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However, its role in oral mucosal immunity remains ambiguous. Periodontitis is a special but prevalent infectious disease characterized as hyperinflammation of oral mucosa and bone resorption. Here, it is reported that genetic deletion of <jats:italic>Mettl3<\/jats:italic> alleviates periodontal destruction via suppressing NLRP3 inflammasome activation. Mechanistically, the stability of <jats:italic>TNFAIP3<\/jats:italic> (also known as A20) transcript is significantly attenuated upon m<jats:sup>6<\/jats:sup>A modification. When silencing METTL3, accumulated TNFAIP3 functioning as a ubiquitin\u2010editing enzyme facilitates the ubiquitination of NEK7 [NIMA (never in mitosis gene a)\u2010related kinase 7], and subsequently impairs NLRP3 inflammasome assembly. Furtherly, Coptisine chloride, a natural small\u2010molecule, is discovered as a novel METTL3 inhibitor and performs therapeutic effect on periodontitis. 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