Role and relevance of dentists in a multiprofessional palliative care team: results of a cross-sectional survey study.

PURPOSE: Despite the multiprofessional concept surrounding palliative care patients (PCPs) and their high prevalence of oral issues, licensed dentists (LDs) are often not included in their treatment team. This study aimed to examine the current state of cooperation and to determine whether and how LDs should be included in the care for PCPs. METHODS: This single-centre cross-sectional study was conducted at the University Hospital Muenster, Germany. We surveyed three participant groups: PCPs, LDs, and healthcare professionals (HCPs). Questionnaires were tailored for each group, with some questions common for comparison. RESULTS: The study encompassed the results of 48 questionnaires from LDs, 50 from PCPs along with 50 from HCPs. Consensus was reached among all parties (LDs: 73% (n = 35/48); HCPs: 94%, n = 47/50; PCPs: 60%, n = 30/50) that involving LDs in the treatment concept is favourable. On the other hand, a significant discrepancy emerged in the perception of the dental treatment effort required by PCPs. While LDs (81%; n = 39/48) and HCPs (64%; n = 32/50) were convinced of increased effort, PCPs (34%; n = 17/50) largely did not share this perspective. To enhance patient care and formulate appropriate treatment plans, LDs consider both training (58%; n = 28/48) and guidebooks (71%; n = 34/48) to be valuable and would attend or use such resources. CONCLUSION: This study sheds light on the current gaps in including LDs in palliative care teams and emphasizes the importance of multidisciplinary collaboration to address oral health needs effectively. Development of continuing education options and collaborative models between LDs and HCPs needs to be further expanded in future.

Downregulation of interleukin 6 signaling might reduce the risk of periodontitis: a drug target Mendelian randomization study.

Aim: Interleukin 6 (IL-6) is considered to play a role in the dysbiotic host response in the development of periodontitis. While the inhibition of the IL-6 receptor using monoclonal antibodies is a well-established therapy for some diseases, so far, its potential benefit in patients with periodontitis has not been examined. We tested the association of genetically proxied downregulation of IL-6 signaling with periodontitis to explore whether downregulation of IL-6 signaling could represent a viable treatment target for periodontitis. Materials and methods: As proxies for IL-6 signaling downregulation, we selected 52 genetic variants in close vicinity of the gene encoding IL-6 receptor that were associated with lower circulating C-reactive protein (CRP) levels in a genome-wide association study (GWAS) of 575 531 participants of European ancestry from the UK Biobank and the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) consortium. Associations with periodontitis were tested with inverse-variance weighted Mendelian randomization in a study of 17 353 cases and 28 210 controls of European descent in the Gene-Lifestyle Interactions in Dental Endpoints (GLIDE) consortium. In addition, the effect of CRP reduction independent of the IL-6 pathway was assessed. Results: Genetically proxied downregulation of IL-6 signaling was associated with lower odds of periodontitis (odds ratio (OR) = 0.81 per 1-unit decrement in log-CRP levels; 95% confidence interval (CI): [0.66;0.99]; P = 0.0497). Genetically proxied reduction of CRP independent of the IL-6 pathway had a similar effect (OR = 0.81; 95% CI: [0.68; 0.98]; P = 0.0296). Conclusion: In conclusion, genetically proxied downregulation of IL-6 signaling was associated with lower odds of periodontitis and CRP might be a causal target for the effect of IL-6 on the risk of periodontitis.

Inhibition of tumor necrosis factor receptor 1 and the risk of periodontitis.

