979 resultados para Periapical periodontitis
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This study evaluated the response of periapical tissues to the endodontic sealer EndoREZ in root canal fillings short of or beyond the apical foramenlike communication. Twenty root canals of premolars and incisors of 2 mongrel dogs were used. After coronal access and pulp extirpation, the canals were instrumented up to a size 55 K-file and the apical cemental barrier was penetrated with a size 15 K-file to create an apical foramenlike communication, which was widened to a size 25 K-file. The canals were irrigated with saline at each change of file. The root canals were obturated either short of or beyond the apical foramenlike opening by the lateral condensation of gutta-percha and EndoREZ, originating 2 experimental groups: G1, EndoREZ/short of the apical foramenlike opening, and G2, EndoREZ/beyond the apical foramenlike opening. The animals were killed by anesthetic overdose 90 days after endodontic treatment. The individual roots were obtained and serial histological sections were prepared for histomorphological analysis (H&E and Brown and Brenn techniques) under light microscopy. The following parameters were examined: closure of the apical foramenlike communication and apical opening of accessory canals, apical cementum resorptions, intensity of the inflammatory infiltrate, presence of giant cells, and thickness and organization of the apical periodontal ligament. Each parameter was scored 1 to 4, 1 being the best result and 4 the worst. Data were analyzed statistically by the Wilcoxon nonparametric tests (P = .05). Comparing the 2 groups, the best result (P = .05) was obtained with root canal filling with EndoREZ short of the apical foramenlike opening. In conclusion, limiting the filling material to the root canal space apically was important to determine the best treatment outcome when EndoREZ was used as the sealer. (Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2010; 109: e94-e99)
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The aim of this study was to evaluate the periapical healing after the use of membrane, bone graft, and mineral trioxide aggregate (MTA) in apical surgery of dogs' teeth. Apical lesions were induced in 48 roots of 6 dogs after coronal access and pulpal removal. Apical surgery consisted of osteotomy with trephine bur for the standardization of the critical surgical cavities, followed by apicoectomy, curettage, preparation of the root-end cavities with the aid of the ultrasonic device, and retrofilling with MTA. The surgical sites were divided into: group 1-filled with blood; group 2-filled with blood and recovered with membrane; group 3-filled with bone graft; and group 4-filled with bone graft and recovered with membrane. The results showed that the inflammatory infiltrate, the periapical healing process, and the behavior of MTA was the same in all groups, including the mineralization stimulation. It was concluded that the use of membranes and bone graft materials isolated or associated in apical surgery did not alter the periapical healing process after the root-end filling with MTA. (Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2010; 109: 309-314)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Background: It is well known that the multiple direct and indirect consequences of hyperglycemia in diabetic individuals have been linked to a number of abnormal host effector mechanisms that could lead to an increased risk of developing periodontal disease.Objective: the aim of this study was to investigate the effect of short-term experimental diabetes and insulin therapy on the severity of alveolar bone loss in rats, and the effect of experimental periodontitis on glycemic control.Methods: Seventy-two male Wistar rats were divided into four groups: group I animals were submitted to dental ligature around lower right first molars (ligated); group II consisted of streptozotocin (STZ)-diabetic, ligated rats; group III represented STZ-diabetic, unligated rats; and group IV consisted of insulin-treated (6 U/day), STZ-diabetic, ligated rats. Blood glucose of all diabetic rats was monitored at regular intervals. Standardized digital radiographs were taken after killing at 7, 15 and 30 days to measure the amount of bone loss about the mesial root surface of the first molar tooth in each rat.Results: No significant (p < 0.05) changes in plasma glucose levels of insulin-treated diabetic rats were found among the different examinations after the beginning of insulin therapy. Rats from group II showed significantly greater increases in mean plasma glucose levels at 15 and 30 days after ligature placement compared with rats from group III (p < 0.05). Furthermore, in spite of the significant alveolar bone loss progression that was observed in groups I, II and IV (p < 0.00001; two-way ANOVA), no significant differences among these groups regarding the severity of bone loss (p = 0.77) and no significant interaction between treatment group and time (p = 0.81) were found.Conclusions: Within the limits of this study, it can be suggested that the severity of periodontal disease was not affected by short-term diabetes, and that experimental periodontitis increased blood glucose levels in uncontrolled diabetic rats.
