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Genetic risk factors play important roles in the etiology of oral, dental, and craniofacial diseases. Identifying the relevant risk loci and understanding their molecular biology could highlight new prevention and management avenues. Our current understanding of oral health genomics suggests that dental caries and periodontitis are polygenic diseases, and very large sample sizes and informative phenotypic measures are required to discover signals and adequately map associations across the human genome. In this article, we introduce the second wave of the Gene-Lifestyle Interactions and Dental Endpoints consortium (GLIDE2) and discuss relevant data analytics challenges, opportunities, and applications. In this phase, the consortium comprises a diverse, multiethnic sample of over 700,000 participants from 21 studies contributing clinical data on dental caries experience and periodontitis. We outline the methodological challenges of combining data from heterogeneous populations, as well as the data reduction problem in resolving detailed clinical examination records into tractable phenotypes, and describe a strategy that addresses this. Specifically, we propose a 3-tiered phenotyping approach aimed at leveraging both the large sample size in the consortium and the detailed clinical information available in some studies, wherein binary, severity-encompassing, and "precision," data-driven clinical traits are employed. As an illustration of the use of data-driven traits across multiple cohorts, we present an application of dental caries experience data harmonization in 8 participating studies ( N = 55,143) using previously developed permanent dentition tooth surface-level dental caries pattern traits. We demonstrate that these clinical patterns are transferable across multiple cohorts, have similar relative contributions within each study, and thus are prime targets for genetic interrogation in the expanded and diverse multiethnic sample of GLIDE2. We anticipate that results from GLIDE2 will decisively advance the knowledge base of mechanisms at play in oral, dental, and craniofacial health and disease and further catalyze international collaboration and data and resource sharing in genomics research.

Genome-wide transcriptomic analyses in whole tissues reflect the aggregate gene expression in heterogeneous cell populations comprising resident and migratory cells, and they are unable to identify cell type-specific information. We used a computational method (population-specific expression analysis [PSEA]) to decompose gene expression in gingival tissues into cell type-specific signatures for 8 cell types (epithelial cells, fibroblasts, endothelial cells, neutrophils, monocytes/macrophages, plasma cells, T cells, and B cells). We used a gene expression data set generated using microarrays from 120 persons (310 tissue samples; 241 periodontitis affected and 69 healthy). Decomposition of the whole-tissue transcriptomes identified differentially expressed genes in each of the cell types, which mapped to biologically relevant pathways, including dysregulation of Th17 cell differentiation, AGE-RAGE signaling, and epithelial-mesenchymal transition in epithelial cells. We validated selected PSEA-predicted, differentially expressed genes in purified gingival epithelial cells and B cells from an unrelated cohort ( n = 15 persons), each of whom contributed with 1 periodontitis-affected and 1 healthy gingival tissue sample. Differential expression of these genes by quantitative reverse transcription polymerase chain reaction corroborated the PSEA predictions and pointed to dysregulation of biologically important pathways in periodontitis. Collectively, our results demonstrate the robustness of the PSEA in the decomposition of gingival tissue transcriptomes and its ability to identify differentially regulated transcripts in particular cellular constituents. These genes may serve as candidates for further investigation with respect to their roles in the pathogenesis of periodontitis.

A practical method to identify people who are most affected by periodontitis in their age group is currently unavailable. We focused on individuals with mean clinical attachment loss (CAL) above the 80th percentile within each of 10 age groups (5-y intervals between 30 and 74 y as well as ≥75 y). We developed predictive models using combined data from 2 cohorts (2009 to 2010 and 2011 to 2012) from the NHANES (National Health and Nutrition Examination Survey; development cohort [DC], n = 6,757), and we carried out external validation using data from a third NHANES cohort (2013 to 2014; validation cohort [VC], n = 3,447). We used 1) age-specific logistic regression models with stepwise selection to identify significant demographic variables, habits, medical conditions, and selected clinical periodontal parameters (proportion of teeth with probing depth ≥4 mm at incisors and molars and with visible [≥2 mm] recession) and to calculate propensity scores (PSs); 2) Youden's J statistic to select optimum PS cutoffs to maximize diagnostic performance using receiver operating characteristic curves; and 3) bootstrap resampling with 1,000 replicates to validate the age-specific models and adjust the PS and optimal PS cutoffs for overfitting. The bootstrap-adjusted PSs were used as single predictors of mean CAL over the 80th percentile in the VC. The age-specific upper quintiles of mean CAL ranged between 1.63 and 3.24 mm in the DC and between 1.87 and 3.20 mm in the VC. The area under the curve of the models exceeded 0.85 in all age groups in the DC and 0.84 in the VC, indicating well-validated diagnostic performance. In the DC, sensitivity values ranged between 0.75 and 0.97 and exceeded 0.83 in 8 of 10 age groups. Corresponding values in the VC ranged between 0.56 and 0.89 and exceeded 0.68 in 8 of 10 age groups. We conclude that modeling that incorporates readily obtainable variables through a brief patient interview and an abbreviated periodontal examination accurately identifies individuals who are most affected by periodontitis in different ages.

Analytic approaches confined to fold-change comparisons of gene expression patterns between states of health and disease are unable to distinguish between primary causal disease drivers and secondary noncausal events. Genome-wide reverse engineering approaches can facilitate the identification of candidate genes that may distinguish between causal and associative interactions and may account for the emergence or maintenance of pathologic phenotypes. In this work, we used the algorithm for the reconstruction of accurate cellular networks (ARACNE) to analyze a large gene expression profile data set (313 gingival tissue samples from a cross-sectional study of 120 periodontitis patients) obtained from clinically healthy (n = 70) or periodontitis-affected (n = 243) gingival sites. The generated transcriptional regulatory network of the gingival interactome was subsequently interrogated with the master regulator inference algorithm (MARINA) and gene expression signature data from healthy and periodontitis-affected gingiva. Our analyses identified 41 consensus master regulator genes (MRs), the regulons of which comprised between 25 and 833 genes. Regulons of 7 MRs (HCLS1, ZNF823, XBP1, ZNF750, RORA, TFAP2C, and ZNF57) included >500 genes each. Gene set enrichment analysis indicated differential expression of these regulons in gingival health versus disease with a type 1 error between 2% and 0.5% and with >80% of the regulon genes in the leading edge. Ingenuity pathway analysis showed significant enrichment of 36 regulons for several pathways, while 6 regulons (those of MRs HCLS1, IKZF3, ETS1, NHLH2, POU2F2, and VAV1) were enriched for >10 pathways. Pathways related to immune system signaling and development were the ones most frequently enriched across all regulons. The unbiased analysis of genome-wide regulatory networks can enhance our understanding of the pathobiology of human periodontitis and, after appropriate validation, ultimately identify target molecules of diagnostic, prognostic, or therapeutic value., (© International & American Associations for Dental Research 2016.)

