Reporting of interventional clinical trial results in an academic center: a survey of completed studies.

BACKGROUND: The dissemination of clinical trial results is an important scientific and ethical endeavour. This survey of completed interventional studies in a French academic center describes their reporting status. METHODS: We explored all interventional studies sponsored by Rennes University Hospital identified on the French Open Science Monitor which tracks trials registered on EUCTR or clinicaltrials.gov, and provides an automatic assessment of the reporting of results. For each study, we ascertained the actual reporting of results using systematic searches on the hospital internal database, bibliographic databases (Google Scholar, PubMed), and by contacting all principal investigators (PIs). We describe several features (including total budget and numbers of trial participants) of the studies that did not report any results. RESULTS: The French Open Science Monitor identified 93 interventional studies, among which 10 (11%) reported results. In contrast, our survey identified 36 studies (39%) reporting primary analysis results and an additional 18 (19%) reporting results for secondary analyses (without results for their primary analysis). The overall budget for studies that did not report any results was estimated to be €5,051,253 for a total of 6,735 trial participants. The most frequent reasons for the absence of results reported by PIs were lack of time for 18 (42%), and logistic difficulties (e.g. delay in obtaining results or another blocking factor) for 12 (28%). An association was found between non-publication and negative results (adjusted Odds Ratio = 4.70, 95% Confidence Interval [1.67;14.11]). CONCLUSIONS: Even allowing for the fact that automatic searches underestimate the number of studies with published results, the level of reporting was disappointingly low. This amounts to a waste of trial participants' implication and money. Corrective actions are needed. TRIAL REGISTRATION: https://osf.io/q5hcs.

Periodontitis and atherosclerotic cardiovascular disease: A critical appraisal.

In spite of intensive research efforts driving spectacular advances in terms of prevention and treatments, cardiovascular diseases (CVDs) remain a leading health burden, accounting for 32% of all deaths (World Health Organization. "Cardiovascular Diseases (CVDs)." WHO, February 1, 2017, https://www.who.int/news-room/fact-sheets/detail/cardiovascular-diseases-(cvds)). Cardiovascular diseases are a group of disorders affecting the heart and blood vessels. They encompass a collection of different conditions, among which atherosclerotic cardiovascular disease (ASCVD) is the most prevalent. CVDs caused by atherosclerosis, that is, ASCVD, are particularly fatal: with heart attack and stroke being together the most prevalent cause of death in the world. To reduce the health burden represented by ASCVD, it is urgent to identify the nature of the "residual risk," beyond the established risk factors (e.g., hypertension) and behavioral factors already maximally targeted by drugs and public health campaigns. Remarkably, periodontitis is increasingly recognized as an independent cardiovascular risk factor.

Poor Masticatory Capacity and Blood Biomarkers of Elevated Cardiovascular Disease Risk in the Community: The Paris Prospective Study III.

[Figure: see text].

Effectiveness of implant-supported fixed partial denture in patients with history of periodontitis: A systematic review and meta-analysis.

AIM: This systematic review investigates the effectiveness of implant-supported fixed partial denture (IS-FPD) in patients with history of periodontitis (HP) vs. patients with no history of periodontitis (NHP). METHODS: A literature search was performed on different databases on May 2020. Prospective and retrospective studies assessing survival (primary outcome), success and biological/mechanical complications of IS-FPDs in HP vs. NHP patients at ≥1 year after implant loading were evaluated. Meta-analyses were conducted by estimating hazard ratio (HR), risk ratio (RR) and standardized mean differences (SMD) with 95% confidence intervals (CI) using random effect models. RESULTS: Of the initially identified 4096 articles, 349 underwent a full-text evaluation. Finally, 17 were included. Pooled data analyses showed that overall implant survival was significantly higher in the NHP than the HP group (HR = 2.06; 95% CI = 1.37-3.09; I2  = 0%). This difference was noted when follow-up ≥5 years. The risk of peri-implantitis was higher in HP than NHP patients (RR = 3.3; 95% CI = 1.31-8.3; I2  = 0%), whereas the mean marginal bone level change over time was not different between the groups (SMD = -0.16 mm; 95% CI = -1.04-0.73; I2  = 98%). CONCLUSIONS: In partially edentulous patients receiving IS-FPDs, a history of periodontitis is associated with poorer survival rate and higher risk of peri-implantitis during a 5-10 years period after implant loading.

