes com periodontite agressiva, que A. actinomycetemcomitans está presente em menor proporção de indivíduos na população estudada e que P. gingivalis parece ser mais comumente encontrada em bolsas mais profundas e em indivíduos mais velhos.
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Herrera, Bustamante Sergio Humberto. "Variabilidad del LPS de Porphyromonas gingivalis y Porphyromonas endodontalis en dientes con periodontitis apical asintomática." Tesis, Universidad de Chile, 2015. http://repositorio.uchile.cl/handle/2250/137646.

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Trabajo de Investigación Requisito para optar al Título de Cirujano Dentista
La Periodontitis Apical Asintomática (PAA) corresponde a una patología periapical de origen infeccioso que se caracteriza por la respuesta negativa a los tests de sensibilidad pulpar del diente afectado y por presentar, al examen radiográfico, un área radiolúcida peri y/o pararadicular. Histológicamente se puede clasificar como quiste radicular inflamatorio (QRI) o granuloma periapical (GP). Las comunidades microbianas asociadas a la PAA se caracterizan por infectar el sistema de canales radiculares (SCR) de los dientes y son muy variables en su composición, existiendo diferencias entre diferentes poblaciones geográficas, así como también dentro de una misma población. Porphyromonas gingivalis y Porphyromonas endodontalis, son especies bacterianas que se han visto asociadas a este tipo de infección, por medio de la interacción de sus factores de virulencia con las células del hospedero. Dentro de estos factores de virulencia está el lipopolisacárido (LPS), constituyente de la membrana externa de la pared celular más abundante de la superficie de ambas especies bacterianas y que podría explicar los efectos deletéreos en la destrucción del ligamento periodontal y del hueso, influyendo así en el aumento del tamaño de las lesiones apicales de origen endodóntico (ALEO). En este trabajo, realizamos una caracterización del perfil estructural del LPS de Porphyromonas gingivalis y Porphyromonas endodontalis y analizamos la variabilidad de éste entre los aislados obtenidos. Con este objetivo, inicialmente analizamos macromorfológicamente los cultivos en medio líquido y sólido de aislados clínicos de P. gingivalis y P. endodontalis, obtenidos de exudado periapical proveniente de dientes con diagnóstico de Periodontitis Apical Asintomática y luego caracterizamos el perfil electroforético del LPS en geles de SDS-poliacrilamida teñido con Nitrato de Plata de ambas especies bacterianas y las comparamos con sus respectivas cepas de referencia. Nuestros resultados mostraron una baja cantidad de canales radiculares infectados con P. gingivalis y P. endodontalis. Las características macromorfológicas de dichos microorganismos resultaron bastante similares a las de las cepas de referencia, sin embargo, se observaron diferencias entre ambas. En cuanto al perfil electroforético del LPS de ambas especies, pese a tener pocos aislados clínicos positivos para ambas, si hubo diferencias en el perfil electroforético de sus LPS, siendo más marcadas en las colonias de P. endodontalis. En síntesis, nuestros resultados indican que P. gingivalis y P. endodontalis están presentes en canales radiculares de dientes diagnosticados con PAA y que existen diferencias en las especies bacterianas estudiadas, tanto en sus características macromorfológicas, como en las características de sus LPS.
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Книги з теми "Porphyromonas gingivalis":

1

Loomer, Peter Michael. The direct effects of Porphyromonas Gingivalis 2561 on bone formation and mineral resorption in vitro. [Toronto: University of Toronto, Faculty of Dentistry], 1997.

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2

Sun, Frank. Identification of Porphyromonas (Bacteroides) Gingivalis outer membrane proteins that bind to and degrade human matrix proteins. [Toronto: Faculty of Dentistry, University of Toronto, 1992.

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3

Biology of the species Porphyromonas gingivalis. Boca Raton: CRC Press, 1993.

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4

Papaioannou, W. The Adhesion of Porphyromonas Gingivalis and Periodontitis. Leuven University Press, 1998.

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5

Andreou, Vana. Resveratrol mediated reversal of aryl hydrocarbon and porphyromonas gingivalis lipopolysaccharide induced inhibition of osteogenesis in vitro. 2002.

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6

Immunization with Porphyromonas Gingivalis Cysteine Protease: Effects on Experimental Gingivitis and Ligature-Induced Periodontitis in Macaca Fascicularis. Storming Media, 1997.

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7

J, Genco Robert, ed. Molecular pathogenesis of periodontaldisease. Washington, D.C: ASM Press, 1994.

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8

Molecular pathogenesis of periodontal disease. Washington, D.C: ASM Press, 1994.

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Частини книг з теми "Porphyromonas gingivalis":

1

Genco, Caroline Attardo, Waltena Simpson, and Teresa Olczak. "Porphyromonas gingivalis." In Iron Transport in Bacteria, 329–43. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555816544.ch21.

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2

Takeuchi, Hiroki, and Atsuo Amano. "Invasion of Gingival Epithelial Cells by Porphyromonas gingivalis." In Periodontal Pathogens, 215–24. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0939-2_21.

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3

Yongqing, Tang, Jan Potempa, Robert N. Pike, and Lakshmi C. Wijeyewickrema. "The Lysine-Specific Gingipain of Porphyromonas gingivalis." In Advances in Experimental Medicine and Biology, 15–29. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-1-4419-8414-2_2.

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4

Arndt, Annette, and Mary Ellen Davey. "Porphyromonas gingivalis: surface polysaccharides as virulence determinants." In Interface Oral Health Science 2009, 382–87. Tokyo: Springer Japan, 2010. http://dx.doi.org/10.1007/978-4-431-99644-6_111.

