[Temporomandibular dysfunction and bruxism in patients with early rheumatoid arthritis and at-risk patients: a cross-sectional study]. / Temporomandibulaire disfunctie en bruxisme bij patiënten met vroege reumatoïde artritis en risicopatiënten: een cross-sectioneel onderzoek.

What is the prevalence of temporomandibular dysfunction in patients with early rheumatoid arthritis and individuals at risk of rheumatoid arthritis? 3 groups (of 50 participants each) were examined for a possible TMD diagnosis: 1. patients with early rheumatoid arthritis, 2. at-risk individuals, and 3. healthy controls. A possible association with bruxism, determined on the basis of self-reporting and clinical features, was also examined. At-risk patients had a higher prevalence of TMD pain diagnoses compared to healthy controls (p = 0.046). Within the early rheumatoid arthritis group, seronegative patients had a higher prevalence of TMD pain diagnoses than seropositive patients (p = 0.048). No further differences in the prevalence of TMD diagnoses were found between the groups. Participants with a TMD pain diagnosis were more often diagnosed with probable sleep bruxism than those without a TMD pain diagnosis. The prevalence of TMD pain is increased in individuals at risk of rheumatoid arthritis and seronegative early rheumatoid arthritis patients, and is associated with signs of bruxism.

[Non-surgical peri-implantitis treatment with or without systemic antibiotics]. / Initiële behandeling van peri-implantitis met of zonder systemische antibiotica.

This study investigated the effect of initial nonsurgical treatment in patients with peri-implantitis with or without prescription of an antibiotic regimen consisting of amoxicillin and metronidazole. For this purpose, patients with peri-implantitis were randomized into a group of initial treatment with antibiotics and a group without antibiotics. They were re-evaluated 12 weeks after treatment. Analyses were performed at the patient level at 1 peri-implant pocket per patient. Both groups showed significant peri-implant pocket depth reductions after initial treatment. Treatment with antibiotics resulted in a higher mean reduction in peri-implant pocket depth than when no antibiotics were used, but this difference did not reach statistical significance. Only 2 implants, 1 in each group, showed a successful outcome of a peri-implant pocket depth ofunder ≤ 5 mm and with an absence of bleeding and pus after probing. Initial treatment with or without antibiotics is ultimately not sufficient to fully treat peri-implantitis; additional surgical procedures will often be required.

Investigating the Role of Spermidine in a Model System of Alzheimer's Disease Using Correlative Microscopy and Super-resolution Techniques.

Background: Spermidine has recently received major attention for its potential therapeutic benefits in the context of neurodegeneration, cancer, and aging. However, it is unclear whether concentration dependencies of spermidine exist, to differentially enhance autophagic flux. Moreover, the relationship between low or high autophagy activity relative to basal neuronal autophagy flux and subsequent protein clearance as well as cellular toxicity has remained largely unclear. Methods: Here, we used high-resolution imaging and biochemical techniques to investigate the effects of a low and of a high concentration of spermidine on autophagic flux, neuronal toxicity, and protein clearance in in vitro models of paraquat (PQ) induced neuronal toxicity and amyloid precursor protein (APP) overexpression, as well as in an in vivo model of PQ-induced rodent brain injury. Results: Our results reveal that spermidine induces autophagic flux in a concentration-dependent manner, however the detectable change in the autophagy response critically depends on the specificity and sensitivity of the method employed. By using correlative imaging techniques through Super-Resolution Structured Illumination Microscopy (SR-SIM) and Focused Ion Beam Scanning Electron Microscopy (FIB-SEM), we demonstrate that spermidine at a low concentration induces autophagosome formation capable of large volume clearance. In addition, we provide evidence of distinct, context-dependent protective roles of spermidine in models of Alzheimer's disease. In an in vitro environment, a low concentration of spermidine protected against PQ-induced toxicity, while both low and high concentrations provided protection against cytotoxicity induced by APP overexpression. In the in vivo scenario, we demonstrate brain region-specific susceptibility to PQ-induced neuronal toxicity, with the hippocampus being highly susceptible compared to the cortex. Regardless of this, spermidine administered at both low and high dosages protected against paraquat-induced toxicity. Conclusions: Taken together, our results demonstrate that firstly, administration of spermidine may present a favourable therapeutic strategy for the treatment of Alzheimer's disease and secondly, that concentration and dosage-dependent precision autophagy flux screening may be more critical for optimal autophagy and cell death control than previously thought.

