Renata Oliveira Samuel1, Edilson Ervolino2, Índia Olinta de Azevedo Queiroz3, Mariane Maffei Azuma4, Gabriela Tiago Ferreira5, Luciano Tavares Angelo Cintra6. 1. Department of Clinical Dentistry, Universidade de Uberaba Dental School, Uberaba, Minas Gerais, Brazil; Department of Endodontics, School of Dentistry, São Paulo State University - UNESP, Araçatuba, São Paulo, Brazil. 2. Department of Basic Science, School of Dentistry, São Paulo State University - UNESP, Araçatuba, São Paulo, Brazil. 3. Department of Endodontics, School of Dentistry, São Paulo State University - UNESP, Araçatuba, São Paulo, Brazil. 4. Department of Endodontics, School of Dentistry, São Paulo State University - UNESP, Araçatuba, São Paulo, Brazil; Department of Cariology, Restorative Sciences and Endododontics, University of Michigan, Ann Arbor, Michigan. 5. Department of Clinical Dentistry, Universidade de Uberaba Dental School, Uberaba, Minas Gerais, Brazil. 6. Department of Endodontics, School of Dentistry, São Paulo State University - UNESP, Araçatuba, São Paulo, Brazil. Electronic address: luciano.cintra@unesp.br.
Abstract
INTRODUCTION: The aim of this study was to evaluate the inflammatory profile of T helper (Th) cells in normoglycemic (N) and diabetic rats with apical periodontitis (AP). METHODS: Twenty male Wistar rats were divided in 2 groups: N rats and rats with diabetes mellitus (DM). DM was induced using streptozotocin, and AP was induced by dental pulp exposure of the first mandibular molar to the oral environment. After 30 days, the mandibles were removed and processed for histologic analysis, bacterial analysis, and immunochemical assays for interleukin (IL)-6, tumor necrosis factor alpha, IL-17, IL-23, interferon gamma, and IL-10. The Mann-Whitney U test and Student t test were used for statistical analysis (P < .05). RESULTS: The DM group showed more intense inflammatory infiltrate with larger sizes of bone reabsorption and a greater presence of bacteria than the N group (P < .05). Proinflammatory cytokine levels in the DM group were also greater than those in the N group (P < .05). However, interferon gamma was more intense in the N group than in the DM group (P < .05). CONCLUSIONS: The inflammatory profile of AP in DM is different from that in the N group, suggesting that Th1 is a secondary strain and the Th17 strain is predominant in DM.
INTRODUCTION: The aim of this study was to evaluate the inflammatory profile of T helper (Th) cells in normoglycemic (N) and diabeticrats with apical periodontitis (AP). METHODS: Twenty male Wistar rats were divided in 2 groups: Nrats and rats with diabetes mellitus (DM). DM was induced using streptozotocin, and AP was induced by dental pulp exposure of the first mandibular molar to the oral environment. After 30 days, the mandibles were removed and processed for histologic analysis, bacterial analysis, and immunochemical assays for interleukin (IL)-6, tumor necrosis factor alpha, IL-17, IL-23, interferon gamma, and IL-10. The Mann-Whitney U test and Student t test were used for statistical analysis (P < .05). RESULTS: The DM group showed more intense inflammatory infiltrate with larger sizes of bone reabsorption and a greater presence of bacteria than the N group (P < .05). Proinflammatory cytokine levels in the DM group were also greater than those in the N group (P < .05). However, interferon gamma was more intense in the N group than in the DM group (P < .05). CONCLUSIONS: The inflammatory profile of AP in DM is different from that in the N group, suggesting that Th1 is a secondary strain and the Th17 strain is predominant in DM.
Authors: Jiachen Liu; Wei Yin; Lisa S Westerberg; Pamela Lee; Quan Gong; Yan Chen; Lingli Dong; Chaohong Liu Journal: Front Immunol Date: 2021-09-01 Impact factor: 7.561