IL1B and periodontitis: The RT-qPCR analyses first demonstrated that IL-36γ acted on OECs by enhancing the expression of inflammatory cytokines, which have been clearly established as participating in the pathogenic mechanisms of periodontitis including IL-1β, IL-6 and TNF-α with a 1.4-, 12.3- and 5.03-fold increase (Fig. 6A), respectively.