The Effect of Periodontal Treatment on the Reactive Hyperemia Index. A 1-Year Follow-Up Pilot Study.

Background: Periodontitis is a chronic multifactorial inflammatory disease of the supportive tissues of the teeth. In more recent years, remarkable epidemiological and pathophysiological associations between periodontitis and cardiovascular disease (CVD) have been presented. Whether or not treatment of periodontitis is valuable for primary or secondary prevention of cardiovascular disease, has not yet been fully established. In this practice-based pilot study we focused on primary prevention of cardiovascular disease, by investigating the effect of periodontal treatment on the earliest detectable stage of CVD; endothelial dysfunction. Methods: Otherwise healthy periodontitis and non-periodontitis participants 45-70 years of age were included in the study. One year after completing periodontal (non-surgical and surgical) treatment of the periodontitis patients and 1 year after inclusion of the controls, all baseline measurements were repeated. Full-mouth examinations were performed by a periodontist to determine their Periodontal Inflamed Surface Area (PISA) score and other dental parameters. To assess the cardiovascular conditions, endothelial function through the reactive hyperemia index (RHI) assessed by the EndoPAT™, and several physical and biochemical parameters were measured. Results: 21 patients with diagnosed, untreated periodontitis and 21 participants without periodontitis were included in this follow-up study. After periodontal therapy in the periodontitis patients, the PISA reduced significantly. The RHI did not show a significant improvement after treatment of the periodontitis patients (-0.1 ± 0.8, p = 0.524). Similarly, other secondary cardiovascular outcome measurements, hsCRP, total cholesterol, HDL cholesterol, triglycerides, HbA1c, and systolic blood pressure did not improve significantly after periodontal treatment. Controls did not show any significant changes in the RHI, in other CVD parameters and in the PISA after 1-year follow-up. Conclusion: In this practice-based pilot study, periodontal treatment did not improve the endothelial function in otherwise healthy adults with periodontitis. Future studies are needed to be of larger size and could focus on periodontitis patients with co-morbidities to investigate whether periodontal treatment has secondary preventive effect on endothelial function and other CVD parameters. Clinical Trial Registration: [www.ClinicalTrials.gov], identifier [ISRCTN55656827].

The association between periodontitis and cardiovascular risks in asymptomatic healthy patients.

BACKGROUND: Periodontitis is a chronic multifactorial inflammatory disease of the supportive tissues of the teeth. Pathophysiological evidence suggests a possible common inflammatory background between periodontitis and cardiovascular diseases (CVD). Pathological and epidemiological associations between these two diseases have been presented, but are still debated. This study aimed to investigate the association between the inflammatory burden of periodontitis and the presence and extent of coronary calcification. Secondary aims were to study other cardiovascular parameters and cardiovascular risk predictors in relation to periodontitis and dental health. METHODS: Healthy periodontitis or non-periodontitis patients 45-70 years of age were included in a prospective cross-sectional study. Full-mouth examinations were performed by a periodontist to determine their Periodontal Inflamed Surface Area (PISA) score and other dental parameters. To assess the cardiovascular conditions, Coronary Artery Calcium (CAC) scores, endothelial function assessments by the EndoPAT ™, and several physical and biochemical examinations were performed. RESULTS: Seventy-one patients were included. Elevated CAC scores and endothelial dysfunction were not significantly related to PISA or dental health. PISA was significantly related to the Framingham and Reynolds CVD risk predictors, but were no longer significant after correction for confounders. The same applied to the significant relations between tooth loss, dental plaque and bleeding scores and the CVD risk predictors. CONCLUSIONS: Periodontitis is associated with increased CVD risk, but is not an independent risk factor. This link is still important to make to bridge the gap between dentistry and general medicine and to identify patients at risk for CVD in an earlier stage.

