Phenotype Harmonization in the GLIDE2 Oral Health Genomics Consortium.

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.

Cell Type-Specific Decomposition of Gingival Tissue Transcriptomes.

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.

Enhanced monocyte migration and pro-inflammatory cytokine production by Porphyromonas gingivalis infection.

BACKGROUND AND OBJECTIVE: Porphyromonas gingivalis, a major periodontal pathogen, has been reported to be involved in atherogenesis. In order to further understand this pathogen's link with systemic inflammation and vascular disease, we investigated its influence on murine monocytes and macrophages from three different sources. MATERIAL AND METHODS: Concanavalin A-elicited peritoneal macrophages, peripheral blood monocyte-derived macrophages and WEHI 274.1 monocytes were infected with either P. gingivalis 381 or its non-invasive fimbriae-deficient mutant, DPG3. RESULTS: Infection with P. gingivalis 381 markedly induced monocyte migration and significantly enhanced production of the pro-inflammatory cytokines, tumor necrosis factor-alpha and interleukin-6. Consistent with a role for this pathogen's major fimbriae and/or its invasive capacity, infection with DPG3 had a minimal effect on both monocyte attraction and pro-inflammatory cytokine production. CONCLUSION: Since monocyte recruitment and activation are important steps in the development of vascular inflammation and atherosclerosis, these results suggest that P. gingivalis infection may be involved in these processes.

Age-Specific Predictive Models of the Upper Quintile of Periodontal Attachment Loss.

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.

Periodontitis is associated with cognitive impairment among older adults: analysis of NHANES-III.

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 (

Granulocyte chemotactic protein 2 (gcp-2/cxcl6) complements interleukin-8 in periodontal disease.

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 x 10(-16)), in 'diseased' vs. 'healthy' tissue as compared to a 2.6-fold increased expression of interleukin-8 mRNA (p < 1.2 x 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.

Periodontal Medicine: 100 Years of Progress.

Periodontal medicine is a term used to describe how periodontal infection/inflammation may impact extraoral health. Periodontitis has been linked to over 50 systemic diseases and conditions. As part of the Journal of Dental Research's Centennial Celebration, this narrative review discusses periodontal medicine research done over the past 100 y, with particular focus on the effects of periodontal disease on 3 pathological conditions: cardiovascular disease, diabetes mellitus, and adverse pregnancy outcomes. We selected 29 total studies that were the "first" of their kind, as they provided novel observations or contributed to shifting paradigms as well as important studies that made strong contributions to progress in understanding relationships to the systemic conditions. These studies were organized in an overview timeline and broken down into timelines by topic: cardiovascular disease (n = 10), diabetes (n = 12), and adverse pregnancy outcomes (n = 7). Overall, the majority of cross-sectional, case-control, and longitudinal studies have revealed positive associations between poor periodontal status and cardiovascular disease, diabetes metabolic control, and a number of adverse pregnancy outcomes, and these associations are upheld in systematic reviews. Findings from randomized controlled trials testing the effects of periodontal therapy on systemic health outcomes were conflicting and inconsistent. While there has been a great deal of progress, we highlight lessons learned and make comments and suggestions on a number of key aspects, including the heterogeneity of case definitions of periodontal disease across studies, accounting for features of the periodontal phenotype that are most relevant to the biological link between periodontitis and systemic outcomes, the role of other comorbid inflammatory conditions, selection of study participants, and timing and intensity of the periodontal intervention.

Subgingival Microbiota and Longitudinal Glucose Change: The Oral Infections, Glucose Intolerance and Insulin Resistance Study (ORIGINS).

