Cytokine analysis in lesions refractory to endodontic treatment.

Abstract:

INTRODUCTION:Failure in endodontic treatment is often caused by the persistence of microorganisms in the root canal after therapy. When treatment fails, an immune response develops that is characterized by an extensive network of immunologic mechanisms that lead to the production of cytokines and chemokines. METHODS:The objective of this study was to determine the relative messenger RNA (mRNA) expression of IFN-γ, TNF-α, IL-1β, IL-17A, IL-10, and MCP-1 in periapical dental lesions refractory to treatment. Clinical samples were taken from teeth presenting periapical lesions refractory to endodontic treatment (the experimental group) or from healthy teeth with pulp vitality (the control group). Three paper points passing through the root apex (2 mm) were used to collect the samples. The total RNA was extracted from each sample, complementary DNA was synthesized, and quantitative polymerase chain reaction analysis was performed. The Mann-Whitney U test was used to determine the statistical significance of our findings (P < .05). RESULTS:Significant differences in the levels of IFN-γ, TNF-α, IL-17A, and MCP-1 mRNA expression were observed in cases refractory to endodontic treatment as compared with the control group. The expression of IL-1β mRNA was not significantly different between the groups. The expression of IL-10 mRNA was insignificant in both the experimental and control groups. CONCLUSIONS:A significantly increased expression of TNF-α, IFN-γ, IL-17A, and MCP-1 mRNA was observed in the periapical immune response in cases of endodontic failure. These results suggest that a proinflammatory cytokine profile predominates in these types of dental lesions.

journal_name

J Endod

journal_title

Journal of endodontics

authors

Henriques LC,de Brito LC,Tavares WL,Vieira LQ,Ribeiro Sobrinho AP

doi

10.1016/j.joen.2011.08.007

subject

Has Abstract

pub_date

2011-12-01 00:00:00

pages

1659-62

issue

12

eissn

0099-2399

issn

1878-3554

pii

S0099-2399(11)00929-0

journal_volume

37

pub_type

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