Evaluation of Analgesic Mechanisms and NSAIDs for Acute Pain Using the Oral Surgery Model

Abstract

The management of acute pain in dentistry is largely based on observations from the oral surgery model. Generalizations based on these data can be extrapolated to the treatment of acute pain following other forms of minor surgery and the use of analgesics for acute pain in ambulatory patients. The oral surgery model [1] has been used extensively over the past 20 years to evaluate the effects of NSAIDs, opioids, steroids, and other classes of drugs used for acute pain and inflammation. The ability to measure four of the five signs of inflammation and their suppression can be demonstrated over the first 2–3 days following oral surgery [2]. The release of inflammation mediators such as prostaglandin E2, bradykinin, substance P, leukotriene B4, and other products of the lipoxygenase pathway can be measured in the surgical wound [3] and their time course is consistent with the onset of post-operative pain and the effects of NSAIDs. Neuroendocrine responses to the stress of surgery and acute pain are reflected as changes during and following surgery in plasma levels of catecholamines [4] and 13-endorphin [5]. Oral surgery may also be useful as model of central hyperexcitability with levels of pain at 24–48 h reflecting local anaesthetic manipulations on the day of surgery [6,7] and the administration of antagonists of the N-methyl-D -apsartic acid receptor [8] thought to modulate the development of CNS plasticity following pain. These examples illustrate that the surgical extraction of impacted third molars is useful as a model for evaluating analgesic efficacy, the molecular events associated with acute inflammation, neurohumoral responses to surgical stress and acute pain, and central changes associated with neuronal plasticity.