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A Comparative Study of Oral Analgesics for Postoperative Pain After Minor Oral Surgery

Atsushi HanzawaDDS, PhD,

Toshiyuki HandaDDS, PhD,

Yoshihiko KohkitaDDS, PhD,

Tatsuya IchinoheDDS, PhD, and

Ken-Ichi FukudaDDS, PhD

Article Category: Research Article

Volume/Issue: Volume 65: Issue 1

Online Publication Date: Jan 01, 2018

DOI: 10.2344/anpr-65-01-02

Page Range: 24 – 29

are desirable. Preparations recommended for use in postoperative analgesia include opioid analgesics, nonselective nonsteroidal anti-inflammatory drugs (NSAIDs), selective cyclooxygenase (COX)-2 inhibitors, and acetaminophen. 7 In the field of oral surgery, nonselective NSAIDs have been frequently used for postoperative pain relief. 8 However, there is concern about gastrointestinal dysfunction and suppression of platelet function with the administration of nonselective NSAIDs because of inhibition of prostaglandin and thromboxane synthesis by COX-1. 9

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Figure 4; NSAID versus opioid analgesia. The following data were derived from patients who underwent third molar impaction surgery. See text for explanation. (Ibu 400 = ibuprofen 400 mg; Oxy 5 = oxycodone 5 mg)

Daniel E. Becker

Figure 4

NSAID versus opioid analgesia. The following data were derived from patients who underwent third molar impaction surgery. See text for explanation.

(Ibu 400 = ibuprofen 400 mg; Oxy 5 = oxycodone 5 mg)

Figure 2 ; Increased risk of bleeding with selective serotonin reuptake inhibitors (SSRIs) and nonsteroidal anti-inflammatory drug (NSAIDs). Pinto A, Farrar JT, Hersh EV. Compend Contin Educ Dent. 2009;30:142–151.

Mana Saraghi,

Leonard Golden, and

Elliot V. Hersh

Figure 2

Increased risk of bleeding with selective serotonin reuptake inhibitors (SSRIs) and nonsteroidal anti-inflammatory drug (NSAIDs). Pinto A, Farrar JT, Hersh EV. Compend Contin Educ Dent. 2009;30:142–151.

Figure 2.; Response to use of nonsteroidal analgesics. *Ibuprofen and celecoxib, respectively, were considered analgesics separately. †There was no information available about the choice of patient by better response to NSAID or placebo used. Data represent the number of patients who did not make use of supplementary rescue analgesia.

Fábio Wildson Gurgel Costa,

Diego Felipe Silveira Esses,

Paulo Goberlânio de Barros Silva,

Francisco Samuel Rodrigues Carvalho,

Carlos Diego Lopes Sá,

Assis Filipe Medeiros Albuquerque,

Tácio Pinheiro Bezerra,

Thyciana Rodrigues Ribeiro,

Cristiane Sá Roriz Fonteles, and

Eduardo Costa Studart Soares

Figure 2.

Response to use of nonsteroidal analgesics. *Ibuprofen and celecoxib, respectively, were considered analgesics separately. †There was no information available about the choice of patient by better response to NSAID or placebo used. Data represent the number of patients who did not make use of supplementary rescue analgesia.

Figure 1. ; The inflammatory process. Normally, small arterioles deliver blood to capillaries, which are then drained by venules. Vasoactive autacoids trigger the vascular phase, causing arterioles to dilate and endothelial cells to shrink, making capillaries and venules more permeable. Hyperemia produces the cardinal signs of redness and heat. Permeability allows extravasation of plasma leading to swelling and pain. Chemotactic autacoids target leukocytes (WBCs), which adhere to endothelium (margination), squeeze through the openings (diapedesis) and migrate out into the tissues (emigration). Nonsteroidal anti-inflammatory drugs (NSAIDS) inhibit the vascular phase, and the glucocorticoids inhibit both phases.

Daniel E. Becker

Figure 1.

