Additionally, IL-33 may participate in the bone resorption process observed in periodontitis in two ways: by disrupting the RANK (receptor activator of nuclear-kB factor) / RANKL (RANK ligand) / OPG (osteoprotegerin) axis [23, 24] and by increasing the expression of osteoclast precursor transcription factors, favoring the differentiation and activation of these cells [25]. This evidence concerns the gene TNFRSF11B and periodontitis.