In a TNFAIP3-deficient mouse model of periodontitis, IL-17 levels were significantly elevated, accompanied by more severe bone resorption and inflammatory responses, and the primary mechanism is that TNFAIP3 reduces osteoclast differentiation by inhibiting TRAF6 ubiquitination downstream of IL-17R signaling [46,47]. This evidence concerns the gene IL17A and periodontitis.