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The Subgingival Plaque Microbiome, Systemic Antibodies against Bacteria and Citrullinated Proteins following Periodontal Therapy

Periodontitis (PD) shows an association with rheumatoid arthritis (RA) and systemic inflammation. Periodontal pathogens, namely Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans, are proposed to be capable of inducing citrullination of peptides in the gingiva, inducing the formation...

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Autores principales: Davison, Emily, Johnston, William, Piela, Krystyna, Rosier, Bob T., Paterson, Michael, Mira, Alex, Culshaw, Shauna
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7916579/
https://www.ncbi.nlm.nih.gov/pubmed/33578802
http://dx.doi.org/10.3390/pathogens10020193
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author Davison, Emily
Johnston, William
Piela, Krystyna
Rosier, Bob T.
Paterson, Michael
Mira, Alex
Culshaw, Shauna
author_facet Davison, Emily
Johnston, William
Piela, Krystyna
Rosier, Bob T.
Paterson, Michael
Mira, Alex
Culshaw, Shauna
author_sort Davison, Emily
collection PubMed
description Periodontitis (PD) shows an association with rheumatoid arthritis (RA) and systemic inflammation. Periodontal pathogens, namely Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans, are proposed to be capable of inducing citrullination of peptides in the gingiva, inducing the formation of anti-citrullinated protein antibodies (ACPAs) within susceptible hosts. Here, we sought to investigate whether periodontal treatment influenced systemic inflammation and antibody titres to P. gingivalis, A. actinomycetemcomitans, Prevotella intermedia and ACPA in 42 systemically health patients with periodontal disease. Subgingival plaque and serum samples were collected from study participants before (baseline) and 90 days after treatment to analyse the abundance of specific bacteria and evaluate anti-bacterial antibodies, C-reactive protein (CRP), tumour necrosis factor α (TNF-α), interleukin 6 (IL-6) and ACPA in serum. Following treatment, all patients showed reduced periodontal inflammation. Despite observing a weak positive correlation between CRP and IL-6 with periodontal inflammation at baseline, we observed no significant reductions in any indicators of systemic inflammation 90 days after treatment. In contrast, anti-P. gingivalis IgG significantly reduced post-treatment (p < 0.001, Wilcoxon signed rank test), although no changes were observed for other antibody titres. Patients who had detectable P. gingivalis in subgingival plaques had significantly higher anti-P. gingivalis IgG and ACPA titres, suggesting a potential association between P. gingivalis colonisation and systemic antibody titres.
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spelling pubmed-79165792021-03-01 The Subgingival Plaque Microbiome, Systemic Antibodies against Bacteria and Citrullinated Proteins following Periodontal Therapy Davison, Emily Johnston, William Piela, Krystyna Rosier, Bob T. Paterson, Michael Mira, Alex Culshaw, Shauna Pathogens Article Periodontitis (PD) shows an association with rheumatoid arthritis (RA) and systemic inflammation. Periodontal pathogens, namely Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans, are proposed to be capable of inducing citrullination of peptides in the gingiva, inducing the formation of anti-citrullinated protein antibodies (ACPAs) within susceptible hosts. Here, we sought to investigate whether periodontal treatment influenced systemic inflammation and antibody titres to P. gingivalis, A. actinomycetemcomitans, Prevotella intermedia and ACPA in 42 systemically health patients with periodontal disease. Subgingival plaque and serum samples were collected from study participants before (baseline) and 90 days after treatment to analyse the abundance of specific bacteria and evaluate anti-bacterial antibodies, C-reactive protein (CRP), tumour necrosis factor α (TNF-α), interleukin 6 (IL-6) and ACPA in serum. Following treatment, all patients showed reduced periodontal inflammation. Despite observing a weak positive correlation between CRP and IL-6 with periodontal inflammation at baseline, we observed no significant reductions in any indicators of systemic inflammation 90 days after treatment. In contrast, anti-P. gingivalis IgG significantly reduced post-treatment (p < 0.001, Wilcoxon signed rank test), although no changes were observed for other antibody titres. Patients who had detectable P. gingivalis in subgingival plaques had significantly higher anti-P. gingivalis IgG and ACPA titres, suggesting a potential association between P. gingivalis colonisation and systemic antibody titres. MDPI 2021-02-10 /pmc/articles/PMC7916579/ /pubmed/33578802 http://dx.doi.org/10.3390/pathogens10020193 Text en © 2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Davison, Emily
Johnston, William
Piela, Krystyna
Rosier, Bob T.
Paterson, Michael
Mira, Alex
Culshaw, Shauna
The Subgingival Plaque Microbiome, Systemic Antibodies against Bacteria and Citrullinated Proteins following Periodontal Therapy
title The Subgingival Plaque Microbiome, Systemic Antibodies against Bacteria and Citrullinated Proteins following Periodontal Therapy
title_full The Subgingival Plaque Microbiome, Systemic Antibodies against Bacteria and Citrullinated Proteins following Periodontal Therapy
title_fullStr The Subgingival Plaque Microbiome, Systemic Antibodies against Bacteria and Citrullinated Proteins following Periodontal Therapy
title_full_unstemmed The Subgingival Plaque Microbiome, Systemic Antibodies against Bacteria and Citrullinated Proteins following Periodontal Therapy
title_short The Subgingival Plaque Microbiome, Systemic Antibodies against Bacteria and Citrullinated Proteins following Periodontal Therapy
title_sort subgingival plaque microbiome, systemic antibodies against bacteria and citrullinated proteins following periodontal therapy
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7916579/
https://www.ncbi.nlm.nih.gov/pubmed/33578802
http://dx.doi.org/10.3390/pathogens10020193
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