ArticleMolecular oral microbiology2018
Tannerella forsythia-produced methylglyoxal causes accumulation of advanced glycation endproducts to trigger cytokine secretion in human monocytes.
Article in Molecular oral microbiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- Are Inflamed Periodontal Tissues Endogenous Source of Advanced Glycation End-Products (AGEs) in Individuals with and without Diabetes Mellitus? A Systematic Review.Biomolecules · 2022Pooled it
- Effects of Toothpaste Containing 2% Zinc Citrate on Gingival Health and Three Related Bacteria-A Randomized Double-Blind Study.Clinical and experimental dental research · 2024Trial
- Phylogenetic and Functional Analysis of β-Glucanases in Tannerella forsythia Reveals Distinct GH16 Family Glycoside Hydrolase Lineages in Oral Bacteria.Research square · 2026Article
- Oral bacterium contributes to periodontal inflammation by forming advanced glycation end products.Infection and immunity · 2025Article
- Multi-dimensional role of AGEs in periodontitis: from matrix remodeling to neuro-immune crosstalk.Frontiers in immunology · 2025Review
- Periodontal Pathogens and Their Links to Neuroinflammation and Neurodegeneration.Microorganisms · 2023Review
- Pathogenic Molecular Mechanisms in Periodontitis and Peri-Implantitis: Role of Advanced Glycation End Products.Life (Basel, Switzerland) · 2022Review
- Methylglyoxal-Dependent Glycative Stress Is Prevented by the Natural Antioxidant Oleuropein in Human Dental Pulp Stem Cells through Nrf2/Glo1 Pathway.Antioxidants (Basel, Switzerland) · 2021Article
- Oral, Tongue-Coating Microbiota, and Metabolic Disorders: A Novel Area of Interactive Research.Frontiers in cardiovascular medicine · 2021Review
- Persistence ofCurrent oral health reports · 2020Article
- Exploratory Study of Virulence Factors and Protein-Protein Interaction Networks in Major Oral Pathogens.Contemporary clinical dentistryArticle
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
The periodontal pathogen Tannerella forsythia has the unique ability to produce methylglyoxal (MGO), an electrophilic compound which can covalently modify amino acid side chains and generate inflammatory adducts known as advanced glycation endproducts (AGEs). In periodontitis, concentrations of MGO in gingival-crevicular fluid are increased and are correlated with the T. forsythia load. However, the source of MGO and the extent to which MGO may contribute to periodontal inflammation has not been fully explored. In this study we identified a functional homolog of the enzyme methylglyoxal synthase (MgsA) involved in the production of MGO in T. forsythia. While wild-type T.forsythia produced a significant amount of MGO in the medium, a mutant lacking this homolog produced little to no MGO. Furthermore, compared with the spent medium of the T. forsythia parental strain, the spent medium of the T. forsythia mgsA-deletion strain induced significantly lower nuclear factor-kappa B activity as well as proinflammogenic and pro-osteoclastogenic cytokines from THP-1 monocytes. The ability of T. forsythia to induce protein glycation endproducts via MGO was confirmed by an electrophoresis-based collagen chain mobility shift assay. Together these data demonstrated that T. forsythia produces MGO, which may contribute to inflammation via the generation of AGEs and thus act as a potential virulence factor of the bacterium.
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Registered trials
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