Furthermore, the effects of TLR signaling and on RANKL-dependent and -independent mechanisms have been proposed to induce osteoclastogenesis, and other endogenous factors such as miRNA, IL-22, M1/M2 macrophages, and memory B cells have been identified recently as potential contributors in the regulation of osteoclastogenesis and bone loss during periodontal disease pathogenesis [115]. This evidence concerns the gene TNFSF11 and periodontal disorder.