Detalhes bibliográficos
Ano de defesa: |
2015 |
Autor(a) principal: |
Téo, Mirela Anne Quartaroli
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Orientador(a): |
Ishikiriama, Bella Luna Colombini
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Banca de defesa: |
Não Informado pela instituição |
Tipo de documento: |
Dissertação
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Tipo de acesso: |
Acesso aberto |
Idioma: |
por |
Instituição de defesa: |
Universidade do Sagrado Coração
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Programa de Pós-Graduação: |
Biologia Oral
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Departamento: |
Ciências da Saúde e Biológicas
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País: |
Brasil
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Palavras-chave em Português: |
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Palavras-chave em Inglês: |
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Área do conhecimento CNPq: |
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Link de acesso: |
http://tede2.usc.br:8080/jspui/handle/tede/279
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Resumo: |
Secondary occlusal trauma is an injury that occurs in the periodontal support of the teeth, with reduced periodontal height due to the application of occlusal forces that exceed their adaptive capacity. For teeth that suffer this type of injury, inflammatory changes are observed in the periodontal support structures (bone, periodontal ligament and cementum), important inflammatory mediators in this process, as derived from the action of cyclooxygenase enzymes (COX), which may play an important role that is still unknown. Non-steroidal antiinflammatories (NSAIDs), which have action on these different COX isoforms, have been shown to significantly influence other inflammatory processes affecting the periodontal support, particularly the alveolar bone. Thus, the present study aimed to evaluate the action of two NSAIDs: indomethacin, an NSAID with preferential action on COX-1 and celecoxib, a selective NSAID for COX-2, in relation to bone resorption promoted by secondary occlusal trauma. To this end, sixty five male Wistar rats, were randomly divided into 3 groups, namely: G1 - induction of experimental periodontal disease (n=10); G2 – induction of secondary occlusal trauma (n=45) and G3 - negative control (n=10). In the G1 animals, induction of experimental periodontal disease was performed by placing a ligature around their lower left first molars for 7 days, and these animals were administered distilled water throughout the experimental period to attest bone resorption in the experimental periodontal disease. The animals of G2 underwent the same methodology for induction of experimental periodontal disease for 7 days, with subsequent creation of an occlusal interference over the occlusal surfaces of the same molars with the aid of orthodontic wire and composite resin, which remained in place for 14 days. Prior to placement of the ligatures, the animals in this group were randomly divided into 3 subgroups according to the drug to be administered during the 21 days of experiment: celecoxib (10 mg/kg) (n=15), indomethacin (5 mg/kg) (n=15) or water (n=15). The G3 animals were maintained for 21 days without being submitted to any of the experiments and treatments to obtain data for the control. Subsequently, the left hemimandibles of the mice were prepared and submitted for analysis. In G1, histometric analysis confirmed the presence of a statistically greater bone resorption area in the group treated with water compared to the untreated animals. The histometric and morphometric analyses to evaluate the inter-radicular and buccal bone resorption areas, respectively, of groups G2, also detected significant differences in the bone loss area, inter-radicular as well as buccal, among all treatments compared to the control group. However, none of the treatments to which the animals were submitted to altered the resorption profile. Regarding the immuno-staining of the TRAP-positive cells, the statistical analysis did not detect differences in the treated groups compared to the negative control, even between treatments. Thus, it can be concluded that the NSAID indomethacin and celecoxib, on tested doses, did not influence bone resorption in the experimental injuries of secondary occlusal trauma induced for 14 days in rats. |