Eating disorders through the periodontal lens.

People with eating disorders suffer from a mental disorder that negatively affects their physical and/or mental health. The three most frequent eating disorders are binge eating disorder, bulimia nervosa, and anorexia nervosa. Environmental and genetic factors are involved in the pathogenesis of eating disorders in vulnerable persons. Although treatment varies among different types of eating disorders, nutrition, medical care combined with psychotherapy and medications are standard of care. The aim of this review is to give an overview of the oral health impact of eating disorders with a special emphasis on the periodontium. Oral health professionals have a unique role to play in the early diagnosis of eating disorders because of the important impact that eating disorders have on the oral cavity. In vomiting-associated eating disorders, the risk of erosive tooth wear is mainly localized to the palatal surfaces of the incisors. Emerging evidence also indicates a high frequency of gingivitis and gingival recessions associated with compulsive toothbrushing. A holistic approach, including oral health and functional rehabilitation, should be promoted by physicians, psychiatrists, and dentists for people with eating disorders.

Oral microbiota and atherothrombotic carotid plaque vulnerability in periodontitis patients. A cross-sectional study.

BACKGROUND: An increased risk of atherothrombotic vascular events has been reported in periodontitis patients. Periodontitis is associated with dysbiotic subgingival biofilms and bacteremia. OBJECTIVE: We hypothesized (a) that the oral microbiome is associated with the carotid microbiome and (b) that periodontitis could contribute to plaque vulnerability. The aim of this study was to determine the associations between periodontitis, the carotid microbiome, and the local innate immune response in carotid atherothrombotic plaques vulnerable to rupture. METHODS: In this cross-sectional study, 45 patients admitted for carotid endarterectomy underwent a preoperative periodontal examination. The volume of intraplaque hemorrhage reflected by the hemoglobin level released in carotid-conditioned media was considered as a criterion of carotid plaque vulnerability. Levels of antibodies against periodontal bacteria were determined in sera. The signature of the oral microbiota was assessed by microbial whole-genome sequencing, nested PCR, and immunostaining in carotid plaque samples. Markers of neutrophil recruitment (leukotriene B4), neutrophil activation (myeloperoxidase, defensins), and cytokines were measured in carotid-conditioned media and/or plasma. RESULTS: All patients exhibited periodontitis. One hundred and forty-four bacterial genera were detected in the carotid microbiome. While Streptococcus was found in 84% of the carotid samples, periodontitis-associated genera were detected in 21%. P. gingivalis DNA and gingipains were also identified in carotid samples. There were significant inverse correlations between periodontal attachment loss/serum anti-P. gingivalis Immunoglobulin A and cytokine inhibiting neutrophils (all P < .01). There were also significant positive correlations between lipopolysaccharides, myeloperoxidase/human neutrophil peptides1-3, and hemoglobin levels (all P < .01). CONCLUSIONS: In patients at risk of stroke, the carotid plaque microbiome was highly diverse and compatible with an oral origin. Periodontitis was significantly associated with neutrophil activation markers and plaque vulnerability to rupture.

Probiotics, including nisin-based probiotics, improve clinical and microbial outcomes relevant to oral and systemic diseases.

The effects of probiotic supplementation on systemic health and gastrointestinal diseases have been investigated in numerous studies. The aim of this review is to provide an overview of probiotics and their effects on periodontal health. Probiotics show beneficial effects as adjunctive therapeutics and as stand-alone agents in the treatment and prevention of gingivitis as well as specific clinical parameters of periodontitis. This review focuses on the clinical and microbiological aspects of probiotics in the context of health, gingivitis, and periodontitis. In addition, a special focus on nisin-producing probiotics and nisin itself showcase their significant potential for oral and systemic use.

High serum ferritin levels are associated with a reduced periodontium in women with anorexia nervosa.