Periodontitis and type 2 diabetes mellitus are known to be associated. The relationship between periodontal microbiota and early diabetes risk has not been studied. We investigated the association between periodontal bacteria and prediabetes prevalence among diabetes-free adults. ORIGINS (the Oral Infections, Glucose Intolerance and Insulin Resistance Study) cross sectionally enrolled 300 diabetes-free adults aged 20 to 55 y (mean ± SD, 34 ± 10 y; 77% female). Prediabetes was defined as follows: 1) hemoglobin A1c values ranging from 5.7% to 6.4% or 2) fasting plasma glucose ranging from 100 to 125 mg/dL. In 1,188 subgingival plaque samples, 11 bacterial species were assessed at baseline, including Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Treponema denticola, Tannerella forsythia, and Actinomyces naeslundii. Full-mouth clinical periodontal examinations were performed, and participants were defined as having no/mild periodontitis vs. moderate/severe periodontitis per the definition of the Centers for Disease Control and Prevention / American Academy of Periodontology. Modified Poisson regression evaluated prediabetes prevalence across bacterial tertiles. Prevalence ratios and 95% confidence intervals for third vs. first tertiles are presented. All analyses were adjusted for cardiometabolic risk factors. All results presented currently arise from the baseline cross section. Prediabetes prevalence was 18%, and 58% of participants had moderate/severe periodontitis. Prevalence ratios (95% confidence intervals) summarizing associations between bacterial levels and prediabetes were as follows: A. actinomycetemcomitans, 2.48 (1.34, 4.58), P = 0.004; P. gingivalis, 3.41 (1.78, 6.58), P = 0.0003; T. denticola, 1.99 (0.992, 4.00), P = 0.052; T. forsythia, 1.95 (1.0, 3.84), P = 0.05; A. naeslundii, 0.46 (0.25, 0.85), P = 0.01. The prevalence ratio for prediabetes among participants with moderate/severe vs. no/mild periodontitis was 1.47 (0.78, 2.74), P = 0.23. Higher colonization levels of specific periodontal microbiota are associated with higher prediabetes prevalence among diabetes-free adults., (© International & American Associations for Dental Research.)

The currently recognized principal forms of periodontitis-chronic and aggressive-lack an unequivocal, pathobiology-based foundation. We explored whether gingival tissue transcriptomes can serve as the basis for an alternative classification of periodontitis. We used cross-sectional whole-genome gene expression data from 241 gingival tissue biopsies obtained from sites with periodontal pathology in 120 systemically healthy nonsmokers with periodontitis, with available data on clinical periodontal status, subgingival microbial profiles, and serum IgG antibodies to periodontal microbiota. Adjusted model-based clustering of transcriptomic data using finite mixtures generated two distinct clusters of patients that did not align with the current classification of chronic and aggressive periodontitis. Differential expression profiles primarily related to cell proliferation in cluster 1 and to lymphocyte activation and unfolded protein responses in cluster 2. Patients in the two clusters did not differ with respect to age but presented with distinct phenotypes (statistically significantly different whole-mouth clinical measures of extent/severity, subgingival microbial burden by several species, and selected serum antibody responses). Patients in cluster 2 showed more extensive/severe disease and were more often male. The findings suggest that distinct gene expression signatures in pathologic gingival tissues translate into phenotypic differences and can provide a basis for a novel classification.

To gain insights into the in vivo function of miRNAs in the context of periodontitis, we examined the occurrence of miRNAs in healthy and diseased gingival tissues and validated their in silico-predicted targets through mRNA profiling using whole-genome microarrays in the same specimens. Eighty-six individuals with periodontitis contributed 198 gingival papillae: 158 'diseased' (bleeding-on-probing, PD > 4 mm, and AL ≥ 3 mm) and 40 'healthy' (no bleeding, PD ≤ 4 mm, and AL ≤ 2 mm). Expression of 1,205 miRNAs was assessed by microarrays, followed by selected confirmation by quantitative RT-PCR. Predicted miRNA targets were identified and tested for enrichment by Gene Set Enrichment Analysis (GSEA). Enriched gene sets were grouped in functional categories by DAVID and Ingenuity Pathway Analysis. One hundred fifty-nine miRNAs were significantly differentially expressed between healthy and diseased gingiva. Four miRNAs (hsa-miR-451, hsa-miR-223, hsa-miR-486-5p, hsa-miR-3917) were significantly overexpressed, and 7 (hsa-miR-1246, hsa-miR-1260, hsa-miR-141, hsa-miR-1260b, hsa-miR-203, hsa-miR-210, hsa-miR-205*) were underexpressed by > 2-fold in diseased vs. healthy gingiva. GSEA and additional filtering identified 60 enriched miRNA gene sets with target genes involved in immune/inflammatory responses and tissue homeostasis. This is the first study that concurrently examined miRNA and mRNA expression in gingival tissues and will inform mechanistic experimentation to dissect the role of miRNAs in periodontal tissue homeostasis and pathology.

Evidence from epidemiologic studies suggests that periodontal infections are independently associated with subclinical and clinical atherosclerotic vascular disease. Although the strength of the reported associations is modest, the consistency of the data across diverse populations and a variety of exposure and outcome variables suggests that the findings are not spurious or attributable only to the effects of confounders. Analysis of limited data from interventional studies suggests that periodontal treatment generally results in favorable effects on subclinical markers of atherosclerosis, although such analysis also indicates considerable heterogeneity in responses. Experimental mechanistic in vitro and in vivo studies have established the plausibility of a link between periodontal infections and atherogenesis, and have identified biological pathways by which these effects may be mediated. However, the utilized models are mostly mono-infections of host cells by a limited number of 'model' periodontal pathogens, and therefore may not adequately portray human periodontitis as a polymicrobial, biofilm-mediated disease. Future research must identify in vivo pathways in humans that may (i) lead to periodontitis-induced atherogenesis, or (ii) result in treatment-induced reduction of atherosclerosis risk. Data from these studies will be essential for determining whether periodontal interventions have a role in the primary or secondary prevention of atherosclerosis.

Background: Periodontitis is ubiquitous and associated with serological evidence of exposure to periodontal organisms, systemic inflammation and vascular disease. Dementia is a major public health problem likely related to a complex interaction between genetics and diseases associated with systemic inflammation, including diabetes, smoking and stroke., Methods: To assess relationships between systemic exposure to periodontal pathogens and cognitive test outcomes, data were analysed from the Third National Health and Nutrition Examination Survey (NHANES-III), a nationally representative cross sectional observational study among older adults. We included 2355 participants >or=60 years who completed measures of cognition and Poryphyromonas gingivalis IgG. Using SUDAAN, logistic regression models examined the association of P gingivalis IgG with cognitive test performance., Results: Poor immediate verbal memory (<5/9 points) was prevalent in 5.7% of patients, and 6.5% overall had impaired delayed recall (<4/9); 22.1% had difficulty with serial subtractions (<5/5 trials correct). Individuals with the highest P gingivalis IgG (>119 ELISA Units (EU)) were more likely to have poor delayed verbal recall (OR 2.89, 95% CI 1.14 to 7.29) and impaired subtraction (OR 1.95, 95% CI 1.22 to 3.11) than those with the lowest (

