ETIOLOGY AND PATHOGENESIS OF ACUTE PERIODONTITIS

Аннотация

Acute periodontitis is a rapidly progressing inflammatory disease affecting the periapical tissues, primarily triggered by pulpal necrosis and subsequent microbial invasion. This article provides a comprehensive review of the etiological factors and pathogenesis of acute periodontitis based on current scientific literature. The study integrates microbiological, histopathological, and immunological perspectives to offer a deeper understanding of the condition's progression. The most common etiological agents include anaerobic gram-negative bacteria such as Fusobacterium nucleatum, Porphyromonas gingivalis, and Prevotella intermedia. These pathogens produce endotoxins and enzymes that disrupt periapical tissue integrity and stimulate host immune responses. Inflammatory mediators like interleukin-1β (IL-1β), tumor necrosis factor-alpha (TNF-α), and prostaglandin E2 (PGE2) play critical roles in tissue destruction, especially in promoting osteoclast activation and bone resorption. The material and methods section outlines the literature search strategy, which included peer-reviewed articles from PubMed and Scopus databases. Results revealed consistent patterns of acute inflammatory responses marked by polymorphonuclear cell infiltration, vascular changes, and cytokine expression. Discussion highlights the delicate balance between host defense mechanisms and pathogen virulence, emphasizing the need for early diagnosis and intervention. The study concludes that understanding the complex etiopathogenesis of acute periodontitis is essential for effective treatment and prevention. Root canal therapy remains the cornerstone of management, supported by antimicrobial strategies in selected cases. Future research should focus on immunomodulatory approaches to enhance therapeutic outcomes.