Temporomandibular disorders (TMD) are pain conditions that affect the Temporomandibular Joint (TMJ) and masticatory muscles. These conditions present higher prevalent, severity and duration in the female gender and are associated with inflammation. Although none-steroidal anti-inflammatory (NSAIs) drugs have been frequently used in the control of inflammatory pains, many patients can be intolerant to the prolonged treatment or unresponsive to the effect of these medications. It is already known that the inflammatory pain has a sympathetic component that can be predominant in these cases. In this context, recently data of ours laboratory shows that sympathetic amines are released in the rat´s TMJ during the inflammatory process where they contribute with the development of hyperalgesia by activating ²-2 adrenoceptors (ARs). Preliminary datas suggest that ²-ARs maybe participate in the TMJ nociception, but the role of these receptors in this model hasn´t been studied yet. Then, the aims of this project are: 1- Characterize the nociceptive behavior induced by the activation of TMJ ²2-ARs, 2- Verify whether the nociceptive behavior induced by the activation of TMJ ²2-ARs is mediated by a indirect mechanism, 3- Investigate the presence of ²1-ARs RNAm in the trigeminal ganglion in the presence and absent of inflammatory process in the TMJ. This project will be develop in rats by the TMJ injection of the inflammatory agent carragenan, injection of ²2-ARs agonists Salbutamol and Metaproterenol, injection of ²2-ARs antagonist ICI 118.551 and the NSAI Dexamethasone. The understood of peripheral mechanisms involved in the TMJ pain can contribute to the treatment of pain associated with TMD, especially in those cases where patients are unresponsive to the NSAIs treatment.
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