Since P. gingivalis and F. nucleatum can generate inflammation, cell proliferation, and cellular invasion in OSCC through several routes [36], their carcinogenic potential may be critical for oral cavity cancers through the production of interleukin-6, tumor necrosis factor-α, matrix metalloproteinases, reduced apoptosis, and regulation of the p53 tumor suppressor gene. This evidence concerns the gene TP53 and oral cavity cancer.