Microbial communities along mucosal surfaces throughout the digestive tract are hypothesized as risk factors for impaired glucose regulation and the development of clinical cardiometabolic disease. We investigated whether baseline measures of subgingival microbiota predicted fasting plasma glucose (FPG) longitudinally. The Oral Infections, Glucose Intolerance and Insulin Resistance Study (ORIGINS) enrolled 230 diabetes-free adults (77% female) aged 20 to 55 y (mean ± SD, 34 ± 10 y) from whom baseline subgingival plaque and longitudinal FPG were measured. DNA was extracted from subgingival plaque, and V3 to V4 regions of the 16S rRNA gene were sequenced. FPG was measured at baseline and again at 2 y; glucose change was defined as follow-up minus baseline. Multivariable linear models regressed 2-y glucose change onto baseline measures of community diversity and abundances of 369 individual taxa. A microbial dysbiosis index (MDI) summarizing top individual taxa associated with glucose change was calculated and used in regression models. Models were adjusted for age, sex, race/ethnicity, education, smoking status, body mass index, and baseline glucose levels. Statistical significance was based on the false discovery rate (FDR; <0.05) or a Bonferroni-corrected P value of 1 × 10-4, derived from the initial 369 hypothesis tests for specific taxa. Mean 2-y FPG change was 1.5 ± 8 mg/dL. Baseline levels of 9 taxa predicted FPG change (all FDR <0.05), among which Stomatobaculum sp oral taxon 097 and Atopobium spp predicted greater FPG change, while Leptotrichia sp oral taxon 498 predicted lesser FPG change (all 3 P values, Bonferroni significant). The MDI explained 6% of variation in longitudinal glucose change (P < 0.001), and baseline glucose levels explained 10% of variation (P < 0.0001). FPG change values ± SE in the third versus first tertile of the MDI were 4.5 ± 0.9 versus 1.6 ± 0.9 (P < 1 × 10-4). Subgingival microbiota predict 2-y glucose change among diabetes-free men and women.

Infection with a periodontal pathogen induces procoagulant effects in human aortic endothelial cells.

BACKGROUND: Multiple studies have demonstrated a link between periodontal infections and vascular disease. Porphyromonas gingivalis, a major periodontal pathogen, has been shown to adhere to and invade endothelial cells. OBJECTIVE: In order to dissect mechanisms underlying these observations, we assessed the role of P. gingivalis infection in modulating properties of endothelial cells linked to atherothrombosis. METHODS: Primary human aortic endothelial cells (HAEC) were infected with either P. gingivalis 381 or its non-invasive fimbriae-deficient mutant, DPG3. Markers of coagulation and thrombosis were assessed 8 h and 18 h postinfection in cell lysates and supernatants. RESULTS: Infection with P. gingivalis 381 significantly enhanced tissue factor expression and activity, and suppressed levels of tissue factor pathway inhibitor. Furthermore, P. gingivalis infection decreased levels and activity of tissue plasminogen activator, and enhanced plasminogen activator inhibitor-1 antigen and activity. Consistent with an important role for bacterial adhesion/invasion in this setting, infection with DPG3 failed to induce procoagulant properties in HAEC. Most of the above effects of P. gingivalis 381 were more apparent at the later time point (18 h postinfection). This suggests that P. gingivalis infection, rather than having an immediate and direct effect, might activate pathways that, in turn, trigger endothelial procoagulant mechanisms. CONCLUSIONS: Taken together these data demonstrate for the first time that infection with a periodontal pathogen induces procoagulant responses in HAEC.

Identification of Master Regulator Genes in Human Periodontitis.

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.

Periodontal Bacteria and Prediabetes Prevalence in ORIGINS: The Oral Infections, Glucose Intolerance, and Insulin Resistance Study.

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.

Cytokine responses of oral epithelial cells to Porphyromonas gingivalis infection.

Accumulating evidence indicates that epithelia are not merely mechanical barriers but also important elements of the innate immune system. The present study was performed to examine cytokine responses of oral epithelial cells after infection with the periodontal pathogen Porphyromonas gingivalis. The KB-cell line and primary cultures of periodontal pocket epithelium were infected with P. gingivalis for assessment of bacterial invasion by an antibiotic protection assay, and examination of expression of interleukin-1 beta, interleukin-6, interleukin-8, and tumor necrosis factor-alpha by in situ hybridization and immunohistochemistry. We observed that P. gingivalis induces a strong cytokine response, positively correlated with the adhesive/invasive potential of the infecting strain, in both KB cells and primary cultures. These findings indicate that the epithelial cells of the periodontal pocket are an integral part of the immune system, eliciting cytokine responses to a bacterial challenge. In this context, the adhesive/invasive phenotype of P. gingivalis appears to contribute to pathogenicity.

