AimsOur aims were to evaluate the distribution of troponin I concentrations in population cohorts across Europe, to characterize the association with cardiovascular outcomes, to determine the predictive value beyond the variables used in the ESC SCORE, to test a potentially clinically relevant cut-off value, and to evaluate the improved eligibility for statin therapy based on elevated troponin I concentrations retrospectively.Methods and resultsBased on the Biomarkers for Cardiovascular Risk Assessment in Europe (BiomarCaRE) project, we analysed individual level data from 10 prospective population-based studies including 74 738 participants. We investigated the value of adding troponin I levels to conventional risk factors for prediction of cardiovascular disease by calculating measures of discrimination (C-index) and net reclassification improvement (NRI). We further tested the clinical implication of statin therapy based on troponin concentration in 12 956 individuals free of cardiovascular disease in the JUPITER study. Troponin I remained an independent predictor with a hazard ratio of 1.37 for cardiovascular mortality, 1.23 for cardiovascular disease, and 1.24 for total mortality. The addition of troponin I information to a prognostic model for cardiovascular death constructed of ESC SCORE variables increased the C-index discrimination measure by 0.007 and yielded an NRI of 0.048, whereas the addition to prognostic models for cardiovascular disease and total mortality led to lesser C-index discrimination and NRI increment. In individuals above 6 ng/L of troponin I, a concentration near the upper quintile in BiomarCaRE (5.9 ng/L) and JUPITER (5.8 ng/L), rosuvastatin therapy resulted in higher absolute risk reduction compared with individuals <6 ng/L of troponin I, whereas the relative risk reduction was similar.ConclusionIn individuals free of cardiovascular disease, the addition of troponin I to variables of established risk score improves prediction of cardiovascular death and cardiovascular disease.

The relationship between cigarette smoking and periodontal destruction was assessed in young adults. Eighty-two regular dental attenders (21 current cigarette smokers, 61 non-smokers) aged between 20 and 33 years were examined. The smokers consumed on average 15.4 (+/- 7.3) cigarettes per day and had smoked for an average of 11.8 (+/- 7) years. Cigarette smokers had almost the same levels of plaque as non-smokers but had more proximal surfaces with subgingival calculus (P < 0.01) and which bled on probing (P < 0.05). Smokers had significantly more pockets > or = 4 mm (14.6 +/- 19.9) than non-smokers (5.8 +/- 7.9), P < 0.01. Only 2 (10%) of the smokers and 1 (2%) of the non-smokers had deep pocketing (> or = 6 mm). Smokers had significantly more sites (21.8 +/- 24.9) with periodontal attachment loss of > or = 2 mm than non-smokers (9.3 +/- 12.2), P < 0.01. Severe loss of periodontal attachment (> or = 6 mm) was present in 4 (19%) of smokers compared with 2 (3%) of non smokers. In total 4 (19%) of the smokers had "established periodontitis" compared with 1 (2%) of the non-smokers. The odds ratio for the presence of "established periodontitis" and smoking was 14.1 (confidence interval 1.5 to 132.9). It is concluded that cigarette smoking was a major environmental factor associated with accelerated periodontal destruction in this selected group of young adult regular dental attenders.

The aims of the present study were to investigate whether the tachykinins substance P and neurokinin A were present in gingival crevicular fluid in both periodontal health and disease and to study the relationship with periodontal inflammation. Gingival crevicular fluid (GCF) was collected from a healthy, a gingivitis and a periodontitis site in 20 subjects with periodontitis and from a healthy site in 20 subjects without periodontitis. The volume of GCF was measured and each sample subsequently analysed for substance P and neurokinin A by radioimmunoassay. There were significantly increased levels of substance P-like immunoreactivity (SP-LI) and neurokinin A-like immunoreactivity (NKA-LI) in gingivitis and periodontitis sites compared with healthy sites. Both tachykinins were significantly elevated in periodontitis affected subjects, with significantly more tachykinin-like immunoreactivity at healthy sites in periodontitis affected compared with periodontally-healthy subjects. Despite the considerable individual variation in the levels of SP-LI and NKA-LI, both tachykinins were present at levels at which they could have biological activity. It is concluded that substance P and neurokinin A may have a rôle in the pathogenesis of periodontal disease and that further investigations could prove useful in clarifying the mechanisms through which neuropeptides could modulate periodontal health and disease.

Purpose of ReviewThe aim was to assess recent evidence that diabetes, metabolic syndrome (MetS) and obesity impact the progression of periodontitis.Recent FindingsElectronic searches using Embase, Medline, and Web of Science were carried out for epidemiological studies on humans, published between 2014 and 2016. A small number of prospective studies and systematic reviews were identified that in general provide further support for the hypothesis that diabetes, metabolic syndrome and obesity can adversely affect the periodontal condition.SummaryConfounding remains the most challenging issue in the interpretation of the associations found between diabetes, MetS, obesity and periodontal disease. Recent research applying a Mendelian randomisation approach concluded that the association between obesity and periodontitis is confounded and questioned a role for obesity in causation. Further studies are warranted to assess the issue of causality.

