E-cigarettes and flavorings induce inflammatory and pro-senescence responses in oral epithelial cells and periodontal fibroblasts

• DOI: 10.18632/oncotarget.12857
• Publication Date: 2016-10-24T19:08:17Z
• Authors: Isaac K. Sundar; Fawad Javed; Georgios E. Romanos; Irfan Rahman
• Keywords: Proinflammatory cytokine; Senescence; Junctional epithelium

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 important factor in causing inflammation DNA damage. This results stress-induced premature senescence (a state irreversible growth arrest re-enforces chronic inflammation) gingival epithelium, contribute to the pathogenesis diseases. We show that e-cigs with flavorings cause increased oxidative/carbonyl inflammatory cytokine release human periodontal ligament fibroblasts, Human Gingival Epithelium Progenitors pooled (HGEPp), epigingival 3D epithelium. further levels prostaglandin-E2 cycloxygenase-2 are associated upregulation receptor for advanced glycation end products (RAGE) by e-cig exposure-mediated carbonyl epithelium/tissue. Further, responses, damage along histone deacetylase 2 (HDAC2) reduction RAGE-dependent mechanisms A greater response elicited flavored e-cigs. Increased oxidative stress, pro-inflammatory pro-senescence responses (DNA HDAC2 reduction) can result dysregulated repair due proinflammatory cells. These data highlight pathologic role aerosol its flavoring cells tissues cavity compromised health.