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Background: This study determined the prevalence of aggressive (molar-incisor pattern) (Ag/MI) periodontitis and assessed the associated subgingival bacterial-herpesvirus microbiota in Pueblo Indian adolescents in the southwestern United States., Methods: The study included 240 Pueblo Indian adolescents, aged 13-20 years old, residing in three Rio Grande River villages in New Mexico and the Hopi Pueblo reservation in Arizona. Adolescents with Ag/MI periodontitis or periodontal health provided subgingival samples for culture of bacterial pathogens and for polymerase chain reaction detection of periodontal herpesviruses., Results: Ag/MI periodontitis was detected in 22 (9.2%) Pueblo Indian adolescents, with 21 exhibiting a localized molar-incisor breakdown pattern. Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, and other red/orange complex bacterial pathogens predominated in Ag/MI periodontitis, whereas periodontal health yielded mainly viridans streptococci and Actinomyces species. Periodontal herpesviruses demonstrated a 3.5 odds ratio relationship with Ag/MI periodontitis. The only adolescent with generalized Ag/MI periodontitis harbored viral co-infection by cytomegalovirus plus Epstein-Barr virus Type 1, in addition to A. actinomycetemcomitans, P. gingivalis, and several other periodontopathic bacteria., Conclusions: Pueblo Indian adolescents showed an unusually high prevalence of early-age Ag/MI periodontitis predominated by periodontopathic bacteria and herpesviruses suspected to be major etiologic agents of the disease., (© 2023 American Academy of Periodontology.)

Localized juvenile (aggressive) periodontitis starts at puberty in otherwise healthy individuals and involves the proximal surfaces of permanent incisors and first molars. The disease destroys a sizeable amount of periodontal bone within a few months despite minimal dental plaque and gingival tissue inflammation. Cytomegalovirus and Epstein-Barr virus, as well as the two main periodontopathic bacteria Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis, are linked to juvenile periodontitis. Juvenile periodontitis-affected teeth show cementum hypoplasia. We hypothesize that an active herpesvirus infection, at the time of root formation, hampers cementum formation and, at puberty, herpesvirus reactivation triggers an upgrowth of bacterial pathogens which produce rapid periodontal destruction on teeth with a defective periodontium. A pathogenic interaction between active herpesviruses and bacterial pathogens can potentially explain the etiology and incisor-first molar destructive pattern of juvenile periodontitis. Effective treatment of juvenile periodontitis may target the herpesvirus-bacteria co-infection., (© 2023 The Authors. Periodontology 2000 published by John Wiley & Sons Ltd.)

The prevalence of periodontitis among Thai schoolchildren is unknown. In a cross-sectional study, the prevalence and severity of periodontal diseases, in a group of Thai schoolchildren, along with the presence and numbers of bacterial species commonly associated with periodontitis were investigated. A consent form was sent out to 192 schoolchildren in one school (Chanachanupathom School) in Chana, Southern Thailand (in the age range of 12-18 years) and 119 attended for a clinical and microbiological examination. Clinical recordings included number of teeth present, DMFT, plaque index, bleeding index, clinical attachment loss (CAL), and probing pocket depth (PPD). Pooled plaque samples were analyzed with culture and qPCR against bacteria associated with periodontitis. The children had low caries experience (DMFT = 3.2 ± 2.3), poor oral hygiene, high bleeding scores, and 67 (56.3%) had at least one interproximal site with CAL ≥ 1 mm. Thirty-seven (31.1%) of the children were diagnosed with periodontitis stage I, and sixteen (13.4%) were classified as periodontitis Stage II. Aggregatibacter actinomycetemcomitans was sparsely found in all but the healthy clinical groups (gingivitis, periodontitis Stage I and II), while the groups showed a high prevalence of Fusobacterium spp., Prevotella intermedia/nigrescens, and Campylobacter species as well as of the periodontitis-associated species Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia. Thai schoolchildren have poor oral hygiene with abundant amounts of plaque and high presence of bleeding. Early onset periodontitis is common but mostly in its mild form and is not associated with the presence of A. actinomycetemcomitans., (© 2023. The Author(s).)

Periodontal disease is one of the most common disorders in the oral cavity of dogs and humans. Periodontitis, the irreversible periodontal disease, arises progressively from gingivitis, the reversible inflammatory condition caused by dental plaque. Although the etiology of periodontitis has been widely studied in humans, it is still insufficient for the etiological studies on periodontitis in dogs. Many studies have reported that human periodontitis-related bacteria are putative pathogens responsible for periodontitis in dogs. However, most of these studies have focused on the appearance of a specific microbiome, and most of the cohort studies have insufficient sample sizes to generalize their results. In the present study, subgingival samples collected from 336 teeth were categorized into three groups at first, based on clinical outcomes (healthy, gingivitis, periodontitis). Subsequently, the periodontitis samples were further divided into three subgroups (early, moderate, and advanced periodontitis) according to the degree of periodontal attachment loss. Healthy and gingivitis were grouped as a reversible group, and the three subgroups were grouped as an irreversible group. To investigate trends of periodontopathic bacteria in the samples of dogs, a quantitative real-time polymerase chain reaction (PCR) was performed for quantification of 11 human periodontopathic bacteria as follows: Aggregatibacter actinomycetemcomitans (Aa), Porphyromonas gingivalis (Pg), Tannerella forsythia, Treponema denticola (Td), Fusobacterium nucleatum, Prevotella nigrescens, Prevotella intermedia, Parvimonas micra, Eubacterium nodatum, Campylobacter rectus, and Eikenella corrodens. The PCR results showed that Aa and Pg, the representative periodontopathic bacteria, were not significantly correlated or associated with the periodontitis cases in dogs. However, interestingly, Td was strongly associated with the irreversible periodontal disease in dogs, in that it was the most prevalent bacterium detected from the dog samples. These findings indicate that the presence and numbers of Td could be used as a prognostic biomarker in predicting the irreversible periodontal disease and the disease severity in dogs., Competing Interests: The authors have declared that no competing interests exist.

Papillon-Lefèvre syndrome (PLS) is an autosomal recessive rare disease, main characteristics of which include palmoplantar hyperkeratosis and premature edentulism due to advanced periodontitis (formerly aggressive periodontitis). This study aimed to characterize the oral phenotype, including salivary parameters, and the salivary microbiome of three PLS sisters, comparatively. Two sisters were toothless (PLSTL1 and PLSTL2), and one sister had most of the teeth in the oral cavity (PLST). Total DNA was extracted from the unstimulated saliva, and the amplicon sequencing of the 16S rRNA gene fragment was performed in an Ion PGM platform. The amplicon sequence variants (ASVs) were obtained using the DADA2 pipeline, and the taxonomy was assigned using the SILVA v.138. The main phenotypic characteristics of PLS were bone loss and premature loss of primary and permanent dentition. The PLST sister presented advanced periodontitis with gingival bleeding and suppuration, corresponding to the advanced periodontitis as a manifestation of systemic disease, stage IV, grade C. All three PLS sisters presented hyposalivation as a possible secondary outcome of the syndrome. Interestingly, PLST salivary microbiota was dominated by the uncultured bacteria Bacterioidales (F0058), Fusobacterium , Treponema , and Sulfophobococcus ( Archaea domain). Streptococcus , Haemophilus , and Caldivirga ( Archaea ) dominated the microbiome of the PLSTL1 sister, while the PLSTL2 had higher abundances of Lactobacillus and Porphyromonas . This study was the first to show a high abundance of organisms belonging to the Archaea domain comprising a core microbiome in human saliva. In conclusion, a PLST individual does have a microbiota different from that of the periodontitis' aggressiveness previously recognized. Due to an ineffective cathepsin C, the impairment of neutrophils probably provided a favorable environment for the PLS microbiome. The interactions of Bacteroidales F0058, Caldivirga , and Sulfophobococcus with the microbial consortium of PLS deserves future investigation. Traditional periodontal therapy is not efficient in PLS patients. Unraveling the PLS microbiome is essential in searching for appropriate treatment and avoiding early tooth loss., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Lettieri, Santiago, Lettieri, Borges, Marconatto, de Oliveira, Damé-Teixeira and Salles.)

Early acquisition of a pathogenic microbiota and the presence of dysbiosis in childhood is associated with susceptibility to and the familial aggregation of periodontitis. This longitudinal interventional case-control study aimed to evaluate the impact of parental periodontal disease on the acquisition of oral pathogens in their offspring. Subgingival plaque and clinical periodontal metrics were collected from 18 parents with a history of generalized aggressive periodontitis and their children (6-12 years of age), and 18 periodontally healthy parents and their parents at baseline and following professional oral prophylaxis. 16S rRNA amplicon sequencing revealed that parents were the primary source of the child's microbiome, affecting their microbial acquisition and diversity. Children of periodontitis parents were preferentially colonized by Filifactor alocis, Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, Streptococcus parasanguinis, Fusobacterium nucleatum and several species belonging to the genus Selenomonas even in the absence of periodontitis, and these species controlled inter-bacterial interactions. These pathogens also emerged as robust discriminators of the microbial signatures of children of parents with periodontitis. Plaque control did not modulate this pathogenic pattern, attesting to the microbiome's resistance to change once it has been established. This study highlights the critical role played by parental disease in microbial colonization patterns in their offspring and the early acquisition of periodontitis-related species and underscores the need for greater surveillance and preventive measures in families of periodontitis patients.

