Tobacco Use and Periodontal Disease—The Role of Microvascular Dysfunction

SIMPLE SUMMARY: Periodontal disease consists of a wide range of inflammatory conditions that affect the supporting apparatus of teeth, and is highly prevalent in adults worldwide. Tobacco use is currently recognized as the most important risk factor for periodontal disease as it negatively affects both disease evolution and therapeutic strategies. Given close contact with tobacco products, oral microcirculation becomes dysfunctional which, in turn, aggravates periodontal disease. This paper intends to provide a comprehensive review about the impact of tobacco use on oral microcirculation and the mechanisms underlying periodontal disease aggravation. Acute nicotine administration or tobacco use increases oral perfusion (gingiva, lip, tongue) of healthy subjects due to local irritation and increased blood pressure, which overcome neural- and endocrine-mediated vasoconstriction. Chronic tobacco use, particularly smoking, causes several morphological changes to oral microcirculation, namely, increased vascular density and tortuosity, despite a decrease in capillary diameter, and decreased perfusion due to the multiple vasoconstrictive insults. Periodontal disease involves considerable gingival inflammation and angiogenesis in non-smokers which, in chronic smokers, are considerably suppressed, in part due to local immune suppression and oxidative stress. Tobacco exposure, irrespective of form of use, causes long-term microvascular dysfunction which may not be completely reversible upon cessation, and increases the risk of complications due to the natural disease course or secondary to therapeutic strategies. ABSTRACT: Periodontal disease consists in highly prevalent wide-ranging inflammatory conditions that affect the supporting apparatus of teeth. Tobacco use is the most important risk factor for periodontal disease as it increases disease severity and periodontal surgery complications. Tobacco use is harmful for the vasculature by causing microvascular dysfunction, which is known to negatively affect periodontal disease. To the author’s knowledge this paper is the first comprehensive review on the mechanisms by which tobacco use affects oral microcirculation and impacts the pathophysiology of periodontal disease. In healthy subjects, acute nicotine administration or tobacco use (smoking/smokeless forms) increases the blood flow in the oral mucosa due to local irritation and increased blood pressure, which overcome neural- and endocrine-mediated vasoconstriction. Chronic tobacco smokers display an increased gingival microvascular density, which is attributed to an increased capillary recruitment, however, these microcirculatory units show higher tortuosity and lower caliber. These morphological changes, together with the repetitive vasoconstrictive insults, contribute to lower gingival perfusion in chronic smokers and do not completely regress upon smoking cessation. In periodontal disease there is considerable gingival inflammation and angiogenesis in non-smokers which, in chronic smokers, are considerably suppressed, in part due to local immune suppression and oxidative stress. Tobacco exposure, irrespective of the form of use, causes long-term microvascular dysfunction that increases the risk of complications due to the natural disease course or secondary therapeutic strategies.