Aim: To investigate the effect of genetically proxied inhibition of tumor necrosis factor receptor 1 (TNFR1) on the risk of periodontitis. Materials and methods: Genetic instruments were selected from the vicinity of TNFR superfamily member 1A (TNFRSF1A) gene (chromosome 12; base pairs 6,437,923-6,451,280 as per GRCh37 assembly) based on their association with C-reactive protein (N= 575,531). Summary statistics of these variants were obtained from a genome-wide association study (GWAS) of 17,353 periodontitis cases and 28,210 controls to estimate the effect of TNFR1 inhibition on periodontitis using a fixed-effects inverse method. Results: Considering rs1800693 as an instrument, we found no effect of TNFR1 inhibition on periodontitis risk (Odds ratio (OR) scaled per standard deviation increment in CRP: 1.57, 95% confidence interval (CI): 0.38;6.46). Similar results were derived from a secondary analysis that used three variants (rs767455, rs4149570, and rs4149577) to index TNFR1 inhibition. Conclusions: We found no evidence of a potential efficacy of TNFR1 inhibition on periodontitis risk.

Association between bone turnover markers and periodontitis: A population-based cross-sectional study.

AIM: To examine the associations between bone turnover markers and periodontitis in two cross-sectional population-based studies. MATERIALS AND METHODS: We used data from two independent adult samples (N = 4993), collected within the Study of Health in Pomerania project, to analyse cross-sectional associations of N-procollagen type 1 amino-terminal propeptide (P1NP), C-terminal cross-linking telopeptide, osteocalcin, bone-specific alkaline phosphatase (BAP), fibroblast growth factor 23, wingless-type mouse mammary tumour virus integration site family member 5a (WNT5A), and sclerostin values with periodontitis. Confounder-adjusted gamma and fractional response regression models were applied. RESULTS: Positive associations were found for P1NP with mean pocket probing depth (PPD; eß=1.008 ; 95% confidence interval [CI]: 1.001-1.015), mean clinical attachment loss (mean CAL; eß=1.027 ; 95% CI: 1.011-1.044), and proportion of sites with bleeding on probing (%BOP; eß=1.055 ; 95% CI: 1.005-1.109). Similar associations were seen for BAP with %BOP ( eß=1.121 ; 95% CI: 1.042-1.205), proportion of sites with PPD ≥4 mm (%PPD4) ( eß=1.080 ; 95% CI: 1.005-1.161), and sclerostin with %BOP ( eß=1.308 ; 95% CI: 1.005-1.704). WNT5A was inversely associated with mean PPD ( eß=0.956 ; 95% CI: 0.920-0.993) and %PPD4 ( eß=0.794 ; 95% CI: 0.642-0.982). CONCLUSIONS: This study revealed scattered associations of P1NP, BAP, WNT5A, and sclerostin with periodontitis, but the results are contradictory in the overall context. Associations reported in previous studies could not be confirmed.

Understanding the consequences of educational inequalities on periodontitis: A Mendelian randomization study.

AIM: Higher educational attainment is associated with a lower risk of periodontitis, but the extent to which this association is causal and mediated by intermediate factors is unclear. MATERIALS AND METHODS: Using summary data from genetic association studies from up to 1.1 million participants of European descent, univariable and multivariable Mendelian randomization analyses were performed to infer the total effect of educational attainment on periodontitis and to estimate the degree to which income, smoking, alcohol consumption, and body mass index mediate the association. RESULTS: The odds ratio of periodontitis per 1 standard deviation increment in genetically predicted education was 0.78 (95% CI: 0.68-0.89). The proportions mediated of the total effect of genetically predicted education on periodontitis were 64%, 35%, 15%, and 46% for income, smoking, alcohol consumption, and body mass index, respectively. CONCLUSIONS: Using a genetic instrumental variable approach, this study triangulated evidence from existing observational epidemiological studies and suggested that higher educational attainment lowers periodontitis risk. Measures to reduce the burden of educational disparities in periodontitis risk may tackle downstream risk factors, particularly income, smoking, and obesity.

Body Fat Distribution and Risk of Breast, Endometrial, and Ovarian Cancer: A Two-Sample Mendelian Randomization Study.

