This review covers factors influencing COX enzyme activity, the role of their products in the development and maintenance of pain and discusses recent safety concerns of COX-2 inhibitors.
Traditional non-steroidal anti-inflammatory drugs (NSAID) and selective cyclooxygenase-2 (COX-2) inhibitors are widely used in the treatment of pain, including bone fracture pain and orthopaedic post-operative pain.
These results suggest that bupivacaine stimulates COX-2 gene expression after tissue injury, which is associated with higher PGE2 production and pain after the local anesthetic effect dissipates.
The two COX isoforms COX-1 and COX-2 are the targets of the widely used nonsteroidal anti-inflammatory drugs, indicating a role for these enzymes in pain, fever, inflammation, and tumorigenesis.
Controlling for these nongenetic covariates, we found that patients with CC genotypes for PTGS2 exon10+837T>C (rs5275) were at lower risk for severe pain (OR, 0.33; 95% CI, 0.11-0.97) and an additive model for TNFalpha -308GA (rs1800629; OR, 1.67; 95% CI, 1.08-2.58) and NFKBIA Ex6+50C>T (rs8904) was predictive of severe pain (OR, 0.64; 95% CI, 0.43-0.93).
The present findings indicate that not only expression of COX-2 mRNA but also that of COX-1 mRNA is significantly increased in the spine during osteoarthritis pain.
Conventional medical treatment for rheumatoid arthritis and osteoarthritis includes the use of NSAIDs (traditional and selective inhibitors of cyclooxygenase [COX]-2), because they provide unmistakable and significant health benefits in the treatment of pain and inflammation.
Of the 10 SNPs evaluated in LTA and PTGS2 genes, 3 were associated with pain severity (rs5277; rs1799964), social function (rs5277) and mental health (rs5275).
To elucidate the mode of action of chlormadinone acetate (CMA) in reducing dysmenorrheic pain by studying the effects of CMA and dexamethasone (DEX) on messenger RNA (mRNA) abundance of cyclo-oxygenase-2 (COX-2), annexin-1 (ANXA1), glucocorticoid receptor (GR), progesterone receptor (PR), and concentrations of prostaglandin F(2α) (PGF(2α)) and leukotrienes B(4) (LTB(4)) and C(4) (LTC(4)) in human endometrial explants.
Cyclooxygenase-2 (COX-2) is a major prostaglandin E2 (PGE2) synthetic enzyme and is involved in the pathogenesis of chronic inflammation and pain in osteoarthritis (OA).
Finally, we identified genetic variants in COX-2 (haplotype composed of rs2383515 G, rs5277 G, rs5275 T, and rs2206593 A) associated with post-treatment pain after endodontic treatment (P = .025).
At the same location of pain assessment and fibroblast sampling, in situ immunohistochemical (IHC)(+) fibroblasts for IL-6 and Cox-2 were quantified microscopically.
This study investigated whether 14 days of the selective Cox-2 inhibitor etoricoxib (60 mg/day) would modify self-report of pain intensity and quality, and physical measures of hyperalgesia and function in individuals with knee OA.
Treatment with histone acetyl transferase inhibitors have been reported to relieve chronic pain by blocking the up-regulation of chemokines and cyclooxygenase-2, the critical factors associated with histone acetylation-induced pain.
Cyclooxygenase-2 (COX-2) is a membrane-associated enzyme that produces prostaglandin E<sub>2</sub> (PGE<sub>2</sub>) at sites of pulpal injury and inflammation, which leads to tissue swelling, redness and pain.
We examined the analgesic effect of LED therapy on incision pain and the changes in cyclooxygenase 2 (COX-2), prostaglandin E2 (PGE2), and the proinflammatory cytokines interleukin 6 (IL-6), IL-1<i>β</i>, and tumor necrosis factor <i>α</i> (TNF-<i>α</i>).<i>Methods</i>.
Selective COX-2 inhibitors are non-steroidal anti-inflammatory drugs which directly target cyclooxygenase-2 (COX-2), an enzyme mainly responsible for induction of inflammation, pyresis and pain.
The in vivo anti-inflammatory activity of these two novel small molecules is significantly higher than that of widely used selective cyclooxygenase-2 inhibitors.Traditional inflammation and pain relief drugs target both cyclooxygenase 1 and 2 (COX-1 and COX-2), causing severe side effects.