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J Clin Periodontol. 2016 Dec 15. doi: 10.1111/jcpe.12664. [Epub ahead of print]

The subgingival microbiome, systemic inflammation and insulin resistance: The Oral Infections, Glucose Intolerance and Insulin Resistance Study.

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  • 1Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY, USA.
  • 2Division of Molecular Genetics, Departments of Pediatrics and Medicine, Columbia University, New York, NY, USA.
  • 3Dalla Lana School of Public Health, University of Toronto, Toronto, ON, Canada.
  • 4Department of Molecular Genetics, The Forsyth Institute, Cambridge, MA, USA.
  • 5Department of Oral Medicine, Infection, and Immunity, Harvard School of Dental Medicine, Boston, MA, USA.
  • 6Centre de recherche Epidémiologies et Biostatistique, INSERM U1153 Equipe: Méthodes en évaluation thérapeutique des maladies chroniques, Paris, France.
  • 7Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, MN, USA.
  • 8Division of Periodontics, Section of Oral and Diagnostic Sciences, College of Dental Medicine, Columbia University, New York, NY, USA.



Inflammation might link microbial exposures to insulin resistance. We investigated the cross-sectional association between periodontal microbiota, inflammation and insulin resistance.


The Oral Infections, Glucose Intolerance and Insulin Resistance Study (ORIGINS) enrolled 152 diabetes-free adults (77% female) aged 20-55 years (mean = 34 ± 10). Three hundred and four subgingival plaque samples were analysed using the Human Oral Microbe Identification Microarray to measure the relative abundances of 379 taxa. C-reactive protein, interleukin-6, tumour necrosis factor-α and adiponectin were assessed from venous blood and their z-scores were summed to create an inflammatory score (IS). Insulin resistance was defined via the HOMA-IR. Associations between the microbiota and both inflammation and HOMA-IR were explored using multivariable linear regressions; mediation analyses assessed the proportion of the association explained by inflammation.


The IS was inversely associated with Actinobacteria and Proteobacteria and positively associated with Firmicutes and TM7 (p-values < 0.05). Proteobacteria levels were associated with insulin resistance (p < 0.05). Inflammation explained 30-98% of the observed associations between levels of Actinobacteria, Proteobacteria or Firmicutes and insulin resistance (p-values < 0.05). Eighteen individual taxa were associated with inflammation (p < 0.05) and 22 with insulin resistance (p < 0.05). No findings for individual taxa met Bonferroni-adjusted statistical significance.


Bacterial measures were related to inflammation and insulin resistance among diabetes-free adults.


C-reactive protein; adiponectin; diabetes; inflammation; insulin resistance; interleukin-6; microbiome; microbiota; periodontal; tumour necrosis factor-α

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