Periodontal diseases in Thai schoolchildren. Clinical and microbiological observations.

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.

Treponema denticola as a prognostic biomarker for periodontitis in dogs.

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.

Oral Phenotype and Salivary Microbiome of Individuals With Papillon-Lefèvre Syndrome.

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.

Parents with periodontitis impact the subgingival colonization of their offspring.

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.

Interleukin Gene Variability and Periodontal Bacteria in Patients with Generalized Aggressive Form of Periodontitis.

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 IL­10-1087 A/G (rs1800896) and specific IL-10 haplotypes were associated with the development of the disease (P < 0.05, Pcorr > 0.05). Four bacterial species occurred more frequently in AgP than in controls (P < 0.01, Pcorr < 0.05). Elevated IL-10 levels were found in AgP patients, carriers of IL­10-1087GG genotype, and PBMCs stimulated by periodontal bacteria (P < 0.05, Pcorr > 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.

Antibacterial activity of salvia officinalis L. against periodontopathogens: An in vitro study.

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.

Clinical and Microbiological Evaluation of Surgical and Nonsurgical Treatment of Aggressive Periodontitis.

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.

Clinical and microbiological evaluation of surgical and nonsurgical treatment of aggressive periodontitis

Abstract 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.

Resumo O presente estudo teve como objetivo avaliar os efeitos clínicos e microbiológicos de terapia periodontal cirúrgica e não cirúrgica no tratamento da periodontite agressiva generalizada (PAgG). Dezesseis pacientes portadores de PAgG foram incluídos neste estudo clínico, prospectivo, randomizado, de boca dividida. Os quadrantes superiores de cada paciente foram alocados em dois grupos: um grupo de terapia não-cirúrgica (NST) e um grupo de terapia cirúrgica (ST). Os parâmetros clínicos avaliados foram: índice de placa (PI), sangramento à sondagem índice (BoP), profundidade de sondagem (PD), nível clínico de inserção (CAL) e posição da margem gengival (GMP). Também foram determinadas as concentrações de Porphyromonas gingivalis (Pg) e Aggregatibacter actinomycetemcomitans (Aa) no biofilme subgengival. Os parâmetros clínicos e microbiológicos foram avaliados no início, 3, 6 e 12 meses após o tratamento. A terapia cirúrgica foi capaz de promover maior redução de PD em comparação com NST em bolsas profundas aos 12 meses (p<0,05) e em dentes posteriores aos 6 meses (p<0,05). Além disso, houve maior recessão gengival nos dentes posteriores do grupo ST no 6° mês (p<0,05). Entretanto, ST não promoveu ganho adicionais de inserção (CAL) em nenhum período do avaliação. A avaliação microbiológica não mostrou diferença estatística nos níveis de Aa e Pg, para ambos os grupos, em todos os períodos de acompanhamento. O tratamento cirúrgico promoveu benefícios clínicos similares ao tratamento não cirúrgico em pacientes com PAgG. Além disso, ambas as terapias não conseguiram reduzir os níveis Aa e Pg após terapia.

Aggregatibacter actinomycetemcomitans (Aa) Under the Radar: Myths and Misunderstandings of Aa and Its Role in Aggressive Periodontitis.

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.

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

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.

Subgingival microbiome in Chinese patients with generalized aggressive periodontitis compared to healthy controls.

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.

Comparison of Subgingival and Buccal Mucosa Microbiome in Chronic and Aggressive Periodontitis: A Pilot Study.

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_[XI][G-6], Peptostreptococcaceae_[XI][G-5], Bacteroidetes_[G-5], Bacteroidetes_[G-3], Peptostreptococcaceae_[XI][G-4], Peptostreptococcaceae_[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.

Comparison of the oral microbiome of patients with generalized aggressive periodontitis and periodontitis-free subjects.

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.

Effect of periodontal treatment on Aggregatibacter actinomycetemcomitans colonization and serum IgG levels against A. actinomycetemcomitans serotypes and Omp29 of aggressive periodontitis patients.

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.

Efficacy of adjunctive photodynamic therapy in the treatment of generalized aggressive periodontitis: A randomized controlled clinical trial.

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.

Detection of Tannerella forsythia bspA and prtH genotypes among periodontitis patients and healthy subjects-A case-Control study.

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.

Localization and density of Porphyromonas gingivalis and Tannerella forsythia in gingival and subgingival granulation tissues affected by chronic or aggressive periodontitis.

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 polymorphisms affect the key periodontal pathogens in Chinese periodontitis patients.

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.

The Subgingival Microbiome of Periodontal Pockets With Different Probing Depths in Chronic and Aggressive Periodontitis: A Pilot Study.

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_2, Defluviitaleaceae_UCG_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_UCG_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.

Wild-type isolates of Porphyromonas gingivalis derived from periodontitis patients display major variability in platelet activation.

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.