Epigenetic Mechanisms in Periodontal Disease

Periodontal disease arises from a complex interplay between microbial challenge and host response, in which epigenetic mechanisms are now recognised as crucial modulators. DNA methylation, histone modifications and non-coding RNAs adjust the expression of genes that regulate immune detection, cytokine production, matrix remodelling and bone homeostasis within the periodontium. Oral pathogens such as Porphyromonas gingivalis induce site-specific changes in DNA methylation and histone acetylation in gingival cells, amplifying pro-inflammatory cytokine and matrix metalloproteinase expression. Conversely, aberrant epigenetic marks in fibroblasts and periodontal ligament cells can impair tissue repair and osteogenic differentiation. Environmental factors—including smoking, diet and systemic health—further shape the epigenome, creating individual susceptibility profiles. Efforts to reverse pathogenic epigenetic states through small-molecule inhibitors of DNA methyltransferases, histone deacetylases or bromodomain readers have ameliorated inflammation and bone loss in preclinical models. A comprehensive mapping of epigenetic landscapes in health and disease will pave the way for personalised diagnostics and host-modulation therapies in periodontitis.

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Epigenetic Mechanisms in Periodontal Disease publication trend

The graph below shows the total number of articles in epigenetic mechanisms in periodontal disease across all publications each year (not limited to Nature Index journals).

Technical terms

DNA methylation: Addition of methyl groups to cytosine bases in DNA, typically at CpG dinucleotides, modulating gene expression without altering the sequence.

Histone modification: Post-translational changes to histone proteins, such as acetylation or methylation, that influence chromatin structure and gene accessibility.

Epigenetic regulator: Protein or enzyme that writes, erases or reads epigenetic marks, thereby controlling gene activity.

Gingival fibroblast: Connective-tissue cell in the gums that contributes to tissue maintenance and responds to inflammatory stimuli.

S-adenosylmethionine (SAM): Principal methyl group donor in cellular methylation reactions.

CpG site: DNA region where a cytosine nucleotide is followed by a guanine nucleotide, often a key target for methylation.

References

1. Mapping of DNA methylation-sensitive cellular processes in gingival and periodontal ligament fibroblasts in the context of periodontal tissue homeostasis. Frontiers in Immunology (2023).
2. MAT2A inhibition suppresses inflammation in Porphyromonas gingivalis-infected human gingival fibroblasts. Journal of Oral Microbiology (2023).
3. CpG Single-Site Methylation Regulates TLR2 Expression in Proinflammatory PBMCs From Apical Periodontitis Individuals. Frontiers in Immunology (2022).