Exploring the Bidirectional Relationship Between Periodontitis and Rheumatoid Arthritis in a Large Danish Cohort.

OBJECTIVE: We investigated the bidirectional relationship between rheumatoid arthritis (RA) and periodontitis and their cross-sectional association using national administrative health care data. METHODS: The sample included 3,308,903 individuals aged 20 to 79 years who resided in Denmark in 2000 and had remained free of RA and periodontitis in the previous 10 years. RA and periodontitis were defined using diagnosis and treatment codes. Marginal structural survival models were employed to estimate the effects of RA on periodontitis incidence and vice versa from 2000 to 2017. Using a cross-sectional sample of 2,574,536 individuals from 2017, the association of periodontitis with RA was investigated using regression analyses and probabilistic quantitative bias analyses, simulating RA and periodontitis misclassification and unmeasured confounding of smoking. RESULTS: Between 2000 and 2017, 20,348 individuals developed RA and 740,799 developed periodontitis. The estimated hazard ratio (HR) for the effect of periodontitis on incident RA was 1.05 (95% confidence interval [CI] 0.88-1.25), resulting in a restricted mean survival time difference of one day. The HR for the effect of RA on incident periodontitis was 0.84 (95% CI 0.80-0.88), corresponding to a restricted mean survival time difference of 151 days. Cross-sectionally, the unadjusted prevalence ratio for the association was 1.15 (95% CI 1.11-1.19), whereas the estimate adjusted for measured and simulated confounding was practically null (0.99, 95% simulation interval 0.93-1.04). CONCLUSION: These findings challenge previously reported bidirectional relationships between periodontitis and RA, pointing to potential residual confounding as an important link and prompting reconsideration of the biologic plausibility and clinical significance of these associations.

Dental service use among adults with incident type 2 diabetes, rheumatoid arthritis or inflammatory bowel disease.

OBJECTIVES: It is not clear if or how the incidence of systemic conditions like type 2 diabetes mellitus (DM2), rheumatoid arthritis (RA) or inflammatory bowel disease (IBD) affects dental service utilization. Using nationwide Danish register data, the aim of this study was to analyse the use of dental services 7 years before and after being diagnosed with DM2, RA or IBD between 1997 and 2011. METHODS: Information about incident DM2 was obtained from the National Diabetes Register, and incident RA and IBD were defined based on diagnosis codes of hospital contacts identified through the National Patient Register. Separately, for each of the three conditions, each individual with the incident condition was matched to one control individual based on age, gender, country of origin, municipality of residence, highest completed education, the main source of income and income using coarsened exact matching in the year of incidence. The use of dental services and treatments received within each calendar year from 7 years before to 7 years after getting the condition were analysed with generalized estimating equations. RESULTS: People with incident DM2 were less likely (by seven percentage points) to be dental service users within a year than people without incident DM2 for a period extending from up to 7 years prior to 7 years after the diagnosis. This difference even slightly increased after the diagnosis. Those with incident IBD exhibited a consistently but modestly higher proportion of dental service use (three percentage points) than those without incident IBD before and after the diagnosis. Differences in the use of services between those with or without incident RA were minor. For all three systemic diseases, detected differences mainly mirrored differences in the provision of supragingival scaling and restorative treatment. CONCLUSIONS: The findings suggest that the impact of these three systemic conditions on dental service use was minor.

Contesting the conventional wisdom of periodontal risk assessment.

Over the years, several reviews of periodontal risk assessment tools have been published. However, major misunderstandings still prevail in repeated attempts to use these tools for prognostic risk prediction. Here we review the principles of risk prediction and discuss the value and the challenges of using prediction models in periodontology. Most periodontal risk prediction models have not been properly developed according to guidance given for the risk prediction model development. This shortcoming has led to several problems, including the creation of arbitrary risk scores. These scores are often labelled as 'high risk' without explicit boundaries or thresholds for the underlying continuous risk estimates of patient-important outcomes. Moreover, it is apparent that prediction models are often misinterpreted as causal models by clinicians and researchers although they cannot be used as such. Additional challenges like the critical assessment of transportability and applicability of these prediction models, as well as their impact on clinical practice and patient outcomes, are not considered in the literature. Nevertheless, these instruments are promoted with claims regarding their ability to deliver more individualized and precise periodontitis treatment and prevention, purportedly resulting in improved patient outcomes. However, people with or without periodontitis deserve proper information about their risk of developing patient-important outcomes such as tooth loss or pain. The primary objective of disseminating such information should not be to emphasize assumed treatment efficacy, hype individualization of care, or promote business interests. Instead, the focus should be on providing individuals with locally validated and regularly updated predictions of specific risks based on readily accessible and valid key predictors (e.g. age and smoking).

