Neutralizing effect of green tea epigallocatechin-3-gallate on nicotine-induced toxicity and chemokine (C-C motif) ligand 5 secretion in human oral epithelial cells and fibroblasts.

AIM: Tobacco use has been identified as the most important environmental risk factor for periodontitis. The aim of this study was to investigate the effect of green tea epigallocatechin-3-gallate on the nicotine-induced toxic and inflammatory responses in oral epithelial cells and gingival fibroblasts. METHODS: The effect of nicotine, alone and in combination with the lipopolysaccharide of Aggregatibacter actinomycetemcomitans, on the viability of oral epithelial cells and fibroblasts was evaluated using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide colorimetric assay. The ability of epigallocatechin-3-gallate to neutralize the nicotine-induced cytotoxicity was then investigated. The nicotine-induced cytokine secretion in epithelial cells and the inhibitory effect of epigallocatechin-3-gallate were determined by enzyme-linked immunosorbent assay. RESULTS: Our results indicated that nicotine caused a dose-dependent loss of viability in both epithelial cells and fibroblasts. A mixture of nicotine and A. actinomycetemcomitans lipopolysaccharide demonstrated additive instead of synergistic effects on loss of cell viability. Pretreatment of cells with epigallocatechin-3-gallate efficiently neutralized the nicotine-induced toxic effects in epithelial cells and fibroblasts. It also dose dependently inhibited the nicotine-induced secretion of chemokine (C-C motif) ligand 5 by epithelial cells. CONCLUSIONS: The present study suggests that epigallocatechin-3-gallate, the major polyphenol in green tea, may represent a novel preventive/therapeutic agent for smoking-related periodontitis.

Anthocyanin-rich black currant extract and cyanidin-3-O-glucoside have cytoprotective and anti-inflammatory properties.

Periodontal diseases are a group of multifactorial polymicrobial infections characterized by a progressive inflammatory destruction of the periodontium. Flavonoids, including anthocyanins, are receiving increasing attention because of their promising human health benefits. The aim of our study was to investigate the effect of anthocyanins, pure or as part of a standardized black currant extract, on nicotine-induced cytotoxicity and lipopolysaccharide (LPS)-induced inflammatory responses in human cells. Using a colorimetric assay that measures cell viability, it was found that a pretreatment with an anthocyanin-rich black currant extract or cyanidin-3-O-glucoside neutralized the cytotoxic effect of nicotine on epithelial cells and fibroblasts in a dose-dependent manner. The black currant extract and cyanidin-3-O-glucoside also inhibited the LPS-induced secretion of interleukin-6 by human macrophages. The results of the present study suggest that black currant extract and cyanidin-3-O-glucoside may be promising candidates for the development of novel therapies to prevent and/or to treat smoking-related periodontal diseases.

Reduction of bacterial volatile sulfur compound production by licoricidin and licorisoflavan A from licorice.

Halitosis affects a large proportion of the population and is, in most cases, caused by the production of volatile sulfur compounds (VSCs), particularly methyl mercaptan and hydrogen sulfide, by specific bacterial species colonizing the oral cavity. In this study, a supercritical extract of Chinese licorice (Glycyrrhiza uralensis), and its major isoflavans, licoricidin and licorisoflavan A, were investigated for their effect on growth, VSC production and protease activity of Porphyromonas gingivalis, Prevotella intermedia and Solobacterium moorei, which have been associated with halitosis. The effects of licorice extract, licoricidin, and licorisoflavan A on VSC production in a saliva model were also tested. We first showed that licoricidin and licorisoflavan A, and to a lesser extent the licorice extract, were effective in inhibiting the growth of all three bacterial species, with minimal inhibitory concentrations in the range of 2-80 µg ml(-1). The licorice extract and the two isolates licoricidin and licorisoflavan A, were able to dose-dependently reduce VSC production by P. gingivalis, Prev. intermedia, and S. moorei as well as by a human saliva model. Although the extract and isolates did not inhibit the proteolytic activity of bacteria, they blocked the conversion of cysteine into hydrogen sulfide by Prev. intermedia. Lastly, the deodorizing effects of the licorice extract, licoricidin, and licorisoflavan A were demonstrated, as they can neutralize P. gingivalis-derived VSCs. Licorisoflavan A (10 µg ml(-1)) was found to be the most effective by reducing VSC levels by 50%. Within the limitations of this study, it can be concluded that a licorice supercritical extract and its major isoflavans (licoricidin and licorisoflavan A) represent natural ingredients with a potential for reducing bacterial VSC production and therefore for controlling halitosis.