Advertisement
Clinical Research| Volume 40, ISSUE 11, P1752-1757, November 2014

Macrophage Cell Activation with Acute Apical Abscess Contents Determined by Interleukin-1 Beta and Tumor Necrosis Factor Alpha Production

Published:September 06, 2014DOI:https://doi.org/10.1016/j.joen.2014.06.019

      Abstract

      Introduction

      This clinical study has investigated the antigenic activity of bacterial contents from exudates of acute apical abscesses (AAAs) and their paired root canal contents regarding the stimulation capacity by levels of interleukin (IL)-1 beta and tumor necrosis factor alpha (TNF-α) throughout the root canal treatment against macrophage cells.

      Methods

      Paired samples of infected root canals and exudates of AAAs were collected from 10 subjects. Endodontic contents were sampled before (root canal sample [RCS] 1) and after chemomechanical preparation (RCS2) and after 30 days of intracanal medication with calcium hydroxide + chlorhexidine gel (Ca[OH]2 + CHX gel) (RCS3). Polymerase chain reaction (16S rDNA) was used for detection of the target bacteria, whereas limulus amebocyte lysate was used to measure endotoxin levels. Raw 264.7 macrophages were stimulated with AAA exudates from endodontic contents sampled in different moments of root canal treatment. Enzyme-linked immunosorbent assays were used to measure the levels of TNF-α and IL-1 beta.

      Results

      Parvimonas micra, Porphyromonas endodontalis, Dialister pneumosintes, and Prevotella nigrescens were the most frequently detected species. Higher levels of endotoxins were found in samples from periapical exudates at RCS1 (P < .005). In fact, samples collected from periapical exudates showed a higher stimulation capacity at RCS1 (P < .05). A positive correlation was found between endotoxins from exudates with IL-1 beta (r = 0.97) and TNF-α (r = 0.88) production (P < .01). The significant reduction of endotoxins and bacterial species achieved by chemomechanical procedures (RCS2) resulted in a lower capacity of root canal contents to stimulate the cells compared with that at RCS1 (P < .05). The use of Ca(OH)2 + CHX gel as an intracanal medication (RCS3) improved the removal of endotoxins and bacteria from infected root canals (P < .05) whose contents induced a lower stimulation capacity against macrophages cells at RCS1, RCS2, and RCS3 (P < .05).

      Conclusions

      AAA exudates showed higher levels of endotoxins and showed a greater capacity of macrophage stimulation than the paired root canal samples. Moreover, the use of intracanal medication improved the removal of bacteria and endotoxins from infected root canals, which may have resulted in the reduction of the inflammatory potential of the root canal content.

      Key Words

      To read this article in full you will need to make a payment

      Purchase one-time access:

      Academic & Personal: 24 hour online accessCorporate R&D Professionals: 24 hour online access
      One-time access price info
      • For academic or personal research use, select 'Academic and Personal'
      • For corporate R&D use, select 'Corporate R&D Professionals'

      Subscribe:

      Subscribe to Journal of Endodontics
      Already a print subscriber? Claim online access
      Already an online subscriber? Sign in
      Institutional Access: Sign in to ScienceDirect

