926 resultados para Recesión gingival


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Objective: The purpose of this study was to examine the leukotoxin promoter types of Aggregatibacter actinomycetemcomitans clones in subjects with generalized aggressive periodontitis (GAgP) and in their family members (FM). Material and Methods: Thirty-five patients with GAgP (33.9+/-7.1 years), 33 of their FM (22.8+/-11.4 years), and 41 patients with chronic periodontitis (CP) (44.1+/-9.4 years) were clinically analyzed using the plaque index, gingival index, probing depth (PD), and clinical attachment level (CAL). Subgingival biofilm samples were collected from four interproximal periodontal sites (>PD and >CAL) of each patient. The presence of A. actinomycetemcomitans and its leukotoxic clone was confirmed by polymerase chain reaction (PCR). Results: A. actinomycetemcomitans was observed in 23 (51.1%) GAgP patients and 16 (30.1%) CP patients. Thirty-seven (94.8%) patients showed minimally leukotoxic strains and 2 (5.1%) showed highly leukotoxic strains. In the FM group, 10 (30.3%) had aggressive periodontitis (AgP), 12 (36.3%) had CP, 11 (33.3%) were periodontally healthy or had gingivitis, and 12.2% were A. actinomycetemcomitans positive. Greater full mouth PD and CAL were observed in GAgP patients positive for the bacteria than those negative for it (p<0.05), and the presence of A. actinomycetemcomitans positively correlated with GAgP (Odds ratio, 3.1; confidence interval, 1.4-7.0; p=0.009). Conclusions: The presence of A. actinomycetemcomitans was associated with the clinical condition of GAgP, with most patients exhibiting a generalized form of the disease and minimally leukotoxic clones. Most of the relatives of GAgP patients presented either CP or AgP.

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Triclosan is a general membrane-active agent with a broad-spectrum antimicrobial activity that is commonly used in oral care products. In this study, we investigated the effect of sub-minimum inhibitory concentrations (MICs) of triclosan on the capacity of the cariogenic bacterium Streptococcus mutans to form biofilm and adhere to oral epithelial cells. As quantified by crystal violet staining, biofilm formation by two reference strains of S. mutans was dose-dependently promoted, in the range of 2.2- to 6.2-fold, by 1/2 and 1/4 MIC of triclosan. Observations by scanning electron microscopy revealed the presence of a dense biofilm attached to the polystyrene surface. Growth of S. mutans in the presence of triclosan at subMICs also increased its capacity to adhere to a monolayer of gingival epithelial cells. The expression of several genes involved in adherence and biofilm formation in S. mutans was investigated by quantitative RT-PCR. It was found that subMICs of triclosan significantly increased the expression of comD, gtfC, and luxS, and to a lesser extent of gtfB and atlA genes. These findings stress the importance of maintaining effective bactericidal concentrations of therapeutic triclosan since subMICs may promote colonization of the oral cavity by S. mutans.

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Background: The aim of this study is to characterize and evaluate the host response caused by three different models of experimental periodontitis in mice.Methods: C57BL/6 wild-type female mice were distributed into six experimental groups and sacrificed at 7, 15, and 30 days after the induction of periodontal disease: 1) group C: no treatment control group; 2) group L: periodontal disease induced by ligature; 3) group G-Pg: oral gavage with Porphyromonas gingivalis (Pg); 4) group G-PgFn: oral gavage with Fusobacterium nucleatum + Pg; 5) group I-Pg: heat-killed Pg injected into the palatal mucosa between the molars; and 6) group I-V: phosphatebuffered saline injected into the palatal mucosa. The samples were used to analyze the immune-inflammatory process in the gingival tissue via descriptive histologic and real-time polymerase chain reaction analyses. The alveolar bone loss was evaluated using microcomputed tomography. The data were analyzed using the Kruskal-Wallis test, followed by a post hoc Dunn test and analysis of variance, followed by a Tukey test using a 5% significance level.Results: Only the ligature model displayed significant alveolar bone loss in the initial period (7 days), which was maintained with time. The group injected with heat-killed Pg displayed significant alveolar bone loss starting from day 15, which continued to progress with time (P < 0.05). A significant increase (P < 0.05) in the gene expression of proinflammatory cytokines (interleukin-6 and -1b) and proteins involved in osteoclastogenesis (receptor activator of nuclear factor-kB ligand and osteoprotegerin) was observed in the ligature group on day 7.Conclusion: The ligature and injection of heat-killed Pg models were the most representative of periodontal disease in humans, whereas the oral gavage models were not effective at inducing the disease under the experimental conditions.

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Background and Objective: Antimicrobial peptides, such as beta-defensins, secreted by gingival epithelial cells, are thought to play a major role in preventing periodontal diseases. In the present study, we investigated the ability of green tea polyphenols to induce human beta-defensin (hBD) secretion in gingival epithelial cells and to protect hBDs from proteolytic degradation by Porphyromonas gingivalis.Material and Methods: Gingival epithelial cells were treated with various amounts (25-200 mu g/mL) of green tea extract or epigallocatechin-3-gallate (EGCG). The secretion of hBD1 and hBD2 was measured using ELISAs, and gene expression was quantified by real-time PCR. The treatments were also carried out in the presence of specific kinase inhibitors to identify the signaling pathways involved in hBD secretion. The ability of green tea extract and EGCG to prevent hBD degradation by proteases of P. gingivalis present in a bacterial culture supernatant was evaluated by ELISA.Results: The secretion of hBD1 and hBD2 was up-regulated, in a dose-dependent manner, following the stimulation of gingival epithelial cells with a green tea extract or EGCG. Expression of the hBD gene in gingival epithelial cells treated with green tea polyphenols was also increased. EGCG-induced secretion of hBD1 and hBD2 appeared to involve extracellular signal-regulated kinase 1/2 and p38 mitogen-activated protein kinase. Lastly, green tea extract and EGCG prevented the degradation of recombinant hBD1 and hBD2 by a culture supernatant of P. gingivalis.Conclusion: Green tea extract and EGCG, through their ability to induce hBD secretion by epithelial cells and to protect hBDs from proteolytic degradation by P. gingivalis, have the potential to strengthen the epithelial antimicrobial barrier. Future clinical studies will indicate whether these polyphenols represent a valuable therapeutic agent for treating/preventing periodontal diseases.

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