ReviewAnatomy & cell biology2026
Vape flavoring chemicals and oral fibroblast viability.
Review in Anatomy & cell biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The widespread use of electronic cigarettes is due to the variety of appealing flavor additives marketed to consumers. Although perceived as a less harmful alternative to traditional smoking, emerging evidence suggests that inhaled e-cigarettes aerosol poses multiple risks on oral health. Oral fibroblasts which maintain the extracellular matrix and support wound repair, may be vulnerable to chemical injury. While the toxic effects of base e-liquid components such as nicotine have been investigated, limited research has addressed how added flavoring chemicals influence oral fibroblast survival and stress responses. A comprehensive search was conducted across PubMed, ScienceDirect, and Google Scholar to identify peer-reviewed studies evaluating the biological impact of flavored e-cigarette exposure on human oral fibroblasts. Collective findings revealed consistent mechanistic trends: flavoring chemicals, especially aromatic aldehydes such as cinnamaldehyde and vanillin, induced adverse cellular responses, increasing intracellular reactive oxygen species, and triggering oxidative modifications. These oxidative injuries such as protein carbonylation promote pro-inflammatory responses in oral fibroblasts, specifically heightened secretion of cytokine interleukin-8 and lipid mediator prostaglandin E
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Registered trials
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.