Variables associated with oral health-related self-efficacy - results of a cross-sectional study.

BACKGROUND: Oral health-related self-efficacy (OH-SE) is pivotal for oral health and is associated with other oral-health related variables, such as dental fear and anxiety (DF/A) and dental hygiene behaviors (DHB). This study attempts to analyze associations between OH-SE and oral healthrelated variables in a German population to extend previous research by analyzing whether OH-SE can be predicted by these variables, as this might contribute to the development of treatment interventions. METHODS: OH-SE, DF/A, oral health-related quality of life (OHRQoL), self-perceived dental condition, satisfaction with general health, DHB, and socioeconomic status were assessed as a part of the Saxon Longitudinal Study in an adult sample (n = 309, 56.3% female, all Saxon secondary school 8th graders in 1987). The associations of OH-SE with these variables were examined by means of correlation, multiple linear regression analyses, and group comparisons. Significance (p), standardized regression coefficients (ß), and effect size (Cohen's d) were calculated. RESULTS: The correlation analyses revealed increased OH-SE to be accompanied by low levels of DF/A, high levels of OHRQoL, high levels of self-perceived dental condition, increased satisfaction with general health and socioeconomic status (all r ≥ 0.142; all p ≤ 0.013). In the regression analysis, OH-SE was mainly predicted by self-perceived dental condition and satisfaction with general health (R2 = 0.157) as well as by daily frequency of toothbrushing, OHRQoL, and socioeconomic status on a trend-level basis. In the group comparisons OH-SE was lower in participants with moderate for manifest DF/A and higher in individuals with higher OHRQoL, better self-perceived dental condition, increased satisfaction with general health, increased daily frequency of toothbrushing, more dental appointments, and above-average socioeconomic status (trend level; all t ≥ 1.57; p ≤ 0.059). CONCLUSIONS: In this cross-sectional study, high levels of OH-SE were mainly predicted by general health as well as self-perceived dental condition. It was also associated with decreased DF/A, increased DHB, higher OHRQoL, and higher socioeconomic status. Future research should analyze these associations in longitudinal designs to address whether interventions focusing on adherence to good DHB improve (dental) health and thus OH-SE. This might be a promising approach, particularly in relation to the treatment of DF/A.

E-Cigarette Vapor Induces an Apoptotic Response in Human Gingival Epithelial Cells Through the Caspase-3 Pathway.

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.

Antagonistic effect of Candida albicans and IFNγ on E-cadherin expression and production by human primary gingival epithelial cells.

Caused mainly by Candida albicans, oropharyngeal candidiasis is the most common oral complication associated with HIV disease worldwide. Host defenses against C. albicans essentially fall into two categories: specific immune mechanisms and local oral mucosal epithelial cell defenses. Since oral mucosa is the first line of defense in the form of a physical barrier against C. albicans invasion, and since epithelial cells are involved in anti-Candida innate immunity through different cytokines, we wanted to determine whether C. albicans alters E-cadherin expression and production, and whether interferon-γ (INFγ), a TH1 cytokine, is involved in the anti-Candida defense. Using primary human gingival epithelial cells, we demonstrated that C. albicans significantly decreased E-cadherin mRNA expression and protein production. This effect was basically obtained at later infective periods (24 and 48h). Interestingly, when IFNγ was added to C. albicans infected epithelial cell cultures, it prevented the side effect of C. albicans on E-cadherin mRNA expression and protein production and deposition. All together, these results suggested concomitant interactions between oral epithelial cells and IFNγ against C. albicans infection.

Disruption of the ECM33 gene in Candida albicans prevents biofilm formation, engineered human oral mucosa tissue damage and gingival cell necrosis/apoptosis.

In this study we demonstrated that ΔCaecm33 double mutant showed reduced biofilm formation and causes less damage to gingival mucosa tissues. This was confirmed by the reduced level of necrotic cells and Bax/Bcl2 gene expression as apoptotic markers. In contrast, parental and Caecm33 mutant strains decreased basement membrane protein production (laminin 5 and type IV collagen). We thus propose that ECM33 gene/protein represents a novel target for the prevention and treatment of infections caused by Candida.

E-Cigarettes Increase Candida albicans Growth and Modulate its Interaction with Gingival Epithelial Cells.

Electronic cigarette (e-cigarette) vapor comes in contact with the different constituents of the oral cavity, including such microorganisms as Candida albicans. We examined the impact of e-cigarettes on C. albicans growth and expression of different virulent genes, such as secreted aspartic proteases (SAPs), and the effect of e-cigarette vapor-exposed C. albicans on gingival epithelial cell morphology, growth, and lactate dehydrogenase (LDH) activity. An increase in C. albicans growth was observed with nicotine-rich e-cigarettes compared with non-exposed cultures. Following exposure to e-cigarette vapor, C. albicans produced high levels of chitin. E-cigarettes also increased C. albicans hyphal length and the expression of SAP2, SAP3, and SAP9 genes. When in contact with gingival epithelial cells, e-cigarette-exposed C. albicans adhered better to epithelial cells than the control. Indirect contact between e-cigarette-exposed C. albicans and gingival epithelial cells led to epithelial cell differentiation, reduced cell growth, and increased LDH activity. Overall, results indicate that e-cigarettes may interact with C. albicans to promote their pathogenesis, which may increase the risk of oral candidiasis in e-cigarette users.

Cigarette smoke-exposed Candida albicans increased chitin production and modulated human fibroblast cell responses.

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-1ß 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.