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.
Recent updates on electronic cigarette aerosol and inhaled nicotine effects on periodontal and pulmonary tissues.
F. Javed,S. Kellesarian,I. Sundar,G. Romanos,I. Rahman
Published 2017 in Oral Diseases
ABSTRACT
PUBLICATION RECORD
- Publication year
2017
- Venue
Oral Diseases
- Publication date
2017-03-30
- Fields of study
Medicine, Environmental Science
- Identifiers
- External record
- Source metadata
Semantic Scholar, PubMed
CITATION MAP
EXTRACTION MAP
CLAIMS
CONCEPTS
- dna damage
Structural injury to DNA, including adduct formation and other molecular lesions.
Aliases: DNA adducts, genotoxic damage
- dysregulated repair
Abnormal or misdirected tissue repair and remodeling response.
Aliases: dysregulated repair responses
- e-cigarette aerosol
Aerosol generated by electronic cigarettes and used as the exposure source in the review.
Aliases: e-vapor, e-vapor exposure, e-cig vapor
- e-cigarette-derived inhaled nicotine
Nicotine delivered to the body through inhalation of e-cigarette aerosol.
Aliases: inhaled nicotine, nicotine from e-cigarettes
- flavorings aerosol
Flavoring-related constituents present in e-cigarette aerosol mixtures.
Aliases: flavoring aerosol
- gingival fibroblasts
Fibroblast cells from the gingiva used as an oral tissue model.
Aliases: gum fibroblasts
- inflammation
Inflammatory host response discussed in relation to e-cigarette and nicotine exposure.
- myofibroblast differentiation
The transition of fibroblasts into contractile repair cells during tissue healing.
Aliases: fibroblast differentiation into myofibroblasts
- nicotine
The bioactive tobacco alkaloid delivered by e-cigarettes and discussed for its cellular effects.
- oxidative stress
Cellular redox imbalance associated here with reactive oxygen species and related aerosol constituents.
Aliases: reactive oxygen species
- periodontal disease
Disease affecting the supporting tissues of the teeth, including the gums and periodontal ligament.
Aliases: periodontal diseases
- periodontal ligament fibroblasts
Fibroblast cells from the periodontal ligament used as an oral tissue model.
Aliases: PDL fibroblasts
- pulmonary disease
Disease affecting the lungs and lower respiratory tract.
Aliases: lung disease, pulmonary tissues disease
- wound contraction
Reduction in wound size during healing driven by contractile cellular activity.
REFERENCES
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