Efeito da fumaça do cigarro na periodontite apical induzida em ratos: análise do perfil inflamatório e imuno-histoquímica macrofágica.
Data
2022-02-18
Autores
Silva, Ana Claudia Rodrigues da [UNESP]
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Editor
Universidade Estadual Paulista (Unesp)
Resumo
Objetivo: Avaliar a severidade da periodontite apical (PA) em ratos expostos à fumaça do cigarro, por meio da análise histológica do perfil inflamatório e imunomarcação macrofágica. Material e Métodos: Foram utilizados trinta e dois ratos machos Wistar distribuídos em quatro grupos (n=8): PA (ratos com PA induzida); F (ratos expostos à fumaça do cigarro); FPA (ratos com PA induzida expostos à fumaça do cigarro); C (ratos sem PA e sem exposição ao cigarro). Para inalação da fumaça do cigarro, os animais permaneceram em câmara de tabagismo por oito minutos, três vezes ao dia por vinte dias antes da indução da PA. Em seguida, os animais tiveram as polpas coronárias expostas ao meio oral por 30 dias para a indução da PA e continuaram inalando fumaça até completarem 50 dias. No momento da eutanásia, as hemi-maxilas do lado direito foram removidas para avaliar o perfil inflamatório por coloração em hematoxilina e eosina e imuno-histoquímica para marcação macrofágica F4/80 (macrófago), CD206 (M2) e iNOS (M1). Dados não paramétricos foram analisados por Kruskal-Wallis, seguido de post-hoc Dunn e Mann- Whitney (P<.05). Resultados: O infiltrado inflamatório foi moderado no grupo PA e intenso no grupo FPA (P<.05). A análise histomorfométrica de macrófagos M2 revelaram diferenças estatísticas entre os grupos C e PA, e F e FPA (P>.05). Na imunomarcação de macrófagos M1, os grupos C e F apresentaram diferenças significantes quando comparado aos grupos PA e FPA (P<0,05). Enquanto os grupos PA e FPA apresentaram grande quantidade de células imunorreativas, sendo maior para o grupo FPA (P<0,05). No anticorpo F4/80 não houve diferença entre os grupos (P>.05). Conclusão: A inalação da fumaça do cigarro em ratos contribuiu para uma reação inflamatória periapical mais intensa, com presença predominante de macrófagos pró-inflamatórios M1, agravando a severidade da periodontite apical.
Objective: to evaluate the severity of apical periodontitis (AP) in rats exposed to cigarette smoke, via analysis of inflammatory profile and macrophage immunolabeling. Material and Methods: thirty-two male Wistar rats were used, distributed into four groups (n=8): PA (rats with induced AP); F (rats exposed to cigarette smoke); FPA (AP-induced rats exposed to cigarette smoke); C (rats without AP and without exposure to cigarettes). For cigarette smoke inhalation, animals remained in a smoking chamber for eight minutes, three times daily for twenty days before AP induction. Then, animals had the coronary pulp exposed to oral environment for 30 days to induce AP while continued inhaling smoke until completing 50 days of experimental period. During euthanasia process, the right hemimaxillas were removed to assess inflammatory profile by hematoxylin and eosin staining and immunohistochemistry for macrophage immulabeling: F4/80 (macrophage), CD206 (M2) and iNOS (M1). Nonparametric data were analyzed by Kruskal-Wallis, followed by post-hoc Dunn and Mann-Whitney (P<.05). Results: The inflammatory infiltrate was moderate in the PA group and intense in the FPA group (P<.05). Histomorphometric analysis of M2 macrophages revealed statistical differences between groups C and PA, and F and FPA (P>.05). In the immunostaining of M1 macrophages, groups C and F showed significant differences when compared to groups PA and FPA (P<0.05). While the PA and FPA groups presented a large amount of immunoreactive cells, being higher for the FPA group (P<0.05). In the F4/80 antibody there was no difference between the groups (P>.05)Conclusion: Inhalation of cigarette smoke in rats contributed to a more intense periapical inflammatory reaction, with a predominant presence of pro-inflammatory M1 macrophages, aggravating the severity of apical periodontitis.
Objective: to evaluate the severity of apical periodontitis (AP) in rats exposed to cigarette smoke, via analysis of inflammatory profile and macrophage immunolabeling. Material and Methods: thirty-two male Wistar rats were used, distributed into four groups (n=8): PA (rats with induced AP); F (rats exposed to cigarette smoke); FPA (AP-induced rats exposed to cigarette smoke); C (rats without AP and without exposure to cigarettes). For cigarette smoke inhalation, animals remained in a smoking chamber for eight minutes, three times daily for twenty days before AP induction. Then, animals had the coronary pulp exposed to oral environment for 30 days to induce AP while continued inhaling smoke until completing 50 days of experimental period. During euthanasia process, the right hemimaxillas were removed to assess inflammatory profile by hematoxylin and eosin staining and immunohistochemistry for macrophage immulabeling: F4/80 (macrophage), CD206 (M2) and iNOS (M1). Nonparametric data were analyzed by Kruskal-Wallis, followed by post-hoc Dunn and Mann-Whitney (P<.05). Results: The inflammatory infiltrate was moderate in the PA group and intense in the FPA group (P<.05). Histomorphometric analysis of M2 macrophages revealed statistical differences between groups C and PA, and F and FPA (P>.05). In the immunostaining of M1 macrophages, groups C and F showed significant differences when compared to groups PA and FPA (P<0.05). While the PA and FPA groups presented a large amount of immunoreactive cells, being higher for the FPA group (P<0.05). In the F4/80 antibody there was no difference between the groups (P>.05)Conclusion: Inhalation of cigarette smoke in rats contributed to a more intense periapical inflammatory reaction, with a predominant presence of pro-inflammatory M1 macrophages, aggravating the severity of apical periodontitis.
Descrição
Palavras-chave
Fumantes, Inflamação, Macrófagos, Periodontite periapical, Smoking, Inflammation, Macrophages, Periapical periodontitis