Poorly controlled DM generates sustained hyperglycemia, which in turn induces an increase in the inflammatory response in the periodontal tissue; this stimulates the receptor activator of nuclear factor κB (RANK)/RANK-Ligand (RANKL) axis with an increase in osteoclastogenesis and destruction of the alveolar bone, which will conclude with the clinical attachment loss, one of the PD hallmarks. This evidence concerns the gene TNFRSF11A and diabetes mellitus.