Smoking and periodontal disease.
Numerous investigations of the relationship between smoking and periodontal disease have been performed over the last 15 years, and there now exists a substantial body of literature upon which this current review is based. From both cross-sectional and longitudinal studies, there appears to be strong epidemiological evidence that smoking confers a considerably increased risk of periodontal disease. This evidence is further supported by the data emanating from patients who stop smoking. These patients have levels of risk similar to those of non-smokers. Numerous studies of the potential mechanisms whereby smoking tobacco may predispose to periodontal disease have been conducted, and it appears that smoking may affect the vasculature, the humoral immune system, and the cellular immune and inflammatory systems, and have effects throughout the cytokine and adhesion molecule network. The aim of this review is to consider the evidence for the association between smoking and periodontal diseases and to highlight the biological mechanisms whereby smoking may affect the periodontium.
Kinane
D F
DF
Periodontology and Oral Immunology, University of Glasgow Dental Hospital and School, Scotland, UK.
Chestnutt
I G
IG
D001861:Bone Regeneration / Q000187:drug effects; D016207:Cytokines / Q000096:biosynthesis; D003773:Dental Plaque / Q000382:microbiology; D004305:Dose-Response Relationship, Drug; D006801:Humans; D009538:Nicotine / Q000633:toxicity; D018722:Nicotinic Agonists / Q000633:toxicity; D010510:Periodontal Diseases / Q000209:etiology*; D010519:Periodontium / Q000187:drug effects / Q000378:metabolism; D018570:Risk Assessment; D012907:Smoking / Q000009:adverse effects*; D016540:Smoking Cessation; D014662:Vasoconstrictor Agents / Q000633:toxicity; D014945:Wound Healing / Q000187:drug effects
D016207:Cytokines; D018722:Nicotinic Agonists; D014662:Vasoconstrictor Agents; D009538:Nicotine