BACKGROUND: Mounting evidence shows that adiposity increases female-specific cancer risk, but the role of body fat distribution is less clear. We used a two-sample Mendelian randomization (MR) approach to elucidate causal relations of body fat distribution to the risks of breast, endometrial and ovarian cancers and their subtypes. METHODS: Body composition was assessed using segmental bioelectrical impedance analysis, yielding trunk, arm, and leg fat ratios (TFR, AFR, LFR) and BMI including 195,043 and 434,794 European women, respectively. The sample sizes for the outcomes ranged between 58,396 and 228,951. Causal effects were estimated per one standard deviation increment in the respective exposure within the radial regression framework. Robust sensitivity analyses were performed to verify MR assumptions. In a multivariable MR setting, the proportion of risk attributable to overall and abdominal fat content was assessed. RESULTS: TFR, which represents abdominal fat content, was associated with ovarian cancer and its clear cell and endometrioid histotypes independent of overall fat content. BMI was inversely associated with breast cancer and its ER- and ER+ subtypes, but positively with endometrial cancer and ovarian cancer, including its endometrioid histotype. These estimates were confirmed using AFR as proxy for overall body fat. CONCLUSIONS: Visceral adiposity seems to be a driver of elevated ovarian cancer risk, particularly of the endometrioid and clear cell ovarian cancer histotypes. General adiposity decreases the risk of breast cancer but increases the risk of endometrial and ovarian cancer.

Cardiac MRI shows an association of lower cardiorespiratory fitness with decreased myocardial mass and higher cardiac stiffness in the general population - The Sedentary's Heart.

BACKGROUND: The heart has the capacity to adapt to different demands. The pathophysiological mechanisms involved with sedentarism are not fundamentally the opposite of those related with physical activity and regular exercise. We investigated the impact of lower cardiorespiratory fitness (CRF) on heart's plasticity and function in a population-based setting. METHODS: We used data from 1165 participants (539 women; 46.3%) aged 21-81 years from two independent cohorts of the Study of Health in Pomerania (SHIP-2 and SHIP-TREND-0). We analyzed the cross-sectional associations of peak oxygen uptake (VO2peak), determined by symptom-limited cardiopulmonary exercise testing, with structural and functional left ventricular (LV) and left atrial (LA) parameters determined by magnetic resonance imaging (MRI) using multivariable- adjusted linear regression models. RESULTS: A 1 L/min lower VO2peak was associated with a 10.5 g (95% confidence interval: 8.00 to 12.9; p < 0.001) lower LV mass, a 14.8 mL (10.9 to 18.6; p < 0.001) lower LV end-diastolic volume, a 0.29 mm (0.19 to 0.40; p < 0.001) lower LV wall-thickness, a 8.85 mL/beat (6.53 to 11.2; p < 0.001) lower LV stroke volume, a 0.42 L/min (0.25 to 0.60; p < 0.001) lower LV cardiac output and a 7.51 mL (3.88 to 11.1; p < 0.001) lower LA end-diastolic volume. Moreover, there were no associations with a concentric or eccentric remodeling and LV and LA ejection fraction. CONCLUSIONS: Lower CRF was associated with a smaller heart, LV wall-thickness and mass, LV and LA stroke volume and cardiac output. Conversely, there was no association with LA and LV ejection fraction. Our cross-sectional observations are consistent with cardiac adaptations reflecting reduced volume loading demands of a sedentary lifestyle - "the sedentary's heart".

Testing the association between tobacco smoking, alcohol consumption, and risk of periodontitis: A Mendelian randomization study.

