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INTRODUCTION:

The present study aimed to evaluate the antibacterial effect of the combined use of sodium hypochlorite (NaOCl) and root canal sealers on Enterococcus faecalis biofilms using a dentin infection model.

METHODS:

Cells of E. faecalis were introduced into the dentinal tubules by centrifugation and incubated in brain-heart infusion for 3 weeks. The biofilms in dentin were first subjected to 5% NaOCl or sterile water for 10 minutes followed by an equal thickness of AH Plus (Dentsply International Inc, York, PA), Endosequence BC Sealer (Brasseler USA, Savannah, GA), or MTA Fillapex (Angelus Indústria de Produtos Odontológicos S/A, Londrina, Brazil) placed on the root canal wall of the dentin specimens for 7, 30, and 60 days. Gutta-percha and water were used in a similar manner as controls. The proportions of dead and live bacteria inside the dentinal tubules were assessed by confocal laser scanning microscopy and viability staining.

RESULTS:

The combined use of NaOCl and sealers (30 and 60 days) killed significantly more bacteria than NaOCl or sealers alone (P < .05). NaOCl + MTA Fillapex was the most effective antibacterial combination by killing 83% bacteria in dentin tubules in 60 days. Thirty and 60 days of exposure to the sealers resulted in significantly more dead bacteria in dentin biofilms than 7-day exposures (P < .05).

CONCLUSIONS:

The placement of root canal sealer after NaOCl treatment enhanced antibacterial effects against E. faecalis in the dentinal tubules. Little additional effect was obtained after 30 days of exposure to sealers.

Although several epidemiologic studies reported plausible and potentially causal associations between oral infections and cardiometabolic diseases (CMDs), controversy still lingers. This might be due to unrecognized confounding from metabolic inflammation and genetics, both of which alter the immune responses of the host. Low-grade inflammation termed metainflammation is the hallmark of obesity, insulin resistance, type 2 diabetes, and CMDs. According to the common soil theory, the continuum of obesity to CMDs is the same pathology at different time points, and early metainflammations, such as hyperglycemia and obesity, display many adverse cardiometabolic characteristics. Consequently, adipose tissue is now considered a dynamic endocrine organ that expresses many proinflammatory cytokines such as TNF-α, IL-6, plasminogen activator inhibitor 1, and IL-1β. In metainflammation, IL-1β and reactive oxygen species are generated, and IL-1β is a pivotal molecule in the pathogenesis of CMDs. Note that the same cytokines expressed in metainflammation are also reported in oral infections. In metabolic inflammation and oral infections, the innate immune system is activated through pattern recognition receptors-which include transmembrane receptors such as toll-like receptors (TLRs), cytosolic receptors such as nucleotide-binding oligomerization domain-like receptors, and multiprotein complexes called inflammasome. In general, TLR-2s are presumed to recognize lipoteichoic acid of Gram-positive microbes-and TLR-4s, lipopolysaccharide of Gram-negative microbes-while nucleotide-binding oligomerization domain-like receptors detect both Gram-positive and Gram-negative peptidoglycans on the bacterial cell walls. However, a high-fat diet activates TLR-2s, and obesity activates TLR-4s and induces spontaneous increases in serum lipopolysaccharide levels (metabolic endotoxemia). Moreover, genetics controls lipid-related transcriptome and the differentiation of monocyte and macrophages. Additionally, genetics influences CMDs, and this creates a confounding relationship among oral infections, metainflammation, and genetics. Therefore, future studies must elucidate whether oral infections can increase the risk of CMDs independent of the aforementioned confounding factors.

The three conventional resin composites showed good clinical performance during the 30 year evaluation. The chemical cured resin composites showed better performance than the light-cured composite.