| 1. |
- Belibasakis, Georgios N., et al.
(författare)
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Periodontal microbiology and microbial etiology of periodontal diseases : Historical concepts and contemporary perspectives
- 2023
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Ingår i: Periodontology 2000. - : Wiley-Blackwell. - 0906-6713 .- 1600-0757.
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Tidskriftsartikel (refereegranskat)abstract
- This narrative review summarizes the collective knowledge on periodontal microbiology, through a historical timeline that highlights the European contribution in the global field. The etiological concepts on periodontal disease culminate to the ecological plaque hypothesis and its dysbiosis-centered interpretation. Reference is made to anerobic microbiology and to the discovery of select periodontal pathogens and their virulence factors, as well as to biofilms. The evolution of contemporary molecular methods and high-throughput platforms is highlighted in appreciating the breadth and depth of the periodontal microbiome. Finally clinical microbiology is brought into perspective with the contribution of different microbial species in periodontal diagnosis, the combination of microbial and host biomarkers for this purpose, and the use of antimicrobials in the treatment of the disease.
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| 2. |
- Bertl, Kristina, et al.
(författare)
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Bacterial colonisation during regular daily use of a power-driven water flosser and risk for cross-contamination. Can it be prevented?
- 2022
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Ingår i: Clinical Oral Investigations. - : Springer. - 1432-6981 .- 1436-3771. ; 26, s. 1903-1913
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Tidskriftsartikel (refereegranskat)abstract
- Objective To assess whether bacterial colonisation in a power-driven water flosser can be prevented. Materials and methods Twenty-four patients undergoing supportive periodontal treatment used 2 power-driven water flossers [Sonicare AirFloss (SAF), AirFloss Ultra (SAFU)] for 12 weeks each as follows: (a) with bottled water (BW); (b) with BW and cleaning the device extra-orally twice per week with chlorhexidine gluconate or (c) essential-oil-based (EO) mouth-rinse; (d) with EO only. Water-jet samples were taken after 6 and 12 weeks with the used nozzle and after exchanging to a brand-new nozzle. After 12 weeks, all devices underwent an intensive cleaning procedure. Samples were analysed by PCR-based method for cariogenic and periodontal pathogens and culture for staphylococci, aerobe gram-negative bacteria, and Candida sp. Results Contamination of SAF/SAFU with Streptococcus mutans was found in > 95% of the samples; periodontal pathogens and aerobe gram-negative bacteria were detected in 19-56% of the samples, while Staphylococcus aureus and Candida sp. were identified only in few samples. Contamination rate was basically unaffected by time-point, device, or way of use. Further, exchanging the nozzle did not prevent transmission of a contaminated water-jet, but the intensive cleaning reduced most of the pathogens significantly, except of S. mutans. Conclusion Neither a specific way of use nor exchanging the nozzle prevented bacterial colonisation and transmission of biofilm components via the water-jet of SAF/SAFU.
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| 3. |
- Eick, Sigrun, et al.
