Introduction and Objective: Periodontitis (PD), a chronic inflammatory condition, is a leading cause of tooth loss and jawbone deterioration and is associated with an increased risk of diabetes. The persistent inflammation in PD results from an imbalance between pro-inflammatory (M1) and anti-inflammatory (M2) macrophages, contributing significantly to tissue destruction. This study investigates the role of peroxisome proliferator-activated receptor alpha (PPARα), a nuclear hormone receptor, in regulating macrophage polarization during PD, particularly in the context of diabetes.Methods:In vivo: PD was induced in diabetic (db/db) mice. PPARα expression levels were analyzed, and the effects of PPARα activation on periodontal inflammation and alveolar bone loss were assessed.In vitro: Macrophages were treated with Porphyromonas gingivalis (P.g.) lipopolysaccharide (LPS) and analyzed for PPARα activity under normal and high-glucose conditions. M1 and M2 macrophage markers, including CD14 and IL-10, were measured following PPARα agonist treatment.Results: PPARα expression was markedly reduced in diabetic animals with PD. Lack of PPARα exacerbated periodontal inflammation and alveolar bone loss in db/db mice, whereas activation of PPARα ameliorated these effects. LPS treatment inhibited PPARα activity in a dose-dependent manner, an effect partially reversed by PPARα agonists. However, the reversal was less effective under high-glucose conditions. PPARα activation reduced M1 macrophage marker expression (CD14) and increased M2 macrophage marker expression (IL-10) in vitro.Conclusion: PPARα plays a critical role in modulating macrophage polarization during PD, particularly in diabetes. Activation of PPARα attenuates inflammation and promotes a shift from pro-inflammatory to anti-inflammatory macrophages, highlighting its therapeutic potential for managing PD and its complications in diabetic individuals.
A. Hu: None. Y. Chen: None.
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