Search

The acquired enamel pellicle (AEP) is a multi-protein film attached to the surface of teeth, which functions to lubricate the dental surface, form an anti-erosive barrier and exhibits antimicrobial properties. The initiation of AEP formation occurs within seconds of exposure to saliva, a biofluid rich in protein species. While there have been many publications on the formation of human AEP there is little research on the composition of canine AEP during its acquisition. The aim of these studies was to explore the composition of canine AEP formation, utilising hydroxyapatite (HA) discs as a tooth substitute matrix, over time. Qualitative and quantitative proteomics techniques using tandem mass tag labelled peptides and LC-MS/MS were used to follow the formation of canine AEP on hydroxyapatite discs over the course of an hour. Proteins adsorbed to the HA surface included highly abundant proteins in canine saliva, antimicrobial proteins, protease inhibitors and the buffering agent carbonic anhydrase. Greater understanding of the canine AEP deepens fundamental knowledge of the early processes driving bacterial colonisation of the tooth surface and subsequent plaque accumulation.

The aim of this study was to evaluate the association between systemic non-communicable diseases (NCDs; including lung, kidney, mental and cardiovascular diseases, arthritis, cancer and spinal problems), common risk factors, and tooth loss (TL), as an endpoint of prevalent oral NCDs (periodontitis and caries).A total of 60,271 noninstitutionalized adults (≥30 years) were evaluated, using data from the 2019 Brazilian National Health Survey. Negative binomial regressions were performed, adjusting for sex, age, ethnicity, educational attainment, oral hygiene, risk factors for periodontitis and caries (diabetes, smoking, and a cariogenic diet). The dependent variable was TL expressed as a numerical value.Diabetes, current smoking and a frequent cariogenic diet were significantly associated with TL-Incidence Rate Ratio (IRR [95% CI]): 1.11 (1.08 to 1.14), 1.28 (1.25 to 1.31), and 0.97 (0.94 to 0.99), respectively. Significant associations were observed for TL and all assessed NCDs, except kidney diseases, cancer and musculoskeletal diseases related to work, with IRR ranging from 1.06 for hypertension and asthma to 1.16 for rheumatoid arthritis. Regular consumption (4 to 7 d/wk) of vegetables, fruits and beef; alcohol up to 8 doses/wk; and physical exercise were associated with a lower IRR for TL (P 0.05). Obesity, but not overweight, was associated with increased TL (1.05 [1.03 to 1.07]). Smoking, hypertension, arthritis, other mental diseases and spinal problems further increased the IRR for TL in individuals with diabetes (P 0.05).We conclude that certain chronic systemic conditions are associated with TL in Brazilian adults. This is likely because of shared risk factors; however, causal associations cannot be examined in this cross-sectional dataset.

Periodontitis is independently associated with rheumatoid arthritis (RA); however, there are limited data on whether periodontal treatment improves overall RA disease activity. We conducted a pilot feasibility randomised controlled clinical trial to test whether intensive periodontal therapy reduces RA disease activity in patients with active RA and periodontitis.The following inclusion criteria were applied: patients with RA and periodontitis, aged 18+, stable on treatment with DMARDs for ≥ 3 months, disease activity score (DAS28) ≥3.2, and DAS285.1 only if patient unwilling to take biologics. Participants meeting the inclusion criteria were randomised to immediate intensive periodontal therapy or to delayed therapy (control group) administered by a dental hygienist in a secondary care setting. Data were collected at baseline, 3 and 6 months of follow-up. Participants randomised to the control group (delayed therapy) received the standard of care for the duration of the trial, including oral hygiene instructions delivered by a dental hygienist, and the same periodontal therapy as the intervention group after study completion (i.e., 6 months after randomisation). The periodontal inflammation surface area (PISA) was calculated using clinical attachment loss, periodontal probing pocket depth and bleeding on probing. Cumulative probing depth was also measured. We examined the effect of periodontal therapy on periodontal outcomes and on clinical markers of disease activity in RA, as measured by the DAS28-CRP score and musculoskeletal ultrasound grey scale and power Doppler scores.A total of 649 patients with RA were invited to participate in the study. Of these, 296 (46%) RA patients consented to participate in the screening visit. A sample of 201 were assessed for eligibility, of whom 41 (20%) did not meet RA inclusion criteria and 100 (50%) did not meet periodontal disease (PD) criteria. Amongst 60 (30%) eligible participants, 30 were randomised to immediate periodontal therapy and 30 were allocated to the control group. The loss to follow-up was 18% at the end of the trial. There were no major differences with regards to baseline characteristics between groups. Periodontal therapy was associated with reduced periodontal inflamed surface area, cumulative probing depths, RA disease activity scores and ultrasound scores over the course of the trial. There was no change in clinical attachment loss.Overall, the trial was feasible and acceptable to study participants. Recruitment and satisfactory retention into a randomised controlled trial on the effect of periodontal treatment on RA patients is possible, albeit challenging. In this feasibility study of patients with RA and periodontitis, periodontal treatment resulted in significant improvements in periodontal disease outcomes and overall RA disease activity, although complete resolution of periodontal inflammation was difficult to achieve in some cases. This article is protected by copyright. All rights reserved.

