Understanding the link between subgingival microbiome and insulin resistance

Summarised from:

The subgingival microbiome, systemic inflammation, and insulin resistance: The Oral Infections, Glucose Intolerance, and Insulin Resistance Study
(Journal of Clinical Periodontology; doi: 10.1111/jcpe.12664)

Authors:

Ryan T. Demmer, Alexander Breskin, Michael Rosenbaum, Aleksandra Zuk, Charles LeDuc, Rudolph Leibel, Bruce Paster, Moïse Desvarieux, David R. Jacobs Jr, Panos N. Papapanou

Summarised by:

Dr Dominika Antoniszczak

Research Topic:

Background + Aims

  • Diabetes risk and insulin resistance are associated with chronic systemic inflammation, often exacerbated by microbial factors. Inflammation interferes with insulin signalling, increasing diabetes susceptibility.
  • Periodontitis, a chronic infection of the tooth-supporting structures, is linked to systemic inflammation and glucose intolerance. Emerging research suggests that early microbial changes in the subgingival environment may play a pivotal role in insulin resistance.
  • The study aimed to investigate the relationship between subgingival bacterial composition, systemic inflammation, and insulin resistance in individuals living without diabetes.
  • The hypothesis posited that dysbiosis (bacterial imbalances) in the subgingival microbiome would correlate with elevated inflammation and insulin resistance markers and that systemic inflammation would mediate this relationship.
  • By identifying specific microbial signatures linked to inflammation and glucose regulation, the study hoped to improve early detection of diabetes risks and inform future intervention strategies.

Materials + Methods

  • The ORIGINS study enrolled 152 adults aged 20–55 years, without a history of chronic inflammatory or cardiovascular conditions. Participants underwent periodontal examinations, microbial assessments, and blood tests.
  • Subgingival plaque samples were collected and analysed for bacterial DNA using the Human Oral Microbe Identification Microarray. Key inflammatory markers were measured:
    • C-reactive protein
    • Interleukin-6
    • Tumour necrosis factor-alpha
    • Adiponectin
  • Fasting glucose and insulin levels were used to calculate the Homeostasis Model Assessment of Insulin Resistance (HOMA-IR).
  • Relationships between bacterial composition, inflammatory scores, and HOMA-IR were assessed using multivariable regressions. Mediation analysis evaluated whether inflammation explained the link between microbiota and insulin resistance.
  • Relative abundances of bacterial phyla (e.g., Actinobacteria, Firmicutes, Proteobacteria) were examined, with a focus on their associations with inflammation and insulin resistance.

Results

  • Actinobacteria and Proteobacteria were inversely associated with inflammation, while Firmicutes and TM7 were positively associated.
  • Proteobacteria levels were linked to reduced HOMA-IR, and Firmicutes showed positive correlations with insulin resistance.
  • Individual bacterial species, such as Parvimonas micra and Cardiobacterium hominis, displayed strong correlations with inflammatory markers and HOMA-IR.
  • Firmicutes were most frequently associated with pro-inflammatory effects, while Actinobacteria promoted an anti-inflammatory profile.
  • Systemic inflammation accounted for 27–98% of the associations between microbiota and insulin resistance.

Limitations

  • The study cannot establish causality between subgingival dysbiosis, inflammation, and insulin resistance.
  • Limited power to detect significant findings, particularly after adjusting for multiple comparisons.
  • Grouping bacteria at the phylum level may obscure species-specific effects.
  • Changes in microbiota or inflammation over time could not be assessed, hindering understanding of disease progression.
  • Host genetics, dietary habits, or undetected systemic conditions might influence findings.
  • Advanced techniques like next-generation sequencing were not employed, potentially missing functional insights into microbial activity.

Conclusion

  • The results support the hypothesis that subgingival dysbiosis contributes to systemic inflammation, which mediates the development of insulin resistance in individuals living without diabetes. Firmicutes and Actinobacteria emerge as key players, with inflammation mediating these effects.
  • While findings require validation in larger, longitudinal studies, they highlight the importance of oral health in managing inflammation and diabetes risks. Incorporating periodontal care into broader healthcare strategies may help prevent metabolic disorders.
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Research  |  15.12.16

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