Abstract

Introduction: Gingivitis is characterized as an inflammation of the gum and can have different etiologies, however, most cases occur due to poor oral hygiene and accumulation of bacteria in dental plaque, causing periodontal disease, which can progress to tooth loss. Knowing the pathophysiology of gingivitis is necessary for an effective therapeutic intervention by the professional. This work aims to describe the pathophysiological process of gingivitis and discuss the mechanism of action of anti-inflammatory drugs. Methodology: This work is a literature review carried out on Google Scholar, PUBMED and SciELO platforms. Results and Discussion: Bacteria accumulated in the plaque are recognized by phagocytes, which are activated and induce immune and inflammatory responses, in addition to activating oxidative and nitrosative stress pathways, resulting in bacterial death and gingival necrosis. In the face of aggression, gingiva cells activate the arachidonic acid cascade, which gives rise to several pro-inflammatory mediators; Typical anti-inflammatory drugs block enzymes in this cascade, inhibiting the production of these chemical signals. Conclusion: Therefore, immune and inflammatory responses are important for the prognosis of gingivitis, however, in some cases, therapeutic interventions are necessary so that there is no great tissue and tooth loss.

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