Endomorphin-2 demonstrates potent antinociceptive effects in various
pain models. The objectives of the present study were to explore the role of
endomorphin-2 in the modulation of
orofacial pain induced by
orthodontic tooth movement in rats. An orthodontic
pain model was established in male Sprague-Dawley rats by ligating
coiled springs to mimic orthodontic force (40 g). On days 0, 1, 3, 5, 7, and 14 following
orthodontic tooth movement,
bite force was recorded as a surrogate measure of orthodontic
pain. Ipsilateral trigeminal ganglia, trigeminal nucleus caudalis, and periodontal tissues were harvested for immunostaining.
Endomorphin-2, endomorphin-2 + naloxone (a non-selective
opioid receptor antagonist),
naloxone, and saline were injected into trigeminal ganglia and periodontal tissues to explore the role of
endomorphin-2 on orthodontic
pain. The results showed that following
orthodontic tooth movement,
endomorphin-2 expression levels in trigeminal ganglia were elevated on days 1, 3, 5, and 7. Orthodontic
pain levels were increased on days 1, 3, and 5. The administration of
endomorphin-2 into both trigeminal ganglia and periodontal tissues alleviated orthodontic
pain. Moreover, the effects of
endomorphin-2 could be blocked by
naloxone completely in trigeminal ganglia but only partially in periodontal tissues. Therefore,
endomorphin-2 plays an important role in the modulation of orthodontic
pain both centrally and peripherally, probably through different pathways.