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Thematische Bibliographien / Porphyromonas gingivalis infections

Auswahl der wissenschaftlichen Literatur zum Thema „Porphyromonas gingivalis infections“

Autor: Grafiati

Veröffentlicht am 4. Juni 2021

Zuletzt aktualisiert am 1. Februar 2022

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Zeitschriftenartikel zum Thema "Porphyromonas gingivalis infections":

1

Winkelhoff, Arie J., und Jørgen Slots. „Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis in nonoral infections“. Periodontology 2000 20, Nr. 1 (Juni 1999): 122–35. http://dx.doi.org/10.1111/j.1600-0757.1999.tb00160.x.

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2

Condorelli, Francesca, Guido Scalia, Giuditta Calì, Bruno Rossetti, Giuseppe Nicoletti und Anna M. Lo Bue. „Isolation of Porphyromonas gingivalisand Detection of Immunoglobulin A Specific to Fimbrial Antigen in Gingival Crevicular Fluid“. Journal of Clinical Microbiology 36, Nr. 8 (1998): 2322–25. http://dx.doi.org/10.1128/jcm.36.8.2322-2325.1998.

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The present study evaluated the prevalence of Porphyromonas gingivalis and the correlation between the bacterial culture method and the detection of immunoglobulin A (IgA) specific to theP. gingivalis fimbrial antigen in gingival crevicular fluid (GCF). P. gingivalis was isolated from 78.3% of subgingival plaque samples obtained from active sites and 34.7% of those from inactive sites of periodontal patients. P. gingivalis was isolated from only 4.7% of healthy subjects (control group). Immunoglobulins specific to the P. gingivalis fimbrial antigen were detected by enzyme-linked immunosorbent assay (ELISA). The overall agreement between the results of the P. gingivalis culture method and the results of specific IgA detection in periodontal patients was 71.7% for active sites and 58.7% for inactive sites. IgA specific to P. gingivalis was absent in GCF from all of the sites of healthy subjects. The results suggest that P. gingivalis is associated with the local production of specific IgA. The detection of IgA antibodies specific to P. gingivalis in GCF by ELISA may be used as a predictive parameter to reveal the early phase of the activation of recurrent periodontal infections.

3

Hirasawa, Masaaki, und Tomoko Kurita-Ochiai. „Porphyromonas gingivalis Induces Apoptosis and Autophagy via ER Stress in Human Umbilical Vein Endothelial Cells“. Mediators of Inflammation 2018 (29.07.2018): 1–8. http://dx.doi.org/10.1155/2018/1967506.

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It has been reported that periodontitis is associated with an increased risk of atherosclerosis. Accumulating evidence suggests that endothelial dysfunction is an early marker for atherosclerosis. To determine how periodontal infections contribute to endothelial dysfunction, we examined the effect of Porphyromonas gingivalis on human umbilical vein endothelial cells (HUVEC). P. gingivalis significantly suppressed the viability of HUVEC, induced DNA fragmentation and annexin V staining, and increased caspase-3, caspase-8, and caspase-9 activities. P. gingivalis also increased the expression of GADD153 and GRP78 and caspase-12 activity. Further, P. gingivalis induced autophagy, as evidenced by increased LC3-II and Beclin-1 levels. The suppression of P. gingivalis-induced autophagy by silencing of LC3 with siRNA significantly increased P. gingivalis-induced apoptosis. ER stress inhibitor, salubrinal, suppressed apoptosis and autophagy by inhibiting P. gingivalis-induced DNA fragmentation and LC3-II expression. These data suggest that P. gingivalis infection induces ER stress-mediated apoptosis followed by autophagic response that protects HUVEC from P. gingivalis-mediated apoptosis, potentially amplifying proatherogenic mechanisms in the perturbed vasculature.

4

Wu, Jie, und Hua Xie. „Role of Arginine Deiminase of Streptococcus cristatus in Porphyromonas gingivalis Colonization“. Antimicrobial Agents and Chemotherapy 54, Nr. 11 (26.07.2010): 4694–98. http://dx.doi.org/10.1128/aac.00284-10.