External validation of a rapid, non-invasive tool for periodontitis screening in a medical care setting.

OBJECTIVES: Medical professionals should advise their patients to visit a dentist if necessary. Due to the lack of time and knowledge, screening for periodontitis is often not done. To alleviate this problem, a screening model for total (own teeth/gum health, gum treatment, loose teeth, mouthwash use, and age)/severe periodontitis (gum treatment, loose teeth, tooth appearance, mouthwash use, age, and sex) in a medical care setting was developed in the Academic Center of Dentistry Amsterdam (ACTA) [1]. The purpose of the present study was to externally validate this tool in an outpatient medical setting. MATERIALS AND METHODS: Patients were requited in an outpatient medical setting as the validation cohort. The self-reported oral health questionnaire was conducted, demographic data were collected, and periodontal examination was performed. Algorithm discrimination was expressed as the area under the receiver operating characteristic curve (AUROCC). Sensitivity, specificity, and positive and negative predictive values were calculated. Calibration plots were made. RESULTS: For predicting total periodontitis, the AUROCC was 0.59 with a sensitivity of 49% and specificity of 68%. The PPV was 57% and the NPV scored 55%. For predicting severe periodontitis, the AUROCC was 0.73 with a sensitivity of 71% and specificity of 63%. The PPV was 39% and the NPV 87%. CONCLUSIONS: The performance of the algorithm for severe periodontitis is found to be sufficient in the current medical study population. Further external validation of periodontitis algorithms in non-dental school populations is recommended. CLINICAL RELEVANCE: Because general physicians are obligated to screen patients for periodontitis, it is our general goal that they can use a prediction model in medical settings without an oral examination.

Molecular regulation of autophagy in a pro-inflammatory tumour microenvironment: New insight into the role of serum amyloid A.

Chronic inflammation, systemic or local, plays a vital role in tumour progression and metastasis. Dysregulation of key physiological processes such as autophagy elicit unfavourable immune responses to induce chronic inflammation. Cytokines, growth factors and acute phase proteins present in the tumour microenvironment regulate inflammatory responses and alter crosstalk between various signalling pathways involved in the progression of cancer. Serum amyloid A (SAA) is a key acute phase protein secreted by the liver during the acute phase response (APR) following infection or injury. However, cancer and cancer-associated cells produce SAA, which when present in high levels in the tumour microenvironment contributes to cancer initiation, progression and metastasis. SAA can activate several signalling pathways such as the PI3K and MAPK pathways, which are also known modulators of the intracellular degradation process, autophagy. Autophagy can be regarded as having a double edged sword effect in cancer. Its dysregulation can induce malignant transformation through metabolic stress which manifests as oxidative stress, endoplasmic reticulum (ER) stress and DNA damage. On the other hand, autophagy can promote cancer survival during metabolic stress, hypoxia and senescence. Autophagy has been utilised to promote the efficiency of chemotherapeutic agents and can either be inhibited or induced to improve treatment outcomes. This review aims to address the known mechanisms that regulate autophagy as well as illustrating the role of SAA in modulating these pathways and its clinical implications for cancer therapy.

Elevated Coronary Artery Calcium scores are associated with tooth loss.