Aims: The aims of this study were to assess: (i) the distribution of Fcgamma receptor polymorphisms among patients with chronic periodontitis ("cases") and control subjects with no/minimal loss of periodontal tissue support in a Caucasian population; (ii) whether these polymorphisms can serve as severity markers for periodontitis; and (iii) whether they have any bearing on the response to periodontal therapy., Methods: The study sample consisted of 132 cases and 73 controls of comparable age and gender. Full-mouth periodontal status was assessed. Subgingival plaque (PL) samples and blood samples were obtained and analysed with respect to 19 bacterial species and homologous serum immunoglobulin G titres. Polymorphisms in the Fcgamma receptor IIa (131R/H) and IIIb (NA1/NA2) were assessed by polymerase chain reaction. Patients underwent periodontal therapy and were followed up at 4 and 30 months., Results: Neither polymorphism showed a skewed distribution among cases and controls. At baseline, periodontitis patients with Fcgamma RIIa-H/H131 genotype had more PL and deeper pockets than patients in other genotype groups (p < 0.05). Both bacterial levels and antibody titres were unrelated to genotype. The longitudinal analysis failed to detect an association between genotype and response to periodontal therapy., Conclusions: The present data failed to demonstrate a clinically relevant relationship between the Fcgamma receptor IIa (131R/H) or IIIb (NA1/NA2) polymorphism and periodontal status.

Background: The value of seroepidemiology in the study of periodontal infections has not been adequately explored. This study examined serum immunoglobulin (IgG) responses to periodontal bacteria in patients with periodontitis and periodontitis-free individuals over a 30-month period., Methods: Eighty-nine patients with chronic periodontitis and 42 control subjects with no deep periodontal pockets and no or minimal attachment loss (30-72 years old, 43% men) were included. Patients were examined at baseline, after completed periodontal therapy 4 months post-baseline, and at 30 months, and controls, at baseline and 30 months. IgG antibodies to 19 periodontal species were determined by checkerboard immunoblotting., Results: On average, patients displayed at baseline up to 800-fold higher titers than controls to all but three species. Over the 30-month period, titers remained stable at low levels in controls. In patients, periodontal conditions improved from a baseline mean probing depth of 3.6 mm, bleeding on probing of 62% and an average of 21.5 pockets of=6 mm/person, to 2.5 mm mean pocket depth, 30% bleeding on probing, and 1.2 deep pockets, at 30 months. Over time, antibody titers showed a modest decline in patients, but remained significantly elevated at 30 months in comparison with controls. Antibody-level changes over time were not significantly different between subjects that did and did not receive adjunctive systemic antibiotics., Conclusions: Conspicuous differences in IgG titers to periodontal bacteria exist between periodontitis patients and periodontally healthy controls. Despite successful periodontal therapy, titers remained elevated over a 30-month period, suggesting that serology may mark the history of past periodontal infection., ((c) Blackwell Munksgaard, 2004)

Objectives: This case-control study examined polymorphisms at the interleukin-1 gene in relation to periodontal status, subgingival bacteria and systemic antibodies to periodontal microbiota., Methods: 132 periodontitis patients were age- and gender-matched with 73 periodontally intact controls. Full-mouth clinical assessments of the periodontal tissues were performed. Subgingival plaque samples (2440 in total) were analyzed by genomic DNA probes, and serum IgG antibodies to periodontal microbiota were assessed by an immunoassay. Polymorphisms in the IL-1A gene at position +4845 and the IL-1B gene at position +3953 were studied by PCR. A composite positive genotype was defined as at least one rare (#2) allele present at each locus., Results: No skewed distribution of the composite genotype was observed between cases and controls (45.2% vs 41.7%). In cases, both the composite genotype and the number of #2 alleles were positively correlated with the severity of attachment loss. No relationship between genotype and subgingival microbial profiles was observed. Genotype positive patients revealed both overall lower serum antibody levels and specific titers against selected bacteria., Conclusions: The composite genotype failed to distinguish between periodontitis patients and controls but correlated in patients with the severity of the disease and the antibody responses to periodontal microbiota.

Background: This study addresses whether checkerboard assessments of serum IgG antibodies to oral bacteria may serve as surrogate markers of clinical periodontal status in epidemiologic studies., Method: The analysis involved data from 205 subjects, 132 periodontitis patients and 73 periodontally-intact controls, from whom full-mouth clinical periodontal data and serum IgG titers against 19 periodontal bacterial species were available., Results: A logistic regression model involving titers against 6 species (Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans, Eubacterium nodatum, Eikenella corrodens, Capnocytophaga ochracea and Actinomyces naeslundii genospecies 2) classified correctly 74.5% of the subjects examined, with 84% sensitivity, 57.5% specificity, 78% positive predictive value and 66.7% negative predictive value., Conclusions: Checkerboard serology may be useful in providing surrogate markers for clinical periodontal status when such data are not readily available and, thus may serve as a valuable complement in the armamentarium of epidemiologic tools suited for the study of periodontal diseases.

Background: We explored the association between subgingival microbial profiles and serum IgG responses to periodontal microbiota in relation to clinical periodontal status., Methods: One hundred thirty-one (131) periodontitis patients aged 29 to 74 years (mean 51.8) were age- and gender-matched with 74 periodontally intact controls (range 26 to 77, mean 49.3). Smoking habits and health history were recorded and assessments of plaque, bleeding on probing, probing depth, and attachment level were performed at 6 sites per tooth on all present teeth, excluding third molars. Subgingival plaque samples were obtained from each tooth in one upper and one lower quadrant (maximum 14 samples/subject; 2,440 samples total) and analyzed with respect to 19 species by means of whole genomic DNA probes. Serum IgG antibodies against the same 19 species were assessed by an immunoassay., Results: Cases displayed an average of 22.7 teeth, 20.3 sites with probing depth > or =6 mm, and 18.9 sites with attachment loss > or =6 mm. Corresponding figures for controls were 27.1, 0.1, and 1.0, respectively. Heavy smoking was 3 times more frequent among cases than controls (32.1% versus 9.6%). Higher levels of Porphyromonas gingivalis, Porphyromonas endodontalis, Prevotella intermedia, Prevotella nigrescens, Prevotella melaninogenica, Bacteroides forsythus, Fusobacterium nucleatum, Treponema denticola, Eubacterium nodatum, Peptostreptococcus micros, and Campylobacter rectus were found in cases and higher levels of Eikenella corrodens, Veillonella parvula, and Actinomyces naeslundii in controls. Cases displayed higher IgG levels against P. gingivalis and Actinobacillus actinomycetemcomitans, while controls displayed higher levels against F. nucleatum, T. denticola, E. nodatum, and Capnocytophaga ochracea. Positive correlations between bacterial colonization and antibody responses were identified for 9 species in controls. In cases, however, statistically significant correlations were observed for only 3 species out of which only one was positive (V. parvula). Both bacterial levels and antibody responses declined in ages over 55 years. A logistic regression employing selected elements of bacterial colonization and antibody responses as independent variables resulted in 81.1% correct diagnosis, with sensitivity of 83.1%, specificity of 77.8%, positive predictability of 86%, and negative predictability of 73.7%. Smoking did not reach statistical significance in this model., Conclusion: A combined microbial colonization/antibody response profile can effectively discriminate between periodontitis patients and periodontally intact controls.