Five-year radiological findings from a randomized controlled trial of four periodontitis treatment strategies.

Radiographic findings from long-term studies of periodontitis treatment have rarely been reported. Although bone destruction is a prominent feature of periodontitis, the long-term effect on alveolar bone levels of different treatment strategies, with or without adjunctive metronidazole (MTZ), has not been reported. We investigated the 5-year radiographic outcome of therapy in patient groups treated with conventional scaling and root planing (SRP) or same-day full-mouth disinfection (FDIS), with or without adjunctive MTZ. Following a 3-month oral hygiene phase, 184 periodontitis patients were randomly allocated to one of four treatment regimens: (i) FDIS+MTZ; (ii) FDIS+placebo; (iii) SRP+MTZ; or (iv) SRP+placebo. Following active treatment, patients received biannual maintenance. In total, 161 patients (87.5%) completed the 5-year follow-up examination, at which the radiographic bone level (RBL), clinical attachment level, probing pocket depth, presence of plaque, and bleeding were recorded again. At the 5-year follow up examination, minor radiological bone loss was observed in the intervention groups FDIS+placebo, SRP+MTZ, and SRP+placebo; by contrast, the FDIS+MTZ group did not show any change in RBL. Full-mouth disinfection did not generally perform better than conventional SRP performed over a period of 2 to 4 weeks.

Justification for the 2017 periodontitis classification in the light of the Checklist for Modifying Disease Definitions: A narrative review.

Once a while, disease classifications have needed revision because new knowledge has accumulated, and new technologies and better treatments have emerged. Changes made to disease classifications should be trustworthy and openly justified. The periodontitis definition and classification system was changed in 2017 by the 'World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions'. The workshop, comprising clinicians and researchers, resulted in the production of a 23-article special issue that introduced the new definitions and classifications of periodontitis. In this narrative review, we critically review how the changes made to the periodontitis definition and classification were justified in the light of the Checklist for Modifying Disease Definitions. Under each of the eight items of the checklist, we have discussed how the item was or could have been considered in the light of the checklist and its guidance. In our view, the new definition and classification of periodontitis was presented in an understandable way, even though the changes from the previous definition were not made visible. However, the issues of (1) estimated changes in prevalence or incidence, (2) triggers for the change, (3) prognostic ability, (4) repeatability or reproducibility, (5) incremental benefits, (6) incremental harms or (7) net benefits and harms related to the introduction of new classification were not considered in the way suggested in the checklist. Thereby, a balanced assessment of potential benefits and harms associated with the new periodontitis classification system was not presented, and to a large extent it remains unknown if the use of the new classification system will provide more net benefits to patients and to the community than previous systems. It is our view that patients and societies deserve transparent and balanced assessments of the potential benefits and harms associated with the periodontitis classification. Importantly, these should reflect the values and preferences also of the patients and the wider community and consider the impact on resource usage.

Effect of Sample Storage Conditions on Measurements of Salivary Cotinine Levels.