Host genetic predispositions to dysregulated immune response can influence the development of the aggressive form of periodontitis (AgP) through susceptibility to oral dysbiosis and subsequent host-microbe interaction. This case-control study aimed to perform a multilocus analysis of functional variants in selected interleukin ( IL ) genes in patients with the generalized form of AgP in a homogenous population. Twelve polymorphisms in IL-1 gene cluster, IL-6 and its receptor, IL-10 , IL-17A , and IL-18 were determined in 91 AgP patients and 210 controls. Analysis of seven selected periodontal bacteria in subgingival sulci/pockets was performed with a commercial DNA-microarray kit in a subgroup of 76 individuals. The pilot in vitro study included stimulation of peripheral blood monocytes (PBMC) from 20 individuals with periodontal bacteria and measurement of IL-10 levels using the Luminex method. Only the unctional polymorphism IL‑10 -1087 A/G (rs1800896) and specific IL-10 haplotypes were associated with the development of the disease ( P < 0.05, P corr > 0.05). Four bacterial species occurred more frequently in AgP than in controls ( P < 0.01, P corr < 0.05). Elevated IL-10 levels were found in AgP patients, carriers of IL‑10 -1087GG genotype, and PBMCs stimulated by periodontal bacteria ( P < 0.05, P corr > 0.05). We therefore conclude that a combination of genetic predisposition to the altered expression of IL-10 and the presence of specific periodontal bacteria may contribute to Th1/Th2 balance disruption and AgP development.

Being aware of the remarkable antimicrobial potential of S. officinalis L., we aimed to evaluate the antimicrobial activity of the S. officinalis dichloromethane crude extract (SOD), dichloromethane-soluble fractions (SODH and SODD), SODD subfractions (SODD1 and SODD2), and pure substances (manool, salvigenin, and viridiflorol) against periodontopathogens. This bioassay-guided study comprises five antimicrobial tests-determination of the Minimum Inhibitory Concentration (MIC), determination of the Minimum Bactericidal Concentration (MBC), determination of the antibiofilm activity, construction of the Time-kill curve (determination of Bactericidal Kinetics), and determination of the Fractional Inhibitory Concentration Index-on six clinical bacterial isolates and three standard bacterial strains involved in periodontal disease. SOD has moderate activity against most of the tested bacteria, whereas SODD1, SODH1, SODH3, and manool afford the lowest results. The Porphyromonas gingivalis (ATTC and clinical isolate) biofilm is considerably resistant to all the samples. In association with chlorhexidine gluconate, only SODH1 exerts additive action against P. gingivalis (clinical isolate). Therefore, SODH1 and manool are promising antibacterial agents and may provide therapeutic solutions for periodontal infections., Competing Interests: Declarations of competing interest None., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

The present study aimed to evaluate clinical and microbiological effects of surgical and nonsurgical periodontal therapy in generalized aggressive periodontitis (GAgP) treatment. Sixteen GAgP patients were included in this randomized split-mouth design clinical trial. Maxillary quadrants were allocated into two groups: Nonsurgical Therapy (NST) and Surgical Therapy (ST). The following clinical parameters were assessed: plaque index (PI), bleeding on probing index (BoP), probing depth (PD), clinical attachment level (CAL) and gingival margin position (GMP). Concentrations of Porphyromonas gingivalis (Pg) and Aggregatibacter actinomycetemcomitans (Aa) in the subgingival biofilm were also determined. Clinical and microbiological parameters were assessed at baseline (n=16), 3 (n=15), 6 (n=15) and 12 months (n=8) after treatment. ST was able to promote higher PD reduction compared to NST in deep pockets at 12 months (p<0.05) and in posterior teeth at 6 months (p<0.05). In addition, higher gingival recession was observed in posterior teeth of the ST group at the 6th month (p<0.05). However, ST failed to promoted additional CAL gain in any timepoint (p>0.05). Moreover, microbiological evaluation showed no statistical difference in levels of Aa and Pg for both groups at all follow-up periods. Surgical therapy promoted similar clinical benefits to GAgP therapy. Moreover, both therapies failed to reduce Aa and Pg levels at different follow-up times.

Objective: The aim of the study was to profile the subgingival microbiome of Chinese adults with generalized aggressive periodontitis (GAgP) using human oral microbe identification microarray (HOMIM), and to compare the results with matched periodontal healthy controls., Design: 15 subjects with GAgP and 15 age- and gender- matched periodontal healthy controls were included. Subgingival plaque samples were collected from the deepest pockets of patients with GAgP and matched sites in controls and then analyzed by 16S rRNA-based microarrays. Student's paired t-test was used to compare clinical parameters and mean number of bacterial taxa detected between the two groups. Fisher's exact probability test and Wilcoxon Rank Sum were used to compare bacterial species between all samples. A multiple linear regression model was used for correlations among age, gender and bacterial with clinical parameters., Results: From a total sum of 379 strains tested, 171 bacterial strains were detected from subgingival plaques of the GAgP patients, more than the 157 strains detected in control group. Mean number of subgingival bacterial taxa detected in GAgP group was 68 (SD = 21.06) while in control group was 45 (SD = 21.60). 47 bacterial taxa were detected more frequently in GAgP group while 12 taxa were more prevalent in control group. The significantly more prevalent and abundant taxa of bacteria in GAgP group included Filifactor alocis, Desulfobulbus sp., Fretibacterium sp., Porphyromonas gingivalis, Tannerella forsythia, Porphyromon as endodontalis, Peptostreptococcaceae spp., Parvimonas micra, Eubacterium nodatum and Eubacterium saphenum. Meanwhile the more abundant taxa in control group were Streptococcus spp. and Pseudomonas aeruginosa., Conclusions: There are more taxa of bacteria in subgingival plaques of Chinese patients with GAgP than in healthy controls. F. alocis, Desulfobulbus sp., Fretibacterium sp., P. gingivalis and T. forsythia are strongly associated with GAgP. High-throughout microbiological results may help dentists have a better understanding of subgingival microbiome of GAgP., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

Aggregatibacter actinomycetemcomitans (Aa) is a low-abundance Gram-negative oral pathobiont that is highly associated with a silent but aggressive orphan disease that results in periodontitis and tooth loss in adolescents of African heritage. For the most part Aa conducts its business by utilizing strategies allowing it to conceal itself below the radar of the host mucosal immune defense system. A great deal of misinformation has been conveyed with respect to Aa biology in health and disease. The purpose of this review is to present misconceptions about Aa and the strategies that it uses to colonize, survive, and evade the host. In the process Aa manages to undermine host mucosal defenses and contribute to disease initiation. This review will present clinical observational, molecular, and interventional studies that illustrate genetic, phenotypic, and biogeographical tactics that have been recently clarified and demonstrate how Aa survives and suppresses host mucosal defenses to take part in disease pathogenesis. At one point in time Aa was considered to be the causative agent of Localized Aggressive Periodontitis. Currently, it is most accurate to look at Aa as a community activist and necessary partner of a pathogenic consortium that suppresses the initial host response so as to encourage overgrowth of its partners. The data for Aa's activist role stems from molecular genetic studies complemented by experimental animal investigations that demonstrate how Aa establishes a habitat (housing), nutritional sustenance in that habitat (food), and biogeographical mobilization and/or relocation from its initial habitat (transportation). In this manner Aa can transfer to a protected but vulnerable domain (pocket or sulcus) where its community activism is most useful. Aa 's "strategy" includes obtaining housing, food, and transportation at no cost to its partners challenging the economic theory that "there ain't no such thing as a free lunch." This "strategy" illustrates how co-evolution can promote Aa's survival, on one hand, and overgrowth of community members, on the other, which can result in local host dysbiosis and susceptibility to infection.

Periodontal microorganisms not only colonize subgingival pockets, but also are detected on various mucous membranes in patients with periodontitis. The object of this pilot study was, using the next-generation sequencing of 16S RNA gene, to characterize the microbiota in two oral habitats (buccal mucosas and subgingival pockets) in patients with different forms of periodontitis. Thirty-two buccal swab samples and 113 subgingival samples were obtained from eleven subjects with chronic periodontitis (ChP), twelve subjects with aggressive periodontitis (AgP), and nine periodontally healthy individuals (HP). Using Miseq Sequencing of 16S rRNA gene, we found that the subgingival and buccal mucosa microbiome of ChP and AgP patients both differed from HP. Meanwhile, Veillonella, Treponema, Filifactor, Fretibacterium, Peptostreptococcaceae&#95;[XI][G-6], Peptostreptococcaceae&#95;[XI][G-5], Bacteroidetes&#95;[G-5], Bacteroidetes&#95;[G-3], Peptostreptococcaceae&#95;[XI][G-4], Peptostreptococcaceae&#95;[XI][G-2] significantly increased both in buccal and subgingival plaque samples in periodontitis subjects (ChP and AgP) compared with HP. Moreover, the results based on the Unweighted UniFrac distance showed that buccal and subgingival plaque samples from the same individuals show higher community divergence than same habitats from different subject samples. This study demonstrated that the microbiome of buccal mucosa can be influenced by periodontitis. However, subgingival and buccal mucosa microbiome seem to be characterized by species-specific colonization patterns. This pilot study provides a glimpse at the changes of subgingival and buccal mucosa associated with periodontitis from a holistic view. Further studies should be taken to illuminate the interplay between these detected changes and periodontitis development.

