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Periodontitis and vascular inflammatory biomarkers: an experimental in vivo study in rats
The objective of this preclinical in vivo study was to determine changes in vascular inflammatory biomarkers in systemic circulation after injection of lipopolysaccharide (LPS) from Porphyromonas gingivalis (Pg) in rats. Experimental periodontitis was induced by injections of Pg-LPS. Gingival soft a...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer Singapore
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7066291/ https://www.ncbi.nlm.nih.gov/pubmed/31583485 http://dx.doi.org/10.1007/s10266-019-00461-3 |
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author | Leira, Yago Iglesias-Rey, Ramón Gómez-Lado, Noemí Aguiar, Pablo Sobrino, Tomás D’Aiuto, Francesco Castillo, José Blanco, Juan Campos, Francisco |
author_facet | Leira, Yago Iglesias-Rey, Ramón Gómez-Lado, Noemí Aguiar, Pablo Sobrino, Tomás D’Aiuto, Francesco Castillo, José Blanco, Juan Campos, Francisco |
author_sort | Leira, Yago |
collection | PubMed |
description | The objective of this preclinical in vivo study was to determine changes in vascular inflammatory biomarkers in systemic circulation after injection of lipopolysaccharide (LPS) from Porphyromonas gingivalis (Pg) in rats. Experimental periodontitis was induced by injections of Pg-LPS. Gingival soft and hard tissues changes were analysed by means of magnetic resonance imaging and micro computed tomography. Serum levels of interleukin (IL)-6, IL-10, pentraxin (PTX) 3, and soluble fragment of tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) were determined at baseline and 24 h, 7, 14, and 21 days after periodontal induction. Significant periodontal inflammation and alveolar bone loss were evident at the end of periodontal induction. Experimental periodontitis posed an acute systemic inflammatory response with increased serum levels of IL-6 and PTX3 at 24 h post-induction, followed by a significant overexpression of sTWEAK at 7 days. This inflammatory state was maintained until the end of the experiment (21 days). As expected, IL-10 serum levels were significantly lower during the follow-up compared to baseline concentrations. In the present animal model, experimental periodontitis is associated with increased systemic inflammation. Further studies are needed to confirm whether PTX3 and sTWEAK could be useful biomarkers to investigate potential mechanisms underlying the relationship between periodontitis and atherosclerotic vascular diseases. |
format | Online Article Text |
id | pubmed-7066291 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Springer Singapore |
record_format | MEDLINE/PubMed |
spelling | pubmed-70662912020-03-23 Periodontitis and vascular inflammatory biomarkers: an experimental in vivo study in rats Leira, Yago Iglesias-Rey, Ramón Gómez-Lado, Noemí Aguiar, Pablo Sobrino, Tomás D’Aiuto, Francesco Castillo, José Blanco, Juan Campos, Francisco Odontology Original Article The objective of this preclinical in vivo study was to determine changes in vascular inflammatory biomarkers in systemic circulation after injection of lipopolysaccharide (LPS) from Porphyromonas gingivalis (Pg) in rats. Experimental periodontitis was induced by injections of Pg-LPS. Gingival soft and hard tissues changes were analysed by means of magnetic resonance imaging and micro computed tomography. Serum levels of interleukin (IL)-6, IL-10, pentraxin (PTX) 3, and soluble fragment of tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) were determined at baseline and 24 h, 7, 14, and 21 days after periodontal induction. Significant periodontal inflammation and alveolar bone loss were evident at the end of periodontal induction. Experimental periodontitis posed an acute systemic inflammatory response with increased serum levels of IL-6 and PTX3 at 24 h post-induction, followed by a significant overexpression of sTWEAK at 7 days. This inflammatory state was maintained until the end of the experiment (21 days). As expected, IL-10 serum levels were significantly lower during the follow-up compared to baseline concentrations. In the present animal model, experimental periodontitis is associated with increased systemic inflammation. Further studies are needed to confirm whether PTX3 and sTWEAK could be useful biomarkers to investigate potential mechanisms underlying the relationship between periodontitis and atherosclerotic vascular diseases. Springer Singapore 2019-10-03 2020 /pmc/articles/PMC7066291/ /pubmed/31583485 http://dx.doi.org/10.1007/s10266-019-00461-3 Text en © The Author(s) 2019 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. |
spellingShingle | Original Article Leira, Yago Iglesias-Rey, Ramón Gómez-Lado, Noemí Aguiar, Pablo Sobrino, Tomás D’Aiuto, Francesco Castillo, José Blanco, Juan Campos, Francisco Periodontitis and vascular inflammatory biomarkers: an experimental in vivo study in rats |
title | Periodontitis and vascular inflammatory biomarkers: an experimental in vivo study in rats |
title_full | Periodontitis and vascular inflammatory biomarkers: an experimental in vivo study in rats |
title_fullStr | Periodontitis and vascular inflammatory biomarkers: an experimental in vivo study in rats |
title_full_unstemmed | Periodontitis and vascular inflammatory biomarkers: an experimental in vivo study in rats |
title_short | Periodontitis and vascular inflammatory biomarkers: an experimental in vivo study in rats |
title_sort | periodontitis and vascular inflammatory biomarkers: an experimental in vivo study in rats |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7066291/ https://www.ncbi.nlm.nih.gov/pubmed/31583485 http://dx.doi.org/10.1007/s10266-019-00461-3 |
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