关键词: 牙周炎, 巨噬细胞极化, 免疫微环境, 生物材料

Abstract: Periodontitis is a chronic inflammatory disease caused by dental plaque biofilm，and its progressive alveolar bone destruction is closely associated with the imbalance of host immune response. As the core cells in the periodontal immune microenvironment，the polarization balance between M1-type（exerting pro-inflammatory and bone resorptive functions）and M2-type（exerting anti-inflammatory and tissue repair-promoting functions）macrophages is a key factor in regulating disease prognosis. This article reviewed the activation mechanisms of macrophages in periodontitis，focusing on elaborating the molecular mechanisms by which dental plaque components，such as lipopolysaccharide，initiated immune signal pathways via pattern recognition receptors such as TLR/NLRP3，and activated signaling pathways including MAPK and NF-κB to regulate M1 polarization，as well as the molecular mechanism of IL-4/IL-10 in mediating M2 polarization through pathways like JAK/STAT6 and PI3K/Akt. Additionally，this article systematically summarized the research progress of biomaterials targeting macrophage polarization，including nanomaterials，exosomes，and sustained-release drug carriers，and compared the immune-modulatory effects and clinical translation potential of different biomaterials，so as to provide a theoretical basis and practical reference for immune-modulatory treatment of periodontitis.

Key words: periodontitis, macrophage polarization, immune microenvironment, biomaterials