AIM: This study explores the association between Coronary Artery Calcium (CAC) scores and dental pathology such as missing teeth, the (peri-apical) health status and restoration grade of the teeth, and the grade of alveolar bone loss seen on a dental panoramic radiograph (Orthopantomograph-OPG). MATERIALS AND METHODS: In this retrospective cross-sectional study, data was collected from three hospitals spread in the Netherlands. Patients were included when a CAC score and an OPG were available, both recorded within a maximum period of 365 days from 2009-2017. The CAC score was measured on a CT scan, using the Agatston method. To assess dental pathology, the number of missing teeth, the number of dental implants, alveolar bone loss, caries, endodontic treatments, peri-apical radiolucencies, bone loss at implants, impacted teeth and dental cysts, were determined on the OPG. All observers were calibrated. The electronic health records provided information about: gender, age, smoking, Diabetes Mellitus, hypercholesterolemia, hypertension and Body Mass Index (BMI). RESULTS: 212 patients were included. We found a statistically significant association between the number of missing teeth and the CAC score. When modeling age, sex, and other well-known risk factors for cardiovascular disease, the significant correlation was no longer present after multivariate correction. Furthermore, the results showed a trend for more teeth with peri-apical lesions and a higher percentage of mean alveolar bone loss in the group with the highest CAC scores. CONCLUSION: This study showed that being edentulous or missing teeth is correlated to higher CAC scores however failed to be an independent predictor of atherosclerotic cardiovascular diseases. The number of (missing) teeth is an easily accessible marker and could be used as a marker for atherosclerotic cardiovascular disease (ACVD) risk by almost any healthcare worker. The current study needs to be considered as an explorative pilot study and could contribute to the design of further (prospective) studies on the relationship between dental pathology and coronary artery calcification by adding clinical information and extra cardiovascular biomarkers.

Gingival epithelium attachment to well- or partially cured resin composites.

Ideal restoration material for caries would allow attachment of gingival epithelia. The attachment of epithelial cells to specimens of the 4 most commercially used well- or partially-cured resin composites, with and without TEGDMA, was assessed. Effects of resin composite on the Ca9-22 gingival epithelial cell-line were assessed by measuring the cytotoxicity, viability and gene expression for attachment, apoptosis, ROS-production, pro-inflammatory cytokines, and matrix metalloproteinases. As controls, cells on tissue culture plastic or bovine tooth enamel specimens were used. Significantly less cell attachment was measured on freshly made resin-composite specimens. Concomitantly, significantly higher cytotoxicity was measured in the presence of freshly made resin-composite specimens. However, after 8 d of leakage, the cell attachment to and cytotoxicity of the resin composite was comparable to bovine tooth enamel. Significantly higher expressions of IL6, MMP2, BCL6 and ITGA4 were measured in cells attached to resin-composite surfaces than controls. There were no significant differences between the results using different conditions of resin composite, with or without TEGDMA and well or partially cured. Less cell attachment and presence of more inflammatory markers were observed on all freshly-made resin-composite surfaces. However, after a leakage period attachment of cells to the resin composite improved to the level of natural tooth materials such as enamel. This indicated that the negative effects of resin composites on epithelial cells might be transient.

[Stress and periodontitis]. / Stress en parodontitis.

Gingivitis and periodontitis can worsen with reduced immune fitness. Various causes can reduce immune fitness in a host, as a result of which the balance between the host and the microbiome is disturbed. Among others, lifestyle factors, such as stress and smoking, can have a negative influence on immune fitness. An association has been demonstrated between stress and periodontitis and also acute necrotising ulcerative gingivitis or periodontitis. There are indications that neurons are able to secrete pro-inflammatory cytokines and chemokines that worsen chronic inflammatory reactions in the periodontium and compromise immune fitness. In vitro studies show high cortisol levels may contribute to the increased growth of P. gingivalis. Stress as a risk factor for periodontitis and the role of stress as a negative influence on the results of periodontal treatment are difficult to estimate clinically. Nevertheless, attention to and awareness of stress as an aspect of the comprehensive set of risk factors for periodontitis can diminish its negative impact on immune fitness.

Periodontitis and Cardiovascular Diseases. Consensus Report.

Background: In Europe cardiovascular disease (CVD) is responsible for 3.9 million deaths (45% of deaths), being ischaemic heart disease, stroke, hypertension (leading to heart failure) the major cause of these CVD related deaths. Periodontitis is also a chronic non-communicable disease (NCD) with a high prevalence, being severe periodontitis, affecting 11.2% of the world's population, the sixth most common human disease. Material and Methods: There is now a significant body of evidence to support independent associations between severe periodontitis and several NCDs, in particular CVD. In 2012 a joint workshop was held between the European Federation of Periodontology (EFP) and the American Academy of Periodontology to review the literature relating periodontitis and systemic diseases, including CVD. In the last five years important new scientific information has emerged providing important emerging evidence to support these associations. Results and Conclusions: The present review reports the proceedings of the workshop jointly organised by the EFP and the World Heart Federation (WHF), which has updated the existing epidemiological evidence for significant associations between periodontitis and CVD, the mechanistic links and the impact of periodontal therapy on cardiovascular and surrogate outcomes. This review has also focused on the potential risk and complications of periodontal therapy in patients on anti thrombotic therapy and has made recommendations for dentists, physicians and for patients visiting both the dental and medical practices.

