Periodontal inflammation: from gingivitis to systemic disease?

Compend Contin Educ Dent. 2004 Jul;25(7 Suppl 1):16-25.


There has been a resurgence of interest in recent years in the systemic effects of oral infections such as periodontal diseases. The study of the various means by which periodontal infections and inflammation may influence a variety of systemic conditions is collectively referred to as periodontal medicine. The periodontium responds to tooth-borne biofilm (dental plaque) by the process of inflammation. Dental biofilms release a variety of biologically active products, such as bacterial lipopolysaccharides (endotoxins), chemotactic peptides, protein toxins, and organic acids. These molecules stimulate the host to produce a variety of responses, among them the production and release of potent agents known as cytokines. These include interleukin-1 beta, interleukin-8, prostaglandins, and tumor necrosis factor-alpha. There is a spectrum of periodontal response to these molecules, from mild gingivitis to severe destructive periodontitis. These and other host products and responses may influence a variety of important disease pathways, including atherosclerosis, mucosal inflammation, and premature parturition. The purpose of this article is to review the possible biological pathways by which periodontal diseases may influence these disease processes.

MeSH terms

  • Animals
  • Bacteremia / complications
  • Bacteremia / etiology
  • Cardiovascular Diseases / etiology
  • Chronic Disease
  • Female
  • Gingivitis / complications*
  • Humans
  • Immunity / physiology
  • Inflammation Mediators / physiology
  • Obstetric Labor, Premature / etiology
  • Pregnancy
  • Pulmonary Disease, Chronic Obstructive / etiology


  • Inflammation Mediators