Involvement of NOS/NO in the development of chronic dental inflammatory pain in rats

Nitric oxide (NO) is believed to be an important messenger molecule in nociceptive transmission. To assess the possible roles of NO in trigeminal sensory system, we examined the distribution and density of histochemical staining for nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d), a marker for nitric oxide synthase (NOS), and immunohistochemical staining for c-Fos, a neuronal activity marker, in the trigeminal ganglion (TG) and trigeminal nucleus caudalis (Vc) following pulp exposure (PX) injured rats. The neurons innervating injured tooth in TG were labeled by the retrograde transport of fluoro-gold (FG). Teeth were processed for H&E staining. We found that NADPH-d activity increased significantly in the TG and Vc following PX pretreatment (7–28 days, especially in 21–28 days). Such changes were closely corresponding to the pattern of c-Fos detected by immunocytochemistry. The results demonstrate that PX-induced chronic pulpal inflammation results in significant alterations in the TG cells and in the Vc, and such changes may underlie the observed NADPH-d activity. It suggests that NOS/NO may play an active role in both peripheral and central processing of nociceptive information following chronic tooth inflammation.