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ABSTRACT The ability to attach to a variety of oral surfaces is an important characteristic of Porphyromonas gingivalis. Previous studies have demonstrated that expression and production of FimA, a major subunit protein of the long fimbriae, is required for P. gingivalis colonization. Here we report that a surface protein, arginine deiminase (ArcA) of Streptococcus cristatus, represses FimA production and inhibits biofilm formation of P. gingivalis. This inhibitory function of ArcA is also observed in the formation of heterotypic P. gingivalis-Streptococcus gordonii biofilms. P. gingivalis is released from streptococcal substrates in the presence of ArcA, likely due to an inhibition of FimA production. This work suggests that ArcA may have the potential to be a specific antibiofilm agent to fight P. gingivalis infections.

5

Rôças, Isabela N., und José F. Siqueira. „Distribution of Porphyromonas gingivalis fimA genotypes in primary endodontic infections“. Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontology 109, Nr. 3 (März 2010): 474–78. http://dx.doi.org/10.1016/j.tripleo.2009.11.009.

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6

Odell, Lynnetta J., J. Craig Baumgartner, Tian Xia und Larry L. David. „Survey for collagenase gene prtC in Porphyromonas gingivalis and Porphyromonas endodontalis isolated from endodontic infections“. Journal of Endodontics 25, Nr. 8 (August 1999): 555–58. http://dx.doi.org/10.1016/s0099-2399(99)80379-3.

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7

Fiorillo, Luca, Gabriele Cervino, Luigi Laino, Cesare D’Amico, Rodolfo Mauceri, Tolga Fikret Tozum, Michele Gaeta und Marco Cicciù. „Porphyromonas gingivalis, Periodontal and Systemic Implications: A Systematic Review“. Dentistry Journal 7, Nr. 4 (11.12.2019): 114. http://dx.doi.org/10.3390/dj7040114.

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In recent scientific literature, oral infections and systemic manifestations, or correlations between oral health and systemic diseases are a topic of discussion. Porphyromonas gingivalis is one of the bacteria implicated in the biofilm formation of bacterial plaque, and plays an important role in the progression of periodontal disease. In this systematic review authors have evaluated the literature of the last 10 years on P. gingivalis and all the systemic implications proven. This study therefore evaluates all the districts of the organism in which this bacterium may have implications. From the results it emerges that P. gingivalis has implications in the onset of different systemic pathologies, including rheumatoid arthritis, cardiovascular pathologies, and neurodegenerative pathologies. Surely, understanding the mechanisms of diffusion of this bacterium, it would be possible to prevent a series of pathologies. Thus, putting the dentist clinician at the center of prevention for these diseases.

8

Maezono, H., Y. Noiri, Y. Asahi, M. Yamaguchi, R. Yamamoto, N. Izutani, H. Azakami und S. Ebisu. „Antibiofilm Effects of Azithromycin and Erythromycin on Porphyromonas gingivalis“. Antimicrobial Agents and Chemotherapy 55, Nr. 12 (12.09.2011): 5887–92. http://dx.doi.org/10.1128/aac.05169-11.

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ABSTRACTAntibiotic resistance of biofilm-grown bacteria contributes to chronic infections, such as marginal and periapical periodontitis, which are strongly associated withPorphyromonas gingivalis. Concurrent azithromycin (AZM) administration and mechanical debridement improve the clinical parameters of periodontal tissuein situ. We examined thein vitroefficacy of AZM againstP. gingivalisbiofilms. The susceptibilities of adherentP. gingivalisstrains 381, HW24D1, 6/26, and W83 to AZM, erythromycin (ERY), ampicillin (AMP), ofloxacin (OFX), and gentamicin (GEN) were investigated using a static model. The optical densities of adherentP. gingivaliscells were significantly decreased by using AZM and ERY at sub-MIC levels compared with those of the controls in all the strains tested, except for the effect of ERY on strain W83. AMP and OFX inhibitedP. gingivalisadherent cells at levels over their MICs, and GEN showed no inhibition in the static model. The effects of AZM and ERY against biofilm cells were investigated using a flow cell model. The ATP levels ofP. gingivalisbiofilms were significantly decreased by AZM at concentrations below the sub-MICs; however, ERY was not effective for inhibition ofP. gingivalisbiofilm cells at their sub-MICs. Furthermore, decreased density ofP. gingivalisbiofilms was observed three-dimensionally with sub-MIC AZM, using confocal laser scanning microscopy. These findings suggest that AZM is effective againstP. gingivalisbiofilms at sub-MIC levels and could have future clinical application for oral biofilm infections, such as chronic marginal and periapical periodontitis.

