Murine Experimental Root Canal Infection: Cytokine Expression in Response to F. nucleatum and E. faecalis

Abstract

The aim of this study was to evaluate the gene expression of proinflammatory (RANKL, TNF-a and IFN-g) and regulatory (TGF-b and IL-10) cytokines as reaction to experimental infection by mono or bi-association of Fusobacterium nucleatum (ATCC 10953) and Enterococcus faecalis (ATCC 19433). F. nucleatum and E. faecalis, either in mono- or bi-association were inoculated into the root canal system (RCS) of Balb/c mice. Animals were sacrificed at 10 and 20 days after infection and periapical tissues surrounding the root were collected. The mRNA expression of the cytokines RANKL, TNF-a, IFN- g, TGF-b and IL-10 was assessed using real-time PCR. The Kruskal-Wallis test was used for statistical analysis. F. nucleatum mono-infection induced high expression of RANKL and TNF-a, while its modulation was due to IL-10. High expression of IFN-g at day 20 was up-regulated by E. faecalis and RANKL; TNF-a was up-regulated by an independent mechanism via IL-10 and TGF-b. Bi-association (F. nucleatum and E. faecalis) stimulated high expression of RANKL, TNF-a and IFN-g, which seemed to be modulated by TGF-b 20 days later. The gene expression of proinflammatory cytokines was more prominent in the earlier periods of the experimental periapical infection, which concomitantly decreased in the later period. This expression may be regulated by IL-10 and TGF-b in an infection-specific condition.

Single nucleotide polymorphisms in inducible nitric oxide synthase gene are not associated with persistent apical periodontitis

“…Prostaglandins mediate the alveolar bone absorption by Porphyromonas gingivalis , Campylobacter rectus and Fusobacterium nucleatum [45]. F. nucleatum can act on osteoblasts reflecting in the reduction of osteogenic gene expression and proteins [46], in the inhibition of, cell differentiation, formation of mineralised nodules and increased production of pro‐inflammatory factors [45].…”

“…Prostaglandins mediate the alveolar bone absorption by Porphyromonas gingivalis, Campylobacter rectus and Fusobacterium nucleatum [45]. F. nucleatum can act on osteoblasts reflecting in the reduction of osteogenic gene expression and proteins [46],…”

The Pathogenic Effects of Fusobacterium nucleatum on the Proliferation, Osteogenic Differentiation, and Transcriptome of Osteoblasts

“…Pathogenic infection is an important cause of bone loss in diseases such as periodontitis, dental cysts, bacterial arthritis, and osteomyelitis ( Bolstad et al, 1996 ; Almstahl and Wikstrom, 1999 ; Reis et al, 2016 ). Pathogens such as Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis ( P. gingivalis ) can produce a group of molecules that have potential effects on osteoblast cells and participate in bone loss ( Nair et al, 1996 ).…”

“…Pathogens such as Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis ( P. gingivalis ) can produce a group of molecules that have potential effects on osteoblast cells and participate in bone loss ( Nair et al, 1996 ). Fusobacterium nucleatum ( F. nucleatum ) has been frequently reported in gingivitis, periodontitis, pulpal necrosis, and dental pulp infection (caused by chronic apical periodontitis) ( Siqueira and Rocas, 2009 ; Reis et al, 2016 ; Kook et al, 2017 ). In periodontitis, the detection rate and quantity of F. nucleatum are positively correlated with gingival inflammation and periodontal tissue damage ( Yang et al, 2014 ).…”

Antibacterial Effect of Xanthorrhizol (Curcuma Xanthorrhiza Roxb.) Against the Biofilm of Fusobacterium Nucleatum

“…The interaction between these two bacteria has contributed significantly to the occurrence of endodontic lesions [10]. Reis et al (2016) have conducted in vivo studies on mice, and results showed that exposure to F. nucleatum biofilms and both F. nucleatum and E. faecalis could induce higher expressions of RANKL, TNF-α, and interferon-gamma than exposure to E. faecalis biofilm on the 10 th day [11]. F. nucleatum may be found in oral cavity infections, such as post-treatment endodontic diseases, acute dental abscess, endodontic flare-ups, and periodontal disease [4,9].…”