Our understanding of the etiology and pathogenesis of periodontal diseases has grown in the recent past, and new findings have led to advances in patient management. This article summarizes important new knowledge and offers a description of traditional and novel diagnostic approaches. These include clinical and radiographic assessments of the periodontal tissues, evaluation of the microbial challenge and the host response, and certain elements of the host genotype that may confer susceptibility to destructive periodontal diseases.

Periodontitis affects up to 50% of individuals worldwide, and 8.5% are diagnosed with diabetes. The high-comorbidity rate of these diseases may suggest, at least in part, a shared etiology and pathophysiology. Changes in oral microbial communities have been documented in the context of severe periodontitis and diabetes, both independently and together. However, much less is known about the early oral microbial markers of these diseases. We used a subset of the ORIGINS project dataset, which collected detailed periodontal and cardiometabolic information from 787 healthy individuals, to identify early microbial markers of periodontitis and its association with markers of cardiometabolic health. Using state-of-the-art compositional data analysis tools, we identified the log-ratio of Treponema to Corynebacterium bacteria to be a novel Microbial Indicator of Periodontitis (MIP), and found that this MIP correlates with poor periodontal health and cardiometabolic markers early in disease pathogenesis in both subgingival plaque and saliva.

INTRODUCTION: We examined the association of clinical, microbiological, and host response features of periodontitis with MRI markers of atrophy/cerebrovascular disease in the Washington Heights Inwood Columbia Aging Project (WHICAP) Ancillary Study of Oral Health. METHODS: We analyzed 468 participants with clinical periodontal data, microbial plaque and serum samples, and brain MRIs. We tested the association of periodontitis features with MRI features, after adjusting for multiple risk factors for Alzheimer's disease/Alzheimer's disease‐related dementia (AD/ADRD). RESULTS: In fully adjusted models, having more teeth was associated with lower odds for infarcts, lower white matter hyperintensity (WMH) volume, higher entorhinal cortex volume, and higher cortical thickness. Higher extent of periodontitis was associated with lower entorhinal cortex volume and lower cortical thickness. Differential associations emerged between colonization by specific bacteria/serum antibacterial IgG responses and MRI outcomes. DISCUSSION: In an elderly cohort, clinical, microbiological, and serological features of periodontitis were associated with MRI findings related to ADRD risk. Further investigation of causal associations is warranted. [ABSTRACT FROM AUTHOR]

Background: There is a sparsity of data describing the periodontal microbiome in elderly individuals. We analyzed the association of subgingival bacterial profiles and clinical periodontal status in a cohort of participants in the Washington Heights-Inwood Columbia Aging Project (WHICAP).Methods: Dentate individuals underwent a full-mouth periodontal examination at six sites/tooth. Up to four subgingival plaque samples per person, each obtained from the mesio-lingual site of the most posterior tooth in each quadrant, were harvested and pooled. Periodontal status was classified according to the Centers for Disease Control/American Academy of Periodontology (CDC/AAP) criteria as well as based on the percentage of teeth/person with pockets ≥4 mm deep. Bacterial DNA was isolated and was processed and analyzed using Human Oral Microbe Identification using Next Generation Sequencing (HOMINGS). Differential abundance across the periodontal phenotypes was calculated using the R package DESeq2. α- and β-diversity metrics were calculated using DADA2-based clustering.Results: The mean age of the 739 participants was 74.5 years, and 32% were male. Several taxa including Sneathia amnii-like sp., Peptoniphilaceae [G-1] bacterium HMT 113, Porphyromonas gingivalis, Fretibacterium fastidiosum, Filifactor alocis, and Saccharibacteria (TM7) [G-1] bacterium HMT 346 were more abundant with increasing severity of periodontitis. In contrast, species such as Veillonella parvula, Veillonella dispar, Rothia dentocariosa, and Lautropia mirabilis were more abundant in health. Microbial diversity increased in parallel with the severity and extent of periodontitis.Conclusions: The observed subgingival bacterial patterns in these elderly individuals corroborated corresponding findings in younger cohorts and were consistent with the concept that periodontitis is associated with perturbations in the resident microbiome. [ABSTRACT FROM AUTHOR]

Background: Successful dissemination of the new classification of periodontitis is facilitated by emphasis on the basic ground rules, clarification of ambiguities, and identification of "gray zones" where thoughtful application of the guidelines by an informed, experienced clinician is paramount to arrive at a correct Stage and Grade.Methods: Highlighted ground rules are (1) Stage is a patient-based, not a tooth-based concept, therefore, a single Stage is assigned per patient; (2) Stage can shift upward over time, if the periodontal status deteriorates, but the initially assigned Stage is retained even after improvement post-therapy; (3) the complexity factors that determine Stage must be evaluated collectively, not in isolation, to arrive at a clinically meaningful assessment; (4) a single Grade is assigned to a patient based on a deliberate evaluation of the "biological fabric" of the case, in terms of history of/risk for further progression, interplay of risk factors, and the two-way effects of periodontitis or its treatment on general health; (v) shift of Grade over time is possible towards either direction, after thorough, collective, evaluation of changes in the above parameters. Exemplified gray zones include a radiographically intact patient with minimal attachment loss in older age; presence of "frank" periodontitis affecting a single tooth; and assessment of factors that do/do not lead to increased complexity of therapy.Conclusion: Differentiating between Stage I/II versus Stage III/IV periodontitis is relatively uncomplicated; further distinction between Stages and correct assignment of Grade requires nuanced, thorough interpretation of a broad array of findings by a knowledgeable clinician. [ABSTRACT FROM AUTHOR]

