The pathogenesis of periodontitis is driven by subgingival microbial dysbiosis, where keystone pathogens such as Porphyromonas gingivalis subvert host immunity via lipopolysaccharide (LPS)-mediated activation of the complement 5a receptor 1-Toll-like receptor 2 (C5aR1-TLR2) crosstalk pathway [8]. This evidence concerns the gene TLR2 and periodontitis.