RÉSUMÉ
Periapical periodontitis arises from the interaction between microbial factors and the inflammatory response of the host's periapical tissues. In this process, bacteria and their byproducts serve as the primary drivers for the initiation, progression, and spread of the disease. Pulp infections and periapical lesions are primarily dominated by gram-negative bacteria. The endotoxin lipopolysaccharide component of these bacteria plays a crucial role in pulp infection, triggering clinical symptoms, inflammatory reactions, and bone tissue resorption. Similarly, lipoteichoic acid and lipopolysaccharide from gram-positive bacteria exhibit similar pathogenic characteristics, causing damage to pulp and periapical tissues. The aim of this review is to delve deeper into the distribution patterns and pathogenesis of periapical microorganisms in chronic periapical periodontitis.