Therefore, the control of inflammation is the cornerstone for managing diabetes-periodontitis risk due to the increased production of advanced glycation end-products (AGEs) and interaction with their receptors (RAGEs) in periodontal tissues, which is responsible for the increased activity of monocytes/macrophages, endothelial cells, the release of pro-inflammatory cytokines, and, finally, the activation of NF-κB receptor ligand/osteoprotegerin (RANKL/OPG). Here, TNFRSF11B is linked to diabetes mellitus.