Whole cigarette smoke promotes human gingival epithelial cell apoptosis and inhibits cell repair processes

Authors


Mahmoud Rouabhia, PhD, Professor, Groupe de Recherche en Écologie Buccale, Faculté de Médecine Dentaire, Université Laval, Québec, QC, Canada G1V 0A6
Tel: +418 656 2131, ext. 16321
Fax: +418 656 2861
e-mail: mahmoud.rouabhia@fmd.ulaval.ca

Abstract

Semlali A, Chakir J, Goulet J-P, Chmielewski W, Rouabhia M. Whole cigarette smoke promotes human gingival epithelial cell apoptosis and inhibits cell repair processes. J Periodont Res 2011; 46: 533–541.
©2011 John Wiley & Sons A/S

Background and Objective:  Smoking cigarettes increases the risk of developing various types of human diseases, including cancers and periodontitis. As gingival epithelial cells are known to play an active role in innate immunity via the secretion of a wide variety of mediators, and as these cells are the first ones exposed to environmental stimuli such as cigarette smoke, we sought to investigate the effects of whole cigarette smoke on normal human gingival epithelial cells and tissue.

Material and Methods:  Human gingival epithelial cells were extracted from healthy nonsmokers and used either as a monolayer or as an engineered human oral mucosa to investigate the effect of whole cigarette smoke on cell growth, apoptosis and wound repair/migration.

Results:  Our findings show that when gingival epithelial cells were exposed once to whole cigarette smoke, this resulted in a significant inhibition of cell growth through an apoptotic pathway, as confirmed by an increase of Bax and a decrease of Bcl-xL and caspase-3 activity. Cigarette smoke also inhibited epithelial cell migration. These effects may explain the disorganization of the engineered human oral mucosa tissue when exposed to whole cigarette smoke.

Conclusion:  Exposure to whole cigarette smoke markedly inhibits epithelial cell growth through an apoptosis/necrosis pathway that involves Bax and Bcl-xL proteins and caspase-3 activity. Cigarette smoke also disrupts epithelial cell migration, which may negatively affect periodontal wound healing.

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