(författare)
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Adhesion of Porphyromonas gingivalis and Tannerella forsythia to dentin and titanium with sandblasted and acid etched surface coated with serum and serum proteins - An in vitro study
- 2017
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Ingår i: Archives of Oral Biology. - : Elsevier. - 0003-9969 .- 1879-1506. ; 75, s. 81-88
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Tidskriftsartikel (refereegranskat)abstract
- Objective: To evaluate the adhesion of selected bacterial strains incl. expression of important virulence factors at dentin and titanium SLA surfaces coated with layers of serum proteins. Methods: Dentin-and moderately rough SLA titanium-discs were coated overnight with human serum, or IgG, or human serum albumin (HSA). Thereafter, Porphyromonas gingivalis, Tannerella forsythia, or a six species mixture were added for 4 h and 24 h. The number of adhered bacteria (colony forming units; CFU) was determined. Arg-gingipain activity of P. gingivalis and mRNA expressions of P. gingivalis and T forsythia proteases and T. forsythia protease inhibitor were measured. Results: Coating specimens never resulted in differences exceeding 1.1 log10 CFU, comparing to controls, irrespective the substrate. Counts of T forsythia were statistically significantly higher at titanium than dentin, the difference was up to 3.7 log10 CFU after 24 h (p = 0.002). No statistically significant variation regarding adhesion of the mixed culture was detected between surfaces or among coatings. Arggingipain activity of P. gingivalis was associated with 1og10 CFU but not with the surface or the coating. Titanium negatively influenced mRNA expression of T. forsythia protease inhibitor at 24 h (p = 0.026 uncoated, p = 0.009 with serum). Conclusions: The present findings indicate that: a) single bacterial species (T forsythia) can adhere more readily to titanium SLA than to dentin, b) low expression of T. forsythia protease inhibitor may influence the virulence of the species on titanium SLA surfaces in comparison with teeth, and c) surface properties (e.g. material and/or protein layers) do not appear to significantly influence multi-species adhesion. (C) 2016 Elsevier Ltd. All rights reserved.
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| 4. |
- Eick, Sigrun, et al.
(författare)
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Gingipains impair attachment of epithelial cell to dental titanium abutment surfaces
- 2019
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Ingår i: Journal of Biomedical Materials Research. Part B - Applied biomaterials. - : John Wiley & Sons. - 1552-4973 .- 1552-4981. ; 107:8, s. 2549-2556
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Tidskriftsartikel (refereegranskat)abstract
- The study investigated in vitro the effect of Porphyromonas gingivalis and its cysteine proteases (gingipains) on epithelial cell adhesion to titanium-zirconium alloy surfaces. Titanium-zirconium discs with a standard machined (M) or chemically modified hydrophilic surface (modM) were coated with lamin-5 and incubated with telomerase-inactivated gingival keratinocytes (TIGK). Three P. gingivalis strains or gingipains were either added simultaneously with TIGK or after TIGK cells were already attached to the disks. Adhered TIGK cells were counted at 24 h. All P. gingivalis strains clearly inhibited adhesion of TIGK cells to M and modM surfaces. Compared with bacteria/gingipain-free TIGK cell cultures, the number of attached TIGK cells was reduced by about 80% and 60% when P. gingivalis was added simultaneously or after TIGK cells were already attached to the disks (each p < 0.01), respectively. Counts of attached cells were similarly reduced when only gingipains were used. Adhesion molecules of TIGK cells, in particular E-cadherin, were cleaved by P. gingivalis. In conclusion, P. gingivalis and gingipains interfere with the adhesion of epithelial cells to titanium-zirconium alloy surfaces by cleaving adhesion molecules, while a chemically modified hydrophilic titanium-zirconium alloy surface did not yield any protection. (c) 2019 Wiley Periodicals, Inc. J Biomed Mater Res B Part B, 2019.
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| 5. |
- Eick, Sigrun, et al.
(författare)
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Honey - a potential agent against Porphyromonas gingivalis: an in vitro study
- 2014
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Ingår i: BMC Oral Health. - : Springer Science and Business Media LLC. - 1472-6831. ; 14:1
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Tidskriftsartikel (refereegranskat)abstract
- Abstract Background Honey has been discussed as a therapeutic option in wound healing since ancient time. It might be also an alternative to the commonly used antimicrobials in periodontitis treatment. The in-vitro study was aimed to determine the antimicrobial efficacy against Porphyromonas gingivalis as a major periodontopathogen. Methods One Manuka and one domestic beekeeper honey have been selected for the study. As a screening, MICs of the honeys against 20 P. gingivalis strains were determined. Contents of methylglyoxal and hydrogen peroxide as the potential antimicrobial compounds were determined. These components (up to 100 mg/l), propolis (up to 200 mg/l) as well as the two honeys (up to 10% w/v) were tested against four P. gingivalis strains in planktonic growth and in a single-species biofilm. Results 2% of Manuka honey inhibited the growth of 50% of the planktonic P. gingivalis, the respective MIC50 of the German beekeeper honey was 5%. Manuka honey contained 1.87 mg/kg hydrogen peroxide and the domestic honey 3.74 mg/kg. The amount of methylglyoxal was found to be 2 mg/kg in the domestic honey and 982 mg/kg in the Manuka honey. MICs for hydrogen peroxide were 10 mg/l - 100 mg/l, for methylglyoxal 5 – 20 mg/l, and for propolis 20 mg/l – 200 mg/l. 10% of both types of honey inhibited the formation of P. gingivalis biofilms and reduced the numbers of viable bacteria within 42 h-old biofilms. Neither a total prevention of biofilm formation nor a complete eradication of a 42 h-old biofilm by any of the tested compounds and the honeys were found. Conclusions Honey acts antibacterial against P. gingivalis. The observed pronounced effects of Manuka honey against planktonic bacteria but not within biofilm can be attributed to methylglyoxal as the characteristic antimicrobial component.
