OBJECTIVE: Periodontitis is induced by an imbalance between bacterial virulence and host defense ability involving increased levels of oxidative stress. The aim of this study was to investigate the influence of vitamin C on the cytotoxic effects of Porphyromonas gingivalis on human gingival fibroblasts (HGF). METHODS: This in vitro study observed the interaction between HGF and P. gingivalis. HGF were cultured with medium containing vitamin C and exposed to P. gingivalis ATCC 33277 for a maximum of 180 min. The assessment of cell viability was followed by a 3-(4,5-dimethylthiazol-2-ly)-2,5-diphenyltetrazolium-bromide (MTT) assay. The apoptosis rate was detected by flow cytometry using Annexin-V-FITC and propidium iodide. Superoxide as an oxidative stress factor was measured photometrically by the reduction of ferricytochrome C. RESULTS: Vitamin C reduced the cytotoxic effects of P. gingivalis on HGF. Vitamin C-treated HGF showed significantly higher cell viability rates (89.0+/-5.7%) in comparison to untreated HGF (77.0+/-5.0%; p<0.05). In vitamin C-treated HGF, lower apoptosis rates (40.0+/-2.2%) were observed after P. gingivalis exposure than in untreated HGF (66.1+/-1.6%; p<0.05). The exposure of HGF to P. gingivalis led to a significant increase of superoxide concentration, but this effect was not influenced by vitamin C. CONCLUSION: Vitamin C reduces the cytotoxic and apoptotic effects of P. gingivalis on HGF in vitro. These results suggest that the benefit of vitamin C should be further investigated clinically. Copyright 2009 Elsevier Ltd. All rights reserved.
OBJECTIVE:Periodontitis is induced by an imbalance between bacterial virulence and host defense ability involving increased levels of oxidative stress. The aim of this study was to investigate the influence of vitamin C on the cytotoxic effects of Porphyromonas gingivalis on human gingival fibroblasts (HGF). METHODS: This in vitro study observed the interaction between HGF and P. gingivalis. HGF were cultured with medium containing vitamin C and exposed to P. gingivalis ATCC 33277 for a maximum of 180 min. The assessment of cell viability was followed by a 3-(4,5-dimethylthiazol-2-ly)-2,5-diphenyltetrazolium-bromide (MTT) assay. The apoptosis rate was detected by flow cytometry using Annexin-V-FITC and propidium iodide. Superoxide as an oxidative stress factor was measured photometrically by the reduction of ferricytochrome C. RESULTS:Vitamin C reduced the cytotoxic effects of P. gingivalis on HGF. Vitamin C-treated HGF showed significantly higher cell viability rates (89.0+/-5.7%) in comparison to untreated HGF (77.0+/-5.0%; p<0.05). In vitamin C-treated HGF, lower apoptosis rates (40.0+/-2.2%) were observed after P. gingivalis exposure than in untreated HGF (66.1+/-1.6%; p<0.05). The exposure of HGF to P. gingivalis led to a significant increase of superoxide concentration, but this effect was not influenced by vitamin C. CONCLUSION:Vitamin C reduces the cytotoxic and apoptotic effects of P. gingivalis on HGF in vitro. These results suggest that the benefit of vitamin C should be further investigated clinically. Copyright 2009 Elsevier Ltd. All rights reserved.
Authors: L Gölz; S Memmert; B Rath-Deschner; A Jäger; T Appel; G Baumgarten; W Götz; S Frede Journal: Mediators Inflamm Date: 2014-10-13 Impact factor: 4.711