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Purpose of Review <p>This review examines the role of short-chain fatty acids (SCFAs), key postbiotic metabolites, in regulating histone modifications and their contribution to the pathogenesis of periodontitis.</p> Recent Findings <p>Drawing on recent evidence, we discuss how these modifications contribute to enhanced inflammatory cascades, gingival epithelial cell apoptosis, and alveolar bone resorption in dysbiotic environments. Furthermore, the bidirectional microbiome-epigenome axis is highlighted, underscoring the potential of SCFAs as therapeutic targets for restoring oral microbial balance and mitigating disease progression.</p> Summary <p> Periodontal disease, a prevalent chronic inflammatory condition affecting the gingival tissues and alveolar bone, arises from dysbiotic shifts in the oral microbiome, leading to aberrant host immune responses. This review explores the intricate interplay between SCFAs—key postbiotic metabolites produced by commensal and pathogenic oral bacteria—and epigenetic mechanisms, particularly histone modifications, in the pathogenesis of periodontitis. SCFAs, such as butyrate and propionate, exert dual effects: they inhibit histone deacetylases (HDACs), promoting histone acetylation and influencing gene expression related to inflammation, cell death, and tissue homeostasis, while also modulating histone methylation patterns.</p>

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SCFA-Mediated Histone Modification Mechanisms in Periodontal Disease

  • 期刊论文

  • 发表日期：

    2026年5月22日

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  • Mohammad Ghasemirad,
  • Wael Sheet Hussein,
  • Karar H. Alfarttoosi,
  • Sada Ghalib Taher,
  • Mariem Alwan,
  • Mahmood Jawad,
  • Hiba Mushtaq,
  • Saiedeh Sadeghi

摘要

Purpose of Review

This review examines the role of short-chain fatty acids (SCFAs), key postbiotic metabolites, in regulating histone modifications and their contribution to the pathogenesis of periodontitis.

Recent Findings

Drawing on recent evidence, we discuss how these modifications contribute to enhanced inflammatory cascades, gingival epithelial cell apoptosis, and alveolar bone resorption in dysbiotic environments. Furthermore, the bidirectional microbiome-epigenome axis is highlighted, underscoring the potential of SCFAs as therapeutic targets for restoring oral microbial balance and mitigating disease progression.

Summary

Periodontal disease, a prevalent chronic inflammatory condition affecting the gingival tissues and alveolar bone, arises from dysbiotic shifts in the oral microbiome, leading to aberrant host immune responses. This review explores the intricate interplay between SCFAs—key postbiotic metabolites produced by commensal and pathogenic oral bacteria—and epigenetic mechanisms, particularly histone modifications, in the pathogenesis of periodontitis. SCFAs, such as butyrate and propionate, exert dual effects: they inhibit histone deacetylases (HDACs), promoting histone acetylation and influencing gene expression related to inflammation, cell death, and tissue homeostasis, while also modulating histone methylation patterns.