Periodontal disease caused chiefly by bacteria is characterized by inflammation, bacteremia, and a strong immune response. It is based on evidence that a continuous long-term exposure to oral bacteremia and bacterial toxins induces inflammatory immune response after immune evasion releases growth factors such as FGF, EGF, TGF-Beta, free radicals such as ROS and NOS, cytokines such as TNFAlfa, IL-1 Beta, IL-6; and matrix metalloproteinase such as MMP-9. Immature myeloid cells such as macrophages, dendritic cells and granulocytes involved in chronic inflammation and tumor progression through immunosuppressive activity against innate and adaptive immunity by factors such as iNOS, Arginase1 and ROS, activate major transcriptional factors such as NF-KB and STAT3 that could contribute to genetic instability, uncontrolled cell proliferation, angiogenesis, resistance to apoptosis, epithelial to mesenchymal transition, immunosuppression, invasion and metastasis. This study is a product of research and analysis on the role of chronic inflammatory mediators of chronic periodontitis in progression to cancer.