Given the potential for synergism between complement and TLRs, C3 inhibition in periodontitis can also inhibit inflammation that is activated by TLR signaling either in response to microbial TLR ligands (e.g., LPS, lipoproteins, and bacterial DNA) (96, 97) or in response to endogenous TLR ligands (e.g., biglycan, hyaluronan, or heparan sulfate fragments) that are released upon tissue injury and act as danger-associated molecular patterns (DAMPs) (98, 99). Here, C3 is linked to periodontitis.