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Cellular expression of epigenetic markers and oxidative stress in periodontitis lesions of smokers and non‐smokers
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 sm...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9542336/ https://www.ncbi.nlm.nih.gov/pubmed/35766184 http://dx.doi.org/10.1111/jre.13030 |
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author | Dionigi, Carlotta Larsson, Lena Difloe‐Geisert, Julia C. Zitzmann, Nicola U. Berglundh, Tord |
author_facet | Dionigi, Carlotta Larsson, Lena Difloe‐Geisert, Julia C. Zitzmann, Nicola U. Berglundh, Tord |
author_sort | Dionigi, Carlotta |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-9542336 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-95423362022-10-14 Cellular expression of epigenetic markers and oxidative stress in periodontitis lesions of smokers and non‐smokers Dionigi, Carlotta Larsson, Lena Difloe‐Geisert, Julia C. Zitzmann, Nicola U. Berglundh, Tord J Periodontal Res Original Articles 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. John Wiley and Sons Inc. 2022-06-29 2022-10 /pmc/articles/PMC9542336/ /pubmed/35766184 http://dx.doi.org/10.1111/jre.13030 Text en © 2022 The Authors. Journal of Periodontal Research published by John Wiley & Sons Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Articles Dionigi, Carlotta Larsson, Lena Difloe‐Geisert, Julia C. Zitzmann, Nicola U. Berglundh, Tord Cellular expression of epigenetic markers and oxidative stress in periodontitis lesions of smokers and non‐smokers |
title | Cellular expression of epigenetic markers and oxidative stress in periodontitis lesions of smokers and non‐smokers |
title_full | Cellular expression of epigenetic markers and oxidative stress in periodontitis lesions of smokers and non‐smokers |
title_fullStr | Cellular expression of epigenetic markers and oxidative stress in periodontitis lesions of smokers and non‐smokers |
title_full_unstemmed | Cellular expression of epigenetic markers and oxidative stress in periodontitis lesions of smokers and non‐smokers |
title_short | Cellular expression of epigenetic markers and oxidative stress in periodontitis lesions of smokers and non‐smokers |
title_sort | cellular expression of epigenetic markers and oxidative stress in periodontitis lesions of smokers and non‐smokers |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9542336/ https://www.ncbi.nlm.nih.gov/pubmed/35766184 http://dx.doi.org/10.1111/jre.13030 |
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