<i>Aggregatibacter (Actinobacillus) actimycetemcomitans</i> leukotoxin and human periodontitis – A historic review with emphasis on JP2

Tsai, Chi‐Cheng; Ho, Ya-Ping; Chou, Yu-Shian; Ho, Kuen‐Yao; Wu, Yimin; Lin, Ying‐Chu

doi:10.1016/j.kjms.2018.01.014

Cited by 30 publications

(28 citation statements)

References 92 publications

(125 reference statements)

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“…When results from the periodontally diseased individuals were separated from that of the healthy, we found that the JP2 genotype was detected at high levels in saliva from the periodontally diseased individuals. This further strengthens the role of the JP2 genotype as a disease‐associated risk factor in this population, in line with previous studies (Haubek, ; Tsai et al, ). High levels of JP2 genotype A. actinomycetemcomitans in saliva may be a risk factor for disease onset but could also be a result of release of bacteria from diseased pockets.…”

Section: Discussionsupporting

confidence: 91%

High salivary levels of JP2 genotype of Aggregatibacter actinomycetemcomitans is associated with clinical attachment loss in Moroccan adolescents

Ennibi

Claesson

Akkaoui

et al. 2019

Clinical & Exp Dental Res

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It has previously been shown that the presence of Aggregatibacter actinomycetemcomitans in subgingival plaque is significantly associated with increased risk for clinical attachment loss. The highly leukotoxic JP2 genotype of this bacterium is frequently detected in adolescents with aggressive forms of periodontitis. The aims of the study were to quantify the levels of JP2 and non‐JP2 genotypes of A. actinomycetemcomitans in saliva of Moroccan adolescents with the JP2 genotype earlier detected in the subgingival plaque. The salivary concentrations of inflammatory proteins were quantified and linked to the clinical parameters and microbial findings. Finally, a mouth rinse with leukotoxin‐neutralizing effect was administrated and its effect on the levels the biomarkers and A. actinomycetemcomitans examined. The study population consisted of 22 adolescents that previously were found to be positive for the JP2 genotype in subgingival plaque. Periodontal registration and sampling of stimulated saliva was performed at baseline. A mouth rinse (active/placebo) was administrated, and saliva sampling repeated after 2 and 4 weeks rinse. The salivary levels of JP2 and non‐JP2 were analyzed by quantitative PCR and inflammatory proteins by ELISA. Both the JP2 and the non‐JP2 genotype were detected in all individuals with significantly higher levels of the non‐JP2. Enhanced levels of the JP2 genotype of A. actinomycetemcomitans was significantly correlated to the presence of attachment loss (≥3 mm). Salivary concentrations of inflammatory biomarkers did not correlate to periodontal condition or levels of A. actinomycetemcomitans . The use of active or placebo leukotoxin‐neutralizing mouth rinse did not significantly interfered with the levels of these biomarkers. Saliva is an excellent source for detection of A. actinomycetemcomitans on individual basis, and high levels of the JP2 genotype were significantly associated with the presence of clinical attachment loss.

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Section: Discussionsupporting

confidence: 91%

High salivary levels of JP2 genotype of Aggregatibacter actinomycetemcomitans is associated with clinical attachment loss in Moroccan adolescents

Ennibi

Claesson

Akkaoui

et al. 2019

Clinical & Exp Dental Res

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“…The JP2 genotype was first identified by Brogan and co-workers [33] and was a serotype b isolate with a 530 base pair (bp) deletion in the ltxCABD promoter. Based on this finding, isolates with such a deletion in the promoter are named JP2 genotype, and those lacking this deletion are non-JP2 genotype [20,34]. The discovery of the JP2 genotype introduced a new terminology of high and low leukotoxic A. actinomycetemcomitans based only on the ltx promoter type [33,35].…”

Section: Ltxa Productionmentioning

confidence: 99%

Virulence and Pathogenicity Properties of Aggregatibacter actinomycetemcomitans

et al. 2019

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Aggregatibacter actinomycetemcomitans is a periodontal pathogen colonizing the oral cavity of a large proportion of the human population. It is equipped with several potent virulence factors that can cause cell death and induce or evade inflammation. Because of the large genetic diversity within the species, both harmless and highly virulent genotypes of the bacterium have emerged. The oral condition and age, as well as the geographic origin of the individual, influence the risk to be colonized by a virulent genotype of the bacterium. In the present review, the virulence and pathogenicity properties of A. actinomycetemcomitans will be addressed.

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“…Streptococcus sanguinis is another plaque-forming strain that has been reported to cause infective endocarditis by forming biofilms on the endocardium and heart valves [ 11 ]. Aggregatibacter actinomycetemcomitans has been strongly associated with localized aggressive periodontitis via its ability to form biofilms in the subgingival cavity [ 12 ]. Apart from causing oral diseases, these pathogenic bacteria also cause systemic diseases, such as arteriosclerosis [ 13 ] and diabetes [ 14 ].…”

Section: Introductionmentioning

confidence: 99%

Rhamnolipids and surfactin inhibit the growth or formation of oral bacterial biofilm

et al. 2020

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Background Bacteria survive in various environments by forming biofilms. Bacterial biofilms often cause significant problems to medical instruments and industrial processes. Techniques to inhibit biofilm formation are essential and have wide applications. In this study, we evaluated the ability of two types of biosurfactants (rhamnolipids and surfactin) to inhibit growth and biofilm formation ability of oral pathogenic bacteria such as Aggregatibacter actinomycetemcomitans, Streptococcus mutans, and Streptococcus sanguinis. Results Rhamnolipids inhibited the growth and biofilm formation ability of all examined oral bacteria. Surfactin showed effective inhibition against S. sanguinis ATCC10556, but lower effects toward A. actinomycetemcomitans Y4 and S. mutans UA159. To corroborate these results, biofilms were observed by scanning electron microscopy (SEM) and confocal microscopy. The observations were largely in concordance with the biofilm assay results. We also attempted to determine the step in the biofilm formation process that was inhibited by biosurfactants. The results clearly demonstrated that rhamnolipids inhibit biofilm formation after the initiation process, however, they do not affect attachment or maturation. Conclusions Rhamnolipids inhibit oral bacterial growth and biofilm formation by A. actinomycetemcomitans Y4, and may serve as novel oral drug against localized invasive periodontitis.

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Aggregatibacter (Actinobacillus) actimycetemcomitans leukotoxin and human periodontitis – A historic review with emphasis on JP2

Cited by 30 publications

References 92 publications

High salivary levels of JP2 genotype of Aggregatibacter actinomycetemcomitans is associated with clinical attachment loss in Moroccan adolescents

High salivary levels of JP2 genotype of Aggregatibacter actinomycetemcomitans is associated with clinical attachment loss in Moroccan adolescents

Virulence and Pathogenicity Properties of Aggregatibacter actinomycetemcomitans

Rhamnolipids and surfactin inhibit the growth or formation of oral bacterial biofilm

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