beta-endorphin and Toothache

The non-steroidal anti-inflammatory drugs (NSAIDs) are among the most widely used classes of drugs for the management of acute and chronic pain in dentistry. Their therapeutic efficacy and toxicity are well-documented and provide evidence that NSAIDs generally provide an acceptable therapeutic ratio of pain relief with fewer adverse effects than the opioid-mild analgesic combination drugs that they have largely replaced for most dental applications. The great many studies done with the oral surgery model of acute pain indicate that a single dose of an NSAID is more effective than combinations of aspirin or acetaminophen plus an opioid, with fewer side-effects, thus making it preferable for ambulatory patients. The combination of an NSAID with an opioid generally results in marginal analgesic activity but with an increased incidence of side-effects, which limits its use to patients in whom the NSAID alone results in inadequate analgesia. The selective COX-2 inhibitors hold promise for clinical efficacy with less toxicity from chronic administration and may prove advantageous for the relief of chronic orofacial pain. The use of repeated doses of NSAIDs for chronic orofacial pain should be re-evaluated in light of a lack of documented efficacy and the potential for serious gastrointestinal and renal toxicity with repeated dosing.

Topics: Analgesics, Opioid; Anti-Inflammatory Agents, Non-Steroidal; beta-Endorphin; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Cyclooxygenase Inhibitors; Drug Combinations; Edema; Facial Pain; Humans; Isoenzymes; Ketorolac; Membrane Proteins; Periodontitis; Prostaglandin-Endoperoxide Synthases; Temporomandibular Joint Disorders; Toothache

Release of beta-endorphin is modulated by physiologic stress and a variety of hormonal and pharmacologic factors. Prostaglandin E2 inhibits release of beta-endorphin and corticotropin from pituitary corticotroph cells, suggesting that suppression of prostaglandin levels should increase beta-endorphin release. This hypothesis was tested by administration of 600 mg ibuprofen before surgical stress in humans in comparison to placebo and methylprednisolone. Plasma samples were analyzed for immunoreactive beta-endorphin with concurrent measurement of pain and apprehension. Levels of immunoreactive beta-endorphin increased during surgery in the placebo group but were significantly greater in the group of patients pretreated with ibuprofen. Methylprednisolone suppressed intraoperative immunoreactive beta-endorphin, compared with both placebo and ibuprofen. Parallel in vivo and in vitro studies indicate that nonsteroidal anti-inflammatory drug potentiation of endorphin release is mediated at the level of the pituitary corticotroph cell. These results show that ibuprofen enhances pituitary release of beta-endorphin by corticotroph cells in response to stress.

Topics: Adult; Analysis of Variance; Animals; Anti-Inflammatory Agents; Anti-Inflammatory Agents, Non-Steroidal; beta-Endorphin; Female; Humans; Ibuprofen; Male; Methylprednisolone; Pain, Postoperative; Pituitary Gland; Rats; Time Factors; Tooth Extraction; Tooth, Impacted; Toothache; Treatment Outcome

Topics: Adrenocorticotropic Hormone; Adult; Aspirin; beta-Endorphin; Dental Caries; Dental Pulp Diseases; Drug Evaluation; Endorphins; Female; Humans; Hydrocortisone; Male; Toothache