Abstract
Introduction
Macrophages are highly activated by endodontic contents. This study investigated the
correlation between different clinical signs/symptoms and radiographic features according
to the levels of interleukin (IL)-1β, tumor necrosis factor α (TNF-α), IL-6, IL-10,
prostaglandin E2 (PGE2), and their networks produced by endodontic content–stimulated macrophages collected
from primary endodontic infection with apical periodontitis (PEIAP).
Methods
Samples were taken from 21 root canals with PEIAP by using paper points. The presence
of exudate (EX), pain on palpation (POP), tenderness to percussion (TTP), and the
size of the radiographic lesion (SRL) were recorded. Polymerase chain reaction (16S
rDNA) was used for bacterial detection and limulus amebocyte lysate (LAL) assay for
endotoxin measurement. Raw 264.7 macrophages were stimulated with bacterial contents
during 24 hs. The amounts of IL-1β, TNF-α, IL-6, IL-10 and PGE2 were measured by enzyme-linked immunosorbent assay. Log-based data were correlated
by multiple logistic regression (P < .05).
Results
Bacteria and endotoxin were detected in 100% of the samples. IL-6 and TNF-α were positively
correlated with SRL and EX, respectively (P < .05). Clinical signs/symptoms and radiographic findings were set as dependent variables
for EX-positive correlations between PGE2, IL-1β, and TNF-α (P < .05), whereas IL-6 and PGE2 were positively correlated to each other in POP but negatively correlated in SRL
(P < .05). When POP and TTP-POP were set as dependent variables, different cytokine
networks were found.
Conclusions
Our findings suggest different roles for each cytokine in the development of apical
periodontitis, whose effects of overlapping networks depend on the signs/symptoms
and radiographic features found in endodontic infection.
Key Words
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Article info
Publication history
Published online: April 20, 2012
Footnotes
Supported by the Brazilian agencies FAPESP (08/57551-0; 08/56425; 10/51113-1; 10/17877-4 10/19136-1; 11/50510-0) and CNPq (302575/2009-0; 150557/2011-6).
Identification
Copyright
© 2012 Published by Elsevier Inc.
