The role of smoking in periodontal diseases: Action mechanisms and clinical implications. A review article

Abstract

Smoking, a major systemic risk factor, has a profound negative impact on the development and course of periodontal disease. The mechanisms by which tobacco influences disease pathogenesis are complex by altering the microbial ecosystem, deregulating the host's immune response, compromising gingival microcirculation, and disrupting the metabolism of periodontal tissues caused by chemical components in cigarette smoke. This complex interaction at the molecular and cellular levels is mediated by the thousands of chemical compounds present in cigarette smoke. Nicotine increases the adhesion of certain pathogenic bacteria to the dental and gingival surfaces, favoring the formation of a more virulent biofilm. As far as the immune response is concerned, smoking not only depresses the function of neutrophils, but also influences the activity of T and B lymphocytes, crucial cells in adaptive immunity, thus unbalancing the entire local immune response. Clinical implications, including the effect on periodontal treatment, the risk of dental complications and loss, and implant considerations, are also essential. Smokers have a significantly higher risk of developing periodontal disease, and its progression is accelerated.