Is oxidative stress involved in the hepatic inflammatory response to apical periodontitis? A comparative study in normal and hyperlipidemic rat.

AP could activate systemic and liver inflammation by promoting serum IL-18, 1L-1β, TOS, OSI expression, enhancing hepatic TOS, OSI expression, and inhibiting serum TOAC expression. AP under hyperlipidemia led to more profound periapical bone destruction in the maxilla and elicit systemic and liver inflammatory responses through elevating serum levels of IL-1β, descending serum IL-4 level, and improving hepatic IL-6, TGF-β1 expression.