PURPOSE: Impaired oral health is a well-known complication in individuals with eating disorders, although this is difficult to identify by mental health professionals. The aim of this study was to evaluate the relationship between routine blood parameters and two oral health outcomes (dental erosion, reduced periodontium) in women with eating disorders. METHODS: A face-to-face interview and a clinical oral examination were carried out in a cohort of 70 women from an addiction and psychiatry hospital unit. Biochemical and hematological parameters were collected in medical records at admission. Biological factors associated with a generalized reduced periodontium (≥ 30% of sites with clinical attachment loss ≥ 3 mm) and dental erosion [a basic erosive wear examination (BEWE) score ≥ 3] were determined by logistic regression models. RESULTS: Forty-five women with either anorexia nervosa (n = 27) or bulimia nervosa (n = 18) were included in the study. None of the women had active periodontitis or other inflammatory comorbidity. Women with ≥ 30% of sites with clinical attachment loss ≥ 3 mm and those with a BEWE score ≥ 3 were older than women that did not exhibit a generalized reduced periodontium or dental erosion (37.1 ± 10.4 versus 28.8 ± 7.4, p < 0.01 and 35.2 ± 9.7 versus 28.1 ± 7.8, p = 0.01), respectively. After adjustments for age and duration of eating disorder, high serum ferritin levels were associated with a generalized reduced periodontium [OR (95%CI) = 1.04 (1.01; 1.07)]. No association was found between biological factors and dental erosion. CONCLUSION: Serum ferritin levels together with age may be helpful to mental health professionals in screening patients with eating disorders for adequate referral to a dentist. LEVEL III: Evidence obtained from a case-control analytic study.

Risk factors in periodontology: a conceptual framework.

AIM: The definition and assessment of risk factors, risk indicators and predisposing factors are of paramount importance in the understanding of the pathogenesis of periodontitis, as well as in its prevention and treatment. This article aims to emphasize the concepts of causal chains and the causal network of risk factors in periodontitis. MATERIALS AND METHODS: This is a narrative review focusing on two main questions: (1) what is a risk in periodontology? and (2) how can a risk be assessed? RESULTS: The probability of the occurrence of an adverse outcome following exposure is not sufficient to analyse the impact of a risk factor on the disease. A network model for the pathway of risk factors in the pathogenesis of periodontitis is described. This article emphasizes the concepts of causal chains and the causal network of risk factors in periodontitis. CONCLUSION: Chronic periodontal diseases are among the most complex non-communicable diseases. A conceptual framework intended to clarify the relationship between risk and causality may improve the understanding of the underlying mechanisms of chronic diseases. The proposed causal network may provide a model to assess the role of risk factors in periodontitis.

Interaction of lifestyle, behaviour or systemic diseases with dental caries and periodontal diseases: consensus report of group 2 of the joint EFP/ORCA workshop on the boundaries between caries and periodontal diseases.

Periodontal diseases and dental caries are the most common diseases of humans and the main cause of tooth loss. Both diseases can lead to nutritional compromise and negative impacts upon self-esteem and quality of life. As complex chronic diseases, they share common risk factors, such as a requirement for a pathogenic plaque biofilm, yet they exhibit distinct pathophysiologies. Multiple exposures contribute to their causal pathways, and susceptibility involves risk factors that are inherited (e.g. genetic variants), and those that are acquired (e.g. socio-economic factors, biofilm load or composition, smoking, carbohydrate intake). Identification of these factors is crucial in the prevention of both diseases as well as in their management. AIM: To systematically appraise the scientific literature to identify potential risk factors for caries and periodontal diseases. METHODS: One systematic review (genetic risk factors), one narrative review (role of diet and nutrition) and reference documentation for modifiable acquired risk factors common to both disease groups, formed the basis of the report. RESULTS & CONCLUSIONS: There is moderately strong evidence for a genetic contribution to periodontal diseases and caries susceptibility, with an attributable risk estimated to be up to 50%. The genetics literature for periodontal disease is more substantial than for caries and genes associated with chronic periodontitis are the vitamin D receptor (VDR), Fc gamma receptor IIA (Fc-γRIIA) and Interleukin 10 (IL10) genes. For caries, genes involved in enamel formation (AMELX, AMBN, ENAM, TUFT, MMP20, and KLK4), salivary characteristics (AQP5), immune regulation and dietary preferences had the largest impact. No common genetic variants were found. Fermentable carbohydrates (sugars and starches) were the most relevant common dietary risk factor for both diseases, but associated mechanisms differed. In caries, the fermentation process leads to acid production and the generation of biofilm components such as Glucans. In periodontitis, glycaemia drives oxidative stress and advanced glycation end-products may also trigger a hyper inflammatory state. Micronutrient deficiencies, such as for vitamin C, vitamin D or vitamin B12, may be related to the onset and progression of both diseases. Functional foods or probiotics could be helpful in caries prevention and periodontal disease management, although evidence is limited and biological mechanisms not fully elucidated. Hyposalivation, rheumatoid arthritis, smoking/tobacco use, undiagnosed or sub-optimally controlled diabetes and obesity are common acquired risk factors for both caries and periodontal diseases.

