Abstract
Evidence shows the polymicrobial etiology of endodontic infections, in which bacteria and their products are the main agents for the development, progression, and dissemination of apical periodontitis. Microbial factors in necrotic root canals (e.g., endotoxin) may spread into apical tissue, evoking and supporting a chronic inflammatory load. Thus, apical periodontitis is the result of the complex interplay between microbial factors and host defense against invasion of periradicular tissues. This review of the literature aims to discuss the complex network between endodontic infectious content and host immune response in apical periodontitis. A better understanding of the relationship of microbial factors with clinical symptomatology is important to establish appropriate therapeutic procedures for a more predictable outcome of endodontic treatment.
Highlights
Declaration of Interest: The authors certify that they have no commercial or associative interest that represents a conflict of interest in connection with the manuscript.Submitted: May 21, 2018 Accepted for publication: May 29, 2018 Last revision: June 12, 2018Apical periodontitis is mainly a consequence of root canal infection, characterized by inflammation and destruction of periradicular tissues resulting from the interaction between microbial factors and host immune response.[1]
Evidence has reinforced the microbial role in apical periodontitis;[2] given the diversity of the endodontic microbiota and its different virulence factors, the exact pathogenic roles of microbial species have been under investigation to determine whether any particular group of bacteria is associated with specific endodontic symptoms and clinical signs
Among the virulence factors of gram-negative bacteria, lipopolysaccharides (LPS/endotoxins) are especially important in endodontic infection because of their biological effects, which lead to a complex interplay with host factors, resulting in clinical symptomatology, inflammatory reaction, and resorption of mineralized tissues.[4,11,12,13,14,15,16,17,18,19,20]
Summary
Declaration of Interest: The authors certify that they have no commercial or associative interest that represents a conflict of interest in connection with the manuscript.Submitted: May 21, 2018 Accepted for publication: May 29, 2018 Last revision: June 12, 2018Apical periodontitis is mainly a consequence of root canal infection, characterized by inflammation and destruction of periradicular tissues resulting from the interaction between microbial factors and host immune response.[1]. There is a correlation between higher levels of endotoxins and a greater area of bone destruction in periapical tissues,[142] as well as with the presence of specific clinical features found in primary endodontic infections.[20,46] Increased endotoxin levels in infected root canals may be associated with the severity of periapical disease, as well as with the development of clinical symptoms.[20]
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