Rodrigues Luciane Lacerda Franco Rocha, Oliveira Maria Cláudia Gonçalves, Pelegrini-da-Silva Adriana, de Arruda Veiga Maria Cecília Ferraz, Parada Carlos Amílcar, Tambeli Cláudia Herrera
Department of Physiology, Laboratory of Orofacial Pain, Faculty of Dentistry of Piracicaba, University of Campinas-UNICAMP, São Paulo, Brazil.
J Pain. 2006 Dec;7(12):929-36. doi: 10.1016/j.jpain.2006.05.006.
The aim of this study was to further validate our carrageenan-induced temporomandibular joint (TMJ) inflammatory hyperalgesia model in rats by showing that administration of indomethacin before the initiation of inflammation would diminish the TMJ hyperalgesia. Using this model, we investigated whether norepinephrine and local beta-adrenoceptors contribute to the development of inflammatory TMJ hyperalgesia. Carrageenan-induced TMJ hyperalgesia was assessed by measuring the behavioral nociceptive responses, such as rubbing the orofacial region and flinching the head, induced by the injection of a low dose of 5-hydroxytryptamine into the TMJ sensitized 1 h before by a TMJ injection of carrageenan. Blockade of prostaglandin synthesis by indomethacin prior to initiation of inflammation by carrageenan significantly attenuated the TMJ hyperalgesia. The guanethidine depletion of norepinephrine or the blockade of beta(2)but not the blockade of the beta(1)-adrenoceptor by the selective adrenoceptor antagonists ICI 118.55 and atenolol, respectively, significantly reduced carrageenan-induced TMJ hyperalgesia. In the present study, we further validated our carrageenan-induced TMJ hyperalgesia model to study the mechanisms involved in inflammatory TMJ hyperalgesia and to test the analgesic effect of different types of peripheral analgesics. We also demonstrated that norepinephrine released at the site of injury contributes to the development of the inflammatory TMJ hyperalgesia by the activation of beta(2)-adrenoceptors.
The findings that local sympathomimetic amines contribute to the inflammatory TMJ hyperalgesia by activating beta(2)-adrenoceptors may be relevant to clinical TMJ inflammatory pain states less sensitive to nonsteroidal anti-inflammatory drugs.
本研究的目的是通过证明在炎症开始前给予吲哚美辛会减轻颞下颌关节（TMJ）痛觉过敏，进一步验证我们的角叉菜胶诱导的大鼠颞下颌关节炎性痛觉过敏模型。使用该模型，我们研究了去甲肾上腺素和局部β-肾上腺素能受体是否参与炎性颞下颌关节痛觉过敏的发生。通过测量行为性伤害性反应来评估角叉菜胶诱导的颞下颌关节痛觉过敏，例如在角叉菜胶注射到颞下颌关节1小时前致敏后，向颞下颌关节注射低剂量5-羟色胺所诱发的口面部区域摩擦和头部退缩。在角叉菜胶引发炎症之前，用吲哚美辛阻断前列腺素合成可显著减轻颞下颌关节痛觉过敏。分别用胍乙啶耗竭去甲肾上腺素或用选择性肾上腺素能受体拮抗剂ICI 118.55和阿替洛尔阻断β₂但不阻断β₁-肾上腺素能受体，可显著降低角叉菜胶诱导的颞下颌关节痛觉过敏。在本研究中，我们进一步验证了我们的角叉菜胶诱导的颞下颌关节痛觉过敏模型，以研究炎性颞下颌关节痛觉过敏的机制，并测试不同类型外周镇痛药的镇痛效果。我们还证明，损伤部位释放的去甲肾上腺素通过激活β₂-肾上腺素能受体促进炎性颞下颌关节痛觉过敏的发生。
局部拟交感胺通过激活β₂-肾上腺素能受体导致炎性颞下颌关节痛觉过敏的发现，可能与对非甾体抗炎药不太敏感的临床颞下颌关节炎性疼痛状态相关。
