Abstract
Introduction
Sickle cell anemia (SCA) is the most prevalent genetic disease worldwide. Patients
with SCA exhibit increased levels of proinflammatory mediators as part of a permanently
activated immunoinflammatory status.
Methods
The aim of this study was to evaluate the mRNA expression levels of the cytokines
interferon (IFN-γ), tumor necrosis factor, interleukin (IL-1β, IL-17A, IL-10), receptor
activator for nuclear factor kappa B ligand, and the chemokines CCL2/MCP-1 and CCL5
in the periapical interstitial fluid from SCA individuals compared with healthy individuals.
Samples were collected from 12 teeth of SCA patients and 12 non-SCA patients with
apical periodontitis. In addition, 12 teeth were sampled from the periapical region
of healthy patients with vital pulp (control). The expression of cytokine mRNA was
detected by using real-time polymerase chain reaction.
Results
The expression of mRNA for the Th1-associated cytokines IFN-γ, tumor necrosis factor-α,
and IL-1β were significantly higher in SCA individuals than in the control individuals
(P < .05). Among Th1-associated cytokines, only IFN-γ was significantly increased in
non-SCA compared with control patients (vital pulp). The expression of IL-17A mRNA
was significant higher in SCA cases than in control samples (P < .05), whereas the IL-10 mRNA expression was significantly increased in SCA and
non-SCA individuals when compared with the control group. Similar levels of receptor
activator for nuclear factor kappa B ligand, CCL2, and CCL5 mRNA expression were observed
in all samples. However, no significant differences were observed in the expression
of cytokine or chemokine mRNA between SCA and non-SCA individuals (P > .05).
Conclusions
The results were able to demonstrate that SCA patients presented prone proinflammatory
ability, despite the fact that any differences in periapical immune responses between
SCA and non-SCA individuals were not observed.
Key Words
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Article info
Publication history
Published online: January 06, 2015
Identification
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© 2015 American Association of Endodontists. Published by Elsevier Inc. All rights reserved.
