Periodontitis regulates renal impairment in obese mice via TGF-ß/Smad pathway.

OBJECTIVE: To determine the impact of periodontitis on renal impairment induced by obesity. METHODS: Periodontitis and obesity models were induced using silk ligatures with bacteria and high-fat diet, respectively. Indicators of renal function were compared. Renal tubular epithelial cells (RTECs) were treated with lipopolysaccharides from periodontal pathogens in a high-fat environment to induce cell models of periodontitis and obesity. The transforming growth factor-ß/mothers against decapentaplegic homolog (Smad) (TGF-ß/Smad) pathway was evaluated both in vivo and in vitro. The indicators of renal function, renal pathological changes, and serum inflammatory cytokines were measured. The viability/apoptosis of RTECs and the expression of inflammatory cytokines were determined. RESULTS: Periodontitis resulted in an increase in TGF-ß/Smad activity in the kidney of obese mice. Moreover, the activity of RTECs was also increased in vitro. Downregulation of TGF-ß led to reduced TGF-ß, p-Smad2, p-Smad3, and Smad7 levels in kidney tissue and RTECs, ameliorated renal function indicators and renal pathological changes, increased viability and apoptosis of RTECs, and decreased levels of inflammatory cytokines. CONCLUSION: Periodontitis regulates renal impairment via the TGF-ß/Smad pathway in obese mice.