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Transcriptomic features of programmed and inflammatory cell death in gingival tissues.

Jeffrey L Ebersole1, Sreenatha S Kirakodu2, Linh M Nguyen1

  • 1Department of Biomedical Sciences, School of Dental Medicine, University of Nevada Las Vegas, Las Vegas, Nevada, USA.

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Summary

This study reveals age-related differences in gingival tissue gene expression linked to regulated cell death pathways. These molecular responses are influenced by bacterial changes during periodontitis, impacting tissue health across different age groups.

Keywords:
cell deathnonhuman primateperiodontitistranscriptome

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Area of Science:

  • Oral biology
  • Molecular biology
  • Immunology

Background:

  • Periodontitis involves significant histological and biological changes in gingival tissues.
  • Understanding the molecular mechanisms of cell death in periodontitis is crucial.

Purpose of the Study:

  • To investigate the gingival transcriptome related to four cell death processes: pyroptosis, necroptosis, ferroptosis, and cuproptosis.
  • To analyze age-associated differences in these pathways in healthy and periodontitis models.

Main Methods:

  • Utilized gingival tissue biopsies from Macaca mulatta primates across various age groups.
  • Conducted microarray analysis of 257 genes related to cell death pathways.
  • Performed 16S rRNA gene analysis of bacterial plaque samples.

Main Results:

  • Identified age-related variations in gene expression for cuproptosis, ferroptosis, necroptosis, and pyroptosis in healthy gingival tissues.
  • Observed significant differences in these pathways during periodontitis initiation, progression, and resolution, influenced by animal age.
  • Found distinct bacterial families significantly correlated with gene expression in cell death pathways.

Conclusions:

  • Gingival tissue exhibits age-associated molecular responses to bacterial shifts in periodontitis.
  • Regulated cell death pathways are implicated in both physiological and pathophysiological processes of periodontitis.
  • Age is a critical factor in the gingival tissue's molecular response to periodontitis.