Objective: The primary objectives of the study were to assess differences in complex subgingival bacterial composition between periodontitis-free persons and patients with generalized aggressive periodontitis (gAgP)., Background: The composition of the oral microbiota plays an important role for both oral and systemic diseases. However, the complex nature of the oral microbiome and its homeostasis is still poorly understood., Material and Methods: We compared the microbiome of 13 periodontitis-free persons to 13 patients with gAgP. The 16S rRNA genes were amplified, targeting the V3/V4 region using the MiSeq platform., Results: In total, 1713 different bacterial species were mapped according to the Greengenes database. Using the Shannon index, no significant differences in alpha diversity were found between the two study groups. In principal component and linear discriminant analyses, disease-specific differences in beta diversity of the microbiome composition were evaluated. Bacteroidetes, Spirochaetes, and Synergistetes were more abundant in gAgP whereas Proteobacteria, Firmicutes, and Actinobacteria were associated with a healthy periodontium. At the bacterial species level, we showed that Porphyromonas gingivalis is the strongest indicator of gAgP. Treponema denticola and Tanerella forsythia of the "red complex" as well as Filifactor alocis were among the ten best biomarkers for gAgP., Conclusions: These results broaden our knowledge of disease-specific differences in the microbial community associated with generalized AgP. A more complex view of the composition of the oral microbiome describes the etiology of generalized AgP in more detail. These results could help to individually adapt periodontal therapy in these patients., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

Objective: To evaluate the effect of the periodontal treatment on Aggregatibacter actinomycetemcomitans JP2 clone, and the IgG serum levels against its outer membrane protein (Omp29) and A. actinomycetemcomitans serotypes in aggressive periodontitis (AgP)., Subjects and Methods: Seventeen patients with generalized (GAgP), 10 with localized (LAgP), and 10 healthy controls were included. AgP participants were submitted to periodontal treatment-scaling and root planing plus antibiotics (SRP+A). Periodontal parameters, for example, probing depth (PD) and clinical attachment loss (CAL), were evaluated at baseline and at 1-year. Serum IgG against Omp29 and serotypes a, b, and c were determined by ELISA. The levels of A. actinomycetemcomitans JP2 clone were determined in subgingival biofilm samples by qPCR., Results: Periodontal treatment resulted in significant reductions of PD, CAL, and IgG levels against Omp29, serotypes b, and c. After therapy, IgG levels against A. actinomycetemcomitans serotypes, as well as the levels of the JP2 clone in AgP, became similar to controls. The reduction in JP2 clone count was correlated with a reduction of PD and IgG response against Omp29., Conclusion: Scaling and root planing plus antibiotics decreased IgG levels response against Omp29 and A. actinomycetemcomitans serotypes involved in the disease (b and c), while the serum response increased against tne commensal serotype (a), similar to what occurs in periodontally healthy individuals., (© 2018 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd. All rights reserved.)

Objectives: Generalized aggressive periodontitis (GAgP) is a distinct type of periodontal disease characterized by rapid loss of attachment and alveolar bone occurring in young individuals. Photodynamic therapy (PDT) was introduced in periodontology as an adjunctive approach to non-surgical periodontal treatment (NPT) in periodontitis patients. In this trial, the aim was to evaluate the clinical and microbiological effects of adjunctive PDT to NPT in patients with GAgP., Methods: In this prospective controlled clinical study, 24 systemically healthy, non-smoking subjects with GAgP were enrolled. Subjects were randomly assigned into a control group (n = 12) treated with NPT only or to a test group (n = 12) treated with NPT and PDT. Plaque index, sulcus bleeding index (SBI), probing depth (PD), relative attachment level, gingival recession, and tooth mobility were recorded at baseline and on day 63. Microbiological samples were obtained from the sites with PD ≥ 5 mm at both time periods and evaluated for Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Prevotella intermedia, Tannerella forsythia, and Treponema denticola via micro-IDent® test., Results: Clinical and microbial parameters declined significantly in both groups after the treatments (P < 0.01). The comparisons between the groups showed that only the full mouth SBI score of the test group was significantly lower than the control group on day 63 (P < 0.05). Although the reduction in periodontopathogens of the test group was greater than the control group, there was no significant difference between the groups (P > 0.05)., Conclusions: Within the limits of this study, it can be concluded that in the treatment of GAgP, usage of PDT as an adjunct to NPT does not lead to any beneficial effects on the investigated clinical and microbiological parameters except for SBI. Nevertheless, the statistically significant difference for the SBI score demonstrates that PDT may have additional effect on the reduction in gingival bleeding. Lasers Surg. Med. 51:167-175, 2019. © 2018 Wiley Periodicals, Inc., (© 2018 Wiley Periodicals, Inc.)

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., Competing Interests: The authors declare that there is no conflict of interest.

Background: T. forsythia a gram negative, anaerobe inhabits the mature biofilm present at sites expressing progressive periodontitis. It is a part of "red complex" group which contributes to the pathogenesis of periodontitis. The BspA protein and prtH gene encoded cysteine protease play a vital role in the virulence of T. forsythia. The present study aims to detect the two genotypes (bspA and prtH) in periodontitis and healthy subjects., Materials & Method: Subgingival plaque samples were collected from periodontitis patients and healthy subjects (Chronic Periodontitis n = 128, Aggressive Periodontitis n = 72, healthy subjects n = 200). The samples were screened for the presence of T. forsythia 16S rRNA, bspA and prtH genotypes by Polymerase Chain Reaction. The prevalence of the genotypes between periodontitis patients and healthy subjects was compared with Pearson's Chi-square test. A P value of < 0.05 was considered to be statistically significant., Results: The prevalence for T. forsythia in Chronic Periodontitis (n = 128), Aggressive Periodontitis (n = 72) and health (n = 200) was 73.4%, 59.7% and 10.5% respectively. The prevalence of T.forsythia bspA/prtH genotypes was 81.90%/43.60%, 88.40%/53.50% and 33.30%/14.3% in Chronic Periodontitis, aggressive Periodontitis and health respectively. Compared to healthy subjects, the odds of detecting T.forsythia 16S rRNA was 18.53 times high in individuals with periodontitis (P = 0.0001)., Conclusion: The high odds ratio of T.forsythia 16S rRNA among periodontitis strongly suggests its role in periodontitis. In addition, the high prevalence of T. forsythia bspA genotype among Chronic Periodontitis signifies it as a useful marker for chronic periodontitis., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

Aim: The aim of the study is to assess the long-term effect of active periodontal therapy on serum inflammatory parameters in patients with aggressive (AgP) and chronic (ChP) periodontitis in a non-randomised clinical study., Methods: Twenty-five ChP and 17 AgP were examined clinically prior to (baseline), 12 weeks and 60 months after subgingival debridement of all pockets within 2 days. Systemic antibiotics were prescribed if Aggregatibacter actinomycetemcomitans was detected (10 AgP, 8 ChP), flap surgery was rendered if required. Neutrophil elastase (NE), C-reactive protein (CRP), lipopolysaccharide binding protein, interleukin 6, 8, and leukocyte counts were assessed at baseline, 12 weeks and 60 months., Results: Clinical parameters improved significantly in both groups from 12 weeks to 60 months. Eleven AgP and 18 ChP patients received surgical treatment after the 12 weeks examination. Only 3 patients in each group attended ≥ 2 supportive maintenance visits per year. NE and CRP were significantly higher in AgP than ChP at baseline and 60 months (p < 0.01). For leukocyte counts in ChP, significant changes were observed (baseline: 6.11 ± 1.44 nl -1 ; 12 weeks: 5.34 ± 1.40 nl -1 ; 60 months: 7.73 ± 2.89 nl -1 ; p < 0.05). Multiple regression analysis identified African origin, surgical treatment and female sex to correlate with better clinical improvement., Conclusion: Despite comprehensive periodontal treatment, AgP patients exhibit higher NE and CRP levels than ChP patients up to 5 years after therapy., Clinical Relevance: Systemic inflammatory burden in AgP patients is higher than in ChP patients even 5 years after periodontal treatment.

