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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 <0.01). NOS2(-) CD206(+) and dual NOS2(+) CD206(+) macrophages dominated in the C and P groups, respectively. The P group had significantly increased M1- and M2-type cytokines in both the periodontium and serum and also had an enhanced IL-6/IL-10 ratio in the serum (P <0.05). M1-type markers were significantly upregulated at the mRNA level, whereas M2-type markers were downregulated at both the mRNA and protein levels in BMMs after LPS stimulation (P <0.01). CONCLUSION: Periodontal inflammation is associated with an enhancement of both the M1 and M2 phenotypes of macrophages, in which a phenotypic switch of M2 to M1 might be a critical mechanism in mediating periodontal tissue damage, including alveolar bone loss.
Yu et al. (Fri,) studied this question.