Periodontitis is a common inflammatory periodontal disease affecting a wide range of population all over the world. The causing bacteria releases chemicals which activate the innate immune system to release proinflammatory cytokines contributing to more progression. This activates the acquired immune system leading to more progression of periodontitis. As the immune response goes on, released cytokines and chemokines can damage the periodontal ligaments, gingiva, and alveolar bone. There are many types of cytokines and chemokines in periodontitis. Cytokines are peptide mediators who are responsible for cell signaling and communication. Chemokines are a large subfamily of cytokines having the ability to coordinate leukocyte recruitment and activation. This paper is a narrative review of the literature.This review ensures that inflammatory mediators in the case of periodontitis can cause a noticeable damage in the whole apparatus of the periodontium. It causes soft tissue inflammation and bone damage affected by the mediators of both innate and acquired immune system.The inflammatory process is accompanied by large network of cytokines and chemokines. There is high expression of proinflammatory cytokines such as interleukin (IL)-1α, IL-1β, IL-6, IL-12, tumor necrosis factor (TNF)-α, and regulatory cytokines such as IL-4, IL-1(RA) receptor antagonist, IL-10, and induced protein (IP)-10. There is also increased production of cytokines IL-10, IL-12, interferon-γ, IP-10, IL-1RA, and IL-4. Cytokines IL-17, IL-6, IL-1β, TNF-α, macrophage colony-stimulating factor, and prostaglandin E trigger the osteoclast activity causing bone resorption.

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