A common chronic inflammatory disease with local and systemic effects is periodontitis. Systemic circulation cytokines and chemokine including C Reactive Protein, acute phase proteins, TNF-, IL-1, IL-2 and IL-6 and Interferon gamma are more prevalent. These substances are identical to those released in coronavirus disease. The likelihood that periodontitis will cause hyper inflammation should be considered. Therefore, a symbiosis of the oral micro biota that interacts with host's immunological responses to cause inflammation and tissue damage is responsible for the beginning and development of periodontal disease. Therefore, rather than focusing just on viral pathogenesis, it is advisable to take into account the possibility that preexisting periodontal disease will affect the severity of COVID 19. Which was before to airways epithelial cells to bacteria, as shown in experimental investigations, worsens the production of cytokines in stimulate the establishment of a biofilm on the cells of the airway epithelium in response to a future viral infection. There haven't been any research on the connection between COVID-19 and periodontal disease (PD); however there may be biological justification. With intriguing findings, our team has investigated many PD and systemic condition-related issues. Since periodontal disease is a condition that can be treated, it is imperative that medical practitioners are aware of this potential and evaluate the oral health of their patients. Additionally, it is essential to promote oral hygiene practices to reduce the likelihood of both local and systemic problems during the pandemic. A systemic inflammatory response known as "cytokine storm syndrome" can be brought on by a variety of things, including some drugs and infections. This is a suggested process for how severe viral diseases, such the Coronavirus sickness that causes a pandemic that is caused by the Coronavirus virus, spread. On the other hand, cytokine hyper-reactivity, which affects systemic inflammatory-immune responses, is a feature of chronic periodontitis, one of the most common chronic inflammation diseases of humans. The modern pathophysiology of periodontitis emphasizes the intricate interactions between dental biofilm, acquired environmental stresses, and host genetic components. Since the individual reaction, which includes lipid and cytokine mediators released by the host, as well as adjustments in periodontal structures like connective tissue and bone tissue, can always be visibly categorized by a particular gene tenancy, metabolite and casein expression, genomic, proteomic, and met genomic aspects are determinants to developing periodontal diseases. It is crucial to understand that chronic periodontal disease is an ongoing, severe inflammatory infiltration in the connective tissue that activates T and B cells through the release of cytokines and affects how the illness develops. With the activation of Th1, Th2, and Th17 cells and the production of a number of pro-inflammatory cytokines, including as IL-1, IL-17E (IL-25), and IL-17, other immune cells, including such neutrophils, dendritic cells, and B cells, there is indeed a deregulation of T cells in periodontitis.