Information on smoking exposure obtained with self-reports may be inaccurate. Cotinine has a large half-life and its salivary levels correlate well with plasmatic levels. The influence of storage conditions on the validity and precision of salivary cotinine assessments has rarely been evaluated. Here, smokers donated saliva samples, which were sent for immediate analysis, mail posting, storage at 4 °C for 30 or 90 days, or storage at -20 °C for 30 or 90 days. Cotinine levels were determined using enzyme-linked immune-sorbent assay. Agreement of cotinine level measurements was assessed using Bland-Altman analyses. Average age (years), duration of smoking (years) and number of cigarettes smoked (/day) were 55.4 (±SD 9.4), 35.1 (±SD 11.3), and 15.3 (±SD 7.6). The mean immediate cotinine level was 457 ng/mL (range 11.3 to 1318 ng/mL). Mean cotinine levels in samples analyzed after delay ranged between 433 ng/mL (-20 °C 30 days) and 468 ng/mL (4 °C 30 days). A dose-response gradient was observed in the relationship between salivary cotinine level and self-reported smoking status. A good agreement between cotinine levels for all storage conditions compared with immediate analysis was observed, with average differences ranging from -11 to 24 ng/mL. Cotinine levels remained stable regardless of the tested condition. The stability of salivary cotinine may enable samples to be obtained in difficult-to-reach areas, reduce study costs, and improve the validity of the information on exposure to smoking.

Periodontitis phenotypes and clinical response patterns to non-surgical periodontal therapy: reflections on the new periodontitis classification.

We aimed to identify response patterns to non-surgical periodontal therapy and to investigate whether the new classification system for periodontitis reflects response to treatment after 1 yr. At baseline, data on sociodemographic status, smoking, and diabetes were obtained from participants with periodontal disease. Clinical periodontal data and subgingival plaque were also collected. Participants underwent non-surgical periodontal therapy, and after 3 and 12 months, clinical data were reassessed. Factor analyses, group-based-trajectory modeling, and mixed-effects regression models were used for data analysis. Factor analysis of the baseline periodontal parameters revealed two different periodontitis dimensions: 'moderate' and 'severe'. Two response patterns for each of these periodontitis dimensions were identified. Periodontal therapy had a beneficial effect on both 'moderate' and 'severe' periodontitis; however, individuals with higher levels of disease at baseline experienced greater treatment effect. Regarding the new classification system, while the staging component distinguished different levels of 'moderate' and 'severe' periodontitis before and after treatment, the grading component did not. This study shows the beneficial effect of non-surgical periodontal therapy on both 'moderate' and 'severe' periodontitis. However, the benefit was limited among individuals with low levels of disease. The new classification system did not adequately reflect the periodontal response to therapy in this patient group.

Oral hygiene revisited. The clinical effect of a prolonged oral hygiene phase prior to periodontal therapy in periodontitis patients. A randomized clinical study.

AIM: The aim of the present study was to investigate the effect of a 3-month strict oral hygiene phase on key parameters of periodontitis: plaque, bleeding on probing (BOP) and probing pocket depth (PPD). MATERIALS AND METHODS: Forty-four patients with severe periodontal disease were randomly allocated to a test or a control group. The test group completed a 3-month strict oral hygiene phase. The control group did not receive any instructions or motivation on oral hygiene until after the 3-month period. Plaque, BOP and PPDs were registered on four sites of each tooth at baseline and after 3 months in both groups, as well as after the postponed hygiene phase in the control group. RESULTS: A statistically significant and profound reduction in plaque, BOP and PPD was observed after the 3 months in the test group. No change to the better occurred in the control group. CONCLUSION: A 3-month strict oral hygiene phase in patients referred for periodontal therapy reduced plaque, BOP and pocket depth to such an extent that it could affect therapy planning.

Fluoride in Saliva and Oral Mucosa after Brushing with 1,450 or 5,000 ppm Fluoride Toothpaste.

