Enhanced Activity of the Macrophage M1/M2 Phenotypes and Phenotypic Switch to M1 in Periodontal Infection

Background: Macrophages are central players in the pathogenesis of periodontitis. However, the phenotypic switch of macrophage M1/M2 remains uncertain. Methods: Adult male mice were divided into periodontitis (P) or control (C) groups. Bone marrow–derived macrophages (BMMs) were stimulated with Porphyromonas gingivalis lipopolysaccharide (LPS). In both the periodontium and serum, macrophage M1 and M2 phenotypes were detected in vivo and in vitro via the following: 1) immunofluorescence; 2) immunohistochemistry; 3) electrochemiluminescence immunoassays; 4) quantitative polymerase chain reaction assays; and 5) enzyme‐linked immunosorbent assays. The M1‐type markers used included the following: 1) nitric oxide synthase (NOS)‐2; 2) tumor necrosis factor‐alpha; 3) interleukin (IL)‐1β; 4) IL‐6; and 5) C‐reactive protein. The M2‐type markers were as follows: 1) arginase‐1; 2) cluster of differentiation (CD) 206; and 3) IL‐10. Results: Compared with the C group, the P group had a 14‐fold increase in F4/80+ NOS2+ cells and four‐fold more F4/80+ CD206+ cells with an enhanced NOS2/CD206 ratio in the periodontium (P