Increased COX2 in the Trigeminal Nucleus Caudalis Is Involved in Orofacial Pain Induced by Experimental Tooth Movement

Abstract

Pain is among the major problems during orthodontic treatment. Recent studies have shown that central Cyclooxygenase2 (COX2) pathway was involved in several pain models. The present study investigated whether inducible COX2 within the trigeminal nucleus caudalis (Vc) contributed to experimental tooth movement pain in freely moving rats. Elastic rubber bands were inserted between the first and second maxillary molars bilaterally to establish tooth movement model. The directed mouth wiping behavior was used to evaluate the pain during tooth movement. COX2 distribution in Vc was studied by immunohistochemistry and the changes of COX2 expression were detected by Western blot at different time point after rubber band insertion. Our results showed that tooth movement significantly increased COX2 expression in Vc and the time spent on mouth wiping, reaching a maximum at 1 day and then decreasing gradually. Furthermore, the rhythm change of COX2 expression in Vc and the mouth wiping behavior were much correlative with each other. All of the COX2-immunoreactive structures in Vc exhibited NeuN-immunopositive staining and most of these COX2-immunoreactive neurons were Fos-immunopositive. Importantly, the mouth wiping behavior could be attenuated by intracisternal injection of NS-398 (a selective COX2 inhibitor) but not by periodontal administration of NS-398. All these results suggested that increased COX2 in Vc was involved in tooth movement pain and thus may be a central target for orthodontic pain treatment. Anat Rec, 293:485-491, 2010. V V C 2010 Wiley-Liss, Inc.

The effect of central administration of alpha‐pinene on capsaicin‐induced dental pulp nociception

“…In accordance with the present finding, Gao & Duan () indicated that the expression of COX‐2 in Vc is up‐regulated following experimental tooth movement inflammation. Moreover, central COX‐2 inhibition decreases temporomandibular joint inflammation induced by formalin in rats (Ahn et al .…”

The effect of CA1 administration of orexin-A on hippocampal expression of COX-2 and BDNF in a rat model of orofacial pain

“…In the central nervous system, COX-2 is highly distributed in hippocampal neurons and its expression is correlated with the induction of pro-inflammatory cytokines and pain molecules 21 . In the study by Gao and Duan, increased COX-2 in the trigeminal subnucleus caudalis of rats was observed following tooth movement pain 5 . Capsaicin activates transient receptor potential vanilloid 1 channels on a subpopulation of primary afferent sensory neurons, specifically C fibers, involved in nociception.…”

Effect of lutein on the acute inflammation‐induced c‐Fos expression of rat trigeminal spinal nucleus caudalis and C1 dorsal horn neurons

“…Most patients undergoing orthodontic treatment experience pain and discomfort, not only from teeth, but also from other areas, such as the cheek and masseter muscle , which spreads as referred pain. Despite its detrimental impact on patients, little is known about the underlying mechanism of this referred pain in orthodontic patients, which makes prevention procedurally more difficult . Tooth‐movement pain has been attributed to associated pressure, ischemia, inflammation, and edema , all of which can lead to the release of inflammatory mediators, such as prostaglandin E 2 .…”

“…Tooth‐movement pain has been attributed to associated pressure, ischemia, inflammation, and edema , all of which can lead to the release of inflammatory mediators, such as prostaglandin E 2 . Recently, using an experimental tooth‐movement model in rats, Gao & Duan demonstrated that tooth‐movement pain involved increased COX‐2 in the SpVc, but not in the periodontal tissue, suggesting that central COX‐2 inhibition holds therapeutic promise in the treatment of orofacial pain induced by orthodontic tooth movement. It can be postulated that lutein administration attenuates mechanical hyperalgesia and this effect is mainly a result of the suppression of excitability of SpVc WDR neurons via inhibition of the COX‐2 signaling cascade pathway.…”