Eighteen 8-week-old female C57BL/6 mice were screened and divided into three groups by genotype： C3ar^+/+ group，C3ar^+/－group and C3ar^－/－ group （n=6）， respectively. The chronic periodontitis models were established by ligating the left maxillary second molars of mice with 4-0 silk thread， and the right maxillary second molars were used as controls. On the 11th day after ligation， the alveolar bone resorption was evaluated； the distance from the cementum enamel junction （CEJ） to the alveolar bone crest （ABC） was detected by Micro-CT；the pathomorphology of the periodontal tissue of the mice in various gorups was observed by HE staining. The levels of inducible nitric oxide synthase （iNOS） and arginase 1 （Arg1） in periodontal tissue of the mice in various groups were detected by immunohistochemical staining. In vitro，the RAW264.7 macrophages were used to establish the inflammatory model by treated with lipopolysaccharide （LPS）；the experiment was divided into blank group， LPS group， C3a group and LPS+C3a group. The polarization of macrophages was observed under light microscope， and the expression levels of iNOS， interleukin-1β （IL-1β） and tumor necrosis factor-α （TNF-α） mRNA were detected by Real-time fluorescence quantitative PCR （RT-qPCR） method.

Compared with C3ar^+/+ and C3ar^+／－ groups， the distance between CEJ and ABC of the mice in C3ar^-/- group was significantly decreased （P<0.01）， inflammatory cell infiltration was decreased； the level of attachment loss was decreased，and the alveolar bone absorption was decreased； the expression level ofiNOS protein was decreased （P<0.05）， whereas the expression level of Arg1 protein was increased （P<0.01）.In the in vitro study， the cells in blank group were round in shape， the cells in C3a group， LPS group and LPS+C3a group were spindled， and the cells in LPS+C3a group showed aggregative growth. The expression levels of iNOS， IL-1β and TNF-α mRNA in LPS group， C3a group and LPS+C3a group were higher than those in blank group （P<0.05）；the expression level IL-1β mRNA in the cells in LPS group and LPS+C3a group were significantly increased（P<0.05）.

In the mouse models of chronic periodontitis， the C3a-C3aR axis may promote the inflammatory response and tissue damage of chronic periodontitis through the polarization of macrophages to M1 type.