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Abstract

Tobacco smoking is the most important preventable risk factor for periodontitis; however, the underlying biological mechanisms responsible for the detrimental effects of smoking on periodontal health remain largely unclear. It is also well established that smoking has a negative impact on several inflammatory diseases, including rheumatoid arthritis, multiple sclerosis and inflammatory bowel disease. The aim of this paper was to review smoking-related changes in local and systemic host responses with a focus on cellular and molecular effects that could explain a hyperinflammatory response leading to periodontal destruction. Biological mechanisms that may be common to periodontal disease and other chronic inflammatory diseases were also explored, together with gene–smoking interactions. An epidemiologic perspective on the burden of smoking on periodontal health and the potential for smoking cessation is also presented. Tobacco smoking seems to induce changes ranging from decreased leukocyte chemotaxis to decreased production of immunoglobulins. Smoking also seems to cause a stronger inflammatory reaction with an increased release of potentially tissue-destructive substances (e.g. reactive oxygen species, collagenase, serine proteases and proinflammatory cytokines). These findings support a hypothesis that periodontitis is a hyperinflammatory condition rather than a hypo-inflammatory condition.