Porphyromonas gingivalis and Tannerella forsythia have been thought to be associated with periodontitis; however comprehensive histopathological localization of bacteria in affected human periodontal tissues is not well documented. In the present study, we examined formalin-fixed paraffin-embedded gingival and subgingival granulation tissues from 71 patients with chronic periodontitis and 11 patients with aggressive periodontitis, using immunohistochemistry with novel monoclonal antibodies specific to P. gingivalis or T. forsythia, together with quantitative real-time polymerase chain reaction for each bacterial DNA. Immunohistochemisty revealed both bacterial species extracellularly, as aggregates or within bacterial plaque, and intracellularly in stromal inflammatory cells, squamous epithelium, and capillary endothelium of granulation tissue. Combined analysis with the results from polymerase chain reaction suggested that localization and density of T. forsythia is closely associated with those of P. gingivalis, and that bacterial density is a factor responsible for the cell-invasiveness and tissue-invasiveness of these periodontal bacteria. Detection of these bacteria in the capillary endothelium in some samples suggested possible bacterial translocation into the systemic circulation from inflamed gingival and subgingival granulation tissues. Immunohistochemistry with the novel antibodies showed high specificity and sensitivity, and can be used to locate these periodontal bacteria in routinely-used formalin-fixed paraffin-embedded human tissue sections from systemic locations.

Interleukin-10 (IL-10) polymorphisms have been shown to affect IL-10 production. This study investigated the influences of IL-10 polymorphisms on the susceptibility to chronic periodontitis (CP) and aggressive periodontitis (AP), and their possible role in the quantity of subgingival bacteria Aggregatibacter Actinomycetemcomitans and Porphyromonas gingivalis. 92 CP patients, 83 AP patients and 91 periodontal healthy controls were recruited. Serum IL-10 concentration was analyzed by enzyme-linked immunosorbent assay (ELISA). Gene polymorphisms were determined by multiplex SNaPshot technique. Bacteria were quantified by real-time polymerase chain reaction with TaqMan MGB probes. Taking into account age, gender and periodontal status, IL-10-592 AA, -819 TT and ATA/ATA genotype occurred more frequently in patients with CP than in healthy controls. In CP cases, higher quantity of subgingival A. actinomycetemcomitans and lower serum IL-10 levels could be detected in homozygous ATA/ATA carriers. These findings indicate that variants in IL-10 promoter gene were not only associated with predisposition to chronic periodontitis but also affected the subgingival number of A. Actinomycetemcomitans in a Chinese Han population.

In vitro studies revealed that Porphyromonas gingivalis (Pg), a pathogen intimately associated with the onset and progression of periodontitis, is able to activate platelets, thus linking periodontal inflammation with the endangerment of vascular health. As wild-type Pg strains are characterized by major genetic heterogeneity, the commonness of platelet-activating Pg strains in periodontitis patients is unknown as of yet. Therefore, this study evaluated the platelet activation capacity of wild-type Pg isolates sampled from patients with aggressive periodontitis., Methods: Extent and velocity of platelet aggregation were determined by light transmission aggregometry. Platelet surface expression of P-selectin was measured by flow cytometry, activation of p38 MAP kinase, and protein kinase C by Western blot using phospho-specific antibodies., Results: Pg isolates displayed high variability regarding extent and velocity of platelet activation, as well as the involved activating pathways. Corresponding results were observed for platelet P-selectin expression, activation of p38 MAP kinase, or protein kinase C. Inhibitors of platelet immune receptor FcγRIIA and protease-activated receptors revealed several, diverging pathways of activation. Some isolates induced platelet aggregation even in the presence of potent therapeutical platelet inhibitors., Conclusions: Chronic bacteremia involving specific, platelet-activating Pg strains may constitute a substantial hazard for the integrity of cardiovascular health., (© 2018 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Periodontitis is a kind of infectious disease initiated by colonization of subgingival periodontal pathogens, which cause destruction of tooth-supporting tissues, and is a predominant threat to oral health as the most common cause of loss of teeth. The aim of this pilot study was to characterize the subgingival bacterial biodiversity of periodontal pockets with different probing depths in patients with different forms of periodontitis. Twenty-one subgingival plaque samples were collected from three patients with chronic periodontitis (ChP), three patients with aggressive periodontitis (AgP) and three periodontally healthy subjects (PH). Each patient with periodontitis was sampled at three sites, at different probing depths (PDs, one each at 4 mm, 5-6 mm, and ≥ 7 mm). Using 16S rRNA gene high-throughput sequencing and bioinformatic analysis, we found that subgingival communities in health and periodontitis samples largely differed. Meanwhile, Acholeplasma, Fretibacterium, Porphyromonas, Peptococcus, Treponema&#95;2, Defluviitaleaceae&#95;UCG&#95;011, Filifactor , and Mycoplasma increased with the deepening of the pockets in ChP, whilst only Corynebacterium was negatively associated with PD. In AgP, Corynebacterium and Klebsiella were positively associated with PD, while Serratia, Pseudoramibacter, Defluviitaleaceae&#95;UCG&#95;011 , and Desulfobulbus were negatively associated with PD. And among these two groups, Corynebacterium shifted differently. Moreover, in subgingival plaque, the unweighted UniFrac distances between samples from pockets with different PD in the same patients were significantly lower than those from pockets within the same PD category from different patients. This study demonstrated the shift of the subgingival microbiome in individual teeth sites during disease development. Within the limitation of the relative small sample size, this pilot study shed new light on the dynamic relationship between the extent of periodontal destruction and the subgingival microbiome.

Aim: To investigate the shift in the subgingival microbiota under scaling and root planing (SRP) in patients with generalized aggressive periodontitis (GAgP)., Materials and Methods: After undergoing supragingival scaling, 12 individuals with GAgP were enrolled in this longitudinal study. Full-mouth SRP was accomplished in 3 weeks and re-evaluated 6 weeks later. Pooled subgingival samples (posterior-mesial, posterior-buccal, anterior-mesial, and anterior-buccal) were obtained from each patient before SRP (pre-treatment group) and at the time of re-evaluation (post-treatment group). 16S rRNA PCR products were generated and sequenced after DNA isolation., Results: Under SRP, the diversity of the subgingival community was consistent, whereas genus-level biomarkers transformed from Porphyromonas, Treponema, and Fretibacterium to Actinomyces, Streptococcus, and Haemophilus. In a network analysis, pathogen-related and non-pathogen-related components were identified in both the pre- and post-treatment groups; the pathogen component was dramatically augmented, while the non-pathogen component shrank after treatment. Hubs were also distributed in both components pre-treatment and were confined to the pathogen component post-treatment., Conclusions: Scaling and root planing decreased periodontal pathogens in the subgingival microbiota of patients with GAgP. However, the shift in the microbiota composition was characterized by the expansion of pathogen-related components and the contraction of non-pathogen-related components 6 weeks after SRP. Clinicaltrials.gov #NCT03090282., (© 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Aggregatibacter (Actinobacillus) actimycetemcomitans (Aa) is a gram-negative bacterium that colonizes the human oral cavity and is causative agent for localized aggressive (juvenile) periodontitis (AgP). In the middle of 1990s, a specific JP2 clone of belonging to the cluster of serotype b strains of Aa with highly leukotoxicity (leukotoxin, LtxA) able to kill human immune cells was isolated. JP2 clone of Aa was strongly associated with in particularly in rapidly progressing forms of aggressive periodontitis. The JP2 clone of Aa is transmitted through close contacts. Therefore, AgP patients need intense monitoring of their periodontal status as the risk for developing severely progressing periodontitis lesions are relatively high. Furthermore, timely periodontal treatment, including periodontal surgery supplemented by the use of antibiotics, is warranted. More importantly, periodontal attachment loss should be prevented by early detection of the JP2 clone of Aa by microbial diagnosis testing and/or preventive means., (Copyright © 2018. Published by Elsevier Taiwan.)

Background: The existence of specific microbial profiles for different periodontal conditions is still a matter of debate. The aim of this study was to test the hypothesis that 40 bacterial species could be used to classify patients, utilising machine learning, into generalised chronic periodontitis (ChP), generalised aggressive periodontitis (AgP) and periodontal health (PH)., Method: Subgingival biofilm samples were collected from patients with AgP, ChP and PH and analysed for their content of 40 bacterial species using checkerboard DNA-DNA hybridisation. Two stages of machine learning were then performed. First of all, we tested whether there was a difference between the composition of bacterial communities in PH and in disease, and then we tested whether a difference existed in the composition of bacterial communities between ChP and AgP. The data were split in each analysis to 70% train and 30% test. A support vector machine (SVM) classifier was used with a linear kernel and a Box constraint of 1. The analysis was divided into two parts., Results: Overall, 435 patients (3,915 samples) were included in the analysis (PH = 53; ChP = 308; AgP = 74). The variance of the healthy samples in all principal component analysis (PCA) directions was smaller than that of the periodontally diseased samples, suggesting that PH is characterised by a uniform bacterial composition and that the bacterial composition of periodontally diseased samples is much more diverse. The relative bacterial load could distinguish between AgP and ChP., Conclusion: An SVC classifier using a panel of 40 bacterial species was able to distinguish between PH, AgP in young individuals and ChP., (© 2017 FDI World Dental Federation.)

