In summary elevated levels of focal death in periodontitis promote the secretion of active inflammatory factors (IL-1β, IL-18), which amplifies the inflammatory response and leads to an overactive immune response; this ultimately reduces bone formation, enhances bone resorption by up-regulating RANKL, exacerbates the destruction of periodontal tissues, and inhibits their regeneration. This evidence concerns the gene TNFSF11 and periodontitis.