Periodontal treatment and vascular cell inflammation in diabetes

Summarised from:

Periodontal treatment modulates gene expression of endothelial progenitor cells in diabetic patients
(Journal of Clinical Periodontology; doi: 10.1111/jcpe.12806)

Authors:

Yi Wang, Hin Nam Liu, Zhe Zhen, Kai Hang Yiu, Hung Fat Tse, George Pelekos, Maurizio Tonetti, Lijian Jin

Summarised by:

Dr Varkha Rattu

Research Topic:

Background + Aims

  • Endothelial progenitor cells (EPCs) contribute to maintaining and repairing the endothelium (the lining of blood vessels).
  • Periodontitis and diabetes may alter these cells’ inflammatory responses, providing a possible biological link between periodontal disease and vascular complications.
  • This study aimed to:
    • Investigate whether non-surgical periodontal treatment modifies inflammation-related gene expression in EPCs from patients with type 2 diabetes and moderate-to-severe periodontitis.

Materials + Methods

  • 18 adults were randomly allocated to periodontal treatment (11 participants) or a control group receiving oral hygiene instruction alone (7 participants).
    • 1 control participant was lost to follow-up.
  • Participants had diabetes for ≥5-years and HbA1c above 6.5%. People with documented cardiovascular disease were excluded.
  • Treatment included oral hygiene instruction, extraction of hopeless teeth, scaling and root debridement, with review visits every 4-6 weeks. Controls received periodontal treatment after the 6-month assessment.
  • Blood samples collected at baseline and 6-months were used to culture early, predominantly monocytic EPCs (cells that support blood vessel formation through signals released to surrounding cells).
  • Researchers initially screened 84 genes related to Toll-like receptor signalling, a system involved in recognising microbes and activating immune responses, in four treated participants.
  • Selected findings were then assessed by quantitative PCR across participants with available follow-up samples.
  • Periodontal measurements, HbA1c, high-sensitivity C-reactive protein and cytokine release into cell-culture fluid were also assessed.

Results

  • In the treatment group, bleeding on probing decreased from 54.6% to 16.0% of sites, while sites with pockets ≥4 mm decreased from 26.9% to 6.0%. Changes were significantly better than in controls.
  • The initial screen identified significant reductions in IL-6 and IL-8 transcripts, the RNA instructions used to produce these inflammatory signalling proteins.
  • Changes in IL-6 and IL-8 gene expression significantly favoured treatment over control (p < .01 and p < .05, respectively), although responses varied between individuals.
  • Reduced gene expression was not accompanied by a significant decrease in IL-6 or IL-8 protein levels in the culture fluid.
  • No demonstrated glycaemic benefit as HbA1c did not improve; mean values increased in both groups, without a significant difference in change between groups.
  • No significant systemic inflammatory effect as changes in high-sensitivity C-reactive protein did not differ significantly between groups.

Limitations

  • The small sample and initial screening of only 4 treated participants limit confidence and may have missed other relevant genes.
  • Measurements at baseline and 6-months could not capture short-term responses.
  • Cultured early EPCs were a mixed cell population, limiting conclusions about specific vascular cell types and their behaviour within the body.
  • Gene-expression changes did not translate into measurable changes in the corresponding secreted proteins.
  • The study did not directly establish improved vascular repair, endothelial function or reduced cardiovascular complications.

Conclusion

  • Periodontal treatment reduced selected inflammatory gene signals in cultured EPCs from people with type 2 diabetes. This provides preliminary evidence of a cellular response beyond the periodontal tissues, but does not establish improved glucose control or vascular outcomes.
Read the full article Back to Research

Research  |  24.10.17

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Periodontitis-Diabetes Hub Position: Diabetes Co-Lead

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Professor Mark Ide

Periodontitis-Diabetes Hub Position: Periodontology Co-Lead

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