Clinical evaluation of two dental implant macrostructures on peri-implant bone loss: a comparative, retrospective study.

OBJECTIVES: To compare the effect of two implant macrostructures on peri-implant bone level. MATERIAL AND METHODS: This retrospective cohort study was conducted in a private practice. Patients received test (Nobel Speedy Groovy implants) or control implants (Mk III implants) or both. Baseline and corresponding follow-up radiographs, taken with a long-cone technique, were analyzed to evaluate mean bone level changes around implants during a mean follow-up of 69 ± 19 months. A chi-squared test was performed to compare the bone level changes between the two types of implants. A multivariate analysis was used to explain the difference between the two groups. RESULTS: After controlling for inclusion and exclusion criteria, 144 dental implants corresponding to 68 implants in the test group and 76 implants in the control group were placed in 59 patients. Nine dental implants (6.25%) were lost during the observation period: five implants in the test group and four implants in the control group. Consequently, a total of 135 implants placed in 58 patients were available for analysis. Our study shows a significant difference of peri-implant bone level overtime between the test and control groups (P < 0.01). At the end of the observation period, a bone growth was observed in the control group (0.02 ± 0.80 mm), whereas a bone loss was found in the test group (-0.43 ± 1.11 mm). The mean bone level at baseline and the type of periodontal therapy and the maintenance care program were involved in this difference (P < 0.001, P = 0.035, P < 0.001, respectively). CONCLUSION: Our study demonstrates a significant difference in peri-implant bone level between test and control groups. The mean bone level at baseline, the type of periodontal therapy, and the maintenance program may explain peri-implant bone level changes overtime.

Nisin lantibiotic prevents NAFLD liver steatosis and mitochondrial oxidative stress following periodontal disease by abrogating oral, gut and liver dysbiosis.

Oral microbiome dysbiosis mediates chronic periodontal disease, gut microbial dysbiosis, and mucosal barrier disfunction that leads to steatohepatitis via the enterohepatic circulation. Improving this dysbiosis towards health may improve liver disease. Treatment with antibiotics and probiotics have been used to modulate the microbial, immunological, and clinical landscape of periodontal disease with some success. The aim of the present investigation was to evaluate the potential for nisin, an antimicrobial peptide produced by Lactococcus lactis, to counteract the periodontitis-associated gut dysbiosis and to modulate the glycolipid-metabolism and inflammation in the liver. Periodontal pathogens, namely Porphyromonas gingivalis, Treponema denticola, Tannerella forsythia and Fusobacterium nucleatum, were administrated topically onto the oral cavity to establish polymicrobial periodontal disease in mice. In the context of disease, nisin treatment significantly shifted the microbiome towards a new composition, commensurate with health while preventing the harmful inflammation in the small intestine concomitant with decreased villi structural integrity, and heightened hepatic exposure to bacteria and lipid and malondialdehyde accumulation in the liver. Validation with RNA Seq analyses, confirmed the significant infection-related alteration of several genes involved in mitochondrial dysregulation, oxidative phosphorylation, and metal/iron binding and their restitution following nisin treatment. In support of these in vivo findings indicating that periodontopathogens induce gastrointestinal and liver distant organ lesions, human autopsy specimens demonstrated a correlation between tooth loss and severity of liver disease. Nisin's ability to shift the gut and liver microbiome towards a new state commensurate with health while mitigating enteritis, represents a novel approach to treating NAFLD-steatohepatitis-associated periodontal disease.