BACKGROUND: The recently published clinical practice guideline (CPG) for the treatment of periodontitis in stages I-III provided evidence-based recommendations for the treatment of periodontitis patients, defined according to the 2018 classification. Stage IV periodontitis shares the severity and complexity characteristics of stage III periodontitis, but includes the anatomical and functional sequelae of tooth and periodontal attachment loss (tooth flaring and drifting, bite collapse, etc.), which require additional interventions following completion of active periodontal therapy.AIM: To develop an S3 Level CPG for the treatment of stage IV periodontitis, focusing on the implementation of inter-disciplinary treatment approaches required to treat/rehabilitate patients following associated sequelae and tooth loss.MATERIALS AND METHODS: This S3 Level CPG was developed by the European Federation of Periodontology (EFP), following methodological guidance from the Association of Scientific Medical Societies in Germany and the Grading of Recommendations Assessment, Development and Evaluation (GRADE) process. A rigorous and transparent process included synthesis of relevant research in 13 specifically commissioned systematic reviews, evaluation of the quality and strength of evidence, the formulation of specific recommendations and a structured consensus process with leading experts and a broad base of stakeholders.RESULTS: The S3 Level CPG for the treatment of stage IV periodontitis culminated in recommendations for different interventions, including orthodontic tooth movement, tooth splinting, occlusal adjustment, tooth- or implant-supported fixed or removable dental prostheses and supportive periodontal care. Prior to treatment planning, it is critically important to undertake a definitive and comprehensive diagnosis and case evaluation, obtain relevant patient information, and engage in frequent re-evaluations during and after treatment. The periodontal component of therapy should follow the CPG for the treatment of periodontitis in stages I-III.CONCLUSIONS: The present S3 Level CPG informs clinical practice, health systems, policymakers and, indirectly, the public on the available and most effective modalities to treat patients with stage IV periodontitis and to maintain a healthy dentition over lifetime, according to the available evidence at the time of publication.

Introduction Fusobacterium nucleatum is an opportunistic oral pathogen with five subspecies: animalis, fusiforme, nucleatum, polymorphumandvincentii. These play an important role in biofilms associated with chronic gum disease (periodontitis). Neutrophils form the first line of defence against these and other oral pathogens, employing a multitude of anti-microbial strategies, which, alongside bacterial killing, also cause collateral host-tissue damage. The immunogenic properties of F. nucleatum subspecies are poorly understood. The purpose of this study was to investigate specific neutrophil responses to all F. nucleatum subspecies. Methods AllF. nucleatumsubspecieswere grown planktonically overnight and inactivated using 10% neutral buffered formalin. Peripheral blood neutrophils (PBN) and neutrophil-like cells (differentiated from HL-60 cells) were challenged with inactivated bacteria (MOI 100) and production of reactive oxygen species (ROS) was quantified by Luminol/Iso-luminol enhanced chemiluminescence assays. Release of neutrophil extracellular traps (NETs) was quantified fluorescently using Sytox-green. Additionally, phagocytosis of fluorescently labelled F. nucleatum subspecies was analysed in both cell groups by flow cytometry. Results In addition to differences in ROS generation by PBN and neutrophil-like cells in response to individual F. nucleatum subspecies, variations in the amount of extracellular DNA extruded during NETosis was evident. Moreover, distinct levels of phagocytic activity of both cell types will be shown. Conclusion F. nucleatum pathogenicity has been reported in oral as well as systemic diseases (colorectal cancer, cardiovascular disease). Understanding subspecies-specific effects of F. nucleatum on neutrophils will enhance our knowledge of the interactions between this bacterium and the host immune response and may help to identify new therapeutic targets.

