Evidence map›Paper›PMID 27791204›Full record

ArticleOncotarget2016

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

Isaac K Sundar, Fawad Javed, Georgios E Romanos, Irfan Rahman

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 131 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
131citing papers in PubMed, 4 pooled it
12.8field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

131 citing papers in PubMed, 4 syntheses or guidelines pooled it, 229 citations in OpenAlex.

  1. Guideline
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  4. Pulmonary effects of e-liquid flavors: a systematic review.Journal of toxicology and environmental health. Part B, Critical reviews · 2022
    Pooled it
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71 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 1 country.

Isaac K SundarDepartment of Environmental Medicine, University of Rochester Medical Center, Rochester, NY, USA.
Fawad JavedDepartment of General Dentistry, Eastman Institute for Oral Health University of Rochester, Rochester, NY, USA.
Georgios E RomanosDepartment of Periodontology, School of Dental Medicine, Stony Brook University, Stony Brook, NY, USA.
Irfan RahmanDepartment of Environmental Medicine, University of Rochester Medical Center, Rochester, NY, USA.
University of Rochester Medical Center · USStony Brook School · USUniversity of Rochester · US

Funding

MECHANISMS OF CIGARETTE SMOKE-INDUCED LUNG CELLULAR SENESCENCER01HL085613 · NHLBI · UNIVERSITY OF ROCHESTER · PI RAHMAN, IRFAN · 2007 to 2017
$4.0M
NHLBI NIH HHS R01 HL085613
6 · The paper itself

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.

Indexed as

Cells, CulturedCellular SenescenceCytokinesDNA DamageElectronic Nicotine Delivery SystemsEpithelial CellsFibroblastsFlavoring AgentsGingivaGlycation End Products, AdvancedHistone Deacetylase 2HumansInflammationMouthOxidative StressPeriodontal LigamentCytokinesFlavoring AgentsGlycation End Products, AdvancedHDAC2 protein, humanHistone Deacetylase 2COX2e-cigarettese-juicesPGE2RAGE

Identifiers

PMID27791204
PMCPMC5363580
OpenAlexW2536294440

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.