A classification scheme for periodontal and peri‐implant diseases and conditions is necessary for clinicians to properly diagnose and treat patients as well as for scientists to investigate etiology, pathogenesis, natural history, and treatment of the diseases and conditions. This paper summarizes the proceedings of the World Workshop on the Classification of Periodontal and Peri‐implant Diseases and Conditions. The workshop was co‐sponsored by the American Academy of Periodontology (AAP) and the European Federation of Periodontology (EFP) and included expert participants from all over the world. Planning for the conference, which was held in Chicago on November 9 to 11, 2017, began in early 2015. An organizing committee from the AAP and EFP commissioned 19 review papers and four consensus reports covering relevant areas in periodontology and implant dentistry. The authors were charged with updating the 1999 classification of periodontal diseases and conditions and developing a similar scheme for peri‐implant diseases and conditions. Reviewers and workgroups were also asked to establish pertinent case definitions and to provide diagnostic criteria to aid clinicians in the use of the new classification. All findings and recommendations of the workshop were agreed to by consensus. This introductory paper presents an overview for the new classification of periodontal and peri‐implant diseases and conditions, along with a condensed scheme for each of four workgroup sections, but readers are directed to the pertinent consensus reports and review papers for a thorough discussion of the rationale, criteria, and interpretation of the proposed classification. Changes to the 1999 classification are highlighted and discussed. Although the intent of the workshop was to base classification on the strongest available scientific evidence, lower level evidence and expert opinion were inevitably used whenever sufficient research data were unavailable. The scope of this workshop was to align and update the classification scheme to the current understanding of periodontal and peri‐implant diseases and conditions. This introductory overview presents the schematic tables for the new classification of periodontal and peri‐implant diseases and conditions and briefly highlights changes made to the 1999 classification. It cannot present the wealth of information included in the reviews, case definition papers, and consensus reports that has guided the development of the new classification, and reference to the consensus and case definition papers is necessary to provide a thorough understanding of its use for either case management or scientific investigation. Therefore, it is strongly recommended that the reader use this overview as an introduction to these subjects. Accessing this publication online will allow the reader to use the links in this overview and the tables to view the source papers (Table 1). [ABSTRACT FROM AUTHOR]

A new periodontitis classification scheme has been adopted, in which forms of the disease previously recognized as "chronic" or "aggressive" are now grouped under a single category ("periodontitis") and are further characterized based on a multi‐dimensional staging and grading system. Staging is largely dependent upon the severity of disease at presentation as well as on the complexity of disease management, while grading provides supplemental information about biological features of the disease including a history‐based analysis of the rate of periodontitis progression; assessment of the risk for further progression; analysis of possible poor outcomes of treatment; and assessment of the risk that the disease or its treatment may negatively affect the general health of the patient. Necrotizing periodontal diseases, whose characteristic clinical phenotype includes typical features (papilla necrosis, bleeding, and pain) and are associated with host immune response impairments, remain a distinct periodontitis category. Endodontic‐periodontal lesions, defined by a pathological communication between the pulpal and periodontal tissues at a given tooth, occur in either an acute or a chronic form, and are classified according to signs and symptoms that have direct impact on their prognosis and treatment. Periodontal abscesses are defined as acute lesions characterized by localized accumulation of pus within the gingival wall of the periodontal pocket/sulcus, rapid tissue destruction and are associated with risk for systemic dissemination. [ABSTRACT FROM AUTHOR]

Objective: We used epidemiologic data of clinical periodontal status from two population‐based samples in two countries, United States and Germany, to examine 1) the impact of age on the relative contribution of recession and pocketing on the distribution of clinical attachment loss, and 2) whether it is feasible to define age‐dependent thresholds for severe periodontitis. Methods: The analytical sample was based on persons aged ≥30 and included 10,713 individuals in the United States, participants in NHANES 2009 to 2014, and 3,071 individuals in Pomerania, Germany, participants in the SHIP‐Trend 2008 to 2012. NHANES used a full‐mouth examination protocol to collect data on recession (R), pocket depth (PD) and clinical attachment loss (CAL) for six sites/tooth on a maximum of 28 teeth; SHIP‐Trend used a half‐mouth examination at four sites/tooth. In both samples, percentile distributions of mean CAL/person were generated for each 5‐year age interval. Age‐dependent thresholds defining the upper quintile of mean CAL were calculated for both samples. The topographic intraoral distribution of CAL and the relative contribution of R and PD on CAL was assessed. Results: Mean CAL increased linearly with age in both samples and was higher in SHIP‐Trend than NHANES across the age spectrum. In contrast, mean PD was constant across age groups in both populations. R contributed increasingly to CAL with age, especially after 45 to 49 years. Upper quintile mean CAL thresholds in NHANES were < 3 mm for ages up to 39 years, and under 3.58 mm in all other age groups. Corresponding values in SHIP‐Trend were also < 3 mm in ages up to 39 years but increased linearly with age up to 7.21 mm for ages ≥75 years. Conclusions: Despite substantial differences in the overall severity of attachment loss between the two samples, common patterns of CAL and of the relative contribution of R and PD to CAL with increasing age were identified. Although periodontitis severity may vary in different populations, empirical evidence‐driven definitions of CAL thresholds signifying disproportionate severity of periodontitis by age are feasible. [ABSTRACT FROM AUTHOR]

A classification scheme for periodontal and peri-implant diseases and conditions is necessary for clinicians to properly diagnose and treat patients as well as for scientists to investigate etiology, pathogenesis, natural history, and treatment of the diseases and conditions. This paper summarizes the proceedings of the World Workshop on the Classification of Periodontal and Peri-implant Diseases and Conditions. The workshop was co-sponsored by the American Academy of Periodontology (AAP) and the European Federation of Periodontology (EFP) and included expert participants from all over the world. Planning for the conference, which was held in Chicago on November 9 to 11, 2017, began in early 2015. An organizing committee from the AAP and EFP commissioned 19 review papers and four consensus reports covering relevant areas in periodontology and implant dentistry. The authors were charged with updating the 1999 classification of periodontal diseases and conditions and developing a similar scheme for peri-implant diseases and conditions. Reviewers and workgroups were also asked to establish pertinent case definitions and to provide diagnostic criteria to aid clinicians in the use of the new classification. All findings and recommendations of the workshop were agreed to by consensus. This introductory paper presents an overview for the new classification of periodontal and peri-implant diseases and conditions, along with a condensed scheme for each of four workgroup sections, but readers are directed to the pertinent consensus reports and review papers for a thorough discussion of the rationale, criteria, and interpretation of the proposed classification. Changes to the 1999 classification are highlighted and discussed. Although the intent of the workshop was to base classification on the strongest available scientific evidence, lower level evidence and expert opinion were inevitably used whenever sufficient research data were unavailable. The scope of this workshop was to align and update the classification scheme to the current understanding of periodontal and peri-implant diseases and conditions. This introductory overview presents the schematic tables for the new classification of periodontal and peri-implant diseases and conditions and briefly highlights changes made to the 1999 classification. It cannot present the wealth of information included in the reviews, case definition papers, and consensus reports that has guided the development of the new classification, and reference to the consensus and case definition papers is necessary to provide a thorough understanding of its use for either case management or scientific investigation. Therefore, it is strongly recommended that the reader use this overview as an introduction to these subjects. Accessing this publication online will allow the reader to use the links in this overview and the tables to view the source papers (Table 1). [ABSTRACT FROM AUTHOR]

