Transcriptomics and methylomics in chronic periodontitis with tobacco use: a pilot study

Cho, Young‐Dan; Kim, Pil-Jong; Kim, Hong-Gee; Seol, Yang‐Jo; Lee, Yong-Moo; Rhyu, In‐Chul; Ryoo, Hyun‐Mo

doi:10.1186/s13148-017-0381-z

Cited by 25 publications

(42 citation statements)

References 41 publications

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“…It is known that smokers and males are at risk for the development of periodontitis [38–46]. Smoking tobacco was an epigenetic factor and may change the transcription and methylation states of extracellular matrix organization-related genes, which exacerbate the periodontal condition [47]. In our study, smokers with periodontitis were more frequent (40.4%) than the total population of Brazilian smokers, which accounts for 17.2% [48].…”

Section: Discussionmentioning

confidence: 68%

The Influence ofTLR4,CD14,OPG, andRANKLPolymorphisms in Periodontitis: A Case-Control Study

Zacarias

Alencar

Tsuneto

et al. 2019

Mediators of Inflammation

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The pathogenesis of periodontitis involves a complex interaction between the microbial challenge and the host immune response. The individual immunoinflammatory response has a great contribution in the pathogenesis of the disease and becomes a trigger in the process of bone remodeling which is a characteristic of the disease. Thus, the aim of this study was to evaluate the influence of the TLR4 A896G (rs4986790), TLR4 C1196T (rs4986791), CD14 C-260T (rs2569190), RANKL (TNFSF11, rs2277438), and OPG (TNFSF11B C163T, rs3102735) polymorphisms in periodontitis. A case-control study was conducted on patients with periodontitis (N=203) and controls (N=213) over 30 years of age, without diabetes mellitus, acute infections, and osteoarthritis, and patients without aggressive periodontitis, i.e., stage IV and C degree of periodontitis, and any periodontal treatment performed in the last 6 months. Genotypes were determined by the PCR-RFLP and sequencing method. The frequency comparisons between case and controls were performed using the chi-square test and logistic regression (OpenEpi and SNPStats software). The risk (OR) was evaluated for values of P<0.05. Differences in TLR4, CD14, RANKL, and OPG genotype and allele frequency distributions were not observed between patients and controls. However, some variants were a risk factor for the development of periodontitis when considering gender and smoking habits. The TLR4 896 A/G genotype was a risk factor for periodontitis in males (OR=2.86), and the TLR4 1196C/C genotype was a risk factor for nonsmoking males (OR=1.85) when compared to women. The RANKL A/A and the OPG T/C genotype was associated with the risk of the disease in nonsmoking men compared to nonsmoking women with the same genotype (OR=1.96 and OR=2.9, respectively). In conclusion, TLR4, CD14, RANKL, and OPG variants were not associated with periodontitis. However, TLR4, RANKL, and OPG polymorphisms could be a risk for periodontitis in males regardless of smoking habits.

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Section: Discussionmentioning

confidence: 68%

The Influence ofTLR4,CD14,OPG, andRANKLPolymorphisms in Periodontitis: A Case-Control Study

Zacarias

Alencar

Tsuneto

et al. 2019

Mediators of Inflammation

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“…environmental factors (4,(26)(27)(28)(29)(30), with methylation/demethylation as a pivotal mechanism (31,32).…”

Section: Discussionmentioning

confidence: 99%

Colorectal cancer-associated microbiota contributes to oncogenic epigenetic signatures

Sobhani

Bergsten

Couffin

et al. 2019

Proc. Natl. Acad. Sci. U.S.A.

