da Silva Machado Nathália Evelyn, Segura-Egea Juan José, Faria Flávio Duarte, Cantiga-Silva Cristiane, Ribeiro Ana Paula Fernandes, Ervolino Edilson, Matsushita Dóris Hissako, Estrela Carlos, Cruz Alvaro, Gomes-Filho João Eduardo, Sivieri-Araújo Gustavo, Cintra Luciano Tavares Angelo
Endodontic Section, Department of Preventive and Restorative Dentistry, Araçatuba School of Dentistry, São Paulo State University (UNESP), R: José Bonifácio, 1193. Vila Mendonça, Araçatuba, SP, Brazil.
Endodontic Section, Department of Stomatology, School of Dentistry, University of Sevilla, Seville, Spain.
Odontology. 2025 Jul 9. doi: 10.1007/s10266-025-01147-9.
The aim of this study was to investigate the inflammatory profile and immunostaining expression of Toll-like receptors 2 and 4 (TLR2 and TLR4) in periapical tissues of control and diabetic rats (DM) with induced apical periodontitis (AP), correlating these findings with the progression of root canal contamination. Forty male Wistar rats were divided into four groups: Group C-control rats, Group AP-rats with AP, Group DM-rats with diabetes, and Group DM + AP-rats with DM and AP. 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 jaws were removed and processed for histologic and bacterial analysis, as well as immunochemical assays for TLR2 and TLR4. Two-way analysis of variance was used (P < 0.05). Inflammatory infiltrate was moderate in the AP group and severe in the DM + AP group (P < 0.05). There was a greater presence of bacteria disseminated in the apical region in the DM + AP group when compared with the AP group (P < 0.05). TLR2 and TLR4 levels were significantly higher in the DM + AP group when compared to the AP group (P < 0.05). Diabetes increases the inflammatory infiltrate in AP, causing significant overexpression of TLR2 and TLR4 in the periapical inflammatory tissues of diabetic rats. By activating TLRs, diabetes exacerbates the immune response in AP, increasing inflammation and influencing the progression of bacterial contamination.
本研究的目的是调查诱导性根尖周炎（AP）的对照大鼠和糖尿病大鼠（DM）根尖周组织中Toll样受体2和4（TLR2和TLR4）的炎症特征和免疫染色表达，并将这些发现与根管污染的进展相关联。40只雄性Wistar大鼠被分为四组：C组-对照大鼠，AP组-患有AP的大鼠，DM组-患有糖尿病的大鼠，以及DM+AP组-患有DM和AP的大鼠。使用链脲佐菌素诱导DM，通过将第一下颌磨牙的牙髓暴露于口腔环境诱导AP。30天后，取出颌骨并进行组织学和细菌分析，以及TLR2和TLR4的免疫化学测定。采用双向方差分析（P<0.05）。AP组炎症浸润为中度，DM+AP组为重度（P<0.05）。与AP组相比，DM+AP组根尖区细菌扩散更多（P<0.05）。与AP组相比，DM+AP组TLR2和TLR4水平显著更高（P<0.05）。糖尿病会增加AP中的炎症浸润，导致糖尿病大鼠根尖周炎症组织中TLR2和TLR4显著过表达。通过激活TLRs，糖尿病会加剧AP中的免疫反应，增加炎症并影响细菌污染的进展。
