LPS Plays a Role in Chronic Periodontitis by Affecting the Proinflammatory Cytokine Secretion of PLSCs and Inhibiting the Osteogenic Differentiation of BMSCS

Chronic periodontitis, a common inflammatory disease, is exacerbated by lipopolysaccharide (LPS), a major gram-negative bacterial component that activates the immune system, triggers proinflammatory responses, and disrupts periodontal ligament stem cell (PLSC) function. The effects of LPS on the osteogenic differentiation of and proinflammatory cytokine secretion by PLSCs were investigated using a cytokine array, RT‒PCR, flow cytometry, and Alkaline phosphatase (ALP) staining. This study focused on analyzing the mechanism by which PLSCs exacerbate chronic periodontitis through the regulation of M1 macrophage polarization. LPS treatment significantly promoted the secretion of proinflammatory cytokines by PLSCs, which not only increased macrophage recruitment but also induced M1 polarization. Further analysis revealed that LPS-induced proinflammatory cytokine secretion by PLSCs inhibits the osteogenic potential of PLSCs through the regulation of M1 macrophage polarization and increases TNF-α expression. LPS, by affecting the paracrine characteristics of PLSCs and immune cell polarization, may be a key factor underlying the persistent inflammation and impaired periodontal tissue repair in chronic periodontitis. Targeting the mechanisms of LPS action, particularly by inhibiting TNF-α and its receptors, may provide new intervention strategies for the treatment of chronic periodontitis. This study offers valuable insights into the pathogenesis of chronic periodontitis and potential therapeutic approaches.