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Actinobacillus actinomycetemcomitans plays a major role in the pathogenesis of aggressive periodontitis. Lipopolysaccharide (LPS) derived from A. actinomycetemcomitans is a key factor in inflammatory cytokine generation within periodontal tissues. In this study, we identify major mitogen-activated protein kinase (MAPK) signaling pathways induced by A. actinomycetemcomitans LPS, Escherichia coli LPS and interleukin-1 beta (IL-1 beta) in a murine periodontal ligament (mPDL) fibroblast cell line. Immunoblot analysis was used to assess the phosphorylated forms of p38, extracellular-regulated kinase (ERK) and c-jun N-terminal kinase (JNK) MAPK following stimulation with A. actinomycetemcomitans LPS, E. coli LPS and IL-1 beta. IL-6 mRNA induction was detected via reverse transcription-polymerase chain reaction, while protein levels were quantified via enzyme-linked immunosorbent assays (ELISA). We utilized biochemical inhibitors of p38, ERK and JNK MAPK to identify the MAPK signaling pathways needed for IL-6 expression. Additional use of stable mPDL cell lines containing dominant negative mutant constructs of MAPK kinase-3 and -6 (MKK-3/6) and p38 null mutant mouse embryonic fibroblast (MEF) cells were used to substantiate the biochemical inhibitor data. Blocking p38 MAPK with SB203580 reduced the induction of IL-6 mRNA by A. actinomycetemcomitans LPS, E. coli LPS and IL-1 beta by > 70%, > 95% and similar to 60%, respectively. IL-6 ELISA indicated that blocking p38 MAPK reduced the IL-6 protein levels induced by A. actinomycetemcomitans LPS, E. coli LPS and IL-1 beta by similar to 60%, similar to 50% and similar to 70%, respectively. All MAPK inhibitors significantly reduced the IL-6 protein levels induced by A. actinomycetemcomitans LPS, E. coli LPS and IL-1 beta whereas only p38 inhibitors consistently reduced the A. actinomycetemcomitans LPS, E. coli LPS and IL-1 beta induction of IL-6 mRNA steady-state levels. The contribution of p38 MAPK LPS-induced IL-6 expression was confirmed using MKK-3/6 dominant negative stable mPDL cell lines. Wild-type and p38 alpha(-/-) MEF cells provided additional evidence to support the role of p38 alpha MAPK in A. actinomycetemcomitans LPS-stimulated IL-6. Our results indicate that induction of IL-6 by E. coli LPS, IL-1 beta and A. actinomycetemcomitans LPS requires signaling through MKK-3-p38 alpha ERK, JNK and p38 MAPK in mPDL cells.
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Objectives: To survey the current radiographic prescriptions in dental implant assessment amongst dentists in Brazil.Methods: Sixty-nine dentists were interviewed during a dental implant meeting by two calibrated graduate students, using a 19-question questionnaire, considering imaging modality options both for pre-operative implant site assessment and for follow-up, particularly with respect to cost, patient radiation dose, and broad coverage of facial bones and teeth. Epi-Info 6.04 software was used to analyse the database file.Results: Approximately 63.8% of the dentists prescribed only panoramic radiography for dental implant assessment and 28.9% ordered panoramic radiography plus periapical radiography and/or conventional tomography and/or computed tomography (CT). Only 7.2% of the dentists ordered conventional tomography or CT as a single examination, although 10.1% ordered it in combination with other imaging modalities. The main reasons given for prescribing panoramic radiography were broad coverage and cost (86.4%).Conclusions: This study has shown that most of the dentists in this study prescribe panoramic radiographs in dental implant assessment based on broad coverage and cost. They are not following the American Academy of Oral and Maxillofacial Radiology recommendations regarding cross-sectional imaging.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Periodontal disease initiation and progression occurs as a consequence of the host immune inflammatory response to oral pathogens. The innate and acquired immune systems are critical for the proper immune response. LPS, an outer membrane constituent of periodontal pathogenic bacteria, stimulates the production of inflammatory cytokines IL-1 beta TNF alpha IL-6 and RANKL either directly or indirectly. In LPS-stimulated cells, the induction of cytokine expression requires activation of several signaling pathways including the p38 MAPK pathway. This review will discuss the significance of the p38 MAPK pathway in periodontal disease progression and the potential therapeutic consequences of pharmacological antagonism of this pathway in the treatment of periodontal diseases.
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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)