Mechanisms of Action of Tobacco Smoking

Objectives: to describe the potential pathogenic mechanisms involved in periodontitis in tobacco smokers. Methods: A comprehensive review of the literature Results: Although smokers may have more severe periodontitis, paradoxically they often appear to have lower signs and symptoms of inflammation. Tobacco smoke contains a large number of noxious agents which may affect the inflammatory and immune responses. Smoking has a long-term chronic effect impairing the vasculature of the periodontal tissues that can be observed through less gingival redness, lower bleeding on probing, and fewer vessels visible clinically and histologically. The detrimental effects on neutrophil function are well established. Although smoking induces a significant systemic neutrophilia, neutrophil transmigration across the periodontal microvasculature is impeded and resultant induction of protease release within the tissues may be important in disease progression. The suppression of neutrophil cell spreading, chemokinesis, chemotaxis and phagocytosis in smokers contribute to impaired defence. Tobacco smoke, especially the particulate phase, has also been shown to affect both humoral immunity and cell-mediated immunity. Acute or chronic exposure to hydrocarbons may stimulate or inhibit the immune response, the net effect being dependent upon the dose and duration of the exposure to components of tobacco smoke. Smoking has a detrimental effect on healing through its affects on the vasculature, revascularisation, the inflammatory response and many aspects of fibroblast function. 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.