SUMMARY Acute apical abscess is the most common form of dental abscess and is caused by infection of the root canal of the tooth. It is usually localized intraorally, but in some cases the apical abscess may spread and result in severe complications or even mortality. The reasons why dental root canal infections can become symptomatic and evolve to severe spreading and sometimes life-threatening abscesses remain elusive. Studies using culture and advanced molecular microbiology methods for microbial identification in apical abscesses have demonstrated a multispecies community conspicuously dominated by anaerobic bacteria. Species/phylotypes commonly found in these infections belong to the genera Fusobacterium , Parvimonas , Prevotella , Porphyromonas , Dialister , Streptococcus , and Treponema . Advances in DNA sequencing technologies and computational biology have substantially enhanced the knowledge of the microbiota associated with acute apical abscesses and shed some light on the etiopathogeny of this disease. Species richness and abundance and the resulting network of interactions among community members may affect the collective pathogenicity and contribute to the development of acute infections. Disease modifiers, including transient or permanent host-related factors, may also influence the development and severity of acute abscesses. This review focuses on the current evidence about the etiology and treatment of acute apical abscesses and how the process is influenced by host-related factors and proposes future directions in research, diagnosis, and therapeutic approaches to deal with this disease.

Objective. This clinical study was undertaken to compare the effectiveness of 2.5% sodium hypochlorite (NaOCl) and 0.12% chlorhexidine digluconate as irrigants in reducing the cultivable bacterial populations in infected root canals of teeth with apical periodontitis. Study design. According to stringent inclusion/exclusion criteria, 32 teeth with primary intraradicular infections and chronic apical periodontitis were selected and followed in the study. Bacterial samples were taken at the baseline (S1) and after chemomechanical preparation using either NaOCl (n ϭ 16) or chlorhexidine (n ϭ 16) as irrigants (S2). Cultivable bacteria recovered from infected root canals at the 2 stages were counted. Isolates from S2 samples were identified by means of 16S rRNA gene sequencing analysis.

Bacteria located at the apical portion of the root canals are conceivably in a strategic position to induce damage to the periradicular tissues and resulting inflammatory diseases. This study sought to investigate the prevalence of 11 selected putative endodontic pathogens in the apical third of infected root canals associated with periradicular lesions. The apical root portion of 23 extracted teeth with carious pulpal exposures and attached periradicular lesions was sectioned, and the root canals were sampled for microbiological investigation. DNA was extracted from the samples and analyzed for the presence of 11 bacterial species using a nested polymerase chain reaction assay. The results showed that Pseuramibacter alactolyticus occurred in 10 cases (44%), Treponema denticola in 6 (26%), Fusobacterium nucleatum in 6 (26%), Porphyromonas endodontalis in 4 (17%), Filifactor alocis in 2 (9%), Dialister pneumosintes in 1 (4%), Porphyromonas gingivalis in 1 (4%), and Tannerella forsythensis in 1 (4%). No sample yielded Prevotella intermedia, Prevotella nigrescens, or Campylobacter rectus. Of the samples examined, 17 were positive for at least 1 of the target species. Occurrence of these bacterial species in the apical third of infected root canals suggests that they can be involved in causation of periradicular lesions.