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If you don't brush your teeth, it's really terrible! The latest research: These bacteria in the mouth may increase the risk of heart disease

Usually, people brush their teeth 2 to 3 times a day. But there are always people who are lazy, such as brushing in the morning and missing the evening time, and in the long run, there will naturally be various oral problems, such as toothache and inflammation.

In fact, dental problems are not trivial, and their health problems are not as simple as everyone thinks! As the saying goes: a toothache is not a disease, it hurts really badly! Dental health is strongly linked to a wide range of diseases – a previous long-term follow-up of 160,000 people over 10 years showed that frequent brushing and regular scaling were associated with a reduced risk of atrial fibrillation and heart failure.

Recently, a study from the Swiss Federal Institute of Technology in Lausanne showed that infection with bacteria that cause gum disease and bad breath may increase the risk of heart disease. The study, titled "Associations of genetic and infectious risk factors with coronary heart disease," was published in the journal elife.

If you don't brush your teeth, it's really terrible! The latest research: These bacteria in the mouth may increase the risk of heart disease

1. Research background

Coronary heart disease (CHD), the most common type of heart disease, is caused by atherosclerosis (atherosclerosis, plaque that forms within the walls of the arteries that supply blood to the heart). Several clinical studies have identified inflammatory risk factors that predict future cardiovascular events, such as endothelial dysfunction and subintimal cholesterol that have been shown to trigger an inflammatory cascade involving activated macrophages and leading to atherosclerotic lesions.

Nearly 150 years ago, it was discovered that acute infection with Typhoid bacillus causes sclerotic changes in artery walls. Subsequently, several other infectious agents were associated with coronary heart disease, including bacteria and viruses such as Helicobacter pylori (H. pylori), hepatitis C virus (HCV), and human herpesvirus.

Although existing research has made great progress in understanding the pathogenesis of coronary heart disease, the combined and overall picture of the combined impact of infection, inflammation, and genetic factors on the risk of coronary heart disease in the general population remains incomplete. This study used a study from CoLaus| Data from the PsyCoLaus study, a well-characterized longitudinal population study from Switzerland to more fully investigate the impact of these factors on coronary heart disease.

2. Research methods

1. Study cohorts

CoLaus| The PsyCoLaus study is a population-based longitudinal study initiated in Lausanne in 2003; It studies the biological, environmental, and genetic determinants of cardiovascular disease (CVD). The study involved more than 6,500 participants of European ancestry, who were randomly recruited from the general population, representing about 10% of the sample of Lausanne citizens. Of the participants, 47.5% were male and enrolled between 35 and 75 years old. Study participants provided detailed phenotypic information through questionnaires, interviews, and clinical and biological data. Nuclear DNA was also extracted from blood for genome-wide genotyping data. Every 5 years, follow-up interviews were conducted on participants' lifestyle and health status. Three follow-up visits were completed and the fourth began in January 2022.

2. Cardiovascular phenotype

The researchers formed an independent panel of experts to collect and evaluate the medical records of participants who had reported coronary heart disease events over their lifetime. During the study, information on the causes of death of participants was prospectively collected.

3. DNA genotyping data and PRS calculations for cardiovascular phenotypes

BB2 GSK's custom-made Affymetrix Axiom Biobank array was used to genotype DNA samples from 5399 participants, including approximately 800,000 single nucleotide polymorphisms (SNPs). After genotype aggregation and quality control procedures, approximately 9 million SNPs are available for analysis. The researchers then calculated CHD-PRS for each study participant based on the risk impact of common SNPs.

4. Coronary heart disease risk assessment

Each participant's coronary heart disease risk was also assessed using the recent SCORE2 and SCORE2-Older Persons (SCORE2-OP, for individuals >65 years age) algorithms. These two algorithms will be called SCORE2.

SCORE2 is derived, calibrated and validated using data from more than 50 European prospective studies and 13 million people in national registries to predict the risk of a 10-year first CVD. To develop this algorithm, the researchers used competitive risk-adjusted models and age- and sex-specific models, including age, current smoking, systolic blood pressure, and total cholesterol, low-density lipoprotein (LDL), and high-density lipoprotein (HDL) cholesterol. In addition, the researchers defined four risk regions in Europe based on CVD mortality in specific countries.

5. Detection of inflammatory biomarkers

Venous blood samples (50 mL) were drawn from fasting participants. Prior to cytokine evaluation, serum blood samples are stored at -80 °C and then sent to the laboratory with dry ice. Flow cytokine levels of hs-CRP, IL-1β, IL-6, and TNF-α were detected.

6. Serological analysis

The pathogens studied included 15 viruses (BKV, JCV, HPyV6, WUPyV, HSV-1, HSV-2, VZV, EBV, CMV, HHV-6A, HHV-6B, HHV-7, KSHV, PVB-19, and rubella virus); Six species of bacteria (C. Diphteriae, C. tetani, C. trachomatis, F. nucleatum, H. pylori, and S. gallolyticus); and a parasite (Toxoplasma gondii).

7. Statistical analysis

In CoLaus| In the PsyCoLaus study, the relationship between risk factors and the incidence of coronary heart disease was explored using univariate and multivariate Cox proportional hazard models. To determine potential confounding caused by demographics, the researchers also tested the association of the first three major genetic components (PC1, PC2, and PC3) with CHD.

3. Research results

The researchers examined the serological status of the participants against 22 human pathogens. However, rubella, Clostridium tetani, and Clostridium diphtheria were excluded from further analysis, as detectable antibodies against these pathogens are likely to be caused by vaccination.

If you don't brush your teeth, it's really terrible! The latest research: These bacteria in the mouth may increase the risk of heart disease

Once the results of known cardiovascular risk factors were adjusted, the researchers found that antibodies against Fusobacterium nucleatum (signs of previous or current infection with the bacterium) were associated with a slightly increased risk of cardiovascular events. Anti-Fusobacterium nucleatus may increase systemic inflammation through bacteria present in the mouth, or increase cardiovascular risk by colonizing plaque in and within the artery wall.

IV. Summary

Cardiovascular disease is a multifactorial disease caused by demographic, environmental and genetic factors, and inflammation caused by persistent or frequent recurrent infections may contribute to its development. After adjusting for all identified risk factors, the researchers found a statistically significant association between the incidence of coronary heart disease and Fusobacterium nucleatum infection. In addition, the researchers also confirmed that the polygenic risk of CVD individuals calculated according to genome-wide genotypes represents an independent risk factor for coronary heart disease events. The results of this study will help to better identify people at high risk of coronary heart disease and inform future anti-infection prevention trials.

Source: https://elifesciences.org/articles/79742#s3

Written by: Catherine

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