Taken together, the literature shows that an increased level of pyroptosis in periodontitis can promote the secretion of active inflammatory factors (IL-1β, IL-18), thus amplifying the inflammation response, leading to an overactive immune response; this ultimately decreases bone formation, enhances bone resorption by upregulation of RANKL, exacerbates the destruction of periodontal tissue, and suppresses its regeneration (Figure 1). This evidence concerns the gene IL18 and periodontitis.