• Journal of Periodontal and Implant Science
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• v.28 no.4
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• pp.703-721
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• 1998

In order to observe the effects of Nicotine and NNK on cultured human gingival fibroblast, several factors were examined including mutagenicity, the number of cells attached culture plate surface through MTT test, the abundance of collagen & collagenase in mRNA level and collagenolytic activity in extracellular matrix. The results were as follows; 1. Regardless of the co-existence of S9, Nicotine did not show the mutagenicity by itself and NNK by itself showd the same result; However, dose related mutagenicity was shown in NNK with S9. 2. The number of fibroblasts attached cultured plate surface was measured by MTT procedure. The number of cells in Non-smokers increased at all time periods as compared to those of smoker. 3. Non-smoker's fibroblast treated by NNK or Nicotine was dosedependently dosedependently decreased in the number of cells when compared to untreated control. In higher dose, Nicotine showed the cellular toxicity, but NNK did not. 4. No change in the abundance of mRNA for pro${\alpha}1$ and pro${\alpha}2$ was shown in Nicotine treated group but in gingival fibroblasts following treatment with NNK, the abundance of mRNA for pro${\alpha}1$, but not pro${\alpha}2$ collagen was decreased. 5. The abundance of mRNA for collagenase was decreased when NNK was treated but no change occurred in Nicotine treated group. 6. The effect of NNK and Nicotine in collagenolytic activity showed that, collagenase activity exclusively react to type I collagen, was increased in both group, but gelatinase exclusively react to type IV collagen was not influenced at all. Collagenase activity of smoker's fibroblast was also increased as much as Nicotine and NNK group. The findings suggest that both of Nicotine and NNK lead gingival fibroblast to decrease in the abundance of collagen. And it seems to be that Nicotine and NNK have independent pathway toward the gingival fibroblast.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.32 no.3
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• pp.216-221
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• 2006

Cyclosporin A-induced gingival hyperplasia is frequently found in the patients who have been received an immunosuppressant for the organ transplantation. However, its exact mechanism is still unknown. The expression of FGF-5 and FGF-7 were studied in cyclosporine A-induced gingival hyperplasia (CGH) and inflammatory gingival hyperplasia (IGH). Immunohistochemistry and in situ hybridization were used for localization of protein and mRNA. The expression of FGF-5 and FGF-7 was different from CGH and IGH. FGF-5 and FGF-7 was strongly expressed in fibroblast in CGH (P<0.005 and P<0.05, respectively). FGF-5 mRNA was localized in the middle portion of connective tissue. FGF-7 mRNA was also identified in fibroblasts and mast cells. In conclusion, FGF-5 and FGF-7 were produced excessively by fibroblasts in CGH. Considering their known functions, their expression in CGH is important for production of collagen and proliferation of fibroblasts.

• Journal of the korean academy of Pediatric Dentistry
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• v.24 no.1
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• pp.204-219
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• 1997

The use of fluoride is one of the most effective methods for caries prevention. Fluoridation of public water supply has been recognized, for many years, as an effective way to reduce dental caries. The fluoride supplement has been recommended when the natural fluoride was unavailable or below the optimal range. However the mechanism of caries prevention by fluoride has not yet been clarified and it is well known that an overdose of fluoride results inacute and chronic toxicity, especially dental fluorosis. Fluoride mouthrinsing solution is widely used in dentistry due to its effectiveness in carrying anticariogenic action. Understanding the effects of fluoride mouthrinsing solution on human gingival fibroblasts will provide the safety rationale for its use during the caries preventive therapy. The purpose of this study was to evaluate the cytotoxic effect of fluoride mouthrinsing solution on the human gingival fibroblast in vitro. The human gingival fibroblasts were cultured from healthy gingiva on the extracted deciduous teeth of children. Cells were inoculated into a 24-well plate with $1{\times}10^4cells/well$ of medium at $37^{\circ}C$, 100% humidity, 5% $CO_2$ incubator for 24 hours. And the cells were counted by using the hemocytometer at each designed study. Human gingival fibroblasts were cultured in growth medium after one minute application range of 0.02%-0.2% NaF solution and 0.1% $SnF_2$ solution. The cells used in this study were between fifth to eighth passage number. The cell morphology was examined by inverted microscope and cell proliferation was measured by incorporating $[^3H]$-thymidine into DNA. DNA synthesis by human gingival fibroblasts was assessed by $[^3H]$-thymidine uptake assays while the cell activity was measured by MTT assay. Each concentrated fluoride mouthrinsing solution was estimated for its biocompatability with fibroblasts by the tissue culture technique. The results of this study were as follows : 1. It was observed that at 0.05%, 0.2% NaF mouthrinsing solution the cytoplasmic processes became globular. When 0.1% $SnF_2$ mouthrinsing solution was applied, the cytoplasmic process and cell morphology were disappeared. 2. DNA synthetic activity was reduced regardless of the concentration of the fluoride mouthrinsing solution. However, the result is statistically insignificant except 0.1% $SnF_2$ mouthrinsing solution(p<0.05). 3. Our results indicate that 0.02%, 0.05% concentrations of NaF mouthrinsing solution caused minimal cytotoxicity. But 0.2% NaF and 0.1% $SnF_2$ concentration were a significant difference between the cell activity in the experimental group and control group (p<0.05). 4. After appling 0.05% & 0.02% NaF fluoride mouthrinsing solution, cell activity was restored to the control groups level according to incubating time. The results suggest that direct exposure to fluoride solution inhibits gingival fibroblast activity. Therefore, for the most effective use of fluoride use, lowering the concentration of fluoride mouthrinsing is advisable because it maintains biocompatability and free ion in the oral fluid.

