The complement system mediates the body’s defense reactions to protect the host against periodontal chronic inflammatory diseases. This system assists pathogens to exacerbate pathological and destructive inflammation by directly affecting immune cells or via crosstalk and by regulating other host signaling pathways. The complement system induces secretion of interleukin, tumor necrosis factor, and granulocyte-macrophage colony-stimulating factor during immune inflammation. Secretion is stimulated by activating leukocytes, regulating helper T cells and macrophages, and promoting cell immune and T cell-dependent antibody secretion, thus enhancing the regulation of immune effect and improving the body’s immunity. Furthermore, the complement system produces inflammation that exacerbates tissue damage and triggers periodontitis. The antagonists of the complement receptor can significantly clean pathogens and prevent periodontitis by interfering the signaling crosstalk between the complement receptor and Toll-like receptors. Therefore, elucidating the mechanism of the complement system in periodontitis can provide novel targets for periodontitis therapeutics.
