Periodontitis aggravates renal inflammatory response in a mouse model of renal fibrosis

Objectives: To assess the effects of periodontitis on renal interstitial fibrosis in a mouse model. Materials and Methods: Thirty C57BL/6 male mice were divided into control, periodontitis (PD), unilateral ureteral ligation (UUO) and PD+UUO groups. Unilateral ureteral ligation was performed 6 days after periodontitis. After 2 weeks, all mice were sacrificed, and samples were collected for the assessment of gene expression, immune cells, biochemical indicators and renal pathology. Results: Expression of tumour necrosis factor-alpha, interleukin-1 beta, and Ly6G in the kidneys in the PD+UUO group was significantly greater than in the UUO group. The percentage of CD11b(+)Ly6G(+) cells was significantly higher in the PD+UUO than in the UUO group. Fibrotic areas in the kidneys in the PD+UUO group were slightly, but not significantly, greater than those in the UUO group. Kidneys from the PD+UUO group showed markedly higher gene expression of matrix metalloproteinase-9, but not alpha-smooth muscle actin or collagen I, than those in the UUO group. There were no significant differences in blood urea nitrogen, serum creatinine and uric acid between the PD+UUO and UUO groups. Conclusions: Periodontitis increases the renal inflammatory response without showing a significant influence on renal interstitial fibrosis or renal function in the UUO mouse model.

Automated summary

This study found that periodontitis increased renal inflammatory response in the UUO mouse model, but did not have a significant effect on renal interstitial fibrosis or renal function.