Additionally, FADD’s pro-apoptotic function might contribute to this negative regulation by promoting cell death, providing a potential feedback mechanism to prevent excessive or prolonged immune activation and inflammation-associated pathology.61 Overall, our findings demonstrated that sHDL could effectively control the inflammatory reaction and bone resorption associated with apical periodontitis by upregulating Ppara and Fadd and reducing the expression of proinflammatory cytokines, suggesting a partial inhibition of the TLR pathway. The gene discussed is PPARA; the disease is periapical periodontitis.