Temporomandibular joint function, periodontal health, and oral microbiome in early rheumatoid arthritis and at-risk individuals: a prospective cohort study protocol.

OBJECTIVES/AIMS: Rheumatoid arthritis (RA) is an autoimmune disease affecting the joints, including the temporomandibular joint (TMJ). Early diagnosis and treatment can alleviate symptoms and prevent progression. Predictors for disease outcome in individuals at risk for RA are therefore valuable. While limited information is available on the prevalence of TMJ involvement in early RA, previous studies suggest that RA, periodontitis and the oral microbiome are interrelated. Predictive factors for RA development may thus be present in the oral cavity. Our two aims are: (1) to assess the prevalence of TMJ involvement in early RA, and (2) to investigate the predictive value of oral factors in RA development. MATERIALS AND METHODS: We will include 150 individuals in this multi-center, prospective cohort study: 50 patients with early RA, 50 at-risk individuals, and 50 healthy controls. At baseline, the TMJ, periodontal health, and the oral microbiome will be examined. The general health will be followed over time, on four occasions up to 3 years. DISCUSSION: Our results will provide insight into the prevalence and clinical characterization of TMJ involvement in early RA. For at-risk individuals, oral factors can be studied as possible predictors for the development of RA.

Smoking Modifies the Genetic Risk for Early-Onset Periodontitis.

Periodontitis has low-prevalence, highly severe disease manifestations with an early onset and rapid progression. The diagnosis is based on severe destruction of the alveolar bone in adolescents and young adults. Genetic susceptibility variants and smoking are well-established risk factors, but their interactions in modifying disease susceptibility have not been studied. We aimed to identify genetic risk variants of early-onset periodontitis that unmask their effects on tobacco smoke exposure. To this end, we analyzed 79,780,573 common variants in 741 northwest Europeans diagnosed to have >30% bone loss at >2 teeth before 35 y of age, using imputed genotypes of the OmniExpress BeadChip. Never versus ever smokers were compared in a logistic regression analysis via a case-only approach. To explore the effect of tobacco smoke on the expression of the G×S-associated genes, cultures of primary gingival fibroblasts (n = 9) were exposed to cigarette smoke extract, and transcripts were quantified by reverse transcription polymerase chain reaction. We identified 16 loci for which our analysis suggested an association with G×S increased disease risk (P < 5 × 10-5). Nine loci had previously been reported to be associated with spirometric measures of pulmonary function by an earlier G×S genome-wide association study. Genome-wide significant cis expression quantitative trait loci were reported for G×S-associated single-nucleotide polymorphisms at ST8SIA1 and SOST, indicating a causal role of these genes in tobacco-related etiopathology. Notably, SOST is a negative regulator of bone growth, and ST8SIA1 has a role in tissue remodeling. Cigarette smoke extract significantly altered the expression of 2 associated genes: SSH1 (P = 5 × 10-07), which is required for NF-κB activation and innate immune responses to bacterial invasion, and ST8SIA1 (P = 0.0048). We conclude that the genetic predisposition to early-onset periodontitis is in part triggered by smoking and that tobacco smoke directly affects the expression of genes involved in bone homeostasis, tissue repair, and immune response.

Integration of Murine and Human Studies for Mapping Periodontitis Susceptibility.