This is the second in a two-part series that aims to summarise answers to common questions facing dentists in general practice. The first part of this series is entitled 'Periodontal care in general practice: 20 important FAQs - Part one' (Br Dent J 2019;226: 850-854) and contains the first set of ten FAQs.

Antibodies specific for the spike glycoprotein (S) and nucleocapsid (N) SARS-CoV-2 proteins are typically present during severe COVID-19, and induced to S after vaccination. The binding of viral antigens by antibody can initiate the classical complement pathway. Since complement could play pathological or protective roles at distinct times during SARS-CoV-2 infection we determined levels of antibody-dependent complement activation along the complement cascade. Here, we used an ELISA assay to assess complement protein binding (C1q) and the deposition of C4b, C3b, and C5b to S and N antigens in the presence of antibodies to SARS-CoV-2 from different test groups: non-infected, single and double vaccinees, non-hospitalised convalescent (NHC) COVID-19 patients and convalescent hospitalised (ITU-CONV) COVID-19 patients. C1q binding correlates strongly with antibody responses, especially IgG1 levels. However, detection of downstream complement components, C4b, C3b and C5b shows some variability associated with the subject group from whom the sera were obtained. In the ITU-CONV, detection of C3b-C5b to S was observed consistently, but this was not the case in the NHC group. This is in contrast to responses to N, where median levels of complement deposition did not differ between the NHC and ITU-CONV groups. Moreover, for S but not N, downstream complement components were only detected in sera with higher IgG1 levels. Therefore, the classical pathway is activated by antibodies to multiple SARS-CoV-2 antigens, but the downstream effects of this activation may differ depending the disease status of the subject and on the specific antigen targeted.

Antibodies specific for the spike glycoprotein (S) and nucleocapsid (N) SARS-CoV-2 proteins are typically present during severe COVID-19, and induced to S after vaccination. The binding of viral antigens by antibody can initiate the classical complement pathway. Since complement could play pathological or protective roles at distinct times during SARS-CoV-2 infection we determined levels of antibody-dependent complement activation along the complement cascade. Here, we used an ELISA assay to assess complement protein binding (C1q) and the deposition of C4b, C3b, and C5b to S and N antigens in the presence of anti-SARS-CoV-2 antibodies from different test groups: non-infected, single and double vaccinees, non-hospitalised convalescent (NHC) COVID-19 patients and convalescent hospitalised (ITU-CONV) COVID-19 patients. C1q binding correlates strongly with antibody responses, especially IgG1 levels. However, detection of downstream complement components, C4b, C3b and C5b shows some variability associated with the antigen and subjects studied. In the ITU-CONV, detection of C3b-C5b to S was observed consistently, but this was not the case in the NHC group. This is in contrast to responses to N, where median levels of complement deposition did not differ between the NHC and ITU-CONV groups. Moreover, for S but not N, downstream complement components were only detected in sera with higher IgG1 levels. Therefore, the classical pathway is activated by antibodies to multiple SARS-CoV-2 antigens, but the downstream effects of this activation may differ depending on the specific antigen targeted and the disease status of the subject.

