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

• Published in: Scientific reports Vol. 7; no. 1; p. 42818
• Main Authors: Sakanaka, Akito, Kuboniwa, Masae, Hashino, Ei, Bamba, Takeshi, Fukusaki, Eiichiro, Amano, Atsuo
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 21.02.2017; Nature Publishing Group
• Subjects: 631/45/320; 692/53/2421; 692/699/255/1318; Adult; Area Under Curve; Arginine; Biomarkers; Biomarkers - metabolism; Butyric acid; Cadaverine; Cadaverine - metabolism; Chronic Periodontitis - metabolism; Chronic Periodontitis - pathology; Dental plaque; Dental Plaque - metabolism; Dysbacteriosis; Ethanolamine; Etiology; Female; Humanities and Social Sciences; Humans; Inflammation; Lysine; Male; Metabolism; Metabolites; Metabolomics; Middle Aged; multidisciplinary; Next-generation sequencing; Periodontitis; Phenylpropionates - metabolism; Proline; ROC Curve; Saliva; Saliva - metabolism; Science; Severity of Illness Index; Uric acid
• DOI: 10.1038/srep42818
• ISSN: 2045-2322

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.