Recalled body silhouette trajectories over the lifespan and oral conditions in adulthood: A cross-sectional analysis of the Paris Prospective Study 3.

OBJECTIVES: To examine the association between life-course body silhouette changes and oral conditions in adulthood. METHODS: At study recruitment (2008-2012), 5430 adults underwent a full-mouth clinical examination and recalled their body silhouettes at ages 8, 15, 25, 35 and 45. Life-course trajectories of body silhouettes were computed using group-based trajectory modelling. Gingival inflammation, dental plaque, masticatory units, numbers of healthy, missing, decayed and filled teeth at study recruitment were clustered. The associations between body silhouette trajectories and clusters of oral conditions were assessed by multinomial logistic regression. RESULTS: The final analysis included 4472 participants. Five body silhouette trajectories were established: lean-stable (30.0%), lean-increased (19.3%), moderate stable (18.1%), lean-marked increased (25.8%) and heavy stable (6.7%). Three clusters of oral conditions were identified: optimal oral health and preserved masticatory capacity (70.0%, cluster 1), moderate oral health and moderately impaired masticatory capacity (25.4%, cluster 2) and poor oral health and severely impaired masticatory capacity (4.7%, cluster 3). Participants with a lean-increased trajectory were 58% more likely than those with a lean-stable trajectory to be in cluster 3 (aOR 1.58 [95% CI 1.07; 2.35]) relative to cluster 1, independently of covariates measured at study recruitment and including age, sex, smoking, socioeconomic status, BMI, hypertension, type 2 diabetes, cholesterol and triglycerides. CONCLUSIONS: A life-course lean-increased body silhouette trajectory is associated with higher likelihood of poor oral health and severely impaired masticatory capacity in adulthood.

Diet Traps during Eating Disorders among Dentate Patients at an Oral Health Glance.

Persons suffering from eating disorders (ED) may often experience a recurrence/persistence symptoms despite the completion of psychiatric therapy. In most cases, their general health status is linked to current nutritional behaviors. Medical professionals, general practitioners (GPs), dieticians, and dentists may see those patients in their practices. At the same time, due to low sense of illness, some patients may delay or never seek professional medical care. The aim of this article is to analyze the main ED types according to dietary behaviors causing oral health problems and discuss oral health complications in affected dentate patients. The second objective is to update oral preventive measures and technological innovations together with active agents for oral hygiene care that might effectively support oral health maintenance during the presence of long-term symptoms. The research method involved a review of clinical reports as a synthesis of the electronic research in the Pubmed, Web of Science, and Google Scholar databases. Based on the research, ED patients were found to present related incidences of oral complications. Studies have reported that the possible course of an ED and comorbidities may be an imbalance in the oral environment. The results showed an association between biological (malnutrition, etc.), behavioral (binge eating episodes, vomiting, acidic diet, poor oral hygiene), and pharmacotherapeutic (addiction, hyposalivation) factors that may threaten oral health. Early diagnosis of the past and present symptoms is essential to eliminate and take control of destructive behaviors. Oral changes need to be tackled with medical insight, and additionally, the perception of dietary interactions is recommended.

Salivary proteome modifications associated with periodontitis in obese patients.