The 2017 international classification system for periodontal diseases characterises periodontitis patients based upon disease extent, severity and past experience, and in stage IV includes a treatment complexity component. In addition, taking into account well-established risk factors, it aims to estimate the risk for future attachment loss. This classification system draws upon current understanding of disease pathobiology and reflects the complex, multifactorial nature of the periodontitis. It also acknowledges individual patients' risk profiles.Classification and diagnosis are distinct but linked entities, and the inclusion of established risk factors in the system helps signpost the clinician and patient towards a more personalised approach to care provision. The European Federation of Periodontology (EFP) has recently developed an S3-level clinical treatment guideline for stages I to III periodontitis, based upon a rigorous standardised process involving 15 systematic reviews of current evidence and their synthesis by a representative group of experts and stakeholders. The aim is to guide the practitioner through the complex plethora of periodontal management options and to facilitate pragmatic decision-making in full knowledge of the evidence base.Here, we present the structured, stepwise treatment protocols developed by the EFP guideline group and highlight selected specific clinical recommendations. The adapted guidelines for the UK healthcare system will be published in early 2021.

To describe the biology of alveolar bone regeneration.Four comprehensive reviews were performed on (a) mesenchymal cells and differentiation factors leading to bone formation; (b) the critical interplay between bone resorbing and formative cells; (c) the role of osteoimmunology in the formation and maintenance of alveolar bone; and (d) the self-regenerative capacity following bone injury or tooth extraction were prepared prior to the workshop.This summary information adds to the fuller understanding of the alveolar bone regenerative response with implications to reconstructive procedures for patient oral rehabilitation. The group collectively formulated and addressed critical questions based on each of the reviews in this consensus report to advance the field. The report concludes with identified areas of future research.

Background Two systematic reviews have evaluated the quality of research and reporting of observational studies investigating the prevalence of, the incidence of and the risk factors for peri-implant diseases and of experimental clinical studies evaluating the efficacy of preventive and therapeutic interventions. Materials and Methods For the improvement of the quality of reporting for both observational and experimental studies, the STROBE and the Modified CONSORT recommendations were encouraged. Results To improve the quality of research in peri-implant diseases, the following were recommended: the use of unequivocal case definitions; the expression of outcomes at the subject rather than the implant level; the implementation of study validation tools; the reporting of potential sources of bias; and the use of appropriate statistical methods. Conclusions In observational studies, case definitions for peri-implantitis were agreed. For risk factor determination, the progressive use of cross-sectional and case–control studies (univariate analyses), to prospective cohorts (multilevel modelling for confounding), and ultimately to intervention studies were recommended. For preventive and interventional studies of peri-implant disease management, parallel arm RCTs of at least 6-months were encouraged. For studies of non-surgical and surgical management of peri-implantitis, the use of a composite therapeutic end point was advocated. The development of standard control therapies was deemed essential.

Background: Periodontitis remains a major public health issue and current management approaches have failed to impact upon the most high-risk proportion of the population and those with the most severe disease. The objective of this session was to assess if and how, current understanding of periodontitis provides the opportunity to develop new preventive and therapeutic strategies. Materials and Methods: Based on the current understanding of the pathophysiology of periodontal diseases, the Workshop discussed the potential of antimicrobial peptides, probiotics, pro-resolving lipid mediators, and micronutritional approaches. Evidence-based position papers and expert discussions formed the basis of deliberations. Results and Discussion: Current preventive and treatment approaches are only partially effective, and this appears due to the therapeutic focus remaining primarily upon biofilm management rather than embracing a pivotal role for inflammation as a driver of biofilm composition as well as tissue damage. There is a need to develop new, more effective, and efficient preventive and treatment approaches for gingivitis and periodontitis, which embrace recent advances in understanding of host modulation and inflammation resolution, as well as direct management of the microbiota.