Background: Localised aggressive periodontitis (LAgP), characterised by rapid attachment and bone loss, which may occur in children and adolescents, without clinical evidence of systemic disease., Case Report: Three-year-old boy was referred with excessive mobility of 83 and exfoliation of 73. Clinical examination revealed acceptable oral hygiene. Blood tests were performed to evaluate PMNs activity and the parents were advised to apply 0.2% chlorhexidine twice a day. One month later 83 was still excessively mobile. Blood tests were normal., Treatment: A full mouth scaling and curettage were performed under general anaesthesia. Since 83 had been spontaneously exfoliated one day earlier, a biopsy was taken from its socket. The biopsy examination revealed granulation tissue with actinomyces colonies. A course of amoxicillin 250 mg three times a day for 7 days was prescribed. Cultures from periodontal pockets of the child's family members were found negative to Aggregatibacter actinomycetem comitans (Aa)., Follow-Up: Examination 3 months later, no tooth mobility was observed and the cultures from the periodontal pockets were negative to Aa. Thereafter, the child was periodically reviewed every 3 months for 26 months with no signs of periodontal disease., Conclusion: Amoxicillin combined with curettage around the involved teeth may be effective in LAgP treatment.

Background: This study assesses the microbiologic effects of a two-phase antimicrobial periodontal therapy and tested microbiologic, clinical, and biologic markers as prognostic indicators for clinical success., Methods: Eighty patients with chronic or aggressive periodontitis received periodontal treatment supplemented with 375 mg amoxicillin plus 500 mg metronidazole, three times daily for 7 days. In group A, antibiotics were given during the first non-surgical phase (T1); in group B, antibiotics were given during the second surgical phase (T2). Six microorganisms, group assignment, demographic and clinical variables, peak values of 15 cytokines, and nine acute-phase proteins in serum were evaluated as potential predictors of at least one site with probing depth (PD) >4 mm and bleeding on probing (BOP) at 12 months post-therapy., Results: T1 decreased the counts of Porphyromonas gingivalis, Tannerella forsythia, Prevotella intermedia (Pi), and Treponema denticola significantly more in group A than group B. Aggregatibacter actinomycetemcomitans and Parvimonas micra (Pm) showed a significant decrease only if the treatment was supplemented with antibiotics, i.e., T1 in group A, or T2 in group B. After T2, differences between groups were no longer significant. A multivariable model including four parameters revealed a predictive value of Pm (odds ratio [OR] = 4.38, P = 0.02) and Pi (OR = 3.44, P = 0.049) and yielded moderate accuracy for predicting the treatment outcome (area under the curve = 0.72). Host-derived factors and treatment sequence were not significantly associated with the outcome., Conclusions: Long-term microbiologic outcomes of periodontal therapy with adjunctive antibiotics either in T1 or T2 were similar. Detection of Pm before therapy was a predictor for persistence of sites with PD >4 mm and BOP at 12 months post-treatment.

Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans) is a Gram-negative, facultative anaerobic bacillus that causes periodontal diseases such as localized aggressive periodontitis (LAP) and. consequently. bone resorption. The potential virulence factors of this organism are powerful leukotoxin, lipopolysaccharide (LPS), cell surface-associated materials, enzymes, and less well-defined virulence factors that will modulate the activity of the host defenses. This organism can induce bone resorption by various virulence factors in periodontal disease. In this review article, we reviewed the pathogenic roles of A. actinomycetemcomitans in periodontal disease and the mechanism which can induce bone resorption. Findings from several studies indicate that the interaction between virulence factors and the host immune system's response often progress bone resorption in periodontal disease. In this organism, GroEL, DnaK, HtpG, LTX, CDT, LPS, and cell surface-associated materials produce cytokines when exposed to the immune system. The produced cytokines are the main cause of tissue destruction and bone resorption in A. actinomycetemcomitans inflammation in periodontal disease., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Background: Previous studies have provided substantial evidence of the association of Aggregatibacter actinomycetemcomitans, and its highly leukotoxic JP2 genotype, with localized aggressive periodontitis (LAgP). The present study aims to evaluate presence of JP2 in individuals with LAgP after periodontal treatment., Methods: Sixty African-American patients with LAgP, aged 5 to 25 years, were examined. At baseline, probing depth (PD), clinical attachment level (CAL), bleeding on probing, and plaque index were measured, and subgingival plaque was collected from LAgP diseased and healthy sites for each participant. Patients received whole-mouth ultrasonic debridement, scaling and root planing, and a 7-day prescription of amoxicillin and metronidazole. Participants were reevaluated and resampled and received regular maintenance therapy at 3, 6, and 12 months after treatment. Polymerase chain reaction was used to detect presence of the JP2 genotype before and after treatment., Results: At baseline, the JP2 sequence was identified in 75% of LAgP diseased sites and in 56.67% of healthy sites. At 3, 6, and 12 months after treatment, the number of patients was 40, 31, and 31, respectively, and JP2 detection decreased to 17.5%, 6.45%, and 3.23%, respectively, in diseased sites (P <0.001) and to 2.5%, 3.23%, and 0%, respectively, in healthy sites (P <0.001). Clinical parameters of disease were also significantly reduced after therapy (P <0.001). Additionally, significant correlations were observed between JP2 presence and mean PD (P <0.002) and CAL (P <0.001), after therapy., Conclusion: Periodontal therapy was successful in reducing clinical parameters of LAgP and subgingival presence of JP2 in diseased and healthy sites.

Interleukin (IL) 1-ra is a potent endogenous competitive inhibitor of IL-α and β and has an anti-inflammatory role. Study objectives were: 1) to assess the associations of IL-1RN genetic single nucleotide polymorphism (SNP) (rs419598) with generalized chronic periodontitis (GCP), generalized aggressive periodontitis (GAgP), and absence of periodontitis and 2) to assess its association with the load of five periodontopathogenic bacteria and periodontal clinical variables. A cross-sectional analytic study was conducted in 123 patients with GCP, 60 patients with GAgP, and 20 controls. Reverse hybridization PCR was used for genotyping analysis to detect SNPs in IL-1A (rs1800587), IL-1B (rs1143634), and IL-1RN (rs419598) genes and for determination of the load of five periodontopathogenic bacteria. The severity and extension of periodontitis were assessed. Multinomial logistic regression and mediated regression analyses were performed. Considering results for GCP and GAgP patients together, the presence of polymorphism in IL-1A and/or IL-1B gene was associated with a higher likelihood of periodontitis, (OR = 8.11; 95%CI [1.85-35.48]), but this likelihood was reduced when IL-1RN polymorphism was also present, (OR = 5.91; 95%CI [1.08-32.27]). IL-1RN polymorphism was significantly associated with lower counts of red complex bacteria, specifically Porphyromona gingivalis, Tannerella forsythia, and Prevotella intermedia, which were associated with improved clinical outcomes. The polymorphic expression of IL-1RN (rs419598) gene may be associated with a reduced susceptibility to GAgP and GCP in populations of European descent. This effect may be mediated by a decreased load of Porphyromona gingivalis, Tannerella forsythia, and Prevotella intermedia.

