Authors :
Dr. Bhargavi R; Dr. Nagarathna D V; Dr. Disha Rai; Dr. Snehal Umesh
Volume/Issue :
Volume 7 - 2022, Issue 4 - April
Google Scholar :
https://bit.ly/3IIfn9N
Scribd :
https://bit.ly/3sZmCVL
Abstract :
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.
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.
