TLR4 and serum lipopolysaccharide activity: 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.