Pathogenesis of apical periodontitis and the causes of endodontic failures.
Apical periodontitis is a sequel to endodontic infection and manifests itself as the host defense response to microbial challenge emanating from the root canal system. It is viewed as a dynamic encounter between microbial factors and host defenses at the interface between infected radicular pulp and periodontal ligament that results in local inflammation, resorption of hard tissues, destruction of other periapical tissues, and eventual formation of various histopathological categories of apical periodontitis, commonly referred to as periapical lesions. The treatment of apical periodontitis, as a disease of root canal infection, consists of eradicating microbes or substantially reducing the microbial load from the root canal and preventing re-infection by orthograde root filling. The treatment has a remarkably high degree of success. Nevertheless, endodontic treatment can fail. Most failures occur when treatment procedures, mostly of a technical nature, have not reached a satisfactory standard for the control and elimination of infection. Even when the highest standards and the most careful procedures are followed, failures still occur. This is because there are root canal regions that cannot be cleaned and obturated with existing equipments, materials, and techniques, and thus, infection can persist. In very rare cases, there are also factors located within the inflamed periapical tissue that can interfere with post-treatment healing of the lesion. The data on the biological causes of endodontic failures are recent and scattered in various journals. This communication is meant to provide a comprehensive overview of the etio-pathogenesis of apical periodontitis and the causes of failed endodontic treatments that can be visualized in radiographs as asymptomatic post-treatment periapical radiolucencies.
Nair
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PN
Institute of Oral Biology, Section of Oral Structures and Development, Center of Dental and Oral Medicine, University of Zürich, Plattenstrasse 11, CH-8028 Zürich, Switzerland. nair@zzmk.unizh.ch
D000818:Animals; D000907:Antibodies, Bacterial / Q000276:immunology; D016207:Cytokines / Q000378:metabolism; D003790:Dental Pulp Necrosis / Q000150:complications* / Q000382:microbiology* / Q000628:therapy; D019232:Dental Restoration Failure; D006094:Gram-Positive Bacteria / Q000472:pathogenicity; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D007962:Leukocytes / Q000276:immunology; D008070:Lipopolysaccharides / Q000276:immunology; D010485:Periapical Periodontitis / Q000209:etiology* / Q000276:immunology / Q000382:microbiology*; D012389:Root Canal Obturation
D000907:Antibodies, Bacterial; D016207:Cytokines; D018836:Inflammation Mediators; D008070:Lipopolysaccharides