The binding of complement(C)5a and its receptors(C5aR) can stimulate the aggregation of neutrophils and macrophages and generate inflammatory mediators during inflammation. C5aR includes CD88 and C5L2, which are expressed on neutrophils, macrophages, and immature dendritic cells. These cells can initiate inflammation. C5a could inhibit the death of programmed neutrophils to promote inflammation through extracellular signal-regulated kinase 1, 2 and P38 mitogen-activated protein kinase pathways. Restraining the interaction between C5a and C5aR can inhibit neutrophil activation and the generation of reactive oxygen and matrix metalloproteinase. This process reduces inflammation and tissue damage. Further understanding of the role of C5a and C5a receptors in the development of periodontitis may offer a new approach to treat periodontitis.