The benefits of treatment are likely to exceed the costs Periodontitis is the most common chronic inflammatory disease seen in humans, affecting nearly half of adults in the United Kingdom and 60% of those over 65 years.1 It is a major public health problem, causing tooth loss, disability, masticatory dysfunction, and poor nutritional status.2 Periodontitis also compromises speech, reduces quality of life,3 and is an escalating burden to the healthcare economy. In the UK alone it was estimated to cost £2.8bn (€3.4bn; $4.6bn) in 2008,4 not including raised all cause mortality, an association that has been noted in several populations.5 Worryingly, the disease is often silent, being present for decades before diagnosis and treatment. It can leave a substantial pathological footprint on multiple organ systems, as well as the oral cavity. Periodontitis follows the development of a pathogenic microbial biofilm at and below the gingival (gum) margin. In susceptible patients, this triggers an exaggerated and dysfunctional inflammatory immune response, which destroys the bone surrounding the teeth, causing tooth loss.6 The host’s immune response to the initiating microbiota is largely genetically determined, but environmental and lifestyle factors such as smoking, suboptimally controlled diabetes, obesity, poor nutrition (high intake of refined sugar and low intake of antioxidant micronutrients), and stress …

Background: Diabetes and periodontitis are complex chronic diseases with an established bidirectional relationship. There is long-established evidence that hyperglycaemia in diabetes is associated with adverse periodontal outcomes. However, given the ubiquity of periodontal diseases and the emerging global diabetes epidemic, the complications of which contribute to significant morbidity and premature mortality, it is timely to review the role of periodontitis in diabetes. Aims: To report the epidemiological evidence from cross-sectional, prospective and intervention studies for the impact of periodontal disease on diabetes incidence, control and complications and to identify potential underpinning mechanisms. Epidemiology: Over the last 20 years, consistent and robust evidence has emerged that severe periodontitis adversely affects glycaemic control in diabetes and glycaemia in non-diabetes subjects. In diabetes patients, there is a direct and dose-dependent relationship between periodontitis severity and diabetes complications. Emerging evidence supports an increased risk for diabetes onset in patients with severe periodontitis. Biological mechanisms: Type 2 diabetes is preceded by systemic inflammation, leading to reduced pancreatic b-cell function, apoptosis and insulin resistance. Increasing evidence supports elevated systemic inflammation (acute-phase and oxidative stress biomarkers) resulting from the entry of periodontal organisms and their virulence factors into the circulation, providing biological plausibility for the effects of periodontitis on diabetes. AGE (Advanced Glycation Endproducts)– RAGE (Receptor for AGEs) interactions and oxidative-stress-mediated pathways provide plausible mechanistic links in the diabetes to periodontitis direction. Interventions: Randomized controlled trials (RCTs) consistently demonstrate that mechanical periodontal therapy associates with approximately a 0.4% reduction in HbA1C at 3 months, a clinical impact equivalent to adding a second drug to a pharmacological regime for diabetes. RCTs are needed with larger numbers of subjects and longer term follow-up, and if results are substantiated, adjunctive periodontal therapies subsequently need to be evaluated. There is no current evidence to support adjunctive use of antimicrobials for periodontal management of diabetes patients. Guidelines: Given the current evidence, it is timely to provide guidelines for periodontal care in diabetes patients for medical and dental professionals and recommendations for patients/the public.

With increasing survival rates for childhood cancer, late effects are of growing importance. Oral health is central to general health, level of nutrition, quality of life, and is significant in the holistic care of children during cancer therapy.The oral health needs of children treated for solid tumours/lymphoma will be greater than the general population, groups will differ according to tumour and treatment.One hundred and twenty patients, 0-17 years, under follow-up from 01/07/06 to 07/02/07 were investigated for caries, opacities, microdontia, and gingivitis. Analysis was performed with stratification according to tumour and treatment. Comparisons made with the UK 2003 Child Dental Health Survey.The neuroblastoma group and high-dose chemotherapy with stem-cell rescue (HDCSCR) therapy group had increased caries of the primary teeth. Chi-squared analysis revealed a statistically significant relationship (P0.03) between the age at receipt of chemotherapy (3.5 years) and the presence of microdont teeth.Oral health care is important for all patients particularly those with a neuroblastoma, or who received HDCSCR. Patients should be advised about the possibility of microdontia in the permanent dentition following chemotherapy under 3.5 years.