Background: Recreational use of cannabis, following its legalization in some countries, poses emergent oral and periodontal health concerns. The objective of this study is to examine the relationship between frequent recreational cannabis (FRC) (marijuana and hashish) use and periodontitis prevalence among adults in the United States.Methods: Data from the National Health and Nutrition Examination Survey (NHANES) 2011 to 2012 were analyzed. Primary outcome (periodontitis) was defined using the Centers for Disease Control and Prevention/American Academy of Periodontology classification as well as continuous measurements of probing depth (PD) and clinical attachment loss (AL). Exposure of interest was self-reported cannabis use, defined as "FRC use" versus "non-FRC use." Bivariate and multivariable regression models were performed using the entire analytical sample (model 1) as well as those who had never used tobacco (never-users) (model 2).Results: Of 1,938 participants with available cannabis use data and essential covariates, 26.8% were FRC users. Mean number of sites per participant with PD ≥4, ≥6, and ≥8 mm and AL ≥3, ≥5, and ≥8 mm was significantly higher among FRC users than among non-FRC users (mean difference in number of PD sites: 6.9, 5.6, and 5.6; P <0.05; mean difference in number of AL sites: 12.7, 7.6, and 5.6; P <0.05). Average AL was higher among FRC users than among non-FRC users (1.8 versus 1.6 mm; P = 0.004). Bivariate analysis revealed positive (harmful) association between FRC use and severe periodontitis in the entire sample (odds ratio [OR]: 1.7, 95% confidence interval [CI]: 1.3 to 2.4; P = 0.002) as well as in never-smokers (OR: 2.0, 95% CI: 1.2 to 3.5; P = 0.01). This association was retained in multivariable models adjusted for demographics (age, sex, race/ethnicity, and income level), alcohol and tobacco use, diabetes mellitus, and past periodontal treatment (model 1: adjusted OR [aOR]: 1.4, 95% CI: 1.1 to 1.9; P = 0.07; model 2: aOR: 1.9, 95% CI: 1.1 to 3.2; P = 0.03).Conclusion: FRC use is associated with deeper PDs, more clinical AL, and higher odds of having severe periodontitis. [ABSTRACT FROM AUTHOR]

Background: and objectives: There is still debate regarding potential relationships between maternal periodontitis during pregnancy and adverse pregnancy outcomes. The aim of this systematic review was to synthesize the available epidemiological evidence on this association. Data sources: Combined electronic and hand search of MEDLINE, EMBASE, WEB OF SCIENCE and Cochrane Central Register databases. Study eligibility criteria: Original publications reporting data from cross‐sectional, case‐control or prospective cohort epidemiological studies on the association between periodontal status and preterm birth, low birthweight (LBW) or preeclampsia. The search was not limited to publications in English. All selected studies provided data based on professional assessments of periodontal status, and outcome variables, including preterm birth (<37 weeks gestation), LBW (<2500 g), gestational age, small for gestational age, birthweight, pregnancy loss or miscarriage, or pre‐eclampsia. Participants: Pregnant women with or without periodontal disease, and with or without adverse pregnancy outcomes, assessed either during pregnancy or postpartum. No intervention studies were included. Study appraisal and synthesis methods – Publications were assessed based on predefined screening criteria including type of periodontal assessment, consistency in the timing of the periodontal assessment with respect to gestational age, examiner masking and consideration of additional exposures and confounders. Results: Maternal periodontitis is modestly but significantly associated with LBW and preterm birth, but the use of a categorical or a continuous exposure definition of periodontitis appears to impact the findings: Although significant associations emerge from case‐control and cross‐sectional studies using periodontitis “case definitions,” these were substantially attenuated in studies assessing periodontitis as a continuous variable. Data from prospective studies followed a similar pattern, but associations were generally weaker. Maternal periodontitis was significantly associated with pre‐eclampsia. Limitations: There is a high degree of variability in study populations, recruitment and assessment, as well as differences in how data are recorded and handled. As a result, studies included in meta‐analyses show a high degree of heterogeneity. Conclusions and implications: of key findings: Maternal periodontitis is modestly but independently associated with adverse pregnancy outcomes, but the findings are impacted by periodontitis case definitions. It is suggested that future studies employ both continuous and categorical assessments of periodontal status. Further use of the composite outcome preterm LBW is not encouraged. [ABSTRACT FROM AUTHOR]

Background: The purposes of this study were to determine: 1) if periodontal treatment in pregnant women before 21 weeks of gestation alters levels of inflammatory mediators in serum; and 2) if changes in these mediators are associated with birth outcomes. Methods: A total of 823 pregnant women with periodontitis were randomly assigned to receive scaling and root planing before 21 weeks of gestation or after delivery. Serum obtained between 13 and 16 weeks, 6 days (study baseline) and 29 to 32 weeks of gestation was analyzed for C-reactive protein; prostaglandin E2; matrix metalloproteinase-9; fibrinogen; endotoxin; interleukin (IL)-1β, -6, and -8, and tumor necrosis factor-α. Cox regression, multiple linear regression, and the t, Χ², and Fisher exact tests were used to examine associations among the biomarkers, periodontal treatment, and gestational age at delivery and birth weight. Results: A total of 796 women had baseline serum data, and 620 women had baseline and follow-up serum and birth data. Periodontal treatment did not significantly alter the level of any biomarker (P>0.05). Neither baseline levels nor the change from baseline in any biomarker were significantly associated with preterm birth or infant birth weight (P>0.05). In treatment subjects, the change in endotoxin was negatively associated with the change probing depth (P<0.05). Conclusions: Non-surgical mechanical periodontal treatment in pregnant women, delivered before 21 weeks of gestation, did not reduce systemic (serum) markers of inflammation, in pregnant women with periodontitis, levels of these markers at 13 to 17 weeks and 29 to 32 weeks gestation were not associated with infant birth weight or a risk for preterm birth. [ABSTRACT FROM AUTHOR]

Background and Objective: Mucosal inflammatory responses are orchestrated largely by pro-inflammatory chemokines. The chemokine granulocyte chemotactic protein 2 (CXCL6) is involved in neutrophil recruitment and migration. Previous studies have shown that granulocyte chemotactic protein 2 is up-regulated during mucosal inflammation (e.g. in inflammatory bowel disease), similarly to the functionally and structurally related chemokine interleukin-8. Nevertheless, unlike interleukin-8, a role of granulocyte chemotactic protein 2 in gingival inflammation has not been yet demonstrated. In this study we aimed to evaluate the expression of the chemokine granulocyte chemotactic protein 2 in clinically healthy vs. diseased gingival tissues and to explore possible correlations with clinical and microbiological markers of periodontitis. Material and Methods: Gene expression in 184 ‘diseased’ and 63 ‘healthy’ gingival tissue specimens from 90 patients with periodontitis was analyzed using Affymetrix U133Plus2.0 arrays. The expression of granulocyte chemotactic protein 2 was further confirmed by real-time reverse transcription–polymerase chain reaction, western blotting and enzyme-linked immunosorbent assay, while the localization of granulocyte chemotactic protein 2 in gingival tissues was analyzed by immunohistochemistry. Plaque samples from the adjacent periodontal pockets were collected and evaluated for 11 species of periodontal bacteria using checkerboard DNA–DNA hybridizations. Results: Among all known chemokines, GCP-2 expression was the most up-regulated (3.8-fold, p < 1.1 × 10−16), in ‘diseased’ vs. ‘healthy’ tissue as compared to a 2.6-fold increased expression of interleukin-8 mRNA ( p < 1.2 × 10−15). Increased expression of granulocyte chemotactic protein 2 correlated with higher levels of ‘red’ and ‘orange’ complex pathogens and with increased probing depth, but not with attachment loss. Immunohistochemistry showed that granulocyte chemotactic protein 2 was expressed in gingival vascular endothelium. Conclusion: The level of expression of granulocyte chemotactic protein 2 correlates with the severity of periodontitis and appears to act as a hitherto unrecognized functional adjunct to interleukin-8 in diseased gingival tissues. [ABSTRACT FROM AUTHOR]