AIM: To investigate the associations of tobacco smoking and alcohol consumption with periodontitis using Mendelian randomization (MR) analysis. MATERIALS AND METHODS: We used 17 single nucleotide polymorphisms (SNPs) as instrumental variables (IVs) for the number of cigarettes per day from a genome-wide association study (GWAS) of 337,334 individuals, 109 SNPs for a lifetime smoking index from GWAS of 462,690 participants, and 33 SNPs for the number of drinks per week from GWAS of 941,280 individuals. The periodontitis GWAS included 12,289 cases and 22,326 controls. Wald ratios were obtained by dividing the SNP-periodontitis effects by SNP-exposure effects and pooled using an inverse-variance weighted model. RESULTS: Genetic liabilities for higher number of cigarettes per day (odds ratio [OR] per one standard deviation (1SD) increment = 1.56; 95% CI: 1.18-2.07, p-value = .0018, Q-value = .0054), lifetime smoking index (OR per 1SD = 1.26; 95% CI: 1.04-1.53, p-value = .0161, Q-value = .0242), and drinks per week (OR per 1SD = 1.41; 95% CI: 1.04-1.90, p-value = .0265, Q-value = .0265) were associated with increased odds of periodontitis. Estimates were consistent across robust and multivariable MR analyses. CONCLUSIONS: The findings of this MR analysis suggest an association between tobacco smoking and alcohol consumption with periodontitis.

Cannabis Use, Pulmonary Function, and Lung Cancer Susceptibility: A Mendelian Randomization Study.

INTRODUCTION: Because of widespread use, understanding the pulmonary effects of cannabis use is important; but its role independent from tobacco smoking is yet to be elucidated. We used Mendelian randomization (MR) to assess the effect of genetic liability to lifetime cannabis use and cannabis use disorder on pulmonary function and lung cancer. METHODS: We used four single nucleotide polymorphisms associated with lifetime cannabis use (p value <5 × 10-8) from a genome-wide association study (GWAS) of 184,765 individuals of European descent from the International Cannabis Consortium, 23andme, and U.K. Biobank as instrumental variables. Seven single nucleotide polymorphisms (p value <5 × 10-8) were selected as instruments for cannabis use disorder from a GWAS meta-analysis of 17,068 European ancestry cases and 357,219 controls of European descent from Psychiatric Genomics Consortium Substance Use Disorders working group, Lundbeck Foundation Initiative for Integrative PsychiatricResearch, and deCode. To assess lung function, GWAS included 79,055 study participants of the SpiroMeta Consortium, and for lung cancer GWAS from the International Lung Cancer Consortium contained 29,266 cases and 56,450 controls. RESULTS: MR revealed that genetic liability to lifetime cannabis use was associated with increased risk of squamous cell carcinoma (OR = 1.22, 95%, confidence interval = 1.07-1.39, p value = 0.003, q value = 0.025). Pleiotropy-robust methods and positive and negative control analyses did not indicate bias in the primary analysis. CONCLUSIONS: The findings of this MR analysis suggest evidence for a potential causal association between genetic liability for cannabis use and the risk of squamous cell carcinoma. Triangulating MR and observational studies and addressing orthogonal sources of bias are necessary to confirm this finding.

Physical Activity Does Not Lower the Risk of Lung Cancer.

Observational studies have suggested that physical activity might lower the risk of lung cancer in former and current smokers, but not in never-smokers. Using genetic instruments for self-reported and accelerometer-measured physical activity traits implemented through two-sample Mendelian randomization (MR), we sought to strengthen the evidence for causality. We used 18 genome-wide significant (P < 5 × 10-8) single-nucleotide polymorphisms (SNP) for self-reported moderate-to-vigorous physical activity and seven SNP for accelerometer-measured ("average acceleration") physical activity from up to 377,234 UK Biobank participants and evaluated these in relation to risk using 29,266 lung cancer cases (including 11,273 adenocarcinomas, 7,426 squamous cell carcinoma, and 2,664 small-cell carcinoma cases) and 56,450 controls. MR analysis suggested no effect of self-reported physical activity [OR (95% confidence interval (CI)) = 0.67 (0.42-1.05); P = 0.081; Q-value = 0.243] and accelerometer-measured activity [OR (95% CI) = 0.98 (0.93-1.03); P = 0.372; Q-value = 0.562] on lung cancer. There was no evidence for associations of physical activity with histologic types and lung cancer in ever and never smokers. Replication analysis using genetic instruments from a different genome-wide study and sensitivity analysis to address potential pleiotropic effects led to no substantive change in estimates. Collectively, these findings do not support a protective relationship between physical activity and the risk of lung cancer. SIGNIFICANCE: A new genetic study provides little evidence that recommending physical activity would help prevent lung cancer.