      References

        • Siqueira Jr., J.F.
        • Rocas I.N.
        The microbiota of acute apical abscesses.
        J Dent Res. 2009; 88: 61-65
        • Siqueira Jr., J.F.
        • Rocas I.N.
        Microbiology and treatment of acute apical abscesses.
        Clin Microbiol Rev. 2013; 26: 255-273
        • Sousa E.L.
        • Martinho F.C.
        • Nascimento G.G.
        • et al.
        Quantification of endotoxins in infected root canals and acute apical abscess exudates: monitoring the effectiveness of root canal procedures in the reduction of endotoxins.
        J Endod. 2014; 40: 177-181
        • Montagner F.
        • Jacinto R.C.
        • Signoretti F.G.
        • Gomes B.P.
        Treponema species detected in infected root canals and acute apical abscess exudates.
        J Endod. 2010; 36: 1796-1799
        • Montagner F.
        • Jacinto R.C.
        • Signoretti F.G.
        • et al.
        Clustering behavior in microbial communities from acute endodontic infections.
        J Endod. 2012; 38: 158-162
        • Murakami Y.
        • Hanazawa S.
        • Tanaka S.
        • et al.
        A possible mechanism of maxillofacial abscess formation: involvement of Porphyromonas endodontalis lipopolysaccharide via the expression of inflammatory cytokines.
        Oral Microbiol Immunol. 2001; 16: 321-325
        • Martinho F.C.
        • Chiesa W.M.
        • Leite F.R.
        • et al.
        Correlation between clinical/radiographic features and inflammatory cytokine networks produced by macrophages stimulated with endodontic content.
        J Endod. 2012; 38: 740-745
        • Martinho F.C.
        • Leite F.R.
        • Chiesa W.M.
        • et al.
        Signaling pathways activation by primary endodontic infectious contents and production of inflammatory mediators.
        J Endod. 2014; 40: 484-489
        • Martinho F.C.
        • Chiesa W.M.
        • Leite F.R.
        • et al.
        Antigenicity of primary endodontic infection against macrophages by the levels of PGE(2) production.
        J Endod. 2011; 37: 602-607
        • Gomes B.P.
        • Martinho F.C.
        • Vianna M.E.
        Comparison of 2.5% sodium hypochlorite and 2% chlorhexidine gel on oral bacterial lipopolysaccharide reduction from primarily infected root canals.
        J Endod. 2009; 35: 1350-1353
        • Oliveira L.D.
        • Carvalho C.A.
        • Carvalho A.S.
        • et al.
        Efficacy of endodontic treatment for endotoxin reduction in primarily infected root canals and evaluation of cytotoxic effects.
        J Endod. 2012; 38: 1053-1057
        • Martinho F.C.
        • Chiesa W.M.
        • Leite F.R.
        • et al.
        Antigenic activity of bacterial endodontic contents from primary root canal infection with periapical lesions against macrophage in the release of interleukin-1beta and tumor necrosis factor alpha.
        J Endod. 2010; 36: 1467-1474
        • Garcia de Aquino S.
        • Manzolli Leite F.R.
        • Stach-Machado D.R.
        • et al.
        Signaling pathways associated with the expression of inflammatory mediators activated during the course of two models of experimental periodontitis.
        Life Sci. 2009; 84: 745-754
        • Guimaraes M.R.
        • Leite F.R.
        • Spolidorio L.C.
        • et al.
        Curcumin abrogates LPS-induced pro-inflammatory cytokines in RAW 264.7 macrophages. Evidence for novel mechanisms involving SOCS-1, -3 and p38 MAPK.
        Arch Oral Biol. 2013; 58: 1309-1317
        • Martinho F.C.
        • Gomes B.P.
        Quantification of endotoxins and cultivable bacteria in root canal infection before and after chemomechanical preparation with 2.5% sodium hypochlorite.
        J Endod. 2008; 34: 268-272
        • Martinho F.C.
        • Chiesa W.M.
        • Marinho A.C.
        • et al.
        Clinical investigation of the efficacy of chemomechanical preparation with rotary nickel-titanium files for removal of endotoxin from primarily infected root canals.
        J Endod. 2010; 36: 1766-1769
        • Vianna M.E.
        • Zilio D.M.
        • Ferraz C.C.
        • et al.
        Concentration of hydrogen ions in several calcium hydroxide pastes over different periods of time.
        Braz Dent J. 2009; 20: 382-388
        • Montagner F.
        • Gomes B.P.
        • Kumar P.S.
        Molecular fingerprinting reveals the presence of unique communities associated with paired samples of root canals and acute apical abscesses.
        J Endod. 2010; 36: 1475-1479
        • Wang Q.
        • Zhou X.D.
        • Zheng Q.H.
        • et al.
        Distribution of Porphyromonas gingivalis fimA genotypes in chronic apical periodontitis associated with symptoms.
        J Endod. 2010; 36: 1790-1795
        • Hsiao W.W.
        • Li K.L.
        • Liu Z.
        • et al.
        Microbial transformation from normal oral microbiota to acute endodontic infections.
        BMC Genomics. 2012; 13: 345
        • Jacinto R.C.
        • Gomes B.P.
        • Shah H.N.
        • et al.
        Quantification of endotoxins in necrotic root canals from symptomatic and asymptomatic teeth.
        J Med Microbiol. 2005; 54: 777-783
        • Martinho F.C.
        • Chiesa W.M.
        • Zaia A.A.
        • et al.
        Comparison of endotoxin levels in previous studies on primary endodontic infections.
        J Endod. 2011; 37: 163-167
        • Jacinto R.C.
        • Gomes B.P.
        • Desai M.
        • et al.
        Bacterial examination of endodontic infections by clonal analysis in concert with denaturing high-performance liquid chromatography.
        Oral Microbiol Immunol. 2007; 22: 403-410
        • Coats S.R.
        • Jones J.W.
        • Do C.T.
        • et al.
        Human Toll-like receptor 4 responses to P. gingivalis are regulated by lipid A 1- and 4'-phosphatase activities.
        Cell Microbiol. 2009; 11: 1587-1599
        • Stashenko P.
        • Jandinski J.J.
        • Fujiyoshi P.
        • et al.
        Tissue levels of bone resorptive cytokines in periodontal disease.
        J Periodontol. 1991; 62: 504-509
        • Xavier A.C.C.
        • Martinho F.C.
        • Chung A.
        • et al.
        One-visit versus two-visit root canal treatment: effectiveness in the removal of endotoxins and cultivable bacteria.
        J Endod. 2013; 39: 959-964
        • Gomes B.P.
        • Endo M.S.
        • Martinho F.C.
        Comparison of endotoxin levels found in primary and secondary endodontic infections.
        J Endod. 2012; 38: 1082-1086
        • Barthel C.R.
        • Levin L.G.
        • Reisner H.M.
        • Trope M.
        TNF-alpha release in monocytes after exposure to calcium hydroxide treated Escherichia coli LPS.
        Int Endod J. 1997; 30: 155-159
        • Safavi K.E.
        • Nichols F.C.
        Effect of calcium hydroxide on bacterial lipopolysaccharide.
        J Endod. 1993; 19: 76-78
        • Safavi K.E.
        • Nichols F.C.
        Alteration of biological properties of bacterial lipopolysaccharide by calcium hydroxide treatment.
        J Endod. 1994; 20: 127-129
        • Gomes M.S.
        • Blattner T.C.
        • Sant'Ana Filho M.
        • et al.
        Can apical periodontitis modify systemic levels of inflammatory markers? A systematic review and meta-analysis.
        J Endod. 2013; 39: 1205-1217