Mechanistically, WTAP mediated the m6A modification of TP53BP1 mRNA, and the effects of WTAP on P-PDLSC senescence, oxidative stress, and osteogenic differentiation were dependent on TP53BP1.<h4>Conclusion</h4>The WTAP/TP53BP1 axis impairs periodontal tissue regeneration by promoting P-PDLSC senescence and suppressing osteogenic differentiation in an m6A-dependent manner, revealing a new cellular-level target for treating periodontitis. This evidence concerns the gene TP53BP1 and periodontitis.