Title of article :
Effects of electronic cigarette liquid on monolayer and 3D tissue-engineered models of human gingival mucosa
Author/Authors :
Shaikh, Zahab N School of Clinical Dentistry - University of Sheffield - Claremont Crescent - Sheffield - S10 2TA - UK , Alqahtani, Abdullah School of Clinical Dentistry - University of Sheffield - Claremont Crescent - Sheffield - S10 2TA - UK , Almela, Thafar School of Clinical Dentistry - University of Sheffield - Claremont Crescent - Sheffield - S10 2TA - UK , Franklin, Kirsty School of Clinical Dentistry - University of Sheffield - Claremont Crescent - Sheffield - S10 2TA - UK , Tayebi, Lobat Marquette University School of Dentistry - Milwaukee - WI 53233 - USA , Moharamzadeh, Keyvan School of Clinical Dentistry - University of Sheffield - Claremont Crescent - Sheffield - S10 2TA - UK - Marquette University School of Dentistry - Milwaukee - WI 53233 - USA
Abstract :
Background. There is limited data available on potential biological effects of E-cigarettes on human oral tissues. The aim
of this study was to evaluate the effects of E-cigarette liquid on the proliferation of normal and cancerous monolayer and 3D
models of human oral mucosa and oral wound healing after short-term and medium-term exposure.
Methods. Normal human oral fibroblasts (NOF), immortalized OKF6-TERET-2 human oral keratinocytes, and cancerous
TR146 keratinocyte monolayer cultures and 3D tissue engineered oral mucosal models were exposed to different concentrations (0.1%, 1%, 5% and 10%) of E-cigarette liquid (12 mg/ml nicotine) for 1 hour daily for three days and for 7 days. Tissue
viability was monitored using the PrestoBlue assay. Wounds were also produced in the middle surface of the monolayer
systems vertically using a disposable cell scraper. The alterations in the cell morphology and wound healing were visualized
using light microscopy and histological examination.
Results. Statistical analysis showed medium-term exposure of TR146 keratinocytes to 5% and 10% E-liquid concentrations
significantly increased the viability of the cancer cells compared to the negative control. Short-term exposure of NOFs to
10% E-liquid significantly reduced the cell viability, whereas medium-term exposure to all E-liquid concentrations significantly reduced the NOF cells’ viability. OKF6 cells exhibited significantly lower viability following short-term and mediumterm exposure to all E-cigarette concentrations compared to the negative control. 3D oral mucosal model containing normal
oral fibroblasts and keratinocytes showed significant reduction in tissue viability after exposure to 10% E-liquid, whereas
medium-term exposure resulted in significantly lower viability in 5% and 10% concentration groups compared to the negative
control. There was a statistically significant difference in wound healing times of both NOF and OKF6 cells after exposure
to 1%, 5% and 10% E-cigarette liquid.
Conclusion. Medium-term exposure to high concentrations of the E-cigarette liquid had cytotoxic effects on normal human
oral fibroblasts and OKF6 keratinocytes, but a stimulatory cumulative effect on the growth of cancerous TR146 keratinocyte
cells as assessed by the PrestoBlue assay and histological evaluation of 3D oral mucosal models. In addition, E-liquid exposure prolonged the wound healing of NOF and OKF6 oral mucosa cells.
Keywords :
Electronic cigarette , cytotoxicity , keratinocyte , fibroblast , tissue engineering , wound healing
Journal title :
Journal of Advanced Periodontology and Implant Dentistry