Integrated analysis of the salivary microbiome and metabolome in chronic and aggressive periodontitis: A pilot study

This pilot study was designed to identify the salivary microbial community and metabolic characteristics in patients with generalized periodontitis. A total of 36 saliva samples were collected from 13 patients with aggressive periodontitis (AgP), 13 patients with chronic periodontitis (ChP), and 10 subjects with periodontal health (PH). The microbiome was evaluated using 16S rRNA gene high-throughput sequencing, and the metabolome was accessed using gas chromatography-mass spectrometry. The correlation between microbiomes and metabolomics was analyzed by Spearman’s correlation method. Our results revealed that the salivary microbial community and metabolite composition differed significantly between patients with periodontitis and healthy controls. Striking differences were found in the composition of salivary metabolites between AgP and ChP. The genera Treponema, Peptococcus, Catonella, Desulfobulbus, Peptostreptococcaceae_[XI] ([G-2], [G-3] [G-4], [G-6], and [G-9]), Bacteroidetes_[G-5], TM7_[G-5], Dialister, Eikenella, Fretibacterium, and Filifactor were present in higher levels in patients with periodontitis than in the healthy participants. The biochemical pathways that were significantly different between ChP and AgP included pyrimidine metabolism; alanine, aspartate, and glutamate metabolism; beta-alanine metabolism; citrate cycle; and arginine and proline metabolism. The differential metabolites between ChP and AgP groups, such as urea, beta-alanine, 3-aminoisobutyric acid, and thymine, showed the most significant correlations with the genera. These differential microorganisms and metabolites may be used as potential biomarkers to monitor the occurrence and development of periodontitis through the utilization of non-invasive and convenient saliva samples. This study reveals the integration of salivary microbial data and metabolomic data, which provides a foundation to further explore the potential mechanism of periodontitis.