The paradox of painless periodontal disease

Research output: Contribution to journalArticlepeer-review

29 Citations (Scopus)

Abstract

Periodontal diseases, primarily gingivitis and periodontitis, are characterised by progressive inflammation and tissue destruction. However, they are unusual in that they are not also accompanied by the pain commonly seen in other inflammatory conditions. This suggests that interactions between periodontal bacteria and host cells create a unique environment in which the pro-algesic effects of inflammatory mediators and factors released during tissue damage are directly or indirectly inhibited. In this review, we summarise the evidence that periodontal disease is characterised by an accumulation of classically pro-algesic factors from bacteria and host cells. We then discuss several mechanisms by which inflammatory sensitisation of nociceptive fibres could be prevented through inactivation or inhibition of these factors. Further studies are necessary to fully understand the molecular processes underlying the endogenous localised hypoalgesia in human periodontal disease. This knowledge might provide a rational basis to develop future therapeutic interventions, such as host modulation therapies, against a wide variety of other human pain conditions.

Original languageEnglish
JournalOral Diseases
Early online date1 Aug 2016
DOIs
Publication statusE-pub ahead of print - 1 Aug 2016

Keywords

  • Bacteria
  • Inflammation
  • Pain
  • Periodontitis
  • Protease

Fingerprint

Dive into the research topics of 'The paradox of painless periodontal disease'. Together they form a unique fingerprint.

Cite this