Taken together, the suggested mechanism accounting for the association between periodontal disease and each of the components of the metabolic syndrome cluster was similar: an increased inflammatory burden through inflammatory cytokines (mostly IL-1β, IL-6, and TNF-α) which results in systemic elevated oxidative stress and the invasion of Gram-negative bacteria, which further increase the inflammatory burden and the activation of bone-resorbing agents. The gene discussed is TNF; the disease is periodontal disorder.