9

Siqueira, José F., Isabela N. Rôças und Marlei G. Silva. „Prevalence and Clonal Analysis of Porphyromonas gingivalis in Primary Endodontic Infections“. Journal of Endodontics 34, Nr. 11 (November 2008): 1332–36. http://dx.doi.org/10.1016/j.joen.2008.08.021.

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10

Loos, B. G., D. Mayrand, R. J. Genco und D. P. Dickinson. „Genetic Heterogeneity of Porphyromonas (Bacteroides) gingivalis by Genomic DNA Fingerprinting“. Journal of Dental Research 69, Nr. 8 (August 1990): 1488–93. http://dx.doi.org/10.1177/00220345900690080801.

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This study describes the use of total genomic DNA fingerprinting with the use of restriction endonucleases to characterize clinical isolates of Porphyromonas gingivalis (Bacteroides gingivalis) obtained from patients with periodontitis or with root-canal infections. The majority of independent isolates had a unique DNA fingerprint, indicating extensive genetic heterogeneity within this species. Twenty-nine distinct DNA fingerprints were found among the 33 isolates investigated. This is in contrast to biotyping and serotyping, where only one type and three types, respectively, have been reported. The observed heterogeneity indicates that DNA fingerprinting is a sensitive measure of genetic dissimilarity between P. gingivalis isolates and is able to characterize individual isolates. These results have ecological implications, indicating that there is considerable natural diversity in the global population of P. gingivalis, and that there are likely to be relatively large numbers of genetically distinct clonal lines. Furthermore, DNA fingerprinting is a sensitive and powerful tool for longitudinal and cross-sectional epidemiological studies. This technique provides far greater discrimination between isolates than either biotyping or serotyping, and will be most helpful in, for example, the analysis of distribution of clonal lines within one periodontal patient, or the analysis of the transmission to and turnover of strain populations within a patient population, since the probability of two strains with the same DNA fingerprint being found by chance is small.

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Dissertationen zum Thema "Porphyromonas gingivalis infections":

1

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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2

Díaz, Patricia I. „Studies on the oxidative stress response of porphyromonas gingivalis : a thesis submitted in fulfillment of the requirements for admission to the degree of Doctor of Philosophy /“. Title page, summary and table of contents only, 2002. http://web4.library.adelaide.edu.au/theses/09PH/09phd5426.pdf.

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3

Leclerc, Julia. „Etude d’un système respiratoire de Porphyromonas gingivalis, pathogène impliqué dans les infections parodontales“. Thesis, Rennes 1, 2015. http://www.theses.fr/2015REN1B032/document.

