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J Dent Res. 2019 Oct;98(11):1245-1252. doi: 10.1177/0022034519869906. Epub 2019 Aug 27.

Metabolic Profile of Supragingival Plaque Exposed to Arginine and Fluoride.

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Department of Restorative Dental Sciences, Division of Operative Dentistry, College of Dentistry, University of Florida, Gainesville, FL, USA.
College of Dentistry, University of Florida, Gainesville, FL, USA.
Pediatric Dentistry Graduate Program, Department of Pediatric Dentistry, College of Dentistry, University of Florida, Gainesville, FL, USA.
Department of Oral Biology, College of Dentistry, University of Florida, Gainesville, FL, USA.
Division of General Dentistry, Eastman Institute for Oral Health, University of Rochester, Rochester, NY, USA.
Dental Clinical Research Unit, College of Dentistry, University of Florida, Gainesville, FL, USA.
Dental Materials Division, Department of Restorative Dentistry, Piracicaba Dental School, State University of Campinas, Piracicaba, SP, Brazil.
Department of Biological Sciences, College of Science, Clemson University, Clemson, SC, USA.
Department of Pathology, Immunology and Laboratory Medicine, College of Medicine, University of Florida, Gainesville, FL, USA.


Caries lesions develop when acid production from bacterial metabolism of dietary carbohydrates outweighs the various mechanisms that promote pH homeostasis, including bacterial alkali production. Therapies that provide arginine as a substrate for alkali production in supragingival oral biofilms have strong anticaries potential. The objective of this study was to investigate the metabolic profile of site-specific supragingival plaque in response to the use of arginine (Arg: 1.5% arginine, fluoride-free) or fluoride (F: 1,100 ppm F/NaF) toothpastes. Eighty-three adults of different caries status were recruited and assigned to treatment with Arg or F for 12 wk. Caries lesions were diagnosed using International Caries Detection and Assessment System II, and plaque samples were collected from caries-free and carious tooth surfaces. Taxonomic profiles were obtained by HOMINGS (Human Oral Microbe Identification using Next Generation Sequencing), and plaque metabolism was assessed by the levels of arginine catabolism via the arginine deiminase pathway (ADS), acidogenicity, and global metabolomics. Principal component analysis (PCA), partial least squares-discriminant analysis, analysis of variance, and random forest tests were used to distinguish metabolic profiles. Of the 509 active lesions diagnosed at baseline, 70 (14%) were inactive after 12 wk. Generalized linear model showed that enamel lesions were significantly more likely to become inactive compared to dentin lesions (P < 0.0001), but no difference was found when treatment with Arg was compared to F (P = 0.46). Arg significantly increased plaque ADS activity (P = 0.031) and plaque pH values after incubation with glucose (P = 0.001). F reduced plaque lactate production from endogenous sources (P = 0.02). PCA revealed differences between the metabolic profiles of plaque treated with Arg or F. Arg significantly affected the concentrations of 16 metabolites, including phenethylamine, agmatine, and glucosamine-6-phosphate (P < 0.05), while F affected the concentrations of 9 metabolites, including phenethylamine, N-methyl-glutamate, and agmatine (P < 0.05). The anticaries mechanisms of action of arginine and fluoride are distinct. Arginine metabolism promotes biofilm pH homeostasis, whereas fluoride is thought to enhance resistance of tooth minerals to low pH and reduce acid production by supragingival oral biofilms.


bacteria; biofilm; dental caries; metabolite; metabolomics; microbiome


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