The inflammatory process. Normally, small arterioles deliver blood to capillaries, which are then drained by venules. Vasoactive autacoids trigger the vascular phase, causing arterioles to dilate and endothelial cells to shrink, making capillaries and venules more permeable. Hyperemia produces the cardinal signs of redness and heat. Permeability allows extravasation of plasma leading to swelling and pain. Chemotactic autacoids target leukocytes (WBCs), which adhere to endothelium (margination), squeeze through the openings (diapedesis) and migrate out into the tissues (emigration). Nonsteroidal anti-inflammatory drugs (NSAIDS) inhibit the vascular phase, and the glucocorticoids inhibit both phases.

Figure 2. ; Pseudoallergy and altered arachidonic acid metabolism. Aspirin and the nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit 2 families of cyclooxygenases (COX-1 and COX-2) from converting arachidonic acid to various prostanoids, including prostaglandins, prostacyclin, and thromboxanes. This in turn reduces the eventual effects normally produced by these prostanoids and leaves more arachidonic acid available as a substrate for lipoxygenase to produce leukotrienes. Inhibiting COX-1 in particular also diminishes the inhibitory effect of prostaglandin E2 (PGE2) on lipoxygenase activity. The increased synthesis of leukotrienes may produce anaphylactoid syndromes in susceptible patients. Selective inhibition of COX-2 is less likely to produce this altered metabolism.

Daniel E. Becker

Figure 2.

Pseudoallergy and altered arachidonic acid metabolism. Aspirin and the nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit 2 families of cyclooxygenases (COX-1 and COX-2) from converting arachidonic acid to various prostanoids, including prostaglandins, prostacyclin, and thromboxanes. This in turn reduces the eventual effects normally produced by these prostanoids and leaves more arachidonic acid available as a substrate for lipoxygenase to produce leukotrienes. Inhibiting COX-1 in particular also diminishes the inhibitory effect of prostaglandin E₂ (PGE₂) on lipoxygenase activity. The increased synthesis of leukotrienes may produce anaphylactoid syndromes in susceptible patients. Selective inhibition of COX-2 is less likely to produce this altered metabolism.

Figure 2; Analgesic efficacy. This graph illustrates a typical dose-response curve for orally administered (PO) analgesics. The dose-response curve for opioids such as morphine demonstrates unlimited efficacy in which greater doses provide greater analgesia. At equipotent doses, all opioids demonstrate a similar dose response. In contrast, nonopioids demonstrate a “ceiling” effect that generally is adequate for relief of mild to moderate pain (pain relief rating of 4–5 in this scale). For ibuprofen, doses greater than 400 mg do not provide further analgesia. For aspirin (ASA) and acetaminophen (APAP), this ceiling effect is achieved at 1000 mg and is somewhat lower than that provided by nonsteroidal anti-inflammatory drugs (NSAIDs).

Daniel E. Becker

Figure 2

Analgesic efficacy. This graph illustrates a typical dose-response curve for orally administered (PO) analgesics. The dose-response curve for opioids such as morphine demonstrates unlimited efficacy in which greater doses provide greater analgesia. At equipotent doses, all opioids demonstrate a similar dose response. In contrast, nonopioids demonstrate a “ceiling” effect that generally is adequate for relief of mild to moderate pain (pain relief rating of 4–5 in this scale). For ibuprofen, doses greater than 400 mg do not provide further analgesia. For aspirin (ASA) and acetaminophen (APAP), this ceiling effect is achieved at 1000 mg and is somewhat lower than that provided by nonsteroidal anti-inflammatory drugs (NSAIDs).

