979 resultados para Periapical periodontitis


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Estudou-se a influência de diferentes irrigantes no potencial antimicrobiano da pasta de hidróxido de cálcio em dentes de cães com periodontite apical. 48 pré-molares de cães adultos tiveram suas câmaras coronárias abertas e expostas à cavidade bucal por 6 meses. Os canais radiculares foram preparados, irrigados e medicados com diferentes substâncias, de acordo com os seguintes grupos: 1) 2,5% NaOCl + CHP; 2) 2% CHX + CHP; 3) vinagre + CHP; 4) vinagre + vinagre. No grupo 4, a solução irrigante e a medicação intracanal utilizada foi o vinagre. Neste grupo, a cada 7 dias, a solução era renovada. Cada amostra foi coletada, mantendo-se o cone de papel esterilizado em posição por 1 min, e a seguir transportado e imerso em 7 mL de Letheen broth, seguido de incubação a 37ºC por 48 h. O crescimento microbiano foi analisado por dois métodos, turbidade do meio de cultura e subcultura em meio nutritivo específico (brain heart infusion). Os resultados mostraram que em todos os grupos experimentais houve crescimento microbiano após 21 dias, em diferentes percentagens: grupo 1 - 30%; grupo 2 - 30%; grupo 3 - 40%; grupo 4 - 60%. Todos os materiais testados apresentaram potencial antimicrobiano. Entretanto, o processo de cura favorecido pela pasta de hidróxido de cálcio não pode ser esquecido, uma vez que muitos estudos já demonstraram sua ação antimicrobiana.

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Objective. The aim of this study was to evaluate the influence of apical foramen widening on the healing of chronic periapical lesions in dogs' teeth after root canal filling with Sealer 26 or Endomethasone.Study design. Forty root canals of dogs' teeth were used. After pulp extirpation, the canals were exposed to the oral cavity for 180 days for induction of periapical lesions, and then instrumented up to a size 55 K-file at the apical cemental barrier. In 20 roots, the cemental canal was penetrated and widened up to a size 25 K-file; in the other 20 roots, the cemental canal was preserved (no apical foramen widening). All canals received a calcium hydroxide intracanal dressing for 21 days and were filled with gutta-percha and 1 of the 2 sealers: group 1: Sealer 26/apical foramen widening; group 2: Sealer 26/no apical foramen widening; group 3: Endomethasone/apical foramen widening; group 4: Endomethasone/no apical foramen widening. The animals were killed after 180 days, and serial histologic sections from the roots were prepared for histomorphologic analysis. Scores were assigned according to preestablished histomorphologic parameters and analyzed statistically by Kruskal-Wallis and Mann-Whitney U tests.Results. Regarding new cementum formation, repair of cementum and bone resorption areas, presence of microorganisms, inflammatory cell infiltrate and periodontal ligament conditions, significantly better periapical healing was obtained when foramen widening was done and Sealer 26 was used.Conclusion. Apical foramen widening and calcium hydroxide-containing sealer were more favorable to the healing of chronic periapical lesions. (Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2010;109:932-940)

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Objectives: the administration of cyclosporin A has been associated with significant bone loss and increased bone remodeling. The present investigation was designed to evaluate the effects of cyclosporin A on alveolar bone of rats subjected to experimental periodontitis, using serum, stereometric and radiographic analysis.Methods: Twenty-four rats were divided into one of the following groups with six animals each: group I, control rats; group II, in which the animals received a cotton ligature around the lower first molars; group III, in which the rats received a cotton ligature around the lower first molars and were treated with 10 mg/(kg body weight day) of cyclosporin A; group IV, in which the rats were treated with 10 mg/(kg body weight day) of cyclosporin A. At the end of experimental period, at 30 days, animals were killed and the serum calcium and alkaline phosphatase levels were measured in all groups. The distance from the alveolar bone crest to the cemento-enamel junction was measured radiographically for each mesial surface of the lower first molars of each rat. After histological processing, the stereological parameters: volume densities of multinucleated osteoclasts (V-o), alveolar bone (V-b), marrow (V-m), and relation of eroded surface/bone surface (Es/Bs) were assessed at the mesial region of the alveolar bone.Results: Significant decreases in serum calcium were observed in those groups that received cyclosporin A therapy. No significant changes in serum alkaline phosphatase were observed. The therapy with cyclosporin A combined with the ligature placement decreased the V-b and increased the V-o, V-m and Es/Bs at the mesial surface of lower first molars. on the other hand, the radiographic data showed that cyclosporin A therapy diminished the alveolar bone loss at the mesial surface of the lower first molars.Conclusions: Therefore, within the limits of this study, we suggest that cyclosporin A at immunosuppressive levels can bring about an imbalance in the alveolar bone homeostasis in rats. However, in the presence of inflammatory stimulation, the inhibition of the immune system by cyclosporin A may decrease the initial periodontal breakdown.

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Objective: Periodontitis is a well-appreciated example of leukocyte-mediated bone loss and inflammation with pathogenic features similar to those observed in other inflammatory diseases, such as arthritis. Since Tacrolimus, is an immunomodulatory drug used for the treatment of some cases of arthritis, we hypothesized that it may modulate periodontal disease.Design: Using a murine model of ligature-induced periodontal disease, we assessed the effects of daily administrations of Tacrolimus (1 mg/kg body weight) on bone loss, enzymatic (myeloperoxidase) analysis, differential white blood cells counts, airpouch exudate and cytokine expression for 5-30 days.Results: Radiographic, enzymatic (myeloperoxidase) and histological analysis revealed that Tacrolimus reduced the severity of periodontitis. More specifically, Tacrolimus suppressed the expression of serum interleukin (IL-1 beta), tumour necrosis factor (TNF-alpha), IL-6, airpouch exudate PGE(2) and leukocytosis usually observed after the induction of periodontitis. Tacrolimus treatment in periodontitis-induced rats conferred protection against the inflammation-induced tissue and bone loss associated with periodontitis, through a mechanism involving IL-1 beta, TNF-alpha and IL-6.Conclusions: the effects of Tacrolimus on periodontal disease pathogenesis may provide clues to a novel approach to host modulation therapy in destructive periodontal disease. (C) 2007 Elsevier Ltd. All rights reserved.

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