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Les parodontites sont des maladies chroniques inflammatoires causées par un biofilm bactérien. Elles sont la première cause de perte des dents dans les pays industrialisés et représentent donc un coût important pour la société. Le biofilm buccal est composé de plus de 500 espèces différentes, parmi lesquelles Porphyromonas gingivalis est reconnue comme une cause majeure du développement des symptômes. Cette bactérie à Gram négatif est considérée comme anaérobie bien qu’elle tolère des concentrations faibles en oxygène, ce qui favorise la colonisation de la cavité orale. Notre objectif était de mettre en évidence les processus biologiques conférant à P. gingivalis sa résistance à l’oxygène et au stress oxydant, mais également ceux impliqués dans la transition métabolique en concentrations variables d’oxygène. Des analyses in silico des génomes de souches de P. gingivalis ont révélé la présence d’un système respiratoire dépendant de l’oxygène, impliquant une cytochrome bd oxydase CydAB. Nous avons construit un mutant de P. gingivalis ATCC 33277 par délétion des gènes cydAB. Nos travaux ont montré que ce mutant était plus sensible que la souche parentale aux espèces réactives de l’oxygène (ROS) dont le peroxyde d’hydrogène et le générateur d’anion superoxyde paraquat. De plus, nous avons démontré que CydAB était impliquée dans le phénotype aérotolérant de P. gingivalis, et que cette enzyme consommait effectivement l’oxygène grâce à une étude par oxygraphie à haute résolution. Les mécanismes de régulations en réponse aux ROS et à l’oxygène sont encore mal connus, notamment en ce qui concerne la régulation positive de l’expression des gènes cydAB en présence d’oxygène. Deux gènes codant des régulateurs de type FNR ont été identifiés dans le génome de P. gingivalis, l’un d’entre eux codant un régulateur de la réponse au stress nitrosant, HcpR. Le second gène PGN_1569 a fait l’objet de notre étude. Par mutation et par analyses transcriptomiques, nous avons démontré que ce régulateur s’autorégulait négativement et activait l’expression de 4 groupes de gènes en anaérobie, n’incluant pas les gènes cydAB. L’expression de ces gènes est par ailleurs contrôlée par d’autres régulateurs redox, OxyR et/ou SigH et/ ou RprY. Cette étude met donc en évidence une connexion entre FNR et les autres régulateurs de la réponse au stress oxydant chez P. gingivalis. Des études complémentaires permettront de caractériser la fonction encore hypothétique des protéines codées par le régulon FNR. Il est intéressant de noter que l’absence de FNR confère à P. gingivalis une plus grande capacité à former un biofilm en anaérobie
Periodontal diseases are chronic inflammatory infections caused by bacteria in oral biofilm they are the first cause of loss of tooth in industrial countries with an important cost for the society. The biofilm comprises more than 500 bacterial species. Amongst them, Porphyromonas gingivalis, a Gram-negative bacterium, is well known as a major causative agent of periodontitis. Although considered as mainly anaerobe, P. gingivalis tolerates low oxygen concentration, therefore enhancing its ability to colonize the oral cavity. Our aim was to decipher the biological processes underpinning the resistance of P. gingivalis to oxygen and reactive oxygen species (ROS) and to characterise the transition from anaerobiosis to hypoxia. In silico studies of P. gingivalis genomes have revealed the presence of a putative oxygen-dependent respiratory system involving a cytochrome bd oxidase CydAB. We constructed a mutant deleted for cydAB genes in the P. gingivalis ATCC 33277 strain. Our study showed that cydAB mutation increased the sensibility of the mutant to reactive oxygen species such as the anion-superoxide generator paraquat and hydrogen peroxide. Moreover we demonstrated that CydAB is involved in the aerotolerance of P. gingivalis, and in oxygen consumption, as demonstrated by high resolution respirometry assay. Many regulations in response to ROS and oxygen are still unexplained in P. gingivalis, including the activation of cydAB expression by oxygen exposure. Two genes encoding FNR-like regulators were identified in the genome of P. gingivalis. One of them encodes the HcpR regulator which controls part of the nitrosative stress response. The second gene PGN_1569 was the focus of our study. By mutation and transcriptome analysis, we demonstrated that this FNR-like regulator repressed its own transcription and activated the expression of 4 gene clusters in anaerobiosis, but not including cydAB genes. The expression of these 4 gene clusters is also controlled by other redox regulators, OxyR and/or SigH and/or RprY. Therefore, this study pointed out the interplay between FNR and known oxidative stress response regulators of P. gingivalis. Further work will study the functions of the hypothetical proteins encoded by the FNR regulon. Interestingly, the fnr mutant displayed higher ability than the wild-type strain to form biofilm in anaerobiosis

4

Belvin, Benjamin R. „Nitrosative stress sensing in Porphyromonas gingivalis: structure and function of the heme binding transcriptional regulator HcpR“. VCU Scholars Compass, 2017. https://scholarscompass.vcu.edu/etd/5123.

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Porphyromonas gingivalis, a Gram negative anaerobe implicated in the progression of periodontal disease, is capable of surviving and causing infection despite high levels of reactive nitrogen species found in the oral cavity due to its efficient nitrosative stress response. HcpR is an important sensor-regulator that plays a vital step in the initiation of the nitrosative stress response in many Gram negative anaerobic bacteria. We employ a combination of X-ray crystallography, SAXS, resonance Raman spectroscopy, UV-Vis spectroscopy, and molecular biology techniques to better understand this key regulator. Knockout of the hcpR gene in W83 P. gingivalis results in the inability of the bacteria to grow in physiological concentrations of nitrite and complementation of hcpR using the novel plasmid Pg108 rescues this phenotype. HcpR causes a drastic, dose dependent upregulation of PG0893, a gene coding for a putative NO reductase, when exposed to nitrite or nitric oxide. Full transcriptome sequencing reveals that hcp is the only significantly upregulated gene when P. gingivalis is exposed to nitrite and knockout of hcp resulted in a phenotype that is similar to that of the hcpR deficient strain. HcpR directly regulates the expression of hcp via direct binding to an inverted repeat sequence in the promoter region of the hcp gene. We present a 2.6 Å crystal structure of the N-terminal sensing domain of HcpR and show that it is FNR-CRP regulator. A putative hydrophobic heme binding pocket was identified in the junction between the N-terminal domain and the dimerization helix. Mutation of two methionine residues (Met68 and Met145) in this pocket abrogates activation of HcpR thus verifying the binding site. Heme bound to HcpR exhibits heme iron as a hexa-coordinate system in the absence of nitric oxide (NO) and upon nitrosylation transitions to a penta-coordinated system. Finally, Small Angle X-ray Scattering experiments of the full length HcpR reveal that the C-terminal DNA binding domain of HcpR has a high degree of interdomain flexibility.

