Recent updates on electronic cigarette aerosol and inhaled nicotine effects on periodontal and pulmonary tissues

Abstract

E-cigarette-derived inhaled nicotine may contribute to the pathogenesis of periodontal and pulmonary diseases in particular via lung inflammation, injurious, and dysregulated repair responses. Nicotine is shown to have antiproliferative properties and affects fibroblasts in vitro, which may interfere in tissue myofibroblast differentiation in e-cig users. This will affect the ability to heal wounds by decreasing wound contraction. In periodontics, direct exposure to e-vapor has been shown to produce harmful effects in periodontal ligament and gingival fibroblasts in culture. This is due to the generation of reactive oxygen species/aldehydes/carbonyls from e-cig aerosol, leading to protein carbonylation of extracellular matrix and DNA adducts/damage. A limited number of studies regarding the effects of e-cig in oral and lung health are available. However, no reports are available to directly link the deleterious effects on e-cigs, inhaled nicotine, and flavorings aerosol on periodontal and pulmonary health in particular to identify the risk of oral diseases by e-cigarettes and nicotine aerosols. This mini-review summarizes the recent perspectives on e-cigarettes including inhaled nicotine effects on several pathophysiological events, such as oxidative stress, DNA damage, innate host response, inflammation, cellular senescence, profibrogenic and dysregulated repair, leading to lung remodeling, oral submucous fibrosis, and periodontal diseases.

Keywords: e-cigarettes; fibrosis; inflammation, lung; oxidative stress; periodontium.

Fig. 1. Possible mechanism of e-cigarette induced inflammatory and dysregulated repair responses to inhaled nicotine

Inhaled nicotine impact effects on lung and systemic inflammatory mediators in oral fluids and causes dysregulated repair responses via its receptor α7 nicotinic acetylcholine receptor (α7nAChR). Nicotine also causes impaired wound healing due to inhibition of myofibroblasts differentiation and/or epithelial-mesenchymal transition. Oxidative stress and vascular remodeling by inhaled nicotine may trigger inflammatory responses in periodontal tissues. Oxidative stress can lead to carbonylation of extracellular matrix and further deposition of modified matrix. All these responses are associated with initiation of oral submucosal fibrosis.