167

146

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Sporadic colorectal cancer (CRC) is a result of complex interactions between the host and its environment. Environmental stressors act by causing host cell DNA alterations implicated in the onset of cancer. Here we investigate the stressor ability of CRC-associated gut dysbiosis as causal agent of host DNA alterations. The epigenetic nature of these alterations was investigated in humans and in mice. Germ-free mice receiving fecal samples from subjects with normal colonoscopy or from CRC patients were monitored for 7 or 14 wk. Aberrant crypt foci, luminal microbiota, and DNA alterations (colonic exome sequencing and methylation patterns) were monitored following human feces transfer. CRC-associated microbiota induced higher numbers of hypermethylated genes in murine colonic mucosa (vs. healthy controls’ microbiota recipients). Several gene promoters including SFRP1,2,3, PENK, NPY, ALX4, SEPT9, and WIF1 promoters were found hypermethylated in CRC but not in normal tissues or effluents from fecal donors. In a pilot study (n = 266), the blood methylation levels of 3 genes (Wif1, PENK, and NPY) were shown closely associated with CRC dysbiosis. In a validation study (n = 1,000), the cumulative methylation index (CMI) of these genes was significantly higher in CRCs than in controls. Further, CMI appeared as an independent risk factor for CRC diagnosis as shown by multivariate analysis that included fecal immunochemical blood test. Consequently, fecal bacterial species in individuals with higher CMI in blood were identified by whole metagenomic analysis. Thus, CRC-related dysbiosis induces methylation of host genes, and corresponding CMIs together with associated bacteria are potential biomarkers for CRC.

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“…Smoking can influence the oral environment by inducing hypoxia, lowering the periodontal redox potential and affecting the subgingival micro-environment, which is beneficial to the survival of anaerobic bacteria 37 . Smoking may alter the transcription and methylation status of extracellular matrix-related genes, which may exacerbate periodontitis 38 .…”

Section: Oral Environmentmentioning

confidence: 99%

Smoking increases the risk of infectious diseases: A narrative review

Chen¹,

Chen²,

Xie³

2020

Tob. Induc. Dis.

112

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Smoking is one of the most severe public health problems in the world. According to the WHO Global report on trends in prevalence of tobacco use 2000-2025, smoking accounts for 9% of all deaths worldwide, and more than half of smokers die from smoking-related diseases 1. China is the largest producer and consumer of tobacco in the world. In 2018, about 26.6% of adults (aged ≥15 years; 308 million in total) were current smokers and 44.9% of adults (515 million) were exposed to secondhand smoke at home 1. Exposure to cigarette smoke and secondhand smoke is very harmful to human health. There are over 7000 chemical components in tobacco smoke, of these, over 250 are toxic or carcinogenic, such as aldehydes, nitrides, and others that irritate the respiratory tract. Nicotine leads to tobacco addiction; benzpyrene, arsenic, cadmium and other components have carcinogenic effects and nitric oxide can reduce oxygen transport by erythrocytes. Smoking can damage nearly all organs of the human body and is one of the main risk factors for respiratory infection and infectious diseases in other systems, in a dose-dependent manner 2,3. In this review, we discuss the mechanisms and influence of smoking on infections in various systems, including the respiratory system, digestive system, and genital system, among others, in order to provide evidence for the active promotion of smoking cessation. DEVELOPMENTS Mechanisms of susceptibility The potential mechanisms of how cigarette smoke increases the risk of systemic infections are not completely understood. These may include alteration ABSTRACT Smoking is relevant to infectious diseases resulting in increased prevalence and mortality. In this article, we aim to provide an overview of the effects of smoking in various infections and to explain the potential mechanisms. We searched PubMed and other relevant databases for scientific studies that explored the relationship between smoking and infection. The mechanisms of susceptibility to infection in smokers may include alteration of the structural, functional and immunologic host defences. Smoking is one of the main risk factors for infections in the respiratory tract, digestive tract, reproductive tract, and other systems in humans, increasing the prevalence of HIV, tuberculosis, SARS-CoV, and the current SARS-CoV-2. Smoking cessation can reduce the risk of infection. Smoking increases the incidence of infections and aggravates the progress and prognosis of infectious diseases in a dose-dependent manner. Smoking cessation promotion and education are the most practical and economical preventive measures to reduce aggravation of disease infection owing to tobacco use.

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Transcriptomics and methylomics in chronic periodontitis with tobacco use: a pilot study

Cited by 25 publications

References 41 publications

The Influence ofTLR4,CD14,OPG, andRANKLPolymorphisms in Periodontitis: A Case-Control Study

The Influence ofTLR4,CD14,OPG, andRANKLPolymorphisms in Periodontitis: A Case-Control Study

Colorectal cancer-associated microbiota contributes to oncogenic epigenetic signatures

Smoking increases the risk of infectious diseases: A narrative review

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