In vitro effect of smokeless tobacco on gingival epithelial cells
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Department of Periodontology, Faculty of Dentistry, Eskisehir Osmangazi University, Eskisehir, Turkey
Finnish Doctoral Program in Oral Sciences (FINDOS), University of Turku, Institute of Dentistry, Turku, Finland
Department of Restorative Dentistry, and Cariology, and Adhesive Dentistry Research Group, Institute of Dentistry, University of Turku, Finland
Turku University Hospital, TYKS, University of Turku, Turku, Finland
Publish date: 2017-05-25
Submission date: 2017-05-10
Acceptance date: 2017-05-10
Tob. Prev. Cessation 2017;3(May Supplement):87
Cigarette smoking is one of the major risk factors in the pathogenesis of periodontal disease. Despite numerous reports on the general toxic effects of oral smokeless tobacco very few studies have assessed the effect of smokeless tobacco on the viability and inflammatory response of gingival epithelial cells.

Material and Methods:
In this study a reference smokeless tobacco (CORESTA CRP2) was used to stimulate gingival epithelial cells. Once the gingival epithelial cells became confluent, the growth medium were conditioned with aqueous extract of CORESTA CRP2 for 3 and 6 hours. Cell viability was measured by alamar blue assay, and cell culture supernatant was examined for the presence of human interlukin-1beta (IL-1beta) using sandwich enzyme-linked immunosorbant assay (ELISA).

Cells treated with smokeless tobacco reference product resulted in decreased viability compared to non stimulated group (P<0.05). In addition, the smokeless tobacco extract augmented the production of IL-1beta in a time -dependent manner (P< 0.05). The micrographs showed that smokeless tobacco extract resulted in a significant change in cell appearance, from the cells being in close contact to becoming separated from each other.

Epithelial cells are the first line of defense against pathogens in the oral cavity. The results suggest that smokeless tobacco not only inhibits the growth of epithelial cells but also induce the generation of inflammatory cytokines which leads to smokeless tobacco-exacerbated disease.

Arzu Beklen   
Department of Periodontology, Faculty of Dentistry, Eskisehir Osmangazi University, Dede Mahallesi, 26030 Odunpazarı Eskisehir, Turkey