The aim was to measure and compare fluoride concentrations in oral mucosa and saliva following a single brushing with either 1,450 or 5,000 ppm fluoride toothpaste. Fourteen healthy participants provided saliva and oral mucosa samples in the morning before tooth brushing. Then participants brushed their teeth with 1,450 ppm fluoride toothpaste, and saliva and mucosa samples were collected after 1, 2, 4, and 6 h. The experiment was repeated 3-7 days later with 5,000 ppm fluoride toothpaste. All samples were analyzed for fluoride using an ion-selective electrode adapted for microanalysis. Pre-brushing fluoride concentrations were higher in mucosa (mean1,450 0.26 ppm and mean5,000 0.20 ppm) than in saliva (mean1,450 0.08 ppm and mean5,000 0.07 ppm). The mean fluoride concentrations increased in both mucosa and saliva following a single brushing with both 1,450 ppm (meanmuc1,450 (1 h) 1.15 ppm, meansal1,450 (1 h) 0.33 ppm) and 5,000 ppm fluoride toothpaste (meanmuc5,000 (1 h) 3.21 ppm and meansal5,000 (1 h) 0.90 ppm). At 6 h, the fluoride concentrations had returned to pre-brushing levels. Across the 6-h sampling period the fluoride concentration in saliva was statistically significantly 1.4 times higher following brushing with 5,000 ppm compared with 1,450 ppm fluoride toothpaste. For mucosa, this ratio was only 1.1 and not statistically significant. In conclusion, the fluoride level in oral buccal mucosa is higher than in saliva and follows the same fluoride clearance pattern as in saliva. Over the initial 6-h period following a single tooth brushing, the ratio of the fluoride concentration in mucosa to that in saliva is independent of the fluoride concentrations in the toothpastes used.

Oral hygiene phase revisited: How different study designs have affected results in intervention studies.

Every periodontal researcher have been taught, and every textbook in periodontics have advocated, that a phase in which the patient is meticulously motivated and instructed in proper oral hygiene-the oral hygiene phase-must be included in any periodontal intervention. However, how is this oral hygiene phase actually portrayed in periodontal intervention studies, and how much space have this important phase received in the planning and carry-through of intervention studies? The purpose of this letter to the editor was to review current literature in the period 1975/01/01-2017/12/31 on periodontal, mechanical intervention studies in order to see what focus the oral hygiene phase had received in these articles. The result showed that the oral hygiene phase is variable in length and content, variable in claimed result, insufficiently described, and invariably amalgamated with the scaling and root planing which is the intervention or part of an intervention. The consequences of these findings are discussed and suggestions proposed for more harmonized and calibrated oral hygiene phase introduced to avoid biased and inflated results of interventions.

An IgY-based immunoassay to evaluate the biomarker potential of the Tannerella forsythia virulence factor karilysin in human saliva.

Tannerella forsythia is a gram-negative anaerobic bacterium that is associated with the development of destructive periodontal disease. T. forsythia secretes the metalloprotease-like enzyme karilysin. Using in vitro systems karilysin has been shown to modulate the host immune response by degradation of complement system proteins and by inactivation of the antimicrobial peptide LL-37 by proteolytic cleavage. This makes karilysin a highly interesting virulence factor to study in the framework of drug development and diagnostics. However, to date the presence of karilysin in clinical samples has not been demonstrated due to the lack of specific probes. In the present work, a high titer and stable affinity-purified avian IgY antibody against karilysin was developed. By surface plasmon resonance imaging the IgY affinity was found to be in the low nanomolar range. The antibody could be used to detect karilysin in saliva samples by immuno-blotting and was specific when tested towards human MMP-3. Furthermore, an avian IgY-based immunoassay was developed, which demonstrated low intra- and interday assay variability (CV's below 10%). Application of the immunoassay on a well-characterized set of saliva samples from adolescents with or without signs of periodontitis showed that it was possible to detect karilysin in saliva. A significant difference in karilysin concentration was found between saliva from participants with signs of periodontitis and saliva from healthy controls (p = .0024). The median of karilysin levels among periodontitis cases was 957 pg/ml (IQR, 499-2132 pg/ml) and the median for controls was 569 pg/ml (IQR, 210-1343 pg/ml). Collectively our data confirm the presence of karilysin in clinical samples. The described IgY-based immunoassay may prove useful as part of protein-based biomarker screenings in the clinic or in point-of care settings.

Salivary levels of MPO, MMP-8 and TIMP-1 are associated with gingival inflammation response patterns during experimental gingivitis.

