Short-Chain Fatty Acids from Oral Microbiota in Periodontal Pathology: Epigenetic and Oxidative Mechanisms of Cellular Injury

Hiromasa Tsuda^1,2,*, Daichi Horikoshi³, Yoshikazu Mikami⁴
1 Department of Biochemistry, Nihon University School of Dentistry, Tokyo, Japan
2 Division of Functional Morphology, Dental Research Center, Nihon University School of Dentistry, Tokyo, Japan
3 Department of Oral and Maxillofacial Surgery II, Nihon University School of Dentistry, Tokyo, Japan
4 Division of Microscopic Anatomy, Graduate School of Medical and Dental Sciences, Niigata University, Niigata, Japan
* Corresponding Author: Hiromasa Tsuda. Email: email
(This article belongs to the Special Issue: Cellular and Molecular Mechanisms of Gut Microbiota, Oxidative Stress, and Inflammation in Health and Disease)

BIOCELL https://doi.org/10.32604/biocell.2026.081392

Received 01 March 2026; Accepted 27 July 2026; Published online 05 August 2026

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Abstract

Plaque-derived short-chain fatty acids (SCFAs) have emerged as potential contributors to periodontal inflammation and tissue destruction. Gram-negative anaerobic dental plaque bacteria produce millimolar concentrations of SCFAs. SCFAs directly affect gingival epithelial cells and infiltrating neutrophils, inducing membrane-disruptive cell death accompanied by the release of damage-associated molecular patterns, which can cause inflammation. In neutrophils, this process is also associated with the extracellular release of peptidyl-arginine deiminase 4 (PAD4) and citrullinated proteins, suggesting a potential link between periodontal inflammation and rheumatoid arthritis and cardiovascular disease. This review summarizes current knowledge on the mechanisms of SCFA-induced cell death in gingival epithelial cells and neutrophils. Based on these mechanisms, this review also discusses experimental and hypothetical strategies for suppressing SCFA-induced cell death. The main conclusion is that mechanical plaque control remains essential for reducing SCFA production, but adjunctive approaches targeting oxidative stress, epigenetic regulation, and PAD4-related pathways may further help limit SCFA-mediated inflammatory damage.

Keywords

Short-chain fatty acids; gingival epithelial cells; neutrophils; reactive oxygen species; epigenetics; cell death; damage-associated molecular patterns; peptidyl arginine deiminase

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Short-Chain Fatty Acids from Oral Microbiota in Periodontal Pathology: Epigenetic and Oxidative Mechanisms of Cellular Injury

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