High-Fat Diet Influences Dendritic Cells and T-Cell Infiltration in Apical Periodontitis in Mice

Diet-induced metabolic syndrome may influence the progression and healing of apical periodontitis (AP). The aim of this study was to evaluate the inflammatory immune response of dendritic cells (DCs) and T helper (Th) cells in normal versus obese mice with AP.

Twenty male C57BL/6 mice were divided into 2 groups: normal chow (NC) and high-fat diet (HFD) for 12 wk. AP was induced in both groups by creating pulp exposure of the right first maxillary molar to the oral environment. Contralateral first molars from each mouse were used as a control. The animal's body mass was recorded on a weekly basis, and they were euthanized after 30 d. The maxillae were removed and processed for micro-computed tomography (micro-CT), histologic analysis, and immunofluorescence staining for DCs (CD11c), Th17 (IL-17A), and T regulatory cells (FOXP3 and IL-10). Different groups were analyzed by Mann-Whitney U test, Student t test, and ordinary 1-way analysis of variance followed by Tukey's multiple comparisons test. The level of significance (α) was set at 0.05.

The HFD group showed larger AP lesions than the NC group from micro-CT analysis. For the NC group, induction of AP significantly increased immune cell infiltration when compared with control. HFD showed increased DCs and Th17 infiltration in the control group without AP. In addition, there was no significant change in the amount of DCs and Th17 in the HFD-AP group when compared with the NC-AP and HFD-control groups.

HFD resulted in an increased immune cell infiltration in the periapical area without AP. Despite the larger AP lesion observed in HFD-AP than that of NC-AP, the amount of infiltrated inflammatory cells did not differ significantly. The results of this study suggest that the DCs and Th17 inflammatory pathways are affected by HFD in the periapical region, but their contribution toward AP complicated by metabolic syndrome requires further investigation.