AIM: This study aimed to investigate the association between salivary levels of myeloperoxidase (MPO), neutrophil elastase (NE), soluble urokinase-type plasminogen activator receptor (suPAR), matrix metalloproteinase (MMP)-8 and tissue inhibitor of matrix metalloproteinases (TIMP)-1 and gingival inflammation development during an experimental gingivitis study. METHODS: A three-week experimental gingivitis study was conducted. Clinical recordings of dental plaque biofilm (Modified Quigley Hein Plaque Index, TQHPI) and gingival inflammation (Modified Gingival Index, MGI) were made at specific time points for each of the 42 participants. Salivary levels of MPO, NE, suPAR, MMP-8 and TIMP-1 at the same time points were measured using distinct immunoassays. For data analysis growth curve modelling was employed to account for the time-varying outcome (MGI score) and the time-varying covariates (salivary marker levels, and TQHPI score). Analyses were stratified according to the MGI-score trajectory groups previously identified as 'fast', respectively 'slow' responders. RESULTS: Overall, higher MGI scores were statistically significantly positively associated with higher levels of MPO, MMP-8 and TIMP-1. Stratified analysis according to inflammation development trajectory group revealed higher levels of salivary MPO, MMP-8 and MMP-8/TIMP-1 ratio among the 'fast' responders than among 'slow' responders. None of the investigated salivary protein markers was associated with a 'slow' inflammation development response. CONCLUSIONS: Salivary levels of MPO, MMP-8 and TIMP-1 were associated with the extent and severity of gingival inflammation. While the 'fast' gingival inflammation response was associated with increased levels of MPO, MMP-8 and MMP-8/TIMP-1 ratio, the 'slow' response was not associated with any of the salivary protein markers investigated in this study. Neutrophil activity seems to orchestrate a 'fast' gingival inflammatory response among participants previously primed to gingival inflammation.

Identification of inflammatory response patterns in experimental gingivitis studies.

We used novel analytical approaches to identify inflammatory response patterns to plaque accumulation in experimental gingivitis studies in humans. Data from two experimental gingivitis studies [Dataset I (n = 40) and Dataset II (n = 42)], which differed in design and recording methods, were used. Both studies comprised a three-phase program as follows: pre-induction period (oral hygiene as usual for Dataset I; professional tooth cleaning for Dataset II); induction period (plaque accumulation); and resolution period (oral hygiene as usual). Clinical recordings of plaque and gingival inflammation were made on days 0, 4, 9, and 14 for Dataset I and on days -14, 0, 7, 21, and 35 for Dataset II. Group-based-trajectory and growth curve modeling were used for data analysis. In Dataset I, gingival response to plaque accumulation was found to be lagged in time. Different group-based response patterns for gingival inflammation were not identified. However, in Dataset II, 'fast' and 'slow' gingival inflammation responders were identified. 'Slow' responders had lagged inflammation responses, whereas 'fast' responders seemed to respond immediately to plaque. The findings show that analytical approaches which consider the data structure allow investigation of the dynamics of the relationship between plaque accumulation and gingival inflammation and facilitate the identification of differential patterns of gingival inflammation development.

Pattern recognition receptor polymorphisms in early periodontitis.

BACKGROUND: Even though bacteria trigger inflammation, most of the tissue destruction in periodontitis is due to the host inflammatory response. In addition to immunological events that drive development of early periodontitis, numerous environmental factors like genetics and smoking play a role. We investigated whether the carriage of selected single nucleotide polymorphisms (SNP) of toll-like receptors (TLR), NOD-like receptors (NLR) and RIG-I-like receptors (RLR) was associated with the diagnosis of early periodontitis in a case-control study. METHODS: Adolescents with positive (n = 87) and negative (n = 73) diagnosis for periodontitis had blood samples taken. All participants were genotyped for 42 SNP in the genes encoding TLR1-10, NOD1-2, DDX58, and IFIH1 using multiplex assays. Associations between SNP and periodontitis diagnosis were tested. RESULTS: TLR1-rs5743611 showed protective effect for periodontitis (CC versus GG and GC, P = 0.01, odds ratio [OR] 0.10, 95% confidence interval [CI] 0.01-0.78). Carriage of the TLR4-rs7873784 was associated with higher odds for periodontitis (GG versus CC and GC, P = 0.05, OR 2.30, 95% CI 1.00-5.63; GG versus GC, P = 0.05, OR 2.46, 95% CI 1.01-5.99). In male participants, reduced susceptibility to periodontitis was observed in carriers of TLR7-rs3853839 (CC versus GG and CG, P = 0.02, OR 0.30, 95% CI 0.11-0.85) and TLR8-rs3764879 (CC versus GG and CG, P = 0.02, OR 0.31, 95% CI 0.12-0.82). Associations were maintained after adjustments for sex, smoking habits, and mother´s education. CONCLUSION: This study demonstrated an association between TLR1-rs5743611, TLR4-rs7873784, TLR7-rs3853839, and TLR8-rs3764879 and susceptibility to periodontitis in adolescents.

