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Porphyromonas gingivalis as a Model Organism for Assessing Interaction of Anaerobic Bacteria with Host Cells
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Subgingival Host-Microbial Interactions in Hyperglycemic Individuals.

P S Kumar1, M F Monteiro2, S M Dabdoub1

  • 1Division of Periodontology, College of Dentistry, The Ohio State University, Columbus, OH, USA.

Journal of Dental Research
|March 17, 2020
PubMed
Summary
This summary is machine-generated.

Type 2 diabetes mellitus (T2DM) disrupts the crucial balance between the host immune system and oral bacteria in periodontitis. Hyperglycemia worsens this imbalance, hindering the positive effects of nonsurgical therapy on restoring microbial community interactions.

Keywords:
16Scytokinediabetesinteractomemicrobiomeperiodontitis

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Area of Science:

  • Oral microbiology
  • Immunology
  • Periodontology

Background:

  • Type 2 diabetes mellitus (T2DM) is a known risk factor for periodontitis.
  • The precise mechanisms by which hyperglycemia impacts host-bacterial interactions in the subgingival crevice remain unclear.

Purpose of the Study:

  • To quantify the effect of hyperglycemia on host-bacterial interactions in periodontitis.
  • To map changes in these interactions after nonsurgical periodontal therapy.

Main Methods:

  • Recruited T2DM and non-T2DM patients with severe chronic periodontitis, and healthy controls.
  • Collected subgingival biofilm and gingival crevicular fluid samples at baseline and post-therapy (1, 3, 6 months).
  • Analyzed 16S ribosomal DNA sequences and immune mediators using differential network analysis to model microbial and host-microbial interactions.

Main Results:

  • Periodontal health shows sparse interbacterial and connected cytokine-bacterial networks.
  • Periodontitis patients (both normoglycemic and T2DM) exhibit strong bacterial hubs but fewer cytokine-bacterial connections.
  • Nonsurgical therapy increased cytokine-bacterial connections in normoglycemics (2-fold at 1 month, 10-fold at 6 months).
  • In hyperglycemic patients, connections doubled at 1 month but showed no further increase, indicating impaired immune system recovery.
  • Interbacterial interactions, not host-bacterial, primarily drove microbial community assembly in periodontitis.
  • Hyperglycemia exacerbated the breakdown of host-bacterial mutualism.

Conclusions:

  • Periodontitis involves a breakdown of host-bacterial mutualism, with bacterial interactions dominating community structure.
  • Hyperglycemia significantly worsens this dysbiosis and impairs the host's immune response to therapy.
  • Nonsurgical therapy can reset host-microbiome interactions, but this effect is diminished and delayed in individuals with hyperglycemia.