Periodontitis is one of the most common inflammatory human diseases with a strong genetic component. Due to the limited sample size of available periodontitis cohorts and the underlying trait heterogeneity, genome-wide association studies (GWASs) of chronic periodontitis (CP) have largely been unsuccessful in identifying common susceptibility factors. A combination of quantitative trait loci (QTL) mapping in mice with association studies in humans has the potential to discover novel risk loci. To this end, we assessed alveolar bone loss in response to experimental periodontal infection in 25 lines (286 mice) from the Collaborative Cross (CC) mouse population using micro-computed tomography (µCT) analysis. The orthologous human chromosomal regions of the significant QTL were analyzed for association using imputed genotype data (OmniExpress BeadChip arrays) derived from case-control samples of aggressive periodontitis (AgP; 896 cases, 7,104 controls) and chronic periodontitis (CP; 2,746 cases, 1,864 controls) of northwest European and European American descent, respectively. In the mouse genome, QTL mapping revealed 2 significant loci (-log P = 5.3; false discovery rate = 0.06) on chromosomes 1 ( Perio3) and 14 ( Perio4). The mapping resolution ranged from ~1.5 to 3 Mb. Perio3 overlaps with a previously reported QTL associated with residual bone volume in F2 cross and includes the murine gene Ccdc121. Its human orthologue showed previously a nominal significant association with CP in humans. Use of variation data from the genomes of the CC founder strains further refined the QTL and suggested 7 candidate genes ( CAPN8, DUSP23, PCDH17, SNORA17, PCDH9, LECT1, and LECT2). We found no evidence of association of these candidates with the human orthologues. In conclusion, the CC populations enabled mapping of confined QTL that confer susceptibility to alveolar bone loss in mice and larger human phenotype-genotype samples and additional expression data from gingival tissues are likely required to identify true positive signals.

Caries Incidence in a Healthy Young Adult Population in Relation to Diet.

In the past, epidemiological studies focused on cavitated stages of caries. The arrival of the International Caries Detection and Assessment System (ICDAS) in 2004 allowed for clinical measurements of the initial stages of enamel caries. However, since the introduction, most studies applying the ICDAS still have studied the diseased population. The objective of this cross-sectional observational study was to describe early enamel caries in a large healthy young adult population and determine the relationship with diet and oral hygiene measures. The study population consisted of 268 healthy participants without frank cavitation. The examinations were done visually and radiographically using ICDAS on all tooth surfaces. In total, 8.6% of the surfaces (occlusal > approximal > smooth) had caries, of which 92.0% were confined to enamel (28.5% ICDAS score 1, 54.0% score 2, 8.6% score 3). Thirteen percent of the occlusal and 63% of the approximal caries were found with radiography. Thus, radiography is quintessential for the diagnosis of approximal enamel lesions. We found a positive correlation between enamel caries (ICDAS 1 to 3) and the consumption of mono- and disaccharides and carbohydrates ( r = 0.226 and r = 0.188, respectively, both P < 0.01), as well as a negative correlation with alcohol consumption ( r = -0.202, P < 0.01). There was also a positive correlation between enamel caries and the energy intake from mono- and disaccharides (sugar kJ, r = 0.206, P < 0.01), which was independent of body mass index. Only 11 participants consumed less than 10% of total energy as sugar kJ, which is the recommended percentage of kJ from free sugar by the World Health Organization. No clear correlation was found with oral hygiene. In conclusion, in this healthy young adult population, caries was found in 97.8% of the subjects, mostly initial enamel caries (ICDAS 1 to 2) in the occlusal surface of molars, and was related with dietary factors.

Family history of periodontal disease and prevalence of smoking status among adult periodontitis patients: a cross-sectional study.

OBJECTIVES: What is the family history of periodontal disease and the prevalence of smoking status among patients with professionally diagnosed periodontitis? Are these factors related to extent and severity of periodontitis? METHODS: Over a 10-year period, referred patients from a clinic for periodontology in the Netherlands were examined in a cross-sectional study. Patients received at the intake appointment a full-mouth periodontal examination. Data regarding family history of periodontitis and smoking status were recorded. RESULTS: A total of 5375 adult periodontitis patients were included in this study sample with a mean age of 50 years. The prevalence of smoking was 34% and 37% of the subjects had at least one parent or sibling with periodontitis. The chance to have severe periodontitis was higher if the patient was male, smoker or had a brother with periodontitis. Being male, smoker and having a parent with periodontitis were significantly associated with a larger extent of periodontitis. CONCLUSIONS: Within the investigated population familial aggregation, smoking status, age and gender are factors that were related to extent and severity of adult periodontitis.