Figure 1; Synthesis and function of prostanoids. Perturbation of cell membranes can be mediated by diverse endogenous and exogenous stimuli. This triggers activity of phospholipase A2, releasing arachidonic acid from the phospholipids making up the membrane. Two families of cyclooxygenases (COX-1 and COX-2) convert this fatty acid to a variety of so-called prostanoids that are unique to the particular cell or tissue and include prostaglandins, thromboxanes, and prostacyclin. Each of these prostanoids has specific physiological functions, some of which are listed in the table within this figure. Most nonsteroidal anti-inflammatory drugs (NSAIDs) are nonselective and inhibit both COX-1 and COX-2 families. Celecoxib (Celebrex) is representative of agents that selectively inhibit COX-2; it reduces pain and inflammation with little or no influence on gastric mucosa. However, this selective inhibition may promote greater synthesis of prostanoids derived from COX-1, including thromboxane-mediated effects leading to possible thrombotic events (eg, myocardial infarction, stroke). Arachidonic acid is also a substrate for lipoxygenase that catalyzes the formation of leukotrienes known for their anaphylactoid effects, including bronchospasm and upper airway edema. As NSAIDs inhibit the activity of cyclooxygenases, a greater portion of arachidonic acid can be converted to leukotrienes by lipoxygenase. This may not be tolerated by patients with atopy because they experience pseudoallergic syndromes.

Daniel E. Becker

Figure 1

Synthesis and function of prostanoids. Perturbation of cell membranes can be mediated by diverse endogenous and exogenous stimuli. This triggers activity of phospholipase A₂, releasing arachidonic acid from the phospholipids making up the membrane. Two families of cyclooxygenases (COX-1 and COX-2) convert this fatty acid to a variety of so-called prostanoids that are unique to the particular cell or tissue and include prostaglandins, thromboxanes, and prostacyclin. Each of these prostanoids has specific physiological functions, some of which are listed in the table within this figure. Most nonsteroidal anti-inflammatory drugs (NSAIDs) are nonselective and inhibit both COX-1 and COX-2 families. Celecoxib (Celebrex) is representative of agents that selectively inhibit COX-2; it reduces pain and inflammation with little or no influence on gastric mucosa. However, this selective inhibition may promote greater synthesis of prostanoids derived from COX-1, including thromboxane-mediated effects leading to possible thrombotic events (eg, myocardial infarction, stroke). Arachidonic acid is also a substrate for lipoxygenase that catalyzes the formation of leukotrienes known for their anaphylactoid effects, including bronchospasm and upper airway edema. As NSAIDs inhibit the activity of cyclooxygenases, a greater portion of arachidonic acid can be converted to leukotrienes by lipoxygenase. This may not be tolerated by patients with atopy because they experience pseudoallergic syndromes.

Figure 1. ; Box plots for visual analog scale (VAS) scores at 4, 5, and 6 hours after administration of study drug. Data are expressed as medians, percentiles, and ranges. *p < .05 compared with the placebo group; **p < .01 compared with the placebo group by Kruskal-Wallis H test and Mann-Whitney U test with Bonferroni correction.

Atsushi Hanzawa,

Toshiyuki Handa,

Yoshihiko Kohkita,

Tatsuya Ichinohe, and

Ken-Ichi Fukuda

Figure 1.

Box plots for visual analog scale (VAS) scores at 4, 5, and 6 hours after administration of study drug. Data are expressed as medians, percentiles, and ranges. *p < .05 compared with the placebo group; **p < .01 compared with the placebo group by Kruskal-Wallis H test and Mann-Whitney U test with Bonferroni correction.

Figure 2. ; Consumption of fentanyl up to 4, 5, and 6 hours after administration of study drug. Data are expressed as mean ± SD. *p < .05 compared with the placebo group; **p < .01 compared with the placebo group by non–repeated-measures analysis of variance and Student-Newman-Keuls test.

Atsushi Hanzawa,

Toshiyuki Handa,

Yoshihiko Kohkita,

Tatsuya Ichinohe, and

Ken-Ichi Fukuda

Figure 2.

Consumption of fentanyl up to 4, 5, and 6 hours after administration of study drug. Data are expressed as mean ± SD. *p < .05 compared with the placebo group; **p < .01 compared with the placebo group by non–repeated-measures analysis of variance and Student-Newman-Keuls test.