AIM: To identify changes in the salivary protein/peptide profiles by differential proteomics in obese patients with or without periodontitis. MATERIAL AND METHODS: Periodontal examinations and whole saliva samples were obtained from 38 obese patients (mean age: 45.1 ± 7.3 years, mean BMI: 49.3 ± 9 kg/m(2) ) including 13 periodontitis and 25 non-periodontitis subjects, and 19 healthy controls (mean age: 44.2 ± 6.4 years, mean BMI: 21.5 ± 2.1 kg/m(2) ). Surface-enhanced laser desorption/ionization time-of-flight (SELDI-TOF) mass spectrometry (MS) was used to compare the whole saliva polypeptide profiles. RESULTS: The SELDI-TOF-MS analysis detected eight putative markers. Six of them were increased and identified in obese subjects versus controls (albumin, α and ß haemoglobin chains, α-defensins 1, 2 and 3). Alpha-defensins were less abundant in saliva of periodontitis obese patients (36.47 ± 19.84 µA) versus non-periodontitis obese patients (43.44 ± 30.34  µA), whereas α-defensins were more abundant in obese patients (40.99 ± 26.66  µA) versus controls (27.1 ± 23.98  µA). CONCLUSIONS: Periodontal status modifies the salivary proteome in obese patients. Alpha-defensins may play a role in gingival inflammation, and be involved in the higher susceptibility of obese patients to periodontal diseases.

Nisin probiotic prevents inflammatory bone loss while promoting reparative proliferation and a healthy microbiome.

Dysbiosis of the oral microbiome mediates chronic periodontal disease. Realignment of microbial dysbiosis towards health may prevent disease. Treatment with antibiotics and probiotics can modulate the microbial, immunological, and clinical landscape of periodontal disease with some success. Antibacterial peptides or bacteriocins, such as nisin, and a nisin-producing probiotic, Lactococcus lactis, have not been examined in this context, yet warrant examination because of their biomedical benefits in eradicating biofilms and pathogenic bacteria, modulating immune mechanisms, and their safety profile in humans. This study's goal was to examine the potential for nisin and a nisin-producing probiotic to abrogate periodontal bone loss, the host inflammatory response, and changes in oral microbiome composition in a polymicrobial mouse model of periodontal disease. Nisin and a nisin-producing Lactococcus lactis probiotic significantly decreased the levels of several periodontal pathogens, alveolar bone loss, and the oral and systemic inflammatory host response. Surprisingly, nisin and/or the nisin-producing L. lactis probiotic enhanced the population of fibroblasts and osteoblasts despite the polymicrobial infection. Nisin mediated human periodontal ligament cell proliferation dose-dependently by increasing the proliferation marker, Ki-67. Nisin and probiotic treatment significantly shifted the oral microbiome towards the healthy control state; health was associated with Proteobacteria, whereas 3 retroviruses were associated with disease. Disease-associated microbial species were correlated with IL-6 levels. Nisin or nisin-producing probiotic's ability to shift the oral microbiome towards health, mitigate periodontal destruction and the host immune response, and promote a novel proliferative phenotype in reparative connective tissue cells, addresses key aspects of the pathogenesis of periodontal disease and reveals a new biomedical application for nisin in treatment of periodontitis and reparative medicine.

Risk Factors for Oral Health in Anorexia Nervosa: Comparison of a Self-Report Questionnaire and a Face-to-Face Interview.

Behavioral, nutritional, and local risk factors for oral health are frequent in people with anorexia nervosa. However no self-report questionnaire is available for screening in clinical practice or for research purposes. The objective of this study was to design a questionnaire to identify risk factors and symptoms of oral diseases and to test its reliability as a self-report form among people with anorexia nervosa. A 26-item questionnaire was designed based on a sound literature review performed by a group of dentists, psychiatrists, and epidemiologists specialized in the field of eating disorders. Sixty-nine anorexia nervosa inpatients (mean age 18.72 ± 5.1) were included from four specialized units. The questionnaire was first self-reported by the patients, then the same questionnaire was administrated by a dentist during a structured face-to-face interview as the gold standard. The concordance between the two forms was evaluated globally and item per item using Cohen's kappa statistical tests. The overall concordance between the self-report questionnaire and the face-to-face structured interview was 55%. Of the 26 items, 19 showed significant concordance. Items relating to water intake, extracted teeth, gingival status, and oral hygiene had the best concordance (all kappa coefficients > 0.4). A questionnaire that identifies risk factors and symptoms of oral diseases in anorexia nervosa was developed and tested. The 26-item form of the questionnaire (long version) is moderately reliable as a self-reported form. A short version of the questionnaire, including the 10 most reliable items, is recommended for oral risk assessment in patients with anorexia nervosa. The clinical value of the self-administered questionnaire remains to be evaluated.

