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Distinct signatures of dental plaque metabolic byproducts dictated by periodontal inflammatory status

Onset of chronic periodontitis is associated with an aberrant polymicrobial community, termed dysbiosis. Findings regarding its etiology obtained using high-throughput sequencing technique suggested that dysbiosis holds a conserved metabolic signature as an emergent property. The purpose of this stu...

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Autores principales: Sakanaka, Akito, Kuboniwa, Masae, Hashino, Ei, Bamba, Takeshi, Fukusaki, Eiichiro, Amano, Atsuo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5318866/
https://www.ncbi.nlm.nih.gov/pubmed/28220901
http://dx.doi.org/10.1038/srep42818
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author Sakanaka, Akito
Kuboniwa, Masae
Hashino, Ei
Bamba, Takeshi
Fukusaki, Eiichiro
Amano, Atsuo
author_facet Sakanaka, Akito
Kuboniwa, Masae
Hashino, Ei
Bamba, Takeshi
Fukusaki, Eiichiro
Amano, Atsuo
author_sort Sakanaka, Akito
collection PubMed
description Onset of chronic periodontitis is associated with an aberrant polymicrobial community, termed dysbiosis. Findings regarding its etiology obtained using high-throughput sequencing technique suggested that dysbiosis holds a conserved metabolic signature as an emergent property. The purpose of this study was to identify robust biomarkers for periodontal inflammation severity. Furthermore, we investigated disease-associated metabolic signatures of periodontal microbiota using a salivary metabolomics approach. Whole saliva samples were obtained from adult subjects before and after removal of supragingival plaque (debridement). Periodontal inflamed surface area (PISA) was employed as an indicator of periodontal inflammatory status. Based on multivariate analyses using pre-debridement salivary metabolomics data, we found that metabolites associated with higher PISA included cadaverine and hydrocinnamate, while uric acid and ethanolamine were associated with lower PISA. Next, we focused on dental plaque metabolic byproducts by selecting salivary metabolites significantly decreased following debridement. Metabolite set enrichment analysis revealed that polyamine metabolism, arginine and proline metabolism, butyric acid metabolism, and lysine degradation were distinctive metabolic signatures of dental plaque in the high PISA group, which may be related to the metabolic signatures of disease-associated communities. Collectively, our findings identified potential biomarkers of periodontal inflammatory status and also provide insight into metabolic signatures of dysbiotic communities.
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spelling pubmed-53188662017-02-24 Distinct signatures of dental plaque metabolic byproducts dictated by periodontal inflammatory status Sakanaka, Akito Kuboniwa, Masae Hashino, Ei Bamba, Takeshi Fukusaki, Eiichiro Amano, Atsuo Sci Rep Article Onset of chronic periodontitis is associated with an aberrant polymicrobial community, termed dysbiosis. Findings regarding its etiology obtained using high-throughput sequencing technique suggested that dysbiosis holds a conserved metabolic signature as an emergent property. The purpose of this study was to identify robust biomarkers for periodontal inflammation severity. Furthermore, we investigated disease-associated metabolic signatures of periodontal microbiota using a salivary metabolomics approach. Whole saliva samples were obtained from adult subjects before and after removal of supragingival plaque (debridement). Periodontal inflamed surface area (PISA) was employed as an indicator of periodontal inflammatory status. Based on multivariate analyses using pre-debridement salivary metabolomics data, we found that metabolites associated with higher PISA included cadaverine and hydrocinnamate, while uric acid and ethanolamine were associated with lower PISA. Next, we focused on dental plaque metabolic byproducts by selecting salivary metabolites significantly decreased following debridement. Metabolite set enrichment analysis revealed that polyamine metabolism, arginine and proline metabolism, butyric acid metabolism, and lysine degradation were distinctive metabolic signatures of dental plaque in the high PISA group, which may be related to the metabolic signatures of disease-associated communities. Collectively, our findings identified potential biomarkers of periodontal inflammatory status and also provide insight into metabolic signatures of dysbiotic communities. Nature Publishing Group 2017-02-21 /pmc/articles/PMC5318866/ /pubmed/28220901 http://dx.doi.org/10.1038/srep42818 Text en Copyright © 2017, The Author(s) http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
spellingShingle Article
Sakanaka, Akito
Kuboniwa, Masae
Hashino, Ei
Bamba, Takeshi
Fukusaki, Eiichiro
Amano, Atsuo
Distinct signatures of dental plaque metabolic byproducts dictated by periodontal inflammatory status
title Distinct signatures of dental plaque metabolic byproducts dictated by periodontal inflammatory status
title_full Distinct signatures of dental plaque metabolic byproducts dictated by periodontal inflammatory status
title_fullStr Distinct signatures of dental plaque metabolic byproducts dictated by periodontal inflammatory status
title_full_unstemmed Distinct signatures of dental plaque metabolic byproducts dictated by periodontal inflammatory status
title_short Distinct signatures of dental plaque metabolic byproducts dictated by periodontal inflammatory status
title_sort distinct signatures of dental plaque metabolic byproducts dictated by periodontal inflammatory status
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5318866/
https://www.ncbi.nlm.nih.gov/pubmed/28220901
http://dx.doi.org/10.1038/srep42818
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