Improved pH-ratiometry for the three-dimensional mapping of pH microenvironments in biofilms under flow conditions.

Confocal microscopy-based monitoring of pH in biofilms is gaining increasing interest, as it allows for a quick assessment of horizontal pH gradients without mechanically perturbing the biofilm. Ratiometric monitoring of pH with the fluorescent dye C-SNARF-4 has been used to reliably map extracellular pH in the basal layers of biofilms, but only under static conditions. Here, we expand this methodology to measurements of vertical gradients in multispecies in vitro-grown and in situ-grown dental biofilms of different age, and to pH measurements in in vitro-grown biofilms under flow conditions. After static incubation with glucose, young in vitro-grown biofilms (30h) were more acidogenic than older biofilms (120h). However, under dynamic conditions mimicking the oral salivary flow, low pH was only preserved in older biofilms. As both types of biofilm were of similar thickness (~20 µm), these findings highlight the importance of cell density and biofilm matrix maturation for pH developments. In both in vitro-grown and in in situ-grown biofilms, horizontal and vertical pH gradients were observed. Under static conditions, the surface layer of the biofilms tended to be more acidic, whereas the bottom layer became more acidic under dynamic conditions. Compared to in vitro-grown biofilms, 120 h in situ-grown biofilms showed higher acidogenicity during static incubation. This study shows that pH ratiometry with C-SNARF-4 is well-suited to monitor extracellular pH in thin biofilms in all three dimensions. The different pH dynamics observed under static and dynamic conditions argue for the implementation of flow during real-time assessment of biofilm pH.

Soluble urokinase-type plasminogen activator receptor is associated with signs of periodontitis in adolescents.

Owing to its molecular stability in body fluids, soluble urokinase-type plasminogen activator receptor (suPAR) is used as a biomarker for the level of systemic inflammation. This study compares the suPAR levels in serum with those in the saliva of adolescents and evaluates their association with the periodontal conditions. Adolescents identified as screen positive (n = 87) or screen negative (n = 73) for periodontitis had saliva and serum samples taken, along with subgingival plaque samples. The concentrations of suPAR were determined in saliva and serum, and 18 microbial species and the immunoglobulin response to them was evaluated. Factor analyses were used to reduce the number of variables within each of the domains of clinical, microbiological, and immunological findings. The median salivary suPAR concentration was 13.18 [(interquartile range (IQR): 6.20-23.36] µg l-1 and was not associated with the serum suPAR levels (median 2.05; IQR: 1.62-2.46 µg l-1 ). Linear regression analysis showed that the log10 (salivary suPAR concentration) was statistically significantly positively associated with the clinical phenotype 'Periodontitis Extent' (ß = 0.28; 95% CI: 0.16-0.39) along with 'Putative periodontopathogens' (ß = 0.65; 95% CI: 0.51-0.79). The study represents the first determination of salivary suPAR concentration in a larger well-defined adolescent population. Our results suggest the potential for clinical use of suPAR in saliva as an inflammatory risk indicator/biomarker of periodontitis.

Nyvad Criteria for Caries Lesion Activity and Severity Assessment: A Validated Approach for Clinical Management and Research.