This study examined the association between occupational stress and the progression of periodontitis in employed adults. 23 regular dental attenders, enrolled in a longitudinal study of periodontal disease, were examined on 2 occasions at an interval of 5.5 (SD 0.6) years. The mean age at the 2nd examination was 41.1 (SD 7.3) years. Clinical measurements of periodontal status including clinical attachment level were made at four proximal sites on all teeth. A questionnaire, the occupational stress indicator, was used at the second examination to assess stress retrospectively. The mean change in clinical attachment level was 0.63 (SD 0.42) mm and 9.6 (SD 8.6)% of sites measured at both examination lost > or = 3 mm of periodontal attachment. Multiple regression analysis was used to explore the relationship between mean loss of periodontal attachment and measures of occupational stress and sociodemographic data. In the final regression model, an increase in loss of periodontal attachment was significantly predicted by increasing age, lower socio-economic status, lower job satisfaction and type A personality. In addition, locus of control was included in the regression model which explained 65% of the variance in the loss of periodontal attachment. The results suggest that occupational stress may have a relationship to the progression of periodontitis.

This study investigated the extent of and reasons for variation in the periodontal referral patterns of general dental practitioners in Northern Ireland. A questionnaire was circulated to all general dental practitioners in Northern Ireland. This questionnaire investigated the management of periodontal disease in the general dental service and referral for specialist periodontal advice and treatment. A usable return was made by 355 (68%) of those surveyed. The mean number of periodontal referrals by each respondent in the past year was 6.5 (SD 7.7), range 0 to 80. Backward stepwise logistic regression analysis indicated that independent predictors of high referral rate were practice location close to the referral centre (p<0.0001); dissatisfaction with ability to treat periodontal disease under the National Health Service (p=0.001); that previous refusals of referral had not dissuaded a dentist from continuing to offer referral (p=0.002); not offering root planing as a treatment (p=0.005); and perceived inadequate postgraduate education in periodontology (p=0.03). It is concluded that considerable variation exists between general dental practitioners working in Northern Ireland in relation to the referral of patients for specialist periodontal advice and treatment. It is further concluded that in many cases non-disease factors, such as the accessibility of the specialist service, have powerful effects on the decisions made by dentists and patients in relation to periodontal referral.

Objectives:To investigate periodontitis as a risk factor for incident type 2 diabetes mellitus (T2DM) in a group of men aged 58-72 years. Accepted ArticleThis article is protected by copyright. All rights reserved. Methods:1331 dentate, diabetes-free males in Northern Ireland underwent a detailed periodontal examination during [2001][2002][2003]. Follow-up was by bi-annual questionnaire and for those reporting diabetes their general medical practitioner was contacted to validate diabetes type, treatment and diagnosis date. Cox's proportional hazard models were used to estimate the effect of periodontitis on incident diabetes. Multivariable analysis included adjustment for various known confounders. Results:The mean age of the men was 63.7 (SD 3.0) years. There were 80 cases (6.0%) of incident T2DM. Follow-up was for a median period of 7.8 years ). After adjusting for confounding variables, the hazard ratio (HR) for incident T2DM in men with moderate / severe periodontitis versus those with no / mild periodontitis was 1.69 (95% CI 1.06-2.69), p=0.03. Conclusion:There was evidence in this homogenous group of dentate men, that those with moderate to severe periodontitis had a significantly increased risk of incident T2DM. Clinical Relevance Scientific rational for the study:Evidence supporting the role of chronic periodontitis as a putative risk factor for the development of type 2 diabetes mellitus (T2DM) is currently limited. Principal findings: Accepted ArticleThis article is protected by copyright. All rights reserved.This study showed that in a group of 58-72 year-old Caucasian dentate men in Northern Ireland, baseline moderate to severe periodontitis was an independent risk predictor for the development of T2DM. This relationship was independent of known confounders. Practical implications:Dentists should be aware of the potential systemic health implications of patients presenting with moderate to severe periodontitis. Patients who present with obvious risk factors for T2DM and signs of periodontitis should be informed about their risk for developing T2DM.

The aim of this study was to investigate the presence of substance P (SP), neurokinin A (NKA) and calcitonin gene-related peptide (CGRP) in the gingival crevicular fluid of teeth diagnosed with pain of pulpal origin compared with clinically healthy teeth, and to detect any changes in the levels of these neuropeptides in gingival crevicular fluid after removal of the pulp from the painful teeth. Gingival crevicular fluid was collected at baseline from one interproximal site at a painful and a non-painful contralateral tooth from 54 adult patients. Sampling was repeated after 1 wk in a subset of 21 subjects. Samples were analysed for SP, NKA, and CGRP using radioimmunoassay. The mean levels of SP and NKA were significantly higher in gingival crevicular fluid from painful teeth compared with non-painful teeth. The level of SP in the GCF of painful teeth fell significantly 1 wk after pulpectomy. In contralateral teeth, there were no significant differences in the levels of SP and NKA after 1 wk. It is concluded that SP and NKA are present in significantly greater amounts in the GCF of painful teeth compared with healthy teeth.