Glucose and insulin levels are associated with arterial stiffness and concentric remodeling of the heart.

BACKGROUND: Mortality attributable to heart failure remains high. The prevalence of heart failure in patients with diabetes mellitus ranges from 19 to 26%. It is estimated that up to 21.1 million adults in the United States have diagnosed diabetes mellitus and around 80.8 million have impaired fasting glucose. We investigated the associations of fasting glucose (FG) and fasting insulin (FI), the homeostasis model assessment-insulin resistance index (HOMA-IR) and 2-h postload glucose (2HG) and insulin (2HI) with parameters of left ventricular geometry and function and arterial stiffness determined by magnetic resonance imaging in individuals without diagnosed type 2 diabetes. METHODS: Cross-sectional analyses of 1001 individuals (453 women, 45.3%), aged 21 to 80 years, from two independent population-based studies, the Study of Health in Pomerania (SHIP-TREND-0) and KORA FF4 Study. FG, FI, HOMA-IR, 2HG and 2HI, as well as glucose tolerance categories, were analyzed for associations with heart and arterial parameters using multivariable-adjusted linear regression models. RESULTS: In total, 390 individuals (39%) had prediabetes (isolated impaired fasting glucose, isolated glucose tolerance or both), and 49 (4.9%) were found to have unknown type 2 diabetes. In the multivariable-adjusted analysis, positive linear associations of FG, FI, HOMA-IR, 2HG and 2HI with arterial stiffness index and left ventricular wall-thickness and concentricity and inverse linear associations with left ventricular end-diastolic volume were observed. A 1 mmol/l higher FG was associated with a 1.18 ml/m2.7 (1.80 to 0.57; p < 0.001) lower left ventricular end-diastolic volume index, a 0.042 mm/m2.7 (0.014 to 0.070) higher left ventricular wall-thickness index, a 0.12 mmHg m2.7/ml (0.06 to 0.17; p < 0.001) greater arterial stiffness index and a 0.037 g/ml (0.018 to 0.056; p < 0.001) higher left ventricular concentricity. CONCLUSIONS: Our findings suggest that higher glucose levels in the prediabetic range and insulin resistance might lead to higher arterial stiffness and concentric remodeling of the heart.

[Prevalence of Cardiovascular Risk Factors at The Population Level: A Comparison of Ambulatory Physician-Coded Claims Data With Clinical Data From A Population-Based Study]. / Untersuchung der Prävalenz kardiologischer Risikofaktoren in der Allgemeinbevölkerung: Ein Vergleich ambulanter ärztlicher Abrechnungsdaten mit Daten einer populationsbasierten Studie.

OBJECTIVE: The study assesses the validity of ICD-10 coded cardiovascular risk factors in claims data using gold-standard measurements from a population-based study for arterial hypertension, diabetes, dyslipidemia, smoking and obesity as a reference. METHODS: Data of 1941 participants (46 % male, mean age 58±13 years) of the Study of Health in Pomerania (SHIP) were linked to electronic medical records from the regional association of statutory health insurance physicians from 2008 to 2012 used for billing purposes. Clinical data from SHIP was used as a gold standard to assess the agreement with claims data for ICD-10 codes I10.- (arterial hypertension), E10.- to E14.- (diabetes mellitus), E78.- (dyslipidemia), F17.- (smoking) and E65.- to E68.- (obesity). RESULTS: A higher agreement between ICD-coded and clinical diagnosis was found for diabetes (sensitivity (sens) 84%, specificity (spec) 95%, positive predictive value (ppv) 80%) and hypertension (sens 72%, spec 93%, ppv 97%) and a low level of agreement for smoking (sens 18%, spec 99%, ppv 89%), obesity (sens 22%, spec 99%, ppv 99%) and dyslipidemia (sens 40%, spec 60%, ppv 70%). Depending on the investigated cardiovascular risk factor, medication, documented additional cardiovascular co-morbidities, age, sex and clinical severity were associated with the ICD-coded cardiovascular risk factor. CONCLUSION: The quality of ICD-coding in ambulatory care is highly variable for different cardiovascular risk factors and outcomes. Diagnoses were generally undercoded, but those relevant for billing were coded more frequently. Our results can be used to quantify errors in population-based estimates of prevalence based on claims data for the investigated cardiovascular risk factors.

