Department of Control of Physical Functions, Kyushu Dental College, 2-6-1 Manazuru, Kokurakitaku, Kitakyushu, Fukuoka, 803-8580, Japan.
J Dent Res. 2010 Jun;89(6):615-20. doi: 10.1177/0022034510363095. Epub 2010 Mar 23.
Rat models of orofacial cancer exhibit both allodynia and hyperalgesia; however, it is unclear whether cancer-induced pain is secondary to cancer-induced inflammation. To address this question, we compared the effects of an anti-inflammatory drug, indomethacin, on pain and neurochemical changes in the medullary dorsal horn in orofacial inflammation and cancer models. Daily peripheral administration of indomethacin largely suppressed mechanical allodynia and thermal hyperalgesia in the inflammation model. The same procedure suppressed allodynia and hyperalgesia in the cancer model, but the suppression was weak when compared with that in the inflammation model. In the medullary dorsal horn, calcitonin gene-related peptide and substance P levels were significantly increased in the inflammation model, but did not change in the cancer model. These results suggest that pain in the orofacial cancer model is not significantly mediated by cancer-induced peripheral inflammation, although it may have some involvement.
口腔癌的大鼠模型表现出痛觉过敏和痛觉超敏；然而，尚不清楚癌症引起的疼痛是否是由癌症引起的炎症引起的。为了解决这个问题，我们比较了一种抗炎药物吲哚美辛对口腔炎症和癌症模型中髓背角疼痛和神经化学变化的影响。每日外周给予吲哚美辛可在很大程度上抑制炎症模型中的机械性痛觉过敏和热痛觉过敏。相同的程序抑制了癌症模型中的痛觉过敏和痛觉超敏，但与炎症模型相比，抑制作用较弱。在髓背角中，降钙素基因相关肽和 P 物质水平在炎症模型中显著增加，但在癌症模型中没有变化。这些结果表明，口腔癌模型中的疼痛并非主要由癌症引起的外周炎症介导，尽管可能有一定的参与。
