Phosphorylation of ERK in trigeminal spinal nucleus neurons following passive jaw movement in rats with chronic temporomandibular joint inflammation.

AIMS

To elucidate the neuronal mechanisms underlying chronic pain of the temporomandibular joint (TMJ), expression of phosphorylated extracellular signal-regulated kinase (pERK) in the trigeminal spinal nucleus caudalis (Vc) was studied in rats with a chronically inflamed TMJ.

METHODS

Complete Freund's adjuvant (CFA) was injected in the left TMJ region of rats anesthetized with pentobarbital (50 mg/kg intraperitoneally). Face temperature of the TMJ region was measured periodically after CFA injection. Two weeks after CFA injection, passive jaw movement with 4-, 6-, and 15-mm distances was carried out in inflamed and naive rats for 5, 15, and 30 minutes. pERK expression was studied in the medulla and upper cervical cord after passive jaw movement.

RESULTS

Face temperature was significantly increased 2 days after CFA injection and returned to the preoperative level 7 days later. The pERK-like immunoreactive (LI) cells were observed in the dorsal portion of the rostral Vc in inflamed rats after passive jaw movement, and a small number of pERK-LI cells were observed in naive rats after passive jaw movement. No pERK-LI cells were observed in the TMJ of inflamed rats without jaw movement. The number of pERK-LI cells increased following increases in the jaw-movement distance and duration.

CONCLUSION

These findings suggest that the dorsal portion of the rostral Vc may be involved in mediating chronic pain following TMJ inflammation and that the intracellular ERK cascade may be involved.