During periodontitis, activated osteoclasts and inflammatory-related mediators can control the release of ligand-receptor factor kappa B (NF-κB), receptor activator of nuclear factor kappa-Β ligand (RANKL), and osteoprotegerin (OPG), which activates the osteoclast receptor and the relative alveolar bone destruction [21]. This evidence concerns the gene TNFSF11 and periodontitis.