At the International Workshop for Classification of Periodontal Diseases and Conditions in 1999, the classification of aggressive and chronic periodontitis that is presently used was introduced. A literature review of papers published in 2015 and having aggressive periodontitis in the title revealed that most studies use this terminology but it is questionable whether all established criteria were really applied correctly. Review of the literature showed no qualitative differences between aggressive and chronic periodontitis regarding bacterial and viral aspects. It is also unlikely that that there are major immunologic differences between aggressive and chronic periodontitis. Neutrophil function can be compromised in both conditions but may be more genetically related in aggressive periodontitis and be associated more with lifestyle factors in chronic periodontitis. In general, genetics plays a more important role in aggressive periodontitis than in chronic periodontitis. It is likely that periodontitis progresses by recurrent acute episodes during which invasion of bacteria into the connective tissue may occur. Two cases are presented for which invasive periodontitis is treated with systemic antibiotics, showing remarkable periodontal healing in terms of probing attachment gain, as well as radiographic bone gain. Periodontitis in an active state with bacterial invasion is probably accompanied with a significant increase in subgingival temperature. It is hypothesized that elevated subgingival temperature may help to distinguish between bacterial and nonbacterial invasive periodontitis. Scaling and root planing during a burst of disease activity may result in removal of connective tissue fiber attachment and down-growth of epithelium, thereby preventing the reattachment of connective tissue. Because the burst of disease is accompanied by an increase of temperature, assessment of the temperature may help in deciding whether or not to prescribe systemic antibiotics. When the use of systemic antibiotics is indicated, the antibiotic therapy may help to maintain the connective tissue attachment at the most possible coronal level. The above implies that the ability to diagnose bacterial invasive periodontitis is quite important, and future research is needed to determine if assessment of subgingival temperature may help in diagnosing invasive periodontitis. In addition, it is suggested that future classification systems of periodontitis include the item of bacterial invasive periodontitis., (© 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Background and Objectives: There has been limited study of the bacterial species associated with aggressive periodontitis (AgP) in high-risk populations in Africa. The aim of this study was to investigate and quantify the presence of four putative periodontal pathogens in the subgingival plaque of Sudanese subjects with AgP. A secondary aim was to investigate the effect of varying the detection threshold on the reported prevalence of the bacterial species investigated., Materials and Methods: Subgingival plaque samples were collected from AgP cases (n=73) and healthy controls (n=71). Bacterial DNA was extracted and analyzed by quantitative polymerase chain reaction for the detection and quantification of four putative periodontal pathogens: Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, Treponema denticola and Tannerella forsythia., Results: At the lowest detection threshold (>10 1 cells), P. gingivalis (p<0.0001) was more prevalent in AgP cases than controls. T. forsythia and T. denticola had a high prevalence (>70%) in AgP cases at all detection levels. While T. forsythia was significantly more frequently identified in AgP than in controls at all detection thresholds, this was only the case for T. denticola at the intermediate threshold (>10 2 cells). A. actinomycetemcomitans was identified less frequently than the other bacterial species with no difference in its prevalence between AgP cases and controls., Conclusion: The prevalence of the putative periodontal pathogens investigated varied considerably in Sudanese subjects with AgP and in periodontally healthy controls depending on the detection thresholds applied. T. forsythia was identified as having the strongest association with AgP., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Purpose: This study aimed to evaluate the potential risk for localized aggressive periodontitis (LAgP) in African American children by detection of the potential periodontal pathogen Aggregatibacter actinomycetemcomitans (Aa) using polymerase chain reaction (PCR) and microbiome analysis., Methods: Twenty-one pre-adolescents (age range equals 10.7 to 13.1 years old) were recruited, for this IRB-approved study. Oral examination included limited periodontal examination determining bleeding index (BOP) and periodontal probing (PD). An oral mucosa sample was used for analysis., Results: Nine of 21 children were Aa+ by PCR. The Aa+ group had a significantly higher proportion of teeth with BOP and PD greater than four mm than the Aa- group (P=0.014 and 0.006 for percent BOP and percent PD equal to or greater than four mm, respectively; Mann Whitney Test). No significant differences in microbe abundance or composition were found from comparison of Aa+ versus Aa- samples., Conclusions: Detection of Aa from preadolescent African American children was associated with signs of periodontal inflammation. Although none of these children were diagnosed with LAgP, PCR targeting Aa could be a risk factor. Further study is indicated; however, the usefulness of PCR in dental practice setting to assess risk may be cost-effective for early diagnosis and prevention of LAgP.

Aim: The aim of the present study was to evaluate the influence of the baseline detection of Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans) on the clinical outcomes of moxifloxacin (MOX) as an adjunct to full-mouth scaling and root planing (SRP) in generalized aggressive periodontitis (GAgP)., Methods: Forty patients were randomly distributed to two therapy protocols: SRP + placebo or SRP combined with MOX. A. actinomycetemcomitans was detected using culture methods. The significance of the treatment option (MOX or SRP + placebo) on the dependent variables (probing depth [PD] and clinical attachment level [CAL]), considering the interaction with the baseline detection of A. actinomycetemcomitans, was estimated., Results: MOX therapy led to a higher significant PD reduction and CAL gain in A. actinomycetemcomitans-positive patients at baseline. In A. actinomycetemcomitans-positive patients, the reduction of sites ≥5 mm was higher in the MOX group. A. actinomycetemcomitans was not present in sites with PD ≥6 mm in the MOX group. The interactions of A. actinomycetemcomitans and MOX were significantly associated with CAL gain and PD reduction at 6 months., Conclusions: Adjunctive MOX trended toward better clinical responses in A. actinomycetemcomitans-positive patients at baseline. These results suggest that A. actinomycetemcomitans at baseline might modify the effect of adjunctive MOX in GAgP., (© 2015 Wiley Publishing Asia Pty Ltd.)

Aim: To investigate the bacterial microbiome in periodontal and peri-implant biofilms deriving from aggressive periodontitis patients (AgP) in conditions of health and disease., Material and Methods: Ninety-one plaque samples were collected from 18 patients previously diagnosed and treated for AgP. The samples were taken from (i) 24 residual periodontal pockets (TD) (n = 6 patients), (ii) 24 healthy periodontal sites (TH) (n = 6 patients), (iii) 24 dental sites from the same implant patients (TM) (n = 6 patients), (iv) 5 peri-implantitis sites (II) (n = 2 patients), (v) 6 peri-mucositis sites (IM) (n = 2 patients) and (vi) 8 healthy implant sites (IH) (n = 2 patients). All subjects underwent periodontal clinical and radiographic assessments. Bacterial DNA was extracted, PCR amplified using 16S rRNA gene V5-V7 primers (barcoded amplicons 785F;1175R), purified, pooled at equimolar concentrations and sequenced (MiSeq, Illumina) yielding 250 bp paired-end reads. The 16S rRNA reads were filtered, assembled and analysed., Results: The genera Propionibacterium, Paludibacter, Staphylococcus, Filifactor, Mogibacterium, Bradyrhizobium and Acinetobacter were unique to peri-implant sites (P = 0.05). In TM samples, different proportions and bacterial spp. were found when compared with the same patients' samples at implant sites. Specifically, Actinomyces (P = 0.013) and Corynebacterium (P = 0.030) genera showed to be significantly more abundant in the TM group when compared to the II. The highest phylogenetic diversity was observed in residual periodontal pocket sites (TD). Increased annual tooth loss rate and residual pocketing was related to high proportions of the genera Actinomyces, Porphyromonas, Prevotella, Streptococcus, Actinomycetaceae, TM7-3, Selenomonas, and Dialister, Treponema, Parvimonas and Peptostreptococcus in the TD group., Conclusion: Within the limitations of this pilot study, the periodontal and peri-implant microbiome presents a dissimilar taxonomic composition across different niches within AgP patients. The host response, the habitat structure and the vast coexistence of strains and species surrounding implants and teeth in health and disease are likely to be shaping the heterogeneous composition of the subgingival biofilms. The TM7 phylum was found only in TD cases. The investigation of the impact of periodontal and peri-implant keystone species on these complex ecosystems in states of health and disease seems to be essential., (© 2016 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Periodontal disease (PD) is generated by microorganisms. These microbes can enter the general circulation causing a bacteraemia. The result can be adverse systemic effects, which could promote conditions such as cardiovascular disease. Level A evidence supports that PD is independently associated with arterial disease. PD is a common chronic condition affecting the majority of Americans 30 years of age and older. Atherosclerosis remains the largest cause of death and disability. Studies indicate that the adverse cardiovascular effects from PD are due to a few putative or high-risk bacteria: Aggregatibacter actinomycetemcomitans , Porphyromonas gingivalis , Tannerella forsythia , Treponema denticola or Fusobacterium nucleatum There are three accepted essential elements in the pathogenesis of atherosclerosis: lipoprotein serum concentration, endothelial permeability and binding of lipoproteins in the arterial intima. There is scientific evidence that PD caused by the high-risk pathogens can influence the pathogenesis triad in an adverse manner. With this appreciation, it is reasonable to state PD, due to high-risk pathogens, is a contributory cause of atherosclerosis. Distinguishing this type of PD as causal provides a significant opportunity to reduce arterial disease., (Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/.)

The object of this study is to characterize the bacterial community of subgingival plaque of two subjects with generalized aggressive periodontitis (GAgP) pre- and post-treatment. We picked two patients with GAgP and used high-throughput 16S rDNA sequencing. V4 hypervariable region was picked for PCR amplification of subgingival samples. Then, the PCR products were sequenced through Illumina MiSeq platform. One month after therapy, both the clinical features and periodontal parameters improved obviously. Moreover, the composition and structure of subgingival bacterial community changed after initial periodontal therapy. Also, the composition of the subgingival microbiota was highly individualized among different patients. Bacteroidetes, Spirochaetes and Fusobacteria were related to pathogenicity of GAgP while Actinobacteria and Proteobacteria seemed associated with clinical symptoms resolution. In this study, we found the subgingival bacterial community was high in species richness but dominated by a few species or phylotypes, with significant shifts of microbiota that occurred after treatment. This study demonstrated the shift of the subgingival bacterial community before and after treatment by high-throughput 16S rDNA sequencing, and provided a concise method for analysis of microbial community for periodontal diseases.

