Differences between Orofacial Inflammation and Cancer Pain

Differences between Orofacial Inflammation and Cancer Pain
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DOI:
10.1177/0022034510363095
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发表时间:
2010-06-01
影响因子:
7.6
通讯作者:
Inenaga, K.
Inenaga, K.
中科院分区:
医学1区
文献类型:
--
作者:
Harano, N.;Ono, K.;Inenaga, K.

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口面癌大鼠模型表现出异常性疼痛和痛觉过敏;然而,尚不清楚癌症引起的疼痛是否继发于癌症引起的炎症。为了解决这个问题,我们比较了抗炎药吲哚美辛对口面部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很大程度上抑制了炎症模型中的机械性异常性疼痛和热痛觉过敏。相同的程序抑制了癌症模型中的异常性疼痛和痛觉过敏,但与炎症模型中的抑制相比较弱。在延髓背角中,降钙素基因相关肽和P物质水平在炎症模型中显着升高,但在癌症模型中没有变化。这些结果表明,口面癌模型中的疼痛并不是由癌症引起的外周炎症显着介导的,尽管它可能有一定的参与。
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.