Abstract
BackgroundThis study aimed to evaluate the gene expression of cyclooxygenases (COXs) in an oral model of preemptive analgesia. Material and MethodsGingival tissue was collected during extraction of lower third molars from a randomized, triple-blind, split-mouth and placebo-controlled study. The eligible patients were randomly sorted to receive a single dose either of ibuprofen 400mg, or etoricoxib 120 mg or a placebo, one hour prior to surgery. The temporal course of RNAm was evaluated for COX-1 and -2 by means of a quantitative polymerase chain reaction in real time (RT-qPCR) at time zero and 30 minutes after the surgical procedure began, and it was correlated with clinical parameters (pain and maximum mouth opening). ResultsThere was a significant increase in COX-1 expression between T0 and T30 in ibuprofen (p=0.004) and etoricoxib (p=0.010) groups. As regards COX-2, there were increases from T0 to T30 in all groups (placebo, p=0.012; ibuprofen, p<0.001; etoricoxib, p<0.001). All groups showed a significant decrease in COX-2:COX-1 ratio from T0 to T30 (placebo, p=0.013; ibuprofen, p<0.001; etoricoxib, p=0.047). Experimental groups showed a significant correlation between COX-1 and COX-2 levels and clinical pain parameters. ConclusionsThe present preemptive analgesia study concludes that COX-2 RNAm induction was directly linked to third molar-related tissue inflammation and that the relation between COX-1 and COX-2 levels were inversely proportional to the preemptively administered nonsteroidal anti-inflammatory drugs COX-2 selectivity. Key words:Preemptive analgesia, dental extraction, cyclooxygenases, real-time polymerase chain reaction.
Highlights
Cyclooxygenase (COX) catalyzes the initial steps in the synthesis of prostaglandins (PGs) and other eicosanoids from arachidonic acid
The messenger RNA originated from COX-1 expression presents a half-life of approximately 12-15 hours, whereas COX-2 gives rise to mRNA with a shorter half-life of less than 3.5 hours [2]
This objective was formulated to test the hypothesis that the non-steroidal anti-inflammatory drugs (NSAIDs) type used before the surgical procedure may influence the COX gene isoforms expression in gingival tissue collected from patients exposed to the preemptive administration of placebo, ibuprofen, and etoricoxib
Summary
Cyclooxygenase (COX) catalyzes the initial steps in the synthesis of prostaglandins (PGs) and other eicosanoids from arachidonic acid. The messenger RNA (mRNA) originated from COX-1 expression presents a half-life of approximately 12-15 hours, whereas COX-2 gives rise to mRNA with a shorter half-life of less than 3.5 hours [2] These findings suggest an intrinsic temporal connection between tissue injury, COX-2 expression and the observed increase in PGE2 levels during inflammation. The primary objective in this study was to evaluate the association between COX-1 and COX-2 RNAm induction and clinical inflammatory parameters (pain scores, rescue medication intake, and maximum mouth opening) in third molar surgeries. The secondary objective in this investigation was to assess the levels of COX-1 and COX-2 RNAm according to the preemptively administered NSAID in third molars surgeries This objective was formulated to test the hypothesis that the NSAID type used before the surgical procedure may influence the COX gene isoforms expression in gingival tissue collected from patients exposed to the preemptive administration of placebo, ibuprofen, and etoricoxib. Conclusions: The present preemptive analgesia study concludes that COX-2 RNAm induction was directly linked to third molar-related tissue inflammation and that the relation between COX-1 and COX-2 levels were inversely proportional to the preemptively administered nonsteroidal anti-inflammatory drugs COX-2 selectivity
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