Electronic cigarettes represent an increasingly significant proportion of today's consumable tobacco products. E-cigarettes contain several chemicals which may promote oral diseases. The aim of this study was to investigate the effect of e-cigarette vapor on human gingival epithelial cells. Results show that e-cigarette vapor altered the morphology of cells from small cuboidal form to large undefined shapes. Both single and multiple exposures to e-cigarette vapor led to a bulky morphology with large faint nuclei and an enlarged cytoplasm. E-cigarette vapor also increased L-lactate dehydrogenase (LDH) activity in the targeted cells. This activity was greater with repeated exposures. Furthermore, e-cigarette vapor increased apoptotic/necrotic epithelial cell percentages compared to that observed in the control. Epithelial cell apoptosis was confirmed by TUNEL assay showing that exposure to e-cigarette vapor increased apoptotic cell numbers, particularly after two and three exposures. This negative effect involved the caspase-3 pathway, the activity of which was greater with repeated exposure and which decreased following the use of caspase-3 inhibitor. The adverse effects of e-cigarette vapor on gingival epithelial cells may lead to dysregulated gingival cell function and result in oral disease. J. Cell. Physiol. 232: 1539-1547, 2017. © 2016 Wiley Periodicals, Inc.

The predisposition of cigarette smokers for development of respiratory and oral bacterial infections is well documented. Cigarette smoke can also contribute to yeast infection. The aim of this study was to investigate the effect of cigarette smoke condensate (CSC) on C. albicans transition, chitin content, and response to environmental stress and to examine the interaction between CSC-pretreated C. albicans and normal human gingival fibroblasts. Following exposure to CSC, C. albicans transition from blastospore to hyphal form increased. CSC-pretreated yeast cells became significantly (P < 0.01) sensitive to oxidation but significantly (P < 0.01) resistant to both osmotic and heat stress. CSC-pretreated C. albicans expressed high levels of chitin, with 2- to 8-fold recorded under hyphal conditions. CSC-pretreated C. albicans adhered better to the gingival fibroblasts, proliferated almost three times more and adapted into hyphae, while the gingival fibroblasts recorded a significantly (P < 0.01) slow growth rate but a significantly higher level of IL-1β when in contact with CSC-pretreated C. albicans. CSC was thus able to modulate both C. albicans transition through the cell wall chitin content and the interaction between C. albicans and normal human gingival fibroblasts. These findings may be relevant to fungal infections in the oral cavity in smokers.

These results suggest that CSC may contribute to deregulating fibroblast functions. This can compromise fibroblast-epithelial cell interactions, which ultimately increases the risk of gingival tissue damage and the onset of periodontitis.

The goal of this study was to optimize key processes in recreating functional and viable palatal mucosa-like tissue that would be easy to handle and would promote wound healing. Normal human gingival fibroblasts and epithelial cells and a clinically useful biomaterial, CollaTape, were used. Structural and ultrastructural analyses showed that the gingival fibroblasts and epithelial cells adhered to the biomaterial and proliferated. Following a 6-day culture, using 10(5) fibroblasts and 10(6) epithelial cells, a well-organized palatal mucosa-like tissue was engineered. The engineered epithelium displayed various layers, including a stratum corneum, and contained cytokeratin 16-positive cells located in the supra-basal layer. This palatal mucosa-like engineered tissue was designed to meet a variety of surgical needs. The biodegradable collagen membrane (CollaTape) contributed to the flexibility of the engineered tissue. This engineered innovative tissue may contribute to the reconstruction of oral soft-tissue defects secondary to trauma, congenital defects, and acquired diseases.

Abstract:The aim of this study was to evaluate the link between Candida albicans growth and dimorphism and the production of keratins by oral epithelial cells. Various culture models (monolayer and non-keratinized and keratinized engineered human oral mucosa) were produced and used for this purpose. Cell morphology, tissue structure, and the transition of C. albicans were assessed following cell and tissue infections. Keratin production by epithelial cells exposed to C. albicans was evaluated by Western blotting. Following contact with C. albicans, epithelial cells in the monolayer cultures showed differentiating phenotypes. Compared to the keratinized tissue, the non-keratinized mucosa displayed visible disorganization. The transition of C. albicans from blastospore to hyphal form was significantly lower in the keratinized oral mucosa model. This was correlated with the high levels of differentiating (K10) and proliferating (K14, K16, and K19) keratins in the keratinized tissue, suggesting that tissue stratification contributes to controlling C. albicans pathogenicity via keratin production. Thus, the transition of C. albicans from blastospore to hyphal form may be linked to keratin production. This may ultimately have implications in the control of oral candidiasis as well as in denture design to prevent denture stomatitis.