• Title/Summary/Keyword: periodontitis-medical gel

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A Clinical Study of the Effect of Periodontitis-Medical Gel on Human Gingivitis and Periodontitis (수용성 Periodontitis-Medical Gel이 치은염, 치주염에 미치는 영향)

  • Chai, Jung-Kiu;Choi, Jae-Seong;Park, Ji-Sook;Suh, Jong-Gin;Choi, Seong-Ho;Cho, Kyoo-Sung;Kim, Chong-Kwan
    • Journal of Periodontal and Implant Science
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    • v.30 no.1
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    • pp.11-27
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    • 2000
  • The purpose of this study was to evaluate the clinical effects of Dipotassium glycyrrhizinate, Allantoin, Hinokitiol, Cetylpyridinium chloride containing gel($Dentheth^{(R)}$) on periodontitis. 41 patients with sites having pocket depth of 4-6mm were selected for the study. We classified 2 groups which consisted of 21 patients in the test group(exp.) and 20 patients in the control(placebo) respectively. Following a baseline examination, plaque and calculus were removed and then the experimental gel were handed out to the patients and topical application regimens were initiated. During the 4-week experimental period, pocket depth, bleeding on probing, gingival index, plaque index as a clinical parameters were measured in the baseline, 2 weeks, 4 weeks respectively. A questionnaire was delivered to each patients in 2 weeks, 4 weeks respectively. The results were as follows : 1. Probing pocket depth showed a significant difference in the Exp. group compared with the control group in the changes from baseline to 2 weeks(p<0.05), but there was no significant difference between the groups in the changes from baseline to 4 weeks, from 2 weeks to 4 weeks(p<0.05). 2. The Exp. group showed a significant difference compared with the control group in the changes from baseline to 2 weeks, from baseline to 4 weeks, from 2 weeks to 4 weeks in bleeding on probing(p<0.05). 3. The gingival index showed a significant difference compared with the control group in the changes from baseline to 2 weeks, from baseline to 4 weeks, from 2 weeks to 4 weeks after 4 weeks use of a gel(p<0.05). 4. The plaque index showed a significant difference in the Exp. group compared with the control group in the changes from baseline to 2 weeks(p<0.05), but there was no significant difference between the groups in the changes from baseline to 4 weeks, from 2 weeks to 4 weeks(p<0.05). 5. A questionnaire was consisted of 5 kinds as to bleeding, pus discharge, pain, burning sensation, patient's satisfaction and all of the questions showed a significant difference compared with the control group in the changes from 2 weeks to 4 weeks(p<0.05). 6. During the 4-week experimental period, important side-effects were not finded out, but each groups had one patient appealed nausea or discomfort respectively. These results indicate that application of periodontitis medical gel was useful as an additional aid of mechanical treatment.

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Aggregatibacter actinomycetemcomitans Strongly Stimulates Endothelial Cells to Produce Monocyte Chemoattractant Protein-1 and Interleukin-8

  • Choi, Eun-Kyoung;Kang, Mi-Sun;Oh, Byung-Ho;Kim, Sang-Yong;Kim, So-Hee;Kang, In-Chol
    • International Journal of Oral Biology
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    • v.37 no.3
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    • pp.137-145
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    • 2012
  • Aggregatibacter actinomycetemcomitans is the most important etiologic agent of aggressive periodontitis and can interact with endothelial cells. Monocyte chemoattractant protein-1 (MCP-1) and interleukin-8 (IL-8) are chemokines, playing important roles in periodontal pathogenesis. In our current study, the effects of A. actinomycetemcomitans on the production of MCP-1 and IL-8 by human umbilical vein endothelial cells (HUVEC) were investigated. A. actinomycetemcomitans strongly induced the gene expression and protein release of both MCP-1 and IL-8 in a dose- and time-dependent manner. Dead A. actinomycetemcomitans cells were as effective as live bacteria in this induction. Treatment of HUVEC with cytochalasin D, an inhibitor of endocytosis, did not affect the mRNA up-regulation of MCP-1 and IL-8 by A. actinomycetemcomitans. However, genistein, an inhibitor of protein tyrosine kinases, substantially inhibited the MCP-1 and IL-8 production by A. actinomycetemcomitans, whereas pharmacological inhibition of each of three members of mitogen-activated protein (MAP) kinase family had little effect. Furthermore, gel shift assays showed that A. actinomycetemcomitans induces a biphasic activation (early at 1-2 h and late at 8-16 h) of nuclear factor-${\kappa}B$ (NF-${\kappa}B$) and an early brief activation (0.5-2 h) of activator protein-1 (AP-1). Activation of canonical NF-${\kappa}B$ pathway ($I{\kappa}B$ kinase activation and $I{\kappa}B-{\alpha}$ degradation) was also demonstrated in these experiments. Although lipopolysaccharide from A. actinomycetemcomitans also induced NF-${\kappa}B$ activation, this activation profile over time differed from that of live A. actinomycetemcomitans. These results suggest that the expression of MCP-1 and IL-8 is potently increased by A. actinomycetemcomitans in endothelial cells, and that the viability of A. actinomycetemcomitans and bacterial internalization are not required for this effect, whereas the activation of protein tyrosine kinase(s), NF-${\kappa}B$, and AP-1 appears to play important roles. The secretion of high levels of MCP-1 and IL-8 resulting from interactions of A. actinomycetemcomitans with endothelial cells may thus contribute to the pathogenesis of aggressive periodontitis.