The Nyvad classification is a visual-tactile caries classification system devised to enable the detection of the activity and severity of caries lesions with special focus on low-caries populations. The criteria behind the classification reflect the entire continuum of caries, ranging from clinically sound surfaces through noncavitated and microcavitated caries lesions in enamel, to frank cavitation into the dentin. Lesion activity at each severity stage is discriminated by differences in surface topography and lesion texture. The reliability of the Nyvad criteria is high to excellent when used by trained examiners in the primary and permanent dentitions. The Nyvad criteria have construct validity for lesion activity assessments because of their ability to reflect the well-known caries-controlling effect of fluoride. Predictive validity was demonstrated by showing that active noncavitated lesions are at higher risk of progressing to a cavity or filled state than do inactive noncavitated lesions. Lesion activity assessment performed successfully as a screening tool to identify individuals with a poor caries prognosis. Because of their predictive validity, the Nyvad criteria are superior to other current caries lesion descriptors for the detection of changes in the lesion activity status over time. The Nyvad criteria fulfill all the formal requirements for a robust caries lesion classification and are recommended for evidence-based caries management in clinical practice and in research.

Methodological issues in assessing the association between periodontitis and caries among adolescents.

OBJECTIVES: We aimed to investigate the association between dental caries and periodontitis among adolescents participating in a case-control study of periodontitis. In addition, we compared 2 analytical approaches to estimate the association: conventional regression and structural equation modelling (SEM). METHODS: Along with periodontal recordings, data were obtained on caries, just as subgingival plaque samples were collected. Sociodemographic information was collected with a questionnaire. We used factor analyses to express the many correlated clinical periodontal dimensions in a smaller number of factors. The association between caries (counts of enamel and dentin lesions, or dentin lesions only) and periodontitis was tested using negative binomial regression with robust variance (conventional regression) and weighted least squares (SEM) estimation. RESULTS: Factor analysis revealed 2 different latent periodontal variables: "extent" and "severity" of periodontitis. Using conventional regression, the "extent" of periodontitis was positively associated with higher counts of dentin caries lesions, even after adjustments for maternal education and subgingival microbial composition (rate ratio 1.34; 95% CI 1.07-1.68). The "severity" of periodontitis was associated with lower counts of enamel and dentin caries lesions (rate ratio 0.85 95% CI 0.77-0.92). The SEM revealed a positive association between periodontitis "extent" and number of dentin caries lesions (coefficient 0.29; P < .0001). The "severity" of periodontitis was negatively associated with enamel and dentin caries (coefficient -0.44; P < .0001). CONCLUSIONS: We found an association between caries and periodontitis among adolescents. The "severity" of periodontitis was negatively associated with enamel/dentin caries, whereas the "extent" of periodontitis was positively associated with dentin caries irrespective of the analytical approach employed.

Fluoride in saliva and dental biofilm after 1500 and 5000 ppm fluoride exposure.

OBJECTIVES: The aim of this randomized, double-blind, crossover study was to measure fluoride in saliva and 7-day-old biofilm fluid and biofilm solids after rinsing three times per day for 3 weeks with 0, 1500, or 5000 ppm fluoride (NaF). MATERIALS AND METHODS: Following the 3-week wash-in/wash-out period, including 1 week of biofilm accumulation, saliva and biofilm samples were collected from 12 participants immediately before (background fluoride), and 10, 30, and 60 min after a single rinse. Biofilm samples were separated into fluid and solids, and samples were analyzed using a fluoride electrode (microanalysis). RESULTS: The background fluoride concentration was statistically significantly higher in the 5000 compared to the 1500 ppm F rinse group in all three compartments (22.3 and 8.1 µM in saliva, 126.8 and 58.5 µM in biofilm fluid, and 10,940 and 4837 µmol/kg in biofilm solids). The 1-h fluoride accumulation for the 5000 ppm F rinse was higher than for the 1500 ppm F rinse in all three compartments, although not statistically significant for saliva and biofilm solids. CONCLUSION: Regular exposure to 5000 ppm fluoride elevates background fluoride concentrations in saliva, biofilm fluid, and biofilm solids compared to 1500 ppm fluoride. Increasing the fluoride concentration almost 3.5 times (from 1500 to 5000 ppm) only elevates the background fluoride concentrations in saliva, biofilm fluid, and biofilm solids twofold. CLINICAL RELEVANCE: Even though fluoride toothpaste may be diluted by saliva, the results of the present study indicate that use of 5000 ppm fluoride toothpaste might lead to improved caries control.