A review of the evidence for pathogenic mechanisms that may link periodontitis and diabetes

John J. Taylor (Lead / Corresponding author), Philip M. Preshaw, Evanthia Lalla

Research output: Contribution to journalReview articlepeer-review

273 Citations (Scopus)


Aims To review the evidence for the molecular and cellular processes that may potentially link periodontal disease and diabetes. The pathogenic roles of cytokines and metabolic molecules (e.g. glucose, lipids) are explored and the role of periodontal bacteria is also addressed. Paradigms for bidirectional relationships between periodontitis and diabetes are discussed and opportunities for elaborating these models are considered. Methods Database searches were performed using MeSH terms, keywords, and title words. Studies were evaluated and summarized in a narrative review. Results Periodontal microbiota appears unaltered by diabetes and there is little evidence that it may influence glycaemic control. Small-scale clinical studies and experiments in animal models suggest that IL-1β, TNF-α, IL-6, OPG and RANKL may mediate periodontitis in diabetes. The AGE-RAGE axis is likely an important pathway of tissue destruction and impaired repair in diabetes-associated periodontitis. A role for locally activated pro-inflammatory factors in the periodontium, which subsequently impact on diabetes, remains speculative. Conclusion There is substantial information on potential mechanistic pathways which support a close association between diabetes and periodontitis, but there is a real need for longitudinal clinical studies using larger patient groups, integrated with studies of animal models and cells/tissues in vitro.

Original languageEnglish
Pages (from-to)S113-S134
Number of pages22
JournalJournal of Clinical Periodontology
Issue numberSUPPL. 14
Publication statusPublished - 30 Apr 2013


  • adipokines
  • AGE
  • cytokines
  • diabetes
  • hyperglycaemia
  • inflammation
  • periodontal disease
  • plaque bacteria
  • RAGE

ASJC Scopus subject areas

  • Periodontics


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