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Keywords:

  • smoking;
  • periodontitis;
  • bacteria;
  • neutrophils;
  • lymphocytes;
  • fibroblasts

Abstract

Aim: To review the potential biological mechanisms underlying the effects of tobacco smoking on periodontitis.

Main findings: Smoking has major effects on the host response, but there are also a number of studies that show some microbiological differences between smokers and non-smokers.

Smoking has a long-term chronic effect on many important aspects of the inflammatory and immune responses. Histological studies have shown alterations in the vasculature of the periodontal tissues in smokers. Smoking induces a significant systemic neutrophilia, but neutrophil transmigration across the periodontal microvasculature is impeded. The suppression of neutrophil cell spreading, chemokinesis, chemotaxis and phagocytosis have been described. Protease release from neutrophils may be an important mechanism in tissue destruction. Tobacco smoke has been found to affect both cell-mediated immunity and humoral immunity. Research on gingival crevicular fluid has demonstrated that there are lower levels of cytokines, enzymes and possibly polymorphonuclear cells in smokers. In vitro studies have shown detrimental effects of nicotine and some other tobacco compounds on fibroblast function, including fibroblast proliferation, adhesion to root surfaces and cytotoxicity.

Conclusion: Tobacco smoking has widespread systemic effects, many of which may provide mechanisms for the increased susceptibility to periodontitis and the poorer response to treatment.