Evaluation of a long-acting local anesthetic (Bupivacaine) and a selective COX-2 inhibitor (Rofecoxib) in suppression of central sensitization
Date
2005
DOI
Authors
Chuang, Brian Po-Jen
Version
OA Version
Citation
Abstract
Pain of odontogenic origin results from direct activation of nociceptive afferent nerve
fibers and the actions of inflammatory mediators. A positive feedback loop, caused by
the interaction of inflammatory mediators such as prostaglandins, prolongs inflammation
and pain beyond cessation of nociceptive input from the site of injury. Central
mechanisms are activated by both nociceptive barrage during tissue injury and
postoperative inflammation to produce hyperalgesia hours to days after the initiating
events while both surgical nociceptive input and inflammation contribute to central
sensitization. Their respective contributions have not been clearly evaluated. The
purpose of this study was to assess their relative impact using an oral surgery model and
intervention to selectively attenuate postoperative nociceptive barrage or inflammation.
In this randomized, double-blind controlled clinical trial, subjects were allocated to
receive either 2% lidocaine or 0.5% bupivacaine (both with 1:200,000 epinephrine) as
local anesthetic to manage perioperative pain. Subsequently, subjects were provided
either placebo or the selective cyclooxygenase-2 (COX-2) inhibitor rofecoxib 50 mg QD
to manage inflammation in a two by two factorial design resulting in 4 groups:
lidocaine/placebo, lidocaine/rofecoxib, bupivacaine/placebo, and bupivacaine/rofecoxib.
Conscious sedation was induced with midazolam and bilateral impacted mandibular third
molars were extracted. Pain was assessed over the first 4 hours and then at 24 and 48
hours after surgery. Microdialysis samples were collected from the surgical site over the
immediate postoperative period, and subsequently analyzed with an enzyme
immunoassay to demonstrate the level of inflammatory mediators: a product of COX-1, ... [TRUNCATED]
Description
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Thesis (MSD)--Boston University, Henry M. Goldman School of Dental Medicine, 2005 (Endodontics).
Includes bibliography: leaves 60-66.
Thesis (MSD)--Boston University, Henry M. Goldman School of Dental Medicine, 2005 (Endodontics).
Includes bibliography: leaves 60-66.
License
This work is protected by copyright. Downloading is restricted to the BU community. If you are the author of this work and would like to make it publicly available, please contact open-help@bu.edu.