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The effect of low-dose aspirin on aspirin triggered lipoxin, interleukin 1 beta, and prostaglandin E2 levels in periapical fluid: a double-blind randomized clinical trial. | LitMetric

AI Article Synopsis

  • - This study examined how low-dose aspirin affects the levels of pro-inflammatory and pro-resolving mediators in the periapical fluid of patients with necrotic teeth.
  • - Participants were divided into aspirin and placebo groups, with periapical fluid collected before and after 7 days of treatment and analyzed for interleukin-1 beta (IL-1β), prostaglandin E2 (PGE2), and aspirin triggered lipoxin (ATL) levels.
  • - Results showed that low-dose aspirin significantly reduced IL-1β and PGE2 levels while increasing ATL levels, suggesting its potential to modulate inflammation effectively.

Article Abstract

Background: The role of pro-resolving mediators in inflammation is a new concern in research. The effect of low-dose aspirin on production of a special kind of these mediators named aspirin triggered lipoxin (ATL) has been studied on different tissues. This randomized clinical trial evaluated the effect of low-dose aspirin on ATL and pro-inflammatory mediators' level in periapical fluid of necrotic teeth with large lesions.

Methods: Twenty-four patients with necrotic pulp and periapical lesion were randomly assigned to low-dose aspirin and placebo groups. In the first appointment, canals were shaped up to F3 size and #40 K-file and cleaned with 10 milliliters 2.5% sodium hypochlorite and 17% Ethylenediaminetetraacetic acid. Periapical fluid was sampled by a paper cone. The tooth was temporized without any intracanal medication. Tablets were administered for 7 days, then the teeth were re-opened and the sampling were repeated. Interleukin-1 beta (IL-1β), prostaglandin E2 (PGE2) and ATL were analyzed by enzyme-linked immunosorbent assay. Data were analyzed with paired t-test using SPSS statistical software, version 21 (α = 0.05).

Results: A significant reduction in PGE2 and IL-1β was noted in the aspirin-treated group while an increase in ATL was observed (P < 0.001). There was no significant difference in the mediator scores before and after in the placebo-treated group (P > 0.05).

Conclusion: Low-dose aspirin can influence the inflammatory process by reducing pro-inflammatory mediators such as PGE2 and IL-1β, as well as increasing the pro-resolving mediators such as ATL.

Trial Registration: IRCT20191211045702N1.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10388445PMC
http://dx.doi.org/10.1186/s12903-023-03243-0DOI Listing

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