"Checkerboard" assessments of periodontal microbiota and serum antibody responses: a case-control study.

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.

Subgingival microbiota in adult Chinese: prevalence and relation to periodontal disease progression.

The "checkerboard" Dna-Dna hybridization technology was used to study the epidemiology of 18 microbial species associated with various states of periodontal health and disease, in a sample of 148 Chinese subjects never exposed to systematic dental therapeutic intervention, aged 30 to 39 and 50 to 59 years. Our aims were to: 1) describe the prevalence of these microorganisms; 2) correlate the microbiological and clinical profiles of the subjects; and 3) examine the association between the microbiological variables and the longitudinal changes of periodontal status that occurred over a preceding 10-year period. A maximum of 14 subgingival samples were obtained from each subject-1,864 in all. The frequency of occurrence of the 18 species examined was high in this Chinese population, on both the subject and the tooth site level. However, all species were not found equally capable of reaching high numbers in the subgingival samples and, as a rule, colonized heavily only limited proportions of tooth sites within each mouth. There was a profound increase of certain species such as Porphyromonas gingivalis, Treponema denticola, and Bacteroides forsythus in deep pockets or progressing sites. Multivariate techniques using the subgingival profile could effectively discriminate between deep/shallow pockets and progressing/ stable tooth sites. The microbiological variables showed an enhanced discriminating potential when classifications were performed on the individual subject level. Colonization by P. gingivalis, B. forsythus, Campylobacter rectus, and T. denticola at levels exceeding certain thresholds entailed a significantly increased probability (odds ratios > 4) for an individual subject to harbor deep pockets or progressing tooth sites.

CPITN and the epidemiology of periodontal disease.

This paper discusses the purposes of collecting epidemiological data on periodontal disease, and concludes that the severe shortcomings of the CPITN makes it unsuited as a tool for assessing the prevalence and severity of periodontal disease.

Extent and Severity Index based on assessments of radiographic bone loss.

The purpose of the present study was to develop a partial recording system based on the principles of the Extent and Severity Index, aiming at describing the degree of radiographic alveolar bone loss on a population level. The data analyzed were derived from a subject sample comprising 531 individuals aged 25-75 yr. In these subjects alveolar bone level (ABL) was radiographically assessed at all approximal tooth surfaces. An ABL value of greater than 2 mm was required for a tooth site to be included in the computation of a full mouth bivariate Extent and Severity Index (FESI). A partial recording index (PESI-2) based on 18 ad hoc selected tooth sites depicted in one periapical and one vertical bitewing radiograph was evaluated in comparison with the FESI as well as with partial recording indices based on the 9 and 18 tooth sites which displayed the highest correlation with full mouth scores (PESI-9 and PESI-18, respectively). It was shown that all three partial recording systems generated values reasonably close to the full-mouth scores. However, the fitness of all partial indices varied with age. The potential of the partial indices to predict full-mouth scores could be further enhanced via simple regression models. Such an evaluation should, ideally, be carried out in an independent subject sample.

Evaluation of a radiographic partial recording system assessing the extent and severity of periodontal destruction.

The purpose of the present study was to evaluate the validity and reliability of a partial radiographic bivariate index system (PESI-2). The principles of the index were applied to data from a random sample of 192 industrial employees aged 30-65 yr. Estimates of Extent and Severity of radiographic bone loss provided by the PESI-2, as well as adjusted estimates by means of simple regression models, were compared to values obtained by a full mouth radiographic examination. It was shown that the values provided by the PESI-2 were of rather high validity and reliability. The use of the adjusting models resulted in increased validity of the severity estimates and enhanced reliability of both components of the bivariate. The results verified the applicability of the PESI-2 in epidemiologic research of destructive periodontal disease.

