Orthodontic treatment-induced temporal alteration of jaw-opening reflex excitability

The impairment of orofacial motor function during orthodontic treatment needs to be addressed, because most orthodontic patients experience pain and motor excitability would be affected by pain. In the present study, the temporal alteration of the jaw-opening reflex excitability was investigated to determine if orthodontic treatment affects orofacial motor function. The excitability of jaw-opening reflex evoked by electrical stimulation on the gingiva and recorded bilaterally in the anterior digastric muscles was evaluated at 1 (D1), 3 (D3), and 7 days (D7) after orthodontic force application to the teeth of right side; morphological features (e.g., osteoclast genesis and tooth movement) were also evaluated. To clarify the underlying mechanism of orthodontic treatment-induced alteration of orofacial motor excitability, analgesics were administrated for 1 day. At D1 and D3, orthodontic treatment significantly decreased the threshold for inducing the jaw-opening reflex but significantly increased the threshold at D7. Other parameters of the jaw-opening reflex were also evaluated (e.g., latency, duration and area under the curve of anterior digastric muscles activity), and only the latency of the D1 group was significantly different from that of the other groups. Temporal alteration of the jaw-opening reflex excitability was significantly correlated with changes in morphological features. Aspirin (300 mg·kg−1·day−1) significantly increased the threshold for inducing the jaw-opening reflex, whereas a lower dose (75–150 mg·kg−1·day−1) of aspirin or acetaminophen (300 mg·kg−1·day−1) failed to alter the jaw-opening reflex excitability. These results suggest that an increase of the jaw-opening reflex excitability can be induced acutely by orthodontic treatment, possibly through the cyclooxygenase activation. NEW & NOTEWORTHY It is well known that motor function is affected by pain, but the effect of orthodontic treatment-related pain on the trigeminal motor excitability has not been fully understood. We found that, during orthodontic treatment, trigeminal motor excitability is acutely increased and then decreased in a week. Because alteration of trigeminal motor function can be evaluated quantitatively by jaw-opening reflex excitability, the present animal model may be useful to search for alternative approaches to attenuate orthodontic pain.

Morphological study of the sensory nerve which induces jaw opening reflex

Background and objectives