Light to Moderate Alcohol Consumption Is Associated With Lower Risk of Aortic Valve Sclerosis: The Study of Health in Pomerania (SHIP).

OBJECTIVE: In developed countries, sclerotic and calcific degeneration of the aortic valve is a common disorder showing pathophysiologic similarities with atherothrombotic coronary disease. Light to moderate alcohol consumption has been associated with a lower risk for atherothrombotic coronary disease and mortality. Whether alcohol consumption affects the development of aortic valve sclerosis (AVS) is not well known. In the present study, we aim to analyze the cross-sectional association between average daily alcohol consumption and AVS in the general population. APPROACH AND RESULTS: We analyzed cross-sectional data from 2022 men and women, aged 45 to 81 years, from the population-based Study of Health in Pomerania. We used a computer-assisted interview that included beverage-specific questions about quantity and frequency of alcohol over the last 30 days to calculate the average quantity of alcohol consumption (in grams of ethanol per day). AVS was ascertained by echocardiography. The prevalence of AVS was 32.3%. Average daily alcohol intake displayed a J-type relation with AVS (fully adjusted P value: 0.005). Compared with individuals with an average consumption of 10 g of alcohol per day, multivariable-adjusted odds ratios were 1.60 (95% confidence interval, 1.19-2.14) among current abstainers and 1.56 (95% confidence interval, 1.01-2.41) among individuals with an average consumption of 60 g per day. CONCLUSIONS: Our findings indicate that light to moderate alcohol consumption was associated with a lower odd of having AVS. Prospective data need to address whether alcohol consumption and related changes over time in several biological markers affect the progression of AVS.

Effects of smoking on arterial distensibility, central aortic pressures and left ventricular mass.

BACKGROUND: The effects of smoking on central aortic pressures and the age-related increase in left ventricular mass (LVM) are largely unknown. We studied the relationship between smoking, arterial distensibility, central aortic pressures and left ventricular mass in two population-based studies. METHODS: Data was obtained from two German population-based studies (KORA and SHIP, participants' ages 25-84 years). We identified 114 normotensive current smokers and 185 normotensive all-time non-smokers in KORA as well as 400 and 588 such individuals in SHIP. Echocardiographic LVM was obtained at baseline (T0) and follow-up after ten years (T1) in KORA and at follow-up (T1) in SHIP. Additionally, pulse-wave analysis-based central aortic pressure and augmentation index (AIx) were measured at T1 in KORA. RESULTS: Cross-sectional analysis, using KORA T0 and SHIP T1, revealed in both studies a higher covariate-adjusted LVM and left ventricular mass index (LVMI) in smokers as compared with non-smokers. Moreover, in the KORA T1 examination, the smokers demonstrated a more pronounced increase, relative to baseline, of LVM (+13.5%) and LVMI (+13.4%) compared to non-smokers (+8.59% and +8.65%; p=0.036 and 0.042, respectively). Additionally, at KORA T1 smokers had a higher central systolic blood pressure and higher AIx than non-smokers (p=0.012 and p=0.001, respectively). CONCLUSIONS: The difference in central aortic pressure due to enhanced and more prolonged wave reflection may explain our finding of a further pronounced increase in left ventricular wall thickness and mass over time in smokers.