Abstract

Control of pain is the major goal in the management of chronic orofacial pain (COP) patients. The pathogenesis of COP is currently not well understood. Consequently, the treatment of COP may be suboptimal or even harmful. Based on independent observations, we propose that local elevated levels of nitric oxide (NO) may have a central role in the pathogenesis of COP. NO level in the orofacial region of COP patients is elevated. A regional increased level of NO causes excessive vasodilatation. This hyperperfusion is manifested by hyperthermia of the overlying skin, while NO enhances nociception, aggravating orofacial pain. An alternative mechanism involving NO as a neurotransmitter at the CNS level may contribute to orofacial pain, but seems not to account for all the known clinical observations. Two groups of subjects were studied: 5 patients with COP and 59 control subjects. For each subject we collected blood samples for analysis of nitrite\nitrate (or NOx). (1) NOx blood levels for 5 patients diagnosed with COP was 65.9 microM (SD of 10.4) verses 42.7 microM (SD of 24.2) for 59 control subjects, the difference being statistically significant, t-statistic = -2.12 (P > .05). (2) No statistical difference was found for NOx blood levels for 59 control subjects divided by gender (male vs female), with 23 female controls having NOx blood levels of 42.6 microM (SD of 25.2) and male controls having NOx blood levels of 42.8 microM (SD of 24.0), t-statistic = -0.03, P = .98. This pilot study suggests that NO blood levels may have an association with COP. A better understanding of the mechanism of chronic orofacial pain is expected to lead to more precise diagnostic staging and management of this disorder.

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