The plausible mechanisms linking these two conditions are the systemic dissemination of periodontal bacteria and the entrance of the locally-produced pro-inflammatory cytokines to the systemic circulation.17 In fact, current evidence shows that nonspecific inflammatory mediators, such as tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β) and prostaglandin E2 (which plays an important role in the initiation of birth), can also be prematurely induced in periodontitis. The gene discussed is IL1B; the disease is periodontitis.