Immunity and inflammation are governed Through epigenetic mechanisms such as DNA and histoneschanges, which have arisen as imminent focuses for immune modulating drugs. The high commonness and grimness of periodontitis, as well as mounting proof that hereditary, natural, and way of life factors alone are insufficient to fully explain a person's susceptibility to disease development, has sparked interest in epigenetic regulation as a key factor in periodontitis pathogenesis. TLR2, PTGS2, IFNG, IL6, IL8, and TNF all have abnormal promoter methylation profiles in periodontitis patients' gingiva, blood, and buccal mucosa, which corresponds to changes in articulation and sickness seriousness. In periodontitis-impacted gingival tissue, the expression of histone deacetylases (HDACs), which regulate histone acetylation, is also dysregulated. Changes in chromatin-modifying enzyme expression and activity, as well as site-explicit and worldwide changes in DNA methylation designs, histone acetylation, and methylation marks, are all caused by Porphyromonas gingivalis or Treponema denticola. Epigenetic alterations are linked to inflammatory cytokines, chemokines, and matrix-degrading enzymes, and small molecule inhibitors of histone deacetylases (HDACi) or DNA methyltransferases can reduce their production. In animal models of periodontitis, HDACi and inhibitors of bromodomain-containing BET proteins reduce inflammation, osteoclastogenesis, and alveolar bone resorption, implying that they could be used as host modulation treatments in humans.To develop a full picture of epigenetic modifications in periodontitis, however, further epigenomic approaches would be required. Integrating functional research with a global epigenetic landscape analysis will reveal crucial information about epigenetics' restorative and symptomatic potential in periodontal disease.