Background; Our previous studies reported on the obstetric, periodontal, and microbiologic outcomes of women participating in the Obstetrics and Periodontal Therapy (OPT) Study. This article describes the systemic antibody responses to selected periodontal bacteria in the same patients. Methods: Serum samples, obtained from pregnant women at baseline (13 to 16 weeks; 6 days of gestation) and 29 to 32 weeks, were analyzed by enzyme-linked immunosorbent assay for serum immunoglobulin G (IgG) antibody to Aggregatibacter actinomycetemcomitans (previously Actinobacillus actinomycetemcomitans), Campylobacter rectus, Fusobacterium nucleatum, Porphyromonas gingivalis, Prevotella intermedia, Tannerella forsythia (previously T. forsythensis), and Treponema denticola. Results: At baseline, women who delivered live preterm infants had significantly lower total serum levels of IgG antibody to the panel of periodontal pathogens (P= 0.0018), to P. gingivalis (P=0.0013), and to F. nucleatum (P=0.0200) than women who delivered at term. These differences were not significant at 29 to 32 weeks. Changes in IgG levels between baseline and 29 to 32 weeks were not associated with preterm birth when adjusted for treatment group, clinical center, race, or age. In addition, delivery of low birth weight infants was not associated with levels of antibody at baseline or with antibody changes during pregnancy. Conclusions: Live preterm birth is associated with decreased levels of IgG antibody to periodontal pathogens in women with periodontitis when assessed during the second trimester. Changes in IgG antibody during pregnancy are not associated with birth outcomes. [ABSTRACT FROM AUTHOR]

Background: Assessment of periodontal conditions in epidemiologic studies usually requires a clinical examination, which is resource-intensive. We investigated the ability of serum immunoglobulin G (IgG) antibodies to periodontal bacteria to reflect clinical periodontal status. Methods: We used checkerboard immunoblotting to assess serum IgG levels to 19 species, including established/putative periodontal pathogens and non-pathogenic bacteria, in 5,747 dentate adults aged ≥40 years who participated in the third National Health and Nutrition Examination Survey between 1988 and 1994. Three earlier described alternative definitions of periodontitis were used, based on specific combinations of probing depth and attachment level values. Optimized elevated titer thresholds and corresponding sensitivities and specificities were calculated for each definition. Titers significantly associated with periodontitis were identified in univariable and multivariable logistic regression models. Parsimonious models were subsequently developed using age, gender, race/ethnicity, education, smoking, and diagnosed diabetes. Results: In unadjusted models, high titers to Porphyromonas gingivalis were most strongly associated with periodontitis across all definitions (odds ratio, 2.07 to 2.74; P<0.05). In parsimonious models including demographic data, smoking, and diagnosed diabetes, high P. gingivalis titers were consistently associated with periodontitis, whereas high Eubacterium nodatum titers were associated with periodontal health in two of three definitions. Receiver operating characteristic curves for the parsimonious multivariable models showed that the area under the curve ranged between 0.72 and 0.78. Conclusions: Serum IgG titers to selected periodontal species, combined with demographic and behavioral characteristics, resulted in a moderately accurate classification of periodontal status in epidemiologic studies. The external validity of these findings must be examined further. [ABSTRACT FROM AUTHOR]

Background: Clinical and radiographic measures are gold standards for diagnosing periodontitis but offer little information regarding the pathogenesis of the disease. We hypothesized that a comparison of gene expression signatures between healthy and diseased gingival tissues would provide novel insights in the pathobiology of periodontitis and would inform the design of future studies. Methods: Ninety systemically healthy non-smokers with moderate to advanced periodontitis (63 with chronic periodontitis and 27 with aggressive periodontitis) each contributed at least two diseased interproximal papillae (with bleeding on probing [BOP], probing depth [PD] ≥4 mm, and attachment loss [AL] ≥3 mm) and a healthy papilla, if available (no BOP, PD ≤4 mm, and AL ≤2 mm). RNA was extracted, amplified, reverse transcribed, labeled, and hybridized with whole genome microarrays. Differential expression was assayed in 247 individual tissue samples (183 from diseased sites and 64 from healthy sites) using a standard mixed effects linear model approach, with patient effects considered random with a normal distribution and gingival tissue status considered a two level fixed effect. Gene ontology analysis classified the expression patterns into biologically relevant categories Results: Transcriptome analysis revealed that 12,744 probe sets were differentially expressed after adjusting for multiple comparisons (P<9.15 x 10-7). Of those, 5,295 were upregulated and 7,449 were downregulated in disease compared to health. Gene ontology analysis identified 61 differentially expressed groups (adjusted P <0.05), including apoptosis, antimicrobial humoral response, antigen presentation, regulation of metabolic processes, signal transduction, and angiogenesis. Conclusion: Gingival tissue transcriptomes provide a valuable scientific tool for further hypothesis driven studies of the pathobiology of periodontitis. [ABSTRACT FROM AUTHOR]

Background: A recent clinical trial (Obstetrics and Periodontal Therapy [OPT] Study) demonstrated that periodontal therapy during pregnancy improved periodontal outcomes but failed to impact preterm birth. The present study evaluated seven target bacteria, Aggregatibacter actinomycetemcomitans (previously Actinobacillus actinomycetemcomitans), Porphyromonas gingivalis, Treponema denticola, Tannerella forsythia (previously T. forsythensis), Prevotella intermedia, Campylobacter rectus, and Fusobacterium nucleatum, in subgingival dental plaque of pregnant women in the OPT Study and their association with birth outcomes. Methods: Pregnant women were randomly assigned to receive periodontal treatment before 21 weeks' gestation or after delivery. Subgingival plaque was sampled at baseline (13 to 16 weeks; 6 days of gestation) and at 29 to 32 weeks. We analyzed subgingival plaque samples from women who experienced fetal loss, delivered a live preterm infant (preterm women), or delivered a full-term infant (full-term women). Samples were analyzed using quantitative polymerase chain reaction. Associations between preterm birth and bacterial counts and percentages were tested using multiple linear regression. Results: No significant differences were observed at baseline between preterm and full term women for any measured bacterial species or group of species, after accounting for multiple comparisons. Changes in bacterial counts and proportions during pregnancy also were not associated with birth outcomes. In full-term and preterm women, periodontal therapy significantly reduced (P <0.01) counts of all target species except for A. actinomycetemcomitans. Conclusions: In pregnant women with periodontitis, non-surgical periodontal therapy significantly reduced levels of periodontal pathogens. Baseline levels of selected periodontal pathogens or changes in these bacteria resulting from therapy were not associated with preterm birth. [ABSTRACT FROM AUTHOR]

