Traditionally oral cancer has always been associated with tobacco and areca nut chewing habit. An emerging concept is that tumor development and progression is also largely dependent on the cross - talk between immune system and tumor cells. Amongst internal agents, tumor associated macrophages and fibroblasts, play a pivotal role. Cytokines released by fibroblasts crucially affect the carcinoma cell behaviour and the role of chronic inflammation in tumor progression has now widely accepted. Amongst external agents causing infections like, fungal agents(candidiasis) and viruses (HPV and EBV) , with oral cancer have already been discussed by many researchers. It is the bacterial population (H. pylori) in microenvironment, which is now continuously increasing the concern of the scientists towards itself. H. pylori association has already been established with gastric, pancreatic and hepatocellular cancers. It is present in oral cavity with GCF and plaque as its ecological niche and is shown to release inflammatory mediators like cytokines, when associated with chronic gingivitis and periodontitis. These inflammatory mediators when accumulate in the microenvironment of tissues for prolonged periods of time have the capacity to induce cell proliferation and to promote prolonged cell survival through activation of oncogenes and inactivation of tumor suppressor genes. This results in genetic instability with increased risk of oral cancer. Association of H. pylori is still a grey area of study as not many studies have been done in respect to the same. Hence, this study is done to outline the association between H. pylori, its role in chronic inflammation and finally the progression of the disease towards oral cancer. Keywords: oral cancer, tumor microenvironment