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5

McBride, Barry C., Umadatt Singh, and Angela Joe. "Porphyromonas gingivalis: Gene Cloning of Determinants of Pathogenicity." In Brock/Springer Series in Contemporary Bioscience, 552–68. New York, NY: Springer New York, 1993. http://dx.doi.org/10.1007/978-1-4615-7087-5_41.

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6

Amano, Atsuo, Youn-Hee Choi, and Hiroki Takeuchi. "Genotyping of Porphyromonas gingivalis in Relationship to Virulence." In Periodontal Pathogens, 53–59. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0939-2_6.

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7

Hasegawa, Yoshiaki, Keiji Nagano, Yukitaka Murakami, and Richard J. Lamont. "Purification of Native Mfa1 Fimbriae from Porphyromonas gingivalis." In Periodontal Pathogens, 75–86. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0939-2_8.

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8

Heidler, Thomas, and Karina Persson. "Crystallization of Recombinant Fimbrial Proteins of Porphyromonas gingivalis." In Periodontal Pathogens, 87–96. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0939-2_9.

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9

Kadowaki, Tomoko. "Enzymatic Characteristics and Activities of Gingipains from Porphyromonas gingivalis." In Periodontal Pathogens, 97–112. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0939-2_10.

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10

Yoshida, Yasuo. "Analysis of the Butyrate-Producing Pathway in Porphyromonas gingivalis." In Periodontal Pathogens, 167–72. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0939-2_16.

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Тези доповідей конференцій з теми "Porphyromonas gingivalis":

1

De la Garza-Ramos, M. A., A. Alcázar-Pizaña, M. Garza-Enriquez, R. Caffesse, V. Aguirre-Arzola, L. J. Galán-Wong, and B. Pereyra-Alférez. "Streptococcus intermedius trigger quorum-sensing genes in Porphyromonas gingivalis." In Proceedings of the III International Conference on Environmental, Industrial and Applied Microbiology (BioMicroWorld2009). WORLD SCIENTIFIC, 2010. http://dx.doi.org/10.1142/9789814322119_0113.

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2

Sieron, Aleksander, Andrzej Wiczkowski, Mariusz Adamek, Lucja Dyla, Sebastian Mazur, and Beata Wierucka-Mlynarczyk. "Photodynamic destruction of Porphyromonas gingivalis induced by delta-aminolaevulinic acid." In SPIE Proceedings, edited by Leonardo Longo, Alfons G. Hofstetter, Mihail-Lucian Pascu, and Wilhelm R. A. Waidelich. SPIE, 2004. http://dx.doi.org/10.1117/12.584427.

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3

Mahasneh, Arwa M., Michele Darby, Lynn Tolle, Mounir Laroussi, and Wayne Hynes. "Bactericidal effects of low temperature atmospheric pressure plasma on Porphyromonas gingivalis." In 2010 IEEE 37th International Conference on Plasma Sciences (ICOPS). IEEE, 2010. http://dx.doi.org/10.1109/plasma.2010.5534217.

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4

Mechid, Farida, Houda Hafirassou, Malika Meddad, Samir Salah, Saida Merad, Nawel Blidi, and Chafia Makhloufi-Dahou. "AB0255 CLINICO- BIOLOGICAL PROFILE OF RHEUMATOID ARTHRITIS WITH PERIODONTITIS AND PORPHYROMONAS GINGIVALIS." 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.3342.

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5

Jenning, M., B. Marklein, Z. Konthur, U. Nonhoff, G.-R. Burmester, and K. Skriner. "P043 Infection with citrullinating porphyromonas gingivalis can induce autoimmunity to human ribosomal proteins." In 39th European Workshop for Rheumatology Research, 28 February–2 March 2019, Lyon, France. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2018-ewrr2019.35.

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6

De La Garza-Ramos, M. A., A. L. Luna-Ayala, M. Garza-Enriquez, D. S. Martinez-Carreon, B. Pereyra-Alférez, and R. G. Caffesse. "Streptococcus intermedius can module the expression of some virulence factors in Porphyromonas gingivalis." In MICROBES IN APPLIED RESEARCH - Current Advances and Challenges. WORLD SCIENTIFIC, 2012. http://dx.doi.org/10.1142/9789814405041_0116.

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7

Wang, Zhi, Xi Wang, and Yiqun Jia. "Abstract 2358: Porphyromonas gingivalis promotes colorectal cancer development by regulating NLRP3 inflammasome signaling." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-2358.

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8

Wang, Zhi, Xi Wang, and Yiqun Jia. "Abstract 2358: Porphyromonas gingivalis promotes colorectal cancer development by regulating NLRP3 inflammasome signaling." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-2358.

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9

Minasari, Dr, and Dheina Leina Nasution. "The Effectivity of Lemongrass (Cymbopogon Citratus) Extract Against Porphyromonas Gingivalis ATCCr 33277t (IN-VITRO)." In International Dental Conference of Sumatera Utara 2017 (IDCSU 2017). Paris, France: Atlantis Press, 2018. http://dx.doi.org/10.2991/idcsu-17.2018.45.

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M. Alibasyah, Zulfan, Diana Setya Ningsih, Dr Sunnati, Ridha Andayani, and M. Irvan Juliansyah. "Minimum Inhibitory Concentration of Probiotic Soy-Milk Yoghurt (SOYGHURT) Towards Porphyromonas gingivalis [IN VITRO]." In International Dental Conference of Sumatera Utara 2017 (IDCSU 2017). Paris, France: Atlantis Press, 2018. http://dx.doi.org/10.2991/idcsu-17.2018.85.

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