Cellular expression of epigenetic markers and oxidative stress in periodontitis lesions of smokers and non‐smokers

Abstract

Objective To evaluate differences in the cellular expression of epigenetic markers and oxidative stress in periodontitis lesions between current smokers and non‐smokers. Background Tobacco smoking is recognized as one of the major risk factors for periodontitis. However, the mechanisms by which smoking affects the progression of the disease remain to be determined. Methods Twenty‐five current smokers and 21 non‐smokers with generalized severe periodontitis were included. From each patient, one soft tissue biopsy from a periodontitis site was harvested and prepared for histological analysis. The infiltrated connective tissue (ICT) was selected as the region of interest to assess the cellular expression of epigenetic markers and reactive oxygen/nitrogen species (RONS) by immunohistochemistry. Results Although the ICT of smokers and non‐smokers did not differ in size or in the expression of markers for DNA damage or oxidative stress, current smokers presented with significantly lower area proportions and densities of cells positive for the epigenetic markers DNMT1 and AcH3. In addition, periodontitis lesions in current smokers presented with a diminished antimicrobial activity, as indicated by significantly lower densities and area proportions of NOX2‐ and iNOS‐positive cells. Conclusions Components of the host response and epigenetic mechanisms in periodontitis lesions in smokers are downregulated as opposed to lesions of non‐smokers.

Salivary histone deacetylase in periodontal disease: A cross‐sectional pilot study

“…The discordance between these studies and the findings described in the present study is likely related to differences in salivary HDAC expression compared with in vitro cultured cells and gingival tissue samples, with the salivary sample likely to contain material from a wider variety of cellular sources (i.e. endothelial cells or immune cells 41–43 ), including a systemic component. This suggests that epigenetics markers are tissue‐, cell‐ and biofluid‐specific, although further studies are required to validate these speculations.…”

Polymorphism in epigenetic regulating genes in relation to periodontitis, number of teeth, and levels of high‐sensitivity C‐reactive protein and glycated hemoglobin: The Tromsø Study 2015‐2016

“…Few studies have evaluated the expression of markers related to DNA methylation in individuals with periodontitis. 12,13,32 In the present study, we have investigated the presence of SNPs in genes related to the DNA methylation process and their association with periodontitis, tooth loss and biomarkers of low-grade inflammation and hyperglycemia in data from a population-based study.…”

Curcumin Attenuates Periodontal Injury via Inhibiting Ferroptosis of Ligature-Induced Periodontitis in Mice

“…Periodontitis is an inflammatory disease of tooth-supporting structures, which leads to tissue destruction and tooth loss as a result of the interaction of dental plaque microorganisms and the host’s immune response [ 1 ]. In recent years, the importance of increased oxidative stress was highlighted as a potential risk factor in the course of periodontal disease [ 2 , 3 ]. In periodontitis pathogenesis, once activated by subgingival microbes ( P. gingivalis ) and their virulence factors (LPS) [ 4 ], macrophages can not only engulf periodontal pathogens but also release reactive oxygen species (ROS), contributing to the onset of periodontitis as well as the activation of acquired immunity [ 5 , 6 ].…”