The prevalence of Actinobacillus actinomycetemcomitans isolates was examined in a rural population of southern Thailand. Sixty individuals aged 30–39 and 50–59 years were randomly selected from a group of 363 persons, living in four villages, who had been clinically examined previously. A subgingival plaque sample was taken with a curette from the mesial aspect of the two upper and lower first molars. Each sample was dispersed in 3.3 ml of VMGA III transport medium and spread onto Trypticase Soy Broth with Bacitracin and Vancomycin (TSBV)-agar plates on the same day. After incubation in 10% CO2 for 5 days the plates were examined for typical A. actinomycetemcomitans colonies which were tested for catalase activity. Each strain was further tested for biochemical characteristics, serotyped against serotype-specific antisera a–e and ribotyped after DNA digestion using the restriction endonucleases Hin dIII and Eco RI. For 53 (88%) of the 60 individuals, A. actinomycetemcomitans was present in at least one subgingival sample, which is considerably higher than the prevalence in Western European adults. In 11 individuals, two or three different strains were found. Serotypes a and c were the most prevalent, and serotype b was found only once among 46 tested isolates. Eleven ribotypes were found among the 46 strains. While the same ribotype could be found among individuals of the same village, no ribotype of A. actinomycetemcomitans was unique for individuals of any one village. The study demonstrated a high prevalence of A. actinomycetemcomitans among adults of the rural population of southern Thailand and indicates that this species is present as part of the resident oral flora in this population. [ABSTRACT FROM AUTHOR]

The aim of the present study was to compare epidemiological data of periodontal disease obtained from a sample of adults by means of different, commonly employed, partial and full-mouth index systems, in order to explore the amount of discrepancy attributed to the methodology per se. 169 dentate subjects, aged 25 64 years, were subjected to a clinical examination, including circumferential probing assessments of pocket depth (PPD) and attachment level (PAL) at all teeth present. The individual mean % of tooth sites with PPD of &ges; 6 mm and the % of subjects exhibiting at least one such deep pocket were calculated based on (i) full-mouth data, (ii) data derived from the buccal and mesial surfaces from 1 randomly selected upper and 1 lower quadrant, (iii) probing assessments at the 6 "Ramfjord teeth", (iv) the full-mouth community periodontal index for treatment needs (CPITN), and (v) the partial CPITN based on 10 index teeth. The PAL data were analyzed by means of 3 versions of the extent and severity index, 1 generated by full-mourn assessments and 2 by partial assessments based on 28 and 10 tooth sites, respectively. In the entire sample, the individual mean % of sites with PPD of &ges; 6 mm generated by the different systems ranged between 5.0 and 4.2 sites/subject. By full-mouth CPITN scorings, an average of 1.0 score-4 sextants/subject was recorded, while the partial CPITN generated a corresponding value of 0.8 score-4 sextants/subject. The prevalence of subjects with at least one deep pocket was found to be (i) 47% by the full-mouth examination, (ii) 24% by the half-mouth examination, (iii) 26% by the use of the "Ramfjord teeth", and (iv) 44% by the partial CPITN. Variations in the accuracy of the partial recordings were observed in different age groups. Analysis of the PAL data generated extent values ranging between 93 and 96% and severity values between 3.6 and 3.9 mm. It was concluded that partial recording systems (i) provide reasonably valid estimates of the individual mean number of "affected" tooth sites; however, (ii) they grossly underestimate the prevalence of subjects exhibiting deep periodontal pockets. [ABSTRACT FROM AUTHOR]

The prevalence of 18 selected bacterial species was assessed by means of "checkerboard" DNA-DNA hybridisation in a group of 12 Saudi-Arabian adolescents with Papillon-Lefevre syndrome. A total of 36 tooth sites were investigated. The patients exhibited severe periodontal disease with deep pockets. All 12 patients harboured the putative bacterial pathogens P. intermedia. F. nucleaturn. P. micros and S. intermedius while T. denticola, B. forsythus. P. nigrescens. E. corrodens. S. noxia and C. rectus were recovered from 11 patients. P. gingivalis was recovered from 9 patients and 18 sites while corresponding figures for A. actinomyceterncomitans were 8 and 19, respectively. A number of the investigated species (B. forsythus. T. denticola. P. intermedia, C rectus) reached high levels (≥106 cells) in more than 1/2 of the patients. On the other hand. bacteria such as A. actmomyceterncornitans and P. gingivalis were infrequently encountered at high levels in these subgingival samples. In conclusion, the analysis failed to demonstrate a PLS-specific profile of the subgingival infection, since the bacterial composition of the sampled sites closely resembled that characterising deep pockets in adult periodontitis patients. [ABSTRACT FROM AUTHOR]

The present study examined the adhesive and invasive potential of Porphyromonas gingivalis interacting with human pocket epithelium in vitro. Pocket epithelial tissue, obtained during periodontal surgery of patients with advanced periodontal disease, generated a stratified epithelium in culture, P. gingivalis strains W50 and FED 381 (laboratory strains), OMGS 712, 1439, 1738, 1739 and 1743 (clinical isolates) as well as Escherichia coli HB101 (non-adhering control) were tested with respect to epithelial adhesion and invasion. Adhesion was quantitated by scinfillation spectrometry after incubation of radiolabeled bacterial with epithelial cells. The invasive ability of P. gingivalis was measured by means of an antibiotic protection assay. Theepithelial multilayers were infected with the test and control strains and subsequently incubated with an antibiotic mixture (metronidazole 0.1 mg/ml and gentamicin 0.5 mg/ml). The number of internalized bacteria surviving the antibiotic treatment was assessed after plating lyzed epithelial cells on culture media. All tested P. gingivalis strains adhered to an entered pocket epithelial cells. However, considerable variation in their adhesive and invasive potential was observed. E. coli strain HB101 did not adhere or invade. Transmission electron microscopy revealed that internalization of P. gingivalis was preceded by formation of microvilli and coated pits on the epithelial cell surfaces. Intracellular bacteria were most frequently surrounded by endosomal membranes; however, bacteria devoid of such membrances were also. Release of outer membrane vesicles (blebs) by internalized P. gingivalis was observed. These results support and extend previous work from this laboratory which demonstrated invasion of a human oral epithelial cell-line by P. gingivalis. [ABSTRACT FROM AUTHOR]

In vitro interactions between the periodontal pathogen Porphyromonas gingivalis and oral epithelial cells have lately been the subject of study in different laboratories. Authors recently examined the potential of P. gingivalis to adhere to and invade in vitro pocket epithelium. Cultured pocket epithelial tissue, obtained from patients in conjunction with periodontal surgery, generated a stratified epithelium. This epithelium was subsequently infected by laboratory and clinical strains of P. gingivalis. The invasive potential of these strains was quantitated after killing extracellular bacteria with an antibiotic mixture and plating lysed epithelial cells on culture media.