Diabetes mellitus can revise the expression of inflammatory-related cytokines such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β); increase the generation of reactive oxygen species (ROS) and its association with the oxidative stress index; disrupt the receptor activator of nuclear factor-kappa B (NF-κB) ligand (RANKL)/osteoprotegerin (OPG) axis; activate osteoclasts responsible for bone resorption; and destroy polymorphonuclear leucocyte activity, which in turn may accelerate the development of periodontitis (44). This evidence concerns the gene TNFSF11 and diabetes mellitus.