Pathogenetic Mechanisms of Inflammatory Resorption of Jaw Bones in Apical Periodontitis

Apical periodontitis (AP) is characterized by persistent inflammation and resorption of alveolar bone initiated by microorganisms, posing a serious threat to both dental and systemic health. Although non-surgical antimicrobial therapy remains the standard approach in endodontic treatment, many periapical lesions continue to demonstrate resistance to conventional therapy. Improving the outcomes of endodontic treatment requires a deeper understanding of the pathogenetic mechanisms underlying the formation of the inflammatory microenvironment in apical lesions. Current evidence indicates that inflammatory bone resorption in the periapical region results from microbial biofilm activity and activation of immune cells, leading to significant disruption of bone homeostasis. The principal pathways involved in inflammatory tissue destruction include immune dysregulation, oxidative stress, and lipid peroxidation, all of which contribute to damage of periapical tissues. This review discusses the pathogenetic mechanisms of inflammatory jaw bone resorption in apical periodontitis and highlights modern therapeutic strategies aimed at interrupting destructive processes, including targeted antioxidant therapy, cytokine modulation, and adaptive cell-based approaches.