Influência da periodontite apical sobre parâmetros de estresse oxidativo e atividades de ATPases em diferentes órgãos de ratos adultos e jovens

• Ano de defesa: 2020
• Autor(a) principal: Barcelos, Raquel Cristine Silva
• Tipo de documento: Tese
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Santa Maria; Brasil; Odontologia; UFSM; Programa de Pós-Graduação em Ciências Odontológicas; Centro de Ciências da Saúde
• Palavras-chave em Português: Lesão periapical; Bomba de cálcio; Bomba de sódio; Sistema de defesa antioxidante; Periapical lesion; Calcium pump; Sodium pump; Antioxidant defense system; CNPQ::CIENCIAS DA SAUDE::ODONTOLOGIA
• Link de acesso: http://repositorio.ufsm.br/handle/1/22154

Apical periodontitis, inflammatory process around the apex of a tooth root, is primarily a sequel to microbial infection of the pulp space of teeth and is a remarkably widespread problem. P-type ATPases, as Na+/K+-ATPase (NKA) and Ca2+-ATPase (CAA), create electrochemical potential gradients for the different ions essential for various cellular functions. Such transmembrane enzymes have an oxidative regulation and are associated with the pathogenesis of various systemic diseases. However, its relationship with apical periodontitis has not yet been reported. Considering that oxidative stress is related to the pathogenesis of apical periodontitis, this study was designed to evaluate the influence of apical periodontitis on oxidative stress parameters and ATPases activities in different organs of adult and young rats. Adult male Wistar rats were randomly assigned to two experimental groups: control (CT; no periapical lesion; n=8) and apical periodontitis (AP; with apical periodontitis; n=9). Apical periodontitis was induced by pulpal exposure of the right mandibular first molar. After 21 days of apical periodontitis induction, the rats were euthanized and the jaws dissected for radiographic and histological analysis. In addition, the heart, liver, pancreas and kidneys were collected for biochemical analyzes of NKA activity, reactive species (RS) generation and endogenous antioxidant content. Apical periodontitis increased NKA activity in the heart, liver and pancreas; increased RS generation only in the heart. However, the same influence was not observed in the kidney. While in the heart and pancreas was observed a reduction in endogenous antioxidant defenses, in the liver and kidney such levels were increased. NKA activity and endogenous antioxidant defense system modulations observed in this study suggest that alteration of cellular electrochemical gradient and antioxidant status may be involved in the pathophysiology of apical periodontitis. To continue the studies, to verify if there is influence of age and different pulp exposure times on the same parameters analyzed, a second experimental protocol was developed with young male Wistar rats that were also randomly assigned to two experimental groups: control (CT; no apical periodontitis; n = 21) and apical periodontitis (AP; with apical periodontitis; n = 24). Apical periodontitis was induced by pulpal exposure of the right mandibular first molar. After 7, 14 and 21 days of apical periodontitis induction, the rats were euthanized and the mandibles were dissected for radiographic analysis. In addition, the heart, liver, pancreas and kidney were collected for biochemical analyzes of the RS generation, levels of the lipoperoxidation and protein carbonyls, besides NKA and CAA activities. Apical periodontitis induced oxidative damage to the heart, liver and pancreas, observed mainly 21 days after pulp exposure. In addition, apical periodontitis was related to reduced activities in NAK and CAA in all organs analyzed, except the pancreas, in which an increase in CAA activity was observed at all times evaluated. The reduction in the activity of NKA and CAA, the modulation of the endogenous antioxidant defense system and the increase in oxidative damage observed in this study suggest that changes in the cellular electrochemical gradient and oxidative stress may be involved in the pathophysiology of apical periodontitis.