The aim of this study was to determine the variations in periodontal parameters and microbiological composition in periodontal pockets at the baseline and 3 and 6 months post treatmentin patients with Generalized Aggressive Periodontitis(GAP) undergoing non surgical periodontal treatment combined with chlorhexidine and systemic antibiotics. Medical and dental history was taken from 10 subjects, average age 30.6±2.7 years, diagnosed with GAP. A non surgical periodontal treatment combined with 0.12% chlorhexidine, 875 mg amoxicillin and 500 mg metronidazole every 12 hours for ten days was conducted. At each visit, the following measurements wererecorded: bacterial plaque (BP), bleeding on probing (BOP), probing depth (PD), clinical attachment level (CAL), hypermobility, and furcation lesions, and a sample of subgingivalplaque was taken from the site of the deepest probing depth of each sextant to identify Porphyromonas gingivalis, Treponemadenticola, Tannerella forsythia, Prevotella intermedia and Aggregatibacter actinomycetemcomitans using molecular biology techniques. After 6 months, the Wilcoxon test showed an increase of 0.97 mm in CAL (p=0.0047) and 2.54 mm in PD(p=0.009). A healthy site was defined as having a PD <5 mm, negative BOP and no pathogenic bacteria detected at 6 months, indicating significant improvement (p=0.008), with OR (95%CI) =4.7 (1.102220.11).With the treatment protocol used in this study, 6 months after treatment, patients had an approximately 4- fold higher possibility of presenting PD <5 mm and periodontal pockets without periodontal pathogenic bacteria., (Sociedad Argentina de Investigación Odontológica.)

Objectives: To relate five periodontopathogenic bacteria, including the red complex, to the severity, extent, and inflammation of the periodontal lesion in Caucasian patients with generalized aggressive and chronic periodontitis and to explore whether tobacco use is associated with a specific bacterial profile., Materials and Methods: A cross-sectional and analytic study was conducted in patients with aggressive and chronic periodontitis. Data were gathered on socio-demographic and periodontal variables, and RH-PCR was used to determine subgingival bacterial profile. Linear and logistic regression analyses were performed., Results: The study included 60 patients with aggressive and 123 with chronic periodontitis. Total red complex bacteria count was higher in aggressive periodontitis, mainly due to T. denticola (P = 0.015). In both periodontitis types, models showed an association between T. forsythia count and probing depth (B = 0.157, P = 0.030) and between T. denticola count and higher bleeding scores (B = 2.371, P = 0.027). Smoking did not affect the red complex bacteria count in either disease., Conclusions: The prevalence of red complex bacteria was similar between aggressive and chronic periodontitis, but their count was higher in the former. In both diseases, T. forsythia was associated with greater severity and T. denticola with more severe bleeding. Tobacco smoking was not associated with the presence of red complex bacteria in either disease., (© 2016 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Aggregatibacter actinomycetemcomitans is a perio-pathogenic bacteria that has long been associated with localized aggressive periodontitis. The mechanisms of its pathogenicity have been studied in humans and preclinical experimental models. Although different serotypes of A. actinomycetemcomitans have differential virulence factor expression, A. actinomycetemcomitans cytolethal distending toxin (CDT), leukotoxin, and lipopolysaccharide (LPS) have been most extensively studied in the context of modulating the host immune response. Following colonization and attachment in the oral cavity, A. actinomycetemcomitans employs CDT, leukotoxin, and LPS to evade host innate defense mechanisms and drive a pathophysiologic inflammatory response. This supra-physiologic immune response state perturbs normal periodontal tissue remodeling/turnover and ultimately has catabolic effects on periodontal tissue homeostasis. In this review, we have divided the host response into two systems: non-hematopoietic and hematopoietic. Non-hematopoietic barriers include epithelium and fibroblasts that initiate the innate immune host response. The hematopoietic system contains lymphoid and myeloid-derived cell lineages that are responsible for expanding the immune response and driving the pathophysiologic inflammatory state in the local periodontal microenvironment. Effector systems and signaling transduction pathways activated and utilized in response to A. actinomycetemcomitans will be discussed to further delineate immune cell mechanisms during A. actinomycetemcomitans infection. Finally, we will discuss the osteo-immunomodulatory effects induced by A. actinomycetemcomitans and dissect the catabolic disruption of balanced osteoclast-osteoblast-mediated bone remodeling, which subsequently leads to net alveolar bone loss., (© 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

In recent years, several new periodontal taxa have been associated with the etiology of periodontitis. A recent systematic review provides further support for the pathogenic role of 17 species/phylotypes. Thus, the aim of this study was to assess the prevalence and levels of these species in subjects with generalized chronic periodontitis (GChP; n = 30), generalized aggressive periodontitis (GAgP; n = 30), and periodontal health (PH; n = 30). All subjects underwent clinical and microbiological assessment. Nine subgingival plaque samples were collected from each subject and analyzed for their content of 20 bacterial species/phylotypes through the RNA-oligonucleotide quantification technique. Subjects from the GChP and GAgP groups presented the highest mean values for all clinical parameters in comparison with the PH group (P < 0.05). Subjects with GChP and GAgP showed significantly higher mean levels of Bacteroidetes sp. human oral taxon (HOT) 274, Fretibacterium sp. HOT 360, and TM7 sp. HOT 356 phylotypes, as well as higher mean levels of Filifactor alocis, Fretibacterium fastidiosum, Porphyromonas gingivalis, Tannerella forsythia, and Selenomonas sputigena species than PH subjects (P < 0.05). GAgP subjects presented higher mean levels of TM7 sp. HOT 356 and F. alocis than GChP subjects (P < 0.05). A significantly higher mean prevalence of Bacteroidales sp. HOT 274, Desulfobulbus sp. HOT 041, Fretibacterium sp. HOT 360, and Fretibacterium sp. HOT 362 was found in subjects with GChP and GAgP than in PH subjects. Mean levels of P. gingivalis (r = 0.68), T. forsythia (r = 0.62), F. alocis (r = 0.51, P = 0.001), and Fretibacterium sp. HOT 360 (r = 0.41) were correlated with pocket depth (P < 0.001). In conclusion, Bacteroidales sp. HOT 274, Desulfobulbus sp. HOT 041, Fretibacterium sp. HOT 360, Fretibacterium sp. HOT 362, and TM7 sp. HOT 356 phylotypes, in addition to F. alocis, F. fastidiosum, and S. sputigena, seem to be associated with periodontitis, and their role in periodontal pathogenesis should be further investigated., (© International & American Associations for Dental Research 2016.)

Objective: The aim of the study is to compare detection frequency of periodontal pathogens in patients with aggressive/severe chronic periodontitis using pooled plaque samples from the deepest pockets per quadrant/per sextant., Methods: In 100 patients with aggressive/chronic periodontitis, subgingival plaque was sampled from the deepest pockets per quadrant (MT4) and per sextant (MT6). Plaque samples were taken using two sterile paper points simultaneously. One paper point from each pocket was pooled with the three other paper points of the pockets (MT4). Subsequently, the remaining four paper points were pooled with two paper points from the deepest pockets from the two remaining sextants (MT6). The content of each vial was analyzed with nucleic-acid based methods for Aggregatibacter actinomycetemcomitans, Tannerella forsythia, Porphyromonas gingivalis, Treponema denticola, Prevotella intermedia, Parvimonas micra, Fusobacterium nucleatum, Campylobacter rectus, Eubacterium nodatum, Eikenella corrodens, and Capnocytophaga sp., Results: The detection frequency of A. actinomycetemcomitans (MT4/MT6) at 22/24 %, T. forsythia at 93/96 %, P. gingivalis at 78/79 %, T. denticola at 88/90 %, P. intermedia at 40/46 %, P. micra at 75/79 %, F. nucleatum at both 99 %, C. rectus at 84/89 %, E. nodatum at 62/65 %, E. corrodens at 80/87 %, and Capnocytophaga sp. at 49/58 % was higher with MT6 than with MT4. None of these differences were statistically significant., Conclusion: The detection frequency of the investigated periopathogens was statistically insignificant higher with the sampling method MT6 compared with MT4., Clinical Relevance: In daily dental practice, the plaque sampling of the deepest pockets per quadrant seems to be sufficient.

Objective: This study evaluated the clinical, immunological and microbiological results of full-mouth ultrasonic debridement (FMUD) with 10 % povidone iodine (PVPI) as the cooling liquid in the treatment of generalised aggressive periodontitis (GAgP)., Material and Methods: Twenty-eight patients presenting GAgP were randomly assigned to one of the following groups for evaluation: FMUD + SS (n = 14)--single session of FMUD with 0.9 % saline solution as cooling agent and FMUD + PVPI (n = 14)--single session of FMUD with PVPI solution as cooling agent. Probing depth (PD), relative clinical attachment level (RCAL), relative position of gingival margin, plaque index (FMPI) and bleeding score (FMBS), immunological (interleukin-10 and interleukin-1β concentrations in gingival crevicular fluid) and microbiological (Aa and Pg amounts) parameters were evaluated at baseline, first, third and sixth months after treatment., Results: The two groups presented reduction of FMPI and FMBS and had statistically significant PD reductions, RCAL gains and gingival recession (p < 0.05). Both therapies reduced Pg levels in deep and in moderate pockets (p < 0.05). FMUD + PVPI reduced Aa levels in deep pockets. However, no inter-group differences in clinical, immunological and microbiological parameters were observed (p > 0.05)., Conclusions: It could be concluded that 10 % PVPI used as an irrigant solution in FMUD decreased Aa levels in deep pockets but had no additional benefits when compared with saline solution irrigation in terms of clinical, microbiological and immunological results., Clinical Relevance: The FMUD is a valid option for the treatment of GAgP, but the use of 10 % PVPI did not improve the results of the periodontal therapy.