5

Huck, Olivier. „Infection et stimulation de cellules endothéliales par Porphyromonas gingivalis et son lipopolysaccharide : lien entre maladies parodontales et athérosclérose“. Thesis, Strasbourg, 2013. http://www.theses.fr/2013STRAJ021.

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Depuis plusieurs années, l’influence des pathologies parodontales sur certaines pathologies systémiques, notamment les maladies cardio-vasculaires et l’athérosclérose apparait de plus en plus évidente. Dans notre étude, nous nous sommes intéressés à l’évaluation des effets induits par Porphyromonas gingivalis, une des principales bactéries parodontopathogènes, et son lipopolysaccharide sur les cellules endothéliales, qui forment une interface entre le flux sanguin et la paroi vasculaire, d’où un rôle important dans l’initiation et le développement de la plaque d’athérome. Nous avons surtout ciblé les effets induits sur la cathepsine B, une protéase impliquée dans le développement de la plaque d’athérome, et sur l’inflammasome, un complexe impliqué dans la production d’IL-1beta. Les résultats de nos travaux montrent que l’infection par Porphyromonas gingivalis et la stimulation par son LPS sont capables d’induire une augmentation de l’activité enzymatique de la cathepsine B, ceci suivant différentes cinétiques. Dans les deux cas, ces augmentations d’activité se font sans modifications de la synthèse d’ARNm, ni de la concentration protéique de l’enzyme. Nos résultats démontrent également que l’infection par Porphyromonas gingivalis entraine une augmentation de l’expression ARN de l’inflammasome NLRP3, mais celle ci n’est pas observée au niveau protéique du fait d’un processus de protéolyse de la protéine NLRP3 suite à l’infection. Dans un deuxième temps, nous avons développé un modèle de parodontite expérimentale, fiable et reproductible, nous permettant d’envisager une expérimentation in vivo afin d’observer les interactions à distance entre maladies parodontales et athérosclérose sur dessouris apolipoprotéine-E -/-
Periodontal diseases have been linked to systemic diseases especially cardiovascular diseases and atherosclerosis. In our study, we investigated the effects induced by an infection with Porphyromonas gingivalis, a major periodontal pathogen, and stimulation by its lipopolysaccharide on endothelial cells at the interface between the inner part of arteries and blood flow. We focused on the effects induced on cathepsin B, a protease involved in atherosclerosis and on the activation of inflammasome, an intracellular complex linked to secretion of IL-1beta. Results showed that infection with Porphyromonas gingivalis and stimulation by its lipopolysaccharide increase enzymatic activity of cathepsin B with different kinetics. These modifications are observed without any modifications of RNAm expression and protein concentration. We also showed that infection with Porphyromonas gingivalis increases RNAm expression of NLRP3 but this increase at the RNAm level is not associated with an increase of the protein concentration due to an induced proteolysis. Furthermore, we developed a reliable model of experimental periodontitis that will be used to analyze interactions between periodontitis and systemic diseases in vivo, especially in apolipoprotein-E -/- mice

6

Nakka, Sravya Sowdamini. „Development of novel tools for prevention and diagnosis of Porphyromonas gingivalis infection and periodontitis“. Doctoral thesis, Örebro universitet, Institutionen för medicinska vetenskaper, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-52056.