Caloric restriction and the precision-control of autophagy: A strategy for delaying neurodegenerative disease progression.

Caloric restriction (CR) is known to extend lifespan in most organisms, indicating that nutrient and energy regulatory mechanisms impact aging. The greatest risk factor for neurodegeneration is age; thus, the antiaging effects of CR might attenuate progressive cell death and avert the aggregation of abnormal proteins associated with neurodegenerative diseases. CR is a potent inducer of autophagy, a tightly regulated intracellular process that facilitates recycling of abnormal protein aggregates and damaged organelles into bioenergetic and biosynthetic materials to maintain homeostasis. Thus, dysregulated autophagy can lead to cellular dysfunction, abnormal protein accumulation, proteotoxicity and subsequently the onset of several neurodegenerative diseases. Therefore, the targeted and precision-controlled activation of autophagy represents a promising therapeutic strategy. Non-pharmacological therapeutic interventions that delay aging by modulating specific stages of autophagy might be beneficial against premature aging, neurodegeneration and its associated ailments. However, the dynamic and often compensatory cross-talk that exists between the protein degradation pathways makes clinical translational approaches challenging. Here we review the primary autophagy pathways in the context of age-related neurodegenerative diseases, focusing on compensatory mechanisms and pathway failure. By critically assessing each underlying molecular machinery, we reveal their impact on aging and unmask the role of caloric restriction in changing cellular fate by delayed aging through stimulation of autophagy. This may point towards novel and better targeted interventions that exploit the autophagic machinery in the treatment of neurodegenerative diseases.

Microbial profiles at baseline and not the use of antibiotics determine the clinical outcome of the treatment of chronic periodontitis.

Antibiotics are often used in the treatment of chronic periodontitis, which is a major cause of tooth loss. However, evidence in favour of a microbial indication for the prescription of antibiotics is lacking, which may increase the risk of the possible indiscriminate use of antibiotics, and consequent, microbial resistance. Here, using an open-ended technique, we report the changes in the subgingival microbiome up to one year post-treatment of patients treated with basic periodontal therapy with or without antibiotics. Antibiotics resulted in a greater influence on the microbiome 3 months after therapy, but this difference disappeared at 6 months. Greater microbial diversity, specific taxa and certain microbial co-occurrences at baseline and not the use of antibiotics predicted better clinical treatment outcomes. Our results demonstrate the predictive value of specific subgingival bacterial profiles for the decision to prescribe antibiotics in the treatment of periodontitis, but they also indicate the need for alternative therapies based on ecological approaches.

Implementation process of all periodontal competences and assessments as proposed in the 2010 European consensus meeting into the existing local undergraduate curriculum.

AIM: To report on our implementation process within the existing local curriculum of all periodontal competences and assessments as proposed in the 2010 European consensus meeting. MATERIAL AND METHOD: In 2011, a workshop for all teaching staff at the Department of Periodontology, ACTA, an education and assessment blueprint, was developed to test for missing education and assessment of European competences, divided into seven domains. This was repeated in 2013. An oral evaluation of the staff followed both meetings. RESULTS: It appeared that eight of 58 (14%) European competences were not taught, and 21 (35%) competences were not assessed. After evaluation of the results on the actual curriculum and the assessment programme, shared decisions were made about how to teach and assess the missing competences within the local periodontal educational programme. The second workshop in 2013 revealed still 8 (14%) competences were not taught and 8 (14%) competences were not assessed. Staff appreciated the used method of validation; it gave insight and an overview of the curriculum. The existence of the European consensus report for undergraduate periodontal education, based on seven domains, has been instrumental and essential. CONCLUSION: The development of a blueprint from the education programme and concomitant assessment methods in periodontology by participating teaching staff gives a validation and appreciation of the curriculum and will improve the quality of education and assessment. It is advised that for quality control of the curriculum, dental schools could do this exercise for all their specialties if European consensus reports exist.