We report a case of generalized aggressive periodontitis (AgP) requiring periodontal treatment including flap surgery and ridge augmentation. The patient was a 39-year-old woman who presented with the chief complaint of pus discharge from tooth #36. No other obvious signs of gingival inflammation were observed. Periodontal examination revealed multiple sites with a probing depth of ≥10 mm. Radiography showed pro-nounced bone defects in the maxillary incisors and molar region. Real-time PCR was used to detect Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, and Tannerella forsythia in subgingival plaque; all 3 pathogens were found. Based on a clinical diagnosis of generalized AgP, periodontal therapy was initiated, which resulted in an improvement in clinical and microbiological parameters. A modified Widman flap procedure was then performed on sites with residual periodontal pockets. Next, a connective tissue graft was performed for ridge augmentation at #22, which had shown evidence of ridge resorption. Postoperative reevaluation revealed a reduction in probing depth and an improvement in marginal bone levels. Oral function was then restored using a fixed bridge prosthesis and maintenance therapy initiated. The periodontal condition has remained stable over a 2.5-year period. In the present case of AgP, surgical intervention reduced periodontal pockets and periodontal pathogens and improved the architecture of both the hard and soft tissues, allowing subsequent care of the periodontium to be performed efficiently by the patient.

Localized aggressive periodontitis (LAP) is a distinct form of early-onset periodontitis linked to periodontal infection with uncontrolled inflammation and leukocyte-mediated tissue destruction. The resolution of inflammation is an active process orchestrated by specialized proresolving lipid mediators (SPMs). Since the level of the Maresin pathway marker 14-hydroxy-docosahexaenoic acid (14-HDHA) was lower in activated peripheral blood from LAP patients, we investigated the Maresin 1 (MaR1) biosynthetic pathway in these subjects and its role in regulating phagocyte functions. Macrophages from LAP patients had a lower level of expression of 12-lipoxygenase (∼30%) and reduced MaR1 (LAP versus healthy controls [HC], 87.8 ± 50 pg/10(6) cells versus 239.1 ± 32 pg/10(6) cells). Phagocytosis by LAP macrophages was reduced ∼40% compared to that of HC, and killing of periodontal pathogens, including Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans, were similarly reduced. LAP neutrophils also displayed slower kinetics (∼30%) and decreased maximal phagocytosis (∼20% lower) with these pathogens than those of HC. The administration of MaR1 at 1 nM enhanced phagocytosis (31 to 65% increase), intracellular antimicrobial reactive oxygen species production (26 to 71% increase), bacterial killing of these periodontal pathogens (22 to 38% reduction of bacterial titers), and restored impairment of LAP phagocytes. Together, these results suggest that therapeutics targeting the Maresin pathway have clinical utility in treating LAP and other oral diseases associated with infection, inflammation, and altered phagocyte functions., (Copyright © 2016, American Society for Microbiology. All Rights Reserved.)

Periodontal disease (PD) develops from a synergy of complex subgingival oral microbiome, and is linked to systemic inflammatory atherosclerotic vascular disease (ASVD). To investigate how a polybacterial microbiome infection influences atherosclerotic plaque progression, we infected the oral cavity of ApoE null mice with a polybacterial consortium of 4 well-characterized periodontal pathogens, Porphyromonas gingivalis, Treponema denticola, Tannerealla forsythia and Fusobacterium nucleatum, that have been identified in human atherosclerotic plaque by DNA screening. We assessed periodontal disease characteristics, hematogenous dissemination of bacteria, peripheral T cell response, serum inflammatory cytokines, atherosclerosis risk factors, atherosclerotic plaque development, and alteration of aortic gene expression. Polybacterial infections have established gingival colonization in ApoE null hyperlipidemic mice and displayed invasive characteristics with hematogenous dissemination into cardiovascular tissues such as the heart and aorta. Polybacterial infection induced significantly higher levels of serum risk factors oxidized LDL (p < 0.05), nitric oxide (p < 0.01), altered lipid profiles (cholesterol, triglycerides, Chylomicrons, VLDL) (p < 0.05) as well as accelerated aortic plaque formation in ApoE null mice (p < 0.05). Periodontal microbiome infection is associated with significant decreases in Apoa1, Apob, Birc3, Fga, FgB genes that are associated with atherosclerosis. Periodontal infection for 12 weeks had modified levels of inflammatory molecules, with decreased Fas ligand, IL-13, SDF-1 and increased chemokine RANTES. In contrast, 24 weeks of infection induced new changes in other inflammatory molecules with reduced KC, MCSF, enhancing GM-CSF, IFNγ, IL-1β, IL-13, IL-4, IL-13, lymphotactin, RANTES, and also an increase in select inflammatory molecules. This study demonstrates unique differences in the host immune response to a polybacterial periodontal infection with atherosclerotic lesion progression in a mouse model.

Objective: The aim of the study was to compare the agreement and reproducibility of three test kits (IAI Pado Test 4⋅5®, micro-IDent®, and Carpegen® Perio Diagnostik) regarding the detection of Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola, and Aggregatibacter actinomycetemcomitans., Materials and Methods: Periodontal plaque samples from 20 patients suffering from severe chronic or aggressive periodontitis were split into two identical batches. Samples of batch 1 were evaluated immediately. Samples of batch 2 were analyzed after a storage period of 2 weeks at 4 °C., Results: The conformity of results obtained by the evaluated test kits as well as the concordant detection rate of periodontopathogens proved to be low. The agreement of the detection rate depends on the chosen test kit. The intra-test reproducibility of the qualitative analysis of identical plaque samples was perfect only for Carpegen® Perio Diagnostik. The quantitative analysis of the results expressed as n-fold difference of the test results revealed an only poor inter-test agreement between the test systems., Conclusions: Results of test kits for the identification of periodontopathogens are significantly influenced by the detection technology applied. The most advanced technology tended to give the most reliable results., Clinical Relevance: As microbiological test results are supposed to be used for the planning of subsequent treatment strategies, clinicians should be aware of the limitations of results obtained by the different test systems and should use the results only in conjunction with clinical data for subsequent therapeutic decisions.

Aim: Generalized aggressive periodontitis (GAP) is a severe and multifactorial disease in which a familial aggregation and a specific microbiological profile have been suggested. Thus, this case-control study evaluated the clinical and subgingival microbial profile of GAP subjects and their families compared to healthy families., Methods: Fifteen families with parents presenting periodontal health and 15 with parents with a history of GAP were selected. Each family should have at least one child between 6 and 12 years old. Plaque index (PI), gingival index (GI), and periodontal probing depth (PPD), as well as Porphyromonas gingivalis, Tannerella forsythia, and Aggregatibacter actinomycetemcomitans (Aa) amounts (by qPCR), were assessed from all subjects., Results: Children of GAP families showed a higher PI, GI, and PPD when compared to children of healthy families (p ≤ 0.05). A higher frequency of detection and amounts of Aa was observed in GAP children compared to children of healthy families (p ≤ 0.05). Moreover, a significant association between Aa amounts and gingival bleeding was observed in children (p ≤ 0.05, r = 0.37)., Conclusion: Children from GAP families have worst clinical conditions, i.e. higher levels of PI, GI, and PPD, a more pathogenic microbiological profile, and the amount of Aa are associated with a higher marginal inflammation., (© 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Periodontitis is an infectious/inflammatory disease characterized by the loss of periodontal ligament and alveolar bone. Herpesviruses are frequent inhabitants of periodontitis lesions, and the periodontopathogenicity of these viruses is the topic of this review. In 26 recent studies from 15 countries, subgingival cytomegalovirus, Epstein-Barr virus and herpes simplex virus type 1, respectively, yielded median prevalences of 49%, 45% and 63% in aggressive periodontitis, 40%, 32% and 45% in chronic periodontitis, and 3%, 7% and 12% in healthy periodontium. An active herpesvirus infection of the periodontium exhibits site specificity, is a potent stimulant of cellular immunity, may cause upgrowth of periodontopathic bacteria and tends to be related to disease-active periodontitis. Pro-inflammatory cytokines induced by the herpesvirus infection may activate matrix metalloproteinases and osteoclasts, leading to breakdown of the tooth-supportive tissues. The notion that a co-infection of herpesviruses and specific bacteria causes periodontitis provides a plausible etiopathogenic explanation for the disease. Moreover, herpesvirus virions from periodontal sites may dislodge into saliva or enter the systemic circulation and cause diseases beyond the periodontium. Periodontal treatment can diminish significantly the periodontal load of herpesviruses, which may lower the incidence and magnitude of herpesvirus dissemination within and between individuals, and subsequently the risk of acquiring a variety of medical diseases. Novel and more effective approaches to the prevention and treatment of periodontitis and related diseases may depend on a better understanding of the herpesvirus-bacteria-immune response axis., (© 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)