Extent and severity of periodontal destruction based on partial clinical assessments.

The aim of the present study was (i) to identify the 10 approximal tooth sites that provide Extent and Severity estimates of clinical attachment loss which are maximally coherent to the full mouth scores, and (ii) to evaluate the applicability of such a partial recording system. Data from two subject samples, comprising 192 subjects aged 30-64 yr (sample A) and 175 subjects aged 35-80 yr (sample B), were involved in the development and the evaluation of the system, respectively. Approximal probing attachment loss (PAL) measurements were available from all subjects. A PAL value of > 1 mm was required for a tooth site in order to qualify for the Extent and Severity computations. A full mouth bivariate Extent and Severity Index (FESI) was firstly calculated for every subject in sample A. Multiple regression models applied on data derived from the same sample identified the 10 approximal tooth sites which provided the best correlation to the full-mouth scores (correlation coefficients between partial and full mouth scorings of Extent and Severity 0.85 and 0.88, respectively). All tooth types were found to be represented in this set of sites and the ratio of mesial/distal sites was 6/4. The applicability of a partial recording system (PESI) based on these sites was evaluated in sample B. Fully comparable estimates between PESI and FESI values were obtained, but the degree of correlation varied at different ages. Further adjustments by means of regression models failed to increase the validity and reliability of the PESI.(ABSTRACT TRUNCATED AT 250 WORDS)

Periodontal treatment needs assessed by the use of clinical and radiographic criteria.

The aim of the present study was to use a decision making model in order to assess the periodontal treatment needs of a random sample of employees in a large Swedish industrial corporation. The model used provided data on critical bone loss limits for different tooth types and ages, beyond which treatment must be initiated, in order to fulfill the goal of maintaining all teeth in a functional state throughout life. A sample comprising 192 subjects belonging to four age strata (31-35 yr, 41-45 yr, 51-55 yr, and 61-65 yr) was involved. From each subject, a full mouth series of intra-oral radiographs were available. The radiographic bone height was assessed at the mesial and distal aspect of all teeth by measuring the distance between the cementoenamel junction and the bone crest. The clinical examination included assessments of plaque, gingivitis, probing pocket depth, and probing attachment level. The results revealed that (i) only 3.1% of all approximal tooth sites exhibited radiographic bone loss exceeding the critical limit, (ii) all individuals and 70% of the approximal tooth sites were in need periodontal treatment when presence of gingival inflammation (bleeding on probing) was employed as the single criterion for therapeutic intervention, (iii) the proportion of individuals and tooth sites requiring treatment amounted to 98% and 27%. respectively, when a probing pocket depth of at least 4 mm was included as an additional criterion, and 54% and 4.1%, respectively, if a probing depth threshold of 6mm was used, while (iv) the use of bleeding on probing in combination with radiographic bone loss beyond the critical limits disclosed a need of treatment in 40% of the subjects and 2.5% of the approximal tooth sites.

Epidemiology of periodontal diseases: an update.

This article provides a brief review of findings from epidemiological studies of periodontal disease that have been generated over the past five years. In line with the conclusions of the 1996 World Workshop in Periodontics, the recent data support the concept that early onset periodontitis appears to be rather infrequent, while advanced adult periodontitis, leading to severe loss of supporting periodontal tissues and tooth loss, does not exceed a prevalence of 10-15% in most populations. However, a number of important issues remain unresolved. It is still not clear whether the prevalence of these diseases has shown an overall decline in recent years. In fact, retention of teeth in older age may contribute to an increase. Analytical epidemiological studies have been increasingly successful in identifying a handful of risk factors for disease onset and progression. These include colonisation at high levels by certain subgingival bacteria, environmental exposures such as cigarette smoking, and systemic conditions such as diabetes mellitus. Importantly, the molecular basis of host susceptibility has recently begun to be unraveled. Research efforts are now focused on creating multi-factorial models to assess the risk for disease, prior to the development of irreversible damage. Importantly, the role of periodontal infections as a modifier of systemic health is being increasingly explored.