Abstract
Electronic-cigarettes (e-cigs) represent a significant and increasing proportion of tobacco product consumption, which may pose an oral health concern. Oxidative/carbonyl stress via protein carbonylation is an important factor in causing inflammation and DNA damage. This results in stress-induced premature senescence (a state of irreversible growth arrest which re-enforces chronic inflammation) in gingival epithelium, which may contribute to the pathogenesis of oral diseases. We show that e-cigs with flavorings cause increased oxidative/carbonyl stress and inflammatory cytokine release in human periodontal ligament fibroblasts, Human Gingival Epithelium Progenitors pooled (HGEPp), and epigingival 3D epithelium. We further show increased levels of prostaglandin-E2 and cycloxygenase-2 are associated with upregulation of the receptor for advanced glycation end products (RAGE) by e-cig exposure-mediated carbonyl stress in gingival epithelium/tissue. Further, e-cigs cause increased oxidative/carbonyl and inflammatory responses, and DNA damage along with histone deacetylase 2 (HDAC2) reduction via RAGE-dependent mechanisms in gingival epithelium. A greater response is elicited by flavored e-cigs. Increased oxidative stress, pro-inflammatory and pro-senescence responses (DNA damage and HDAC2 reduction) can result in dysregulated repair due to proinflammatory and pro-senescence responses in periodontal cells. These data highlight the pathologic role of e-cig aerosol and its flavoring to cells and tissues of the oral cavity in compromised oral health.
Highlights
The use of electronic-cigarettes (e-cigs) is increasing in the United States, which may pose oral health concerns [1]
IL-8 release was significantly higher in both BLU® Classic Tobacco (16 mg nicotine) and Magnificent Menthol e-cig vapor exposed human periodontal ligament fibroblasts (HPdLFs) cells compared to the controls
We did not see a significant increase in IL-8 release in Human Gingival Epithelium Progenitors pooled (HGEPp) cells exposed to BLU® Magnificent Menthol e-cig vapor compared to control (Figure 1D)
Summary
The use of electronic-cigarettes (e-cigs) is increasing in the United States, which may pose oral health concerns [1]. Aldehyde causes carbonyl/oxidative stress, DNA adducts/damage, as well as stress-induced cellular senescence (a state of irreversible growth arrest which re-enforces chronic inflammation) [4, 5] leading to oral health problems [6,7,8]. It is important to mention that bleeding upon probing (a classical marker of periodontal disease activity) is masked in tobacco smokers than non-smokers [11, 12]. This most likely occurs as a result of the vasoconstrictive effect of nicotine (nicotine is the main component in e-cigs) on gingival blood vessels. Tobacco smokers may remain unaware of ongoing periodontal destruction until the inflammatory process reaches a stage where tooth mobility becomes evident
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