Periodontal tissue inflammation, encompassing acute and chronic periodontitis, represents a multifactorial pathological process affecting the supporting structures of teeth. This condition is primarily initiated by microbial biofilm accumulation; however, its progression is strongly influenced by host immune response, genetic predisposition, and systemic health conditions. The present review aims to critically analyze the etiological factors of periodontitis and explore its bidirectional relationship with systemic diseases. Epidemiological data indicate that periodontitis affects approximately 45–50% of the global adult population, with severe forms observed in nearly 10–15% of cases. Acute periodontitis is characterized by rapid tissue destruction, pain, and inflammatory exudation, whereas chronic periodontitis progresses slowly, often remaining asymptomatic until advanced stages of bone resorption occur. Recent studies highlight a strong association between periodontal inflammation and systemic conditions such as cardiovascular diseases, diabetes mellitus, rheumatoid arthritis, and adverse pregnancy outcomes. The underlying mechanism involves systemic dissemination of inflammatory mediators including interleukin-1β, tumor necrosis factor-alpha, and C-reactive protein. Furthermore, periodontal pathogens such as Porphyromonas gingivalis have been detected in atherosclerotic plaques, suggesting microbial translocation.

Periodontitis, inflammation, periodontal tissues, systemic diseases, etiology, microbiota, cytokines, diabetes, cardiovascular.

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