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Periodontitis is a chronic inflammatory disease caused by exaggerated host immune responses to dysregulated microbiota in dental biofilms leading to degradation of tissues and alveolar bone loss. Porphyromonas gingivalis is a major periodontal pathogen and expresses several potent virulence factors. Among these factors, arginine and lysine gingipains are of special importance, both for the bacterial survival/proliferation and the pathological outcome. The major aim of this thesis was to develop and test novel methods for diagnosis and prevention of P. gingivalis infection and periodontitis. In study I, anti-P. gingivalis antibodies were developed in vitro for immunodetection of bacteria in clinical samples using a surface plasmon resonance (SPR)-based biosensor. Specific binding of the antibodies to P. gingivalis was demonstrated in samples of patients with periodontitis and the results were validated using real-time PCR and DNA-DNA checkerboard analysis. In study II, we elucidated the properties and antimicrobial effects of different lactobacillus species and the two-peptide bacteriocin PLNC8 αβ on P. gingivalis. L. plantarum NC8 and 44048 effectively inhibited P. gingivalis growth and pure PLNC8 αβ induced bacterial lysis by damaging P. gingivalis membrane. In study III, we demonstrated that PLNC8 αβ dose-dependently induces proliferation and release of growth factors in gingival epithelial cells (GECs). Furthermore, PLNC8 αβ decreased P. gingivalis-induced cytotoxic effects in GECs but did not alter the effect of gingipains on cytokine expression. In study IV, we elucidated the effects of anti-P. gingivalis antibodies and PLNC8 αβ in regulating cellular responses during P. gingivalis infection. Both antibodies and PLNC8 αβ modulated P. gingivalis-induced expression of growth factors in GECs, however, their effects were diminished when used in combination. The results of this thesis demonstrate a possible role of anti-P. gingivalis antibodies and PLNC8 αβ in prevention and treatment of P. gingivalis infection and periodontitis with no cytotoxic effects on human cells.

7

Reader, Brenda Faye. „Social Stress Induces Immunoenhancement During Allergic Airway Inflammation and Infection“. The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1385475903.

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8

Gross, Jane Elizabeth. „Local and systemic host immune responses to Porphyromonas gingivalis A7436 infection in a subcutaneous tissue chamber in untreated and lipopolysaccharide-treated mice“. 1999. http://catalog.hathitrust.org/api/volumes/oclc/48199463.html.

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9

Díaz, Patricia I. „Studies on the oxidative stress response of porphyromonas gingivalis : a thesis submitted in fulfillment of the requirements for admission to the degree of Doctor of Philosophy“. 2002. http://web4.library.adelaide.edu.au/theses/09PH/09phd5426.pdf.

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10

Lin, Yuh-Yih. „Characterization of the molecular and cellular events that determine outcome of infection with Porphyromonas gingivalis in a mouse chamber model“. Diss., 1998. http://catalog.hathitrust.org/api/volumes/oclc/47976721.html.

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Bücher zum Thema "Porphyromonas gingivalis infections":

1

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

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2

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

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3

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

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Buchteile zum Thema "Porphyromonas gingivalis infections":

1

Joly, Sophie, Myriam Bélanger, Georgia K. Johnson, Ann Progulske-Fox und Kim A. Brogden. „Infection with Porphyromonas gingivalis, a Potential Risk Factor for Chronic Systemic Disease“. In Sequelae and Long-Term Consequences of Infectious Diseases, 443–57. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555815486.ch25.

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2

Han, Xiaozhe, Xiaoping Lin, Toshihisa Kawai, Karen B. LaRosa und Martin A. Taubman. „Porphyromonas gingivalis infection elicits immune-mediated RANKL-dependent periodontal bone loss in rats“. In Interface Oral Health Science 2009, 400–402. Tokyo: Springer Japan, 2010. http://dx.doi.org/10.1007/978-4-431-99644-6_114.

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3

Khalaf, Hazem, Eleonor Palm und Torbjörn Bengtsson. „Cellular Response Mechanisms in Porphyromonas gingivalis Infection“. In Periodontitis - A Useful Reference. InTech, 2017. http://dx.doi.org/10.5772/intechopen.69019.

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Konferenzberichte zum Thema "Porphyromonas gingivalis infections":

1

Jenning, M., B. Marklein, Z. Konthur, U. Nonhoff, G.-R. Burmester und 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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Jenning, M., B. Marklein, Y. Ytterberg, A. Catarina, D. Schaardenburg, G. Bürmester und K. Skriner. „P013 Porphyromonas gingivalis infection linked to ra onset and ANTI TNF alpha treatment non-response“. In 38th European Workshop for Rheumatology Research, 22–24 February 2018, Geneva, Switzerland. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-ewrr2018.38.

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Jenning, Madeleine, Bianka Marklein, Ute Nonhoff, Zoltan Konthur, Gerd Rüdiger Burmester und Karl Skriner. „SAT0049 INFECTION WITH CITRULLINATING PORPHYROMONAS GINGIVALIS CAN INDUCE AUTOIMMUNITY TO HUMAN RIBOSOMAL PROTEINS AND TNF ALPHA TREATMENT NONRESPONSE“. 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.4653.

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