First, indirect routes: periodontal inflammation and oral dysbiosis increase systemic IL-6/IL-1β and endotoxemia via oral–gut microbial crosstalk (swallowed oral taxa/LPS, gut dysbiosis, barrier dysfunction, portal delivery), activating hepatic innate immune signaling (e.g., TLR4 on Kupffer cells) and promoting steato-inflammatory and fibrotic phenotypes. The gene discussed is IL1B; the disease is serum lipopolysaccharide activity.