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Paula, MAV. Endothelin-1 Participation on the Rats TMJ Synovitis induced by Carrageenan [Master thesis]. São Paulo: Universidade de São Paulo; 2012. Temporomandibular disorders involving the temporomandibular joint (TMJ) are often associated with inflammation and secondary hyperalgesia, allodynia or referred pain. Based on previous studies showing the involvement of ET in some models of nociception, we decided to investigate the role of ET1 in inflammation induced by the carrageenan (CGN) injection in rats TMJ. Intra-articular injections (10 !l) of CGN (500 mg), ET1 or selective ETB receptor agonist (BQ3020) in several different doses (0,3 to 30 pmols) were performed in the cavity of the left TMJ using sterile saline as a vehicle (V). 4 h after, the mechanical allodynia was evaluated by measuring the necessary force threshold to evocate the head withdrawal, using an electronic analgesimeter based on the Von Frey filaments principles. Then the animals were euthanized and the TMJ joint cavities washed with sterile saline in order to determine the total and differential leukocytes in the lavage fluid. Selective ETA (BQ123, 10 pmols) and ETB (BQ78, 10 pmols) receptors antagonists were coinjected with CGN and ET1 in order to characterize the participation of endogenous and exogenous ET1 in nociceptive process induced by both of them. It was also evaluated the effects of the TRPV1 selective antagonist, Capsazepin (600 !g/cavity), on the ET1 evoked nociception. Both ET and the agonist BQ3020 (at doses of 0,3 to 10 pmols/ cavity) evoked hyperalgesia (ie, significant decrease of the necessary force threshold to evocate the head withdrawal). CGN induced significant hypernociception (CGN: vs. -29,0 ± 4,1 V: 6,5 ± 1,6 g, P<0,001) and none of the ET antagonists significantly affected this response when administered separately. However, the simultaneous injection of both antagonists with CGN abolished the nociceptive response (P<0,001), In a similar way, separately both the ET antagonists didn’t abolish completely the nociceptive effect from ET1, but they were able to reduce it, especially the selective ETB antagonist (ETA P<0,05; ETB P<0,01). At all used doses, both ET1 and ETB agonist did not affect the recruitment of inflammatory cells into the TMJ cavity, and none of the ET antagonists affected the cell migration induced by CGN. The selective TRPV1 antagonist didn’t affect the nociceptive affect of ET1 (Capsazepin: P>0,05). The analysis of gene expression alteration for both the TMJ and the trigeminal ganglia region showed no significant increase in the expression from any of the analyzed genes (PPET1, ETA, ETB, ECE1 and TRPV1), but in both region it has been found a decrease in the genic expressions for ETA and ETB (ETA P<0,01 and ETB P<0,001) for the TMJ analysis, and for ETA and TRPV1 (ETA and TRPV1 P<0,001) for the ganglion analysis. These results indicate that ET1 is not only able to evoke hyperalgesia at low doses (up to 10 pmols/ TMJ cavity), but it also appears to be involved in nociception-induced by CGN via ETA and ETB receptors, with no apparent effect on leukocytes migration.

Participação da endotelina-1 na sinovite induzida por carragenina na articulação temporomandibular de ratos.