The increased release of proinflammatory cytokines (IL-1β, IL-6, and TNF-α), an altered RANKL/osteoprotegerin ratio, interactions between advanced glycation end products and their receptors, increased production of reactive oxygen species, and increased interaction between endothelial cells and leukocytes play a crucial role in the two-way relationship between diabetes and periodontitis. Here, IL1B is linked to periodontitis.