Shared detection of Porphyromonas gingivalis in cohabiting family members: a systematic review and meta-analysis.

Introduction: Periodontitis is an inflammatory dysbiotic disease. Among putative dysbiosis causes, transmission of Porphyromonas gingivalis between individuals of the same family remains unclear. The aim of this systematic review and meta-analysis is to assess the likelihood of shared detection of Porphyromonas gingivalis among cohabiting family members. Methods: A literature search was conducted on different databases up to September 2018. Articles assessing the presence of P.gingivalis between members of the same family were screened. Only English literature was retrieved, whereas no limits were applied for bacterial sampling and detection methods. Results: Overall, 26 articles published between 1993 and 2017 met the inclusion criteria. Of these, 18 articles were used for meta-analyses. Based on bacterial culture, the likelihood of an intra-familial transmission of P.gingivalis once a member of the family harbors the bacterium is estimated at 63.5% (n = 132 pairs of family members); this drops to 45% when pooling together culture and Polymerase-Chain-Reaction (n = 481 pairs), whereas it is estimated at 35.7% when genotyping is applied (n = 137 pairs). Conclusion: Pooled results suggest that the likelihood of detecting P.gingivalis within within family members is moderately frequent. Personalized periodontal screening and prevention may consider intra-familial co-occurrence of P.gingivalis as feasible.

Innovative application of nested PCR for detection of Porphyromonas gingivalis in human highly calcified atherothrombotic plaques.

Atherothrombosis, leading to stroke and myocardial infarction, is responsible for most of the deaths in the world. An increased risk of atherothrombotic vascular events has been reported in patients with periodontitis. Periodontitis is a chronic multifactorial inflammatory disease, which involves a dysbiotic microbiota, and leads to a progressive destruction of the tooth-supporting apparatus. Transcient periodontal pathogen blood translocation, mainly bacteremia, has been associated with the severity of gingival inflammation. The identification of periodontal bacteria within atherothrombotic plaques is challenging and unpredictable. This review aims to summarize existing molecular technics for identifying periodontal microbiota in human atherothrombotic samples. A secondary objective is to describe a protocol for the identification of Porphyromonas gingivalis from highly calcified, atherothrombotic human samples that is based on our experience in translational cardiovascular research. Compared to direct real-time PCR, our protocol based on nested PCR has increased the detection of Porphyromonas gingivalis by 22.2% with good specificity.

Polymicrobial periodontal disease triggers a wide radius of effect and unique virome.

Periodontal disease is a microbially-mediated inflammatory disease of tooth-supporting tissues that leads to bone and tissue loss around teeth. Although bacterially-mediated mechanisms of alveolar bone destruction have been widely studied, the effects of a polymicrobial infection on the periodontal ligament and microbiome/virome have not been well explored. Therefore, the current investigation introduced a new mouse model of periodontal disease to examine the effects of a polymicrobial infection on periodontal ligament (PDL) properties, changes in bone loss, the host immune response, and the microbiome/virome using shotgun sequencing. Periodontal pathogens, namely Porphyromonas gingivalis, Treponema denticola, Tannerella forsythia, and Fusobacterium nucleatum were used as the polymicrobial oral inoculum in BALB/cByJ mice. The polymicrobial infection triggered significant alveolar bone loss, a heightened antibody response, an elevated cytokine immune response, a significant shift in viral diversity and virome composition, and a widening of the PDL space; the latter two findings have not been previously reported in periodontal disease models. Changes in the PDL space were present at sites far away from the site of insult, indicating that the polymicrobial radius of effect extends beyond the bone loss areas and site of initial infection and wider than previously appreciated. Associations were found between bone loss, specific viral and bacterial species, immune genes, and PDL space changes. These findings may have significant implications for the pathogenesis of periodontal disease and biomechanical properties of the periodontium. This new polymicrobial mouse model of periodontal disease in a common mouse strain is useful for evaluating the features of periodontal disease.