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| 6. |
- Jusko, Monika, et al.
(författare)
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A Metalloproteinase Karilysin Present in the Majority of Tannerella forsythia Isolates Inhibits All Pathways of the Complement System.
- 2012
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Ingår i: Journal of immunology. - : The American Association of Immunologists. - 1550-6606 .- 0022-1767. ; 188:5, s. 2338-2349
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Tidskriftsartikel (refereegranskat)abstract
- Tannerella forsythia is a poorly studied pathogen despite being one of the main causes of periodontitis, which is an inflammatory disease of the supporting structures of the teeth. We found that despite being recognized by all complement pathways, T. forsythia is resistant to killing by human complement, which is present at up to 70% of serum concentration in gingival crevicular fluid. Incubation of human serum with karilysin, a metalloproteinase of T. forsythia, resulted in a decrease in bactericidal activity of the serum. T. forsythia strains expressing karilysin at higher levels were more resistant than low-expressing strains. Furthermore, the low-expressing strain was significantly more opsonized with activated complement factor 3 and membrane attack complex from serum compared with the other strains. The high-expressing strain was more resistant to killing in human blood. The protective effect of karilysin against serum bactericidal activity was attributable to its ability to inhibit complement at several stages. The classical and lectin complement pathways were inhibited because of the efficient degradation of mannose-binding lectin, ficolin-2, ficolin-3, and C4 by karilysin, whereas inhibition of the terminal pathway was caused by degradation of C5. Interestingly, karilysin was able to release biologically active C5a peptide in human plasma and induce migration of neutrophils. Importantly, we detected the karilysin gene in >90% of gingival crevicular fluid samples containing T. forsythia obtained from patients with periodontitis. Taken together, the newly characterized karilysin appears to be an important virulence factor of T. forsythia and might have several important implications for immune evasion.
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| 7. |
- Jusko, Monika, et al.
(författare)
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A Metalloproteinase Mirolysin of Tannerella forsythia Inhibits All Pathways of the Complement System.
- 2015
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Ingår i: Journal of Immunology. - : The American Association of Immunologists. - 1550-6606 .- 0022-1767. ; 195:5, s. 2231-2240
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Tidskriftsartikel (refereegranskat)abstract
- Recent reports focusing on virulence factors of periodontal pathogens implicated proteinases as major determinants of remarkable pathogenicity of these species, with special emphasis on their capacity to modulate complement activity. In particular, bacteria-mediated cleavage of C5 and subsequent release of C5a seems to be an important phenomenon in the manipulation of the local inflammatory response in periodontitis. In this study, we present mirolysin, a novel metalloproteinase secreted by Tannerella forsythia, a well-recognized pathogen strongly associated with periodontitis. Mirolysin exhibited a strong effect on all complement pathways. It inhibited the classical and lectin complement pathways due to efficient degradation of mannose-binding lectin, ficolin-2, ficolin-3, and C4, whereas inhibition of the alternative pathway was caused by degradation of C5. This specificity toward complement largely resembled the activity of a previously characterized metalloproteinase of T. forsythia, karilysin. Interestingly, mirolysin released the biologically active C5a peptide in human plasma and induced migration of neutrophils. Importantly, we demonstrated that combination of mirolysin with karilysin, as well as a cysteine proteinase of another periodontal pathogen, Prevotella intermedia, resulted in a strong synergistic effect on complement. Furthermore, mutant strains of T. forsythia, devoid of either mirolysin or karilysin, showed diminished survival in human serum, providing further evidence for the synergistic inactivation of complement by these metalloproteinases. Taken together, our findings on interactions of mirolysin with complement significantly add to the understanding of immune evasion strategies of T. forsythia and expand the knowledge on molecular mechanisms driving pathogenic events in the infected periodontium.