• Journal of Periodontal and Implant Science
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• v.19 no.2
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• pp.139.1-139.1
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• 1989

• Journal of Periodontal and Implant Science
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• v.18 no.2
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• pp.125-125
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• 1988

• Journal of Periodontal and Implant Science
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• v.21 no.1
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• pp.177.2-177.2
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• 1991

• International Journal of Oral Biology
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• v.39 no.1
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• pp.41-47
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• 2014

Streptococcus mutans (S. mutans) is a facultative anaerobic bacterium mainly found in the oral cavity and is known to contribute to tooth decay and gingivitis. Recent studies on intestinal microbiota have revealed that microorganisms forming a biofilm play important roles in maintaining tissue homeostasis through their own metabolism. However, the physiological roles of oral microorganisms such as S. mutans are still unclear. In our current study, we identified that constituents released from S. mutans (CR) reduce arecoline-mediated cytotoxicity without producing toxic effects themselves. Arecoline, as a major alkaloid of areca nut, is known to mediate cytotoxicity on oral epithelial cells and induces a sustained intracellular $Ca^{2+}$ ($[Ca^{2+}]_i$) increase that is cytotoxic. The exposure of human gingival fibroblast (HGF) cells to CR not only inhibited the sustained $[Ca^{2+}]_i$ increase but also the initial $[Ca^{2+}]_i$ elevation. In contrast, CR had no effects on the gene regulation mediated by arecoline. These results demonstrate that S. mutans has physiological role in reducing cytotoxicity in HGF cells and may be considered a novel pharmaceutical candidate.

• Journal of Korean society of Dental Hygiene
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• v.14 no.1
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• pp.95-100
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• 2014

Objectives : The purpose of the present study was to investigate the effect of bamboo charcoal on Streptococcus mutans which is one of the most important causative agents of dental caries. Methods : S. mutans was incubated with or without bamboo charcoal and then changes were observed in its cell viability and antibacterial effect. Oral epithelial cells viabillity(human gingival fibroblast, HGF) was performed using MTT assay. Antibacterial effect was analyzed using a dilution plating method and agar diffusion method. Results : Oral epithelial cells, human gingival fibroblast (HGF) showed a tendency to increase in bamboo charcoal treatment solution concentrations(0.5, 1, 2, 3, 5, 10%). The bamboo charcoal had an antibacterial effect on S. mutans. Antibacterial effect of bamboo charcoal for the bacterium was 58%. Charcoal concentration of 2% and 5% in the inhibition zone showed a minimal growth, but the concentration of 10% bamboo charcoal in inhibition zone revealed a conspicuous antibacterial activity. Conclusions : Overall results suggested that the bamboo charcoal proved to be bactericidal effect on S. mutans.

• Journal of Periodontal and Implant Science
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• v.23 no.3
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• pp.507-516
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• 1993

The Chlorhexidine(CHX) has been a widely used adjunt in periodontal therapy due to its bactericidal effect. In spite of the effects of CHX exhibits cytotoxic to human cells and delays granulation tissue formation. Therefore, understanding the effects of CHX on fibroblast attachment and cell growth will provide the rationale for its use during healing phase of periodontal surgery. This study was undertaken to examine the effects of standardized CHX-pretreated dentin slices and direct CHX exposure on human gingival fibroblasts. The results were as follow : 1. In experiment 1, there was a significant reduction in the number of fibroblast attachment in 0.12, 1%-pretreated groups relative to the control, 0.05%-pretreated groups(P<0.05). 2. In experiment 1, the control, 0.05%-pretreated groups showed considerable attachment and typical fibroblastic morphology, but 0.12, 1%-pretreated groups showed irregular, round-up (unattached) fibroblastic morphology. 3. In experiment 2, it appeared that all experimental groups exhibits significant inhibition of cell growth when compared with the control group.

• Journal of Periodontal and Implant Science
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• v.25 no.2
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• pp.181-191
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• 1995

The ability of fibroblasts attach to teeth is of paramount imporance in re-establishing the lost connective tissue attachment after periodontal therapy. Tobacco contains a complex mixture of substances including nicotine. various nitrousamines, trace elements. and a variety of poorly characterized substances. The effects of nicotine on fibroblasts have reported an altered morphology and attachment of fibroblasts to substrates and disturbances in protein synthesis and secretion. This study examined the effect of nicotine, a major component of the particulate phase of tobacco smoke, on human gingival fibroblasts and periodontal ligament cells attachment to tissue culture surfaces and cellular activity of human gingival fibroblasts and periodontal ligament cells. Pooled human gingival fibroblasts made from extraction of 3rd molar were utilized between passage 4 and 5 and plated in 96 well plate at 20,000 cells per well. Cell number were determined using 3-(4,5-dimethylthiazole-2-y)2,5-diphenyltetrazolium bromide(MTI) , which is reflection of mitochondrial dehydrogenase activity. The concentration of nicotine used were 0.025, 0.05, 0.1, 0.2 and $0.4{\mu}M$, the average serum concentration for a smoker being approximately $0.1{\mu}M$. The results were as follows : 1. Attachment effects of nicotine on human gingival fibroblasts and periodontal ligament cells Excepts of $0.4{\mu}M$, the effects on attachment with increasing numbers of cells attaching with increasing nicotine concentrations, compared to control group. But over the 60min, return to control value. 2. The effect of cellular activity on human gingival fibroblasts and periodontal ligament cells. The cellular activity of human gingival fibroblasts and periodontal ligament cells were similar or decrease to control value at 1st incubation day. At 2nd incubation day, 0.05, 0.1, 0.2, $0.4{\mu}M$ concentrations were statistically different from control value on gingival fibroblasts group. But at 3rd incubation day, cellular activities of all experimental group were significantly decrease than control group.