OBJECTIVE: To investigate the effect of periodontitis on the development of kidney damage in obese mice and its possible mechanism. METHODS: C57 BL/6J mice were fed high‑fat (HF) or low‑fat (LF) diet and then divided into four groups: obesity with periodontitis (HFP), obesity without periodontitis (HFC), normal mice with periodontitis (LFP) and normal mice without periodontitis (LFC). Serum indicators of renal function, namely serum total protein (TP), albumin (ALB), creatinine (Cr) and blood urea nitrogen (UREA) were measured. The histopathological examination of kidney tissues was performed. The expressions of transforming growth factor-β1 (TGF-β1), matrix metalloproteinase-2 (MMP2) and tissue inhibitors of metalloproteinases-1 (TIMP1) were detected by immunohistochemistry and real time RT-PCR. RESULTS: Obesity decreased TP and ALB, and increased serum Cr and UREA levels in normal and periodontitis mice groups, as well as induced glomerular and tubulointerstitial pathologic changes. Tubulointerstitial fibrosis was more severe in HFP group. In obese mice, periodontitis caused the downregulation of MMP2, and upregulation of TIMP1 and TGF-β1 at transcriptional and translational levels. CONCLUSIONS: In obese mice, periodontitis may aggravate pathological changes in the kidney. The possible mechanism might lie in downregulation of MMP2 and upregulation of MMP inhibitor, TIMP1, and TGF-β1 (Tab. 1, Fig. 4, Ref. 16).
OBJECTIVE: To investigate the effect of periodontitis on the development of kidney damage in obesemice and its possible mechanism. METHODS: C57 BL/6J mice were fed high‑fat (HF) or low‑fat (LF) diet and then divided into four groups: obesity with periodontitis (HFP), obesity without periodontitis (HFC), normal mice with periodontitis (LFP) and normal mice without periodontitis (LFC). Serum indicators of renal function, namely serum total protein (TP), albumin (ALB), creatinine (Cr) and blood ureanitrogen (UREA) were measured. The histopathological examination of kidney tissues was performed. The expressions of transforming growth factor-β1 (TGF-β1), matrix metalloproteinase-2 (MMP2) and tissue inhibitors of metalloproteinases-1 (TIMP1) were detected by immunohistochemistry and real time RT-PCR. RESULTS:Obesity decreased TP and ALB, and increased serum Cr and UREA levels in normal and periodontitismice groups, as well as induced glomerular and tubulointerstitial pathologic changes. Tubulointerstitial fibrosis was more severe in HFP group. In obesemice, periodontitis caused the downregulation of MMP2, and upregulation of TIMP1 and TGF-β1 at transcriptional and translational levels. CONCLUSIONS: In obesemice, periodontitis may aggravate pathological changes in the kidney. The possible mechanism might lie in downregulation of MMP2 and upregulation of MMP inhibitor, TIMP1, and TGF-β1 (Tab. 1, Fig. 4, Ref. 16).