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| 8. |
- Jusko, Monika, et al.
(författare)
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FACIN, a double-edged sword of the emerging periodontal pathogen filifactor alocis : A metabolic enzyme moonlighting as a complement inhibitor
- 2016
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Ingår i: Journal of Immunology. - : The American Association of Immunologists. - 0022-1767 .- 1550-6606. ; 197:8, s. 3245-3259
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Tidskriftsartikel (refereegranskat)abstract
- Periodontal disease is one of the most common inflammatory infectious diseases worldwide and it is associated with other syndromes, such as cardiovascular disease or rheumatoid arthritis. Recent advances in sequencing allowed for identification of novel periodontopathogens such as Gram-positive Filifactor alocis, but its virulence mechanisms remain largely unknown.We confirmed that F. alocis is a prevalent species in periodontitis patients, and we also observed strong correlation of this bacterium with clinical parameters, highlighting its role in the pathogenesis of the disease. Further, we found that preincubation of human serum with F. alocis resulted in abolished bactericidal activity and that F. alocis was surviving readily in full blood. We demonstrated that one of the key contributors to F. alocis complement resistance is a unique protein, FACIN (F. alocis complement inhibitor), which binds to C3, resulting in suppression of all complement pathways. Interestingly, FACIN is a nonclassical cell surface protein, a cytosolic enzyme acetylornithine transaminase, for which we now identified a moonlighting function. FACIN binds to C3 alone, but more importantly it also captures activated complement factor 3 within the complex with factor B, thereby locking in the convertase in an inactive state. Because of the indispensable role of alternative pathway convertase in amplifying complement cascades, its inhibition by FACIN results in a very potent downregulation of activated complement factor 3 opsonization on the pathogen surface, accompanied by reduction of downstream C5 cleavage.
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| 9. |
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| 10. |
- Malm, Sven, et al.
(författare)
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Acquisition of Complement Inhibitor Serine Protease Factor I and Its Cofactors C4b-Binding Protein and Factor H by Prevotella intermedia.
- 2012
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Ingår i: PLoS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 7:4
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Tidskriftsartikel (refereegranskat)abstract
- Infection with the Gram-negative pathogen Prevotella intermedia gives rise to periodontitis and a growing number of studies implies an association of P. intermedia with rheumatoid arthritis. The serine protease Factor I (FI) is the central inhibitor of complement degrading complement components C3b and C4b in the presence of cofactors such as C4b-binding protein (C4BP) and Factor H (FH). Yet, the significance of complement inhibitor acquisition in P. intermedia infection and FI binding by Gram-negative pathogens has not been addressed. Here we show that P. intermedia isolates bound purified FI as well as FI directly from heat-inactivated human serum. FI bound to bacteria retained its serine protease activity as shown in degradation experiments with (125)I-labeled C4b. Since FI requires cofactors for its activity we also investigated the binding of purified cofactors C4BP and FH and found acquisition of both proteins, which retained their activity in FI mediated degradation of C3b and C4b. We propose that FI binding by P. intermedia represents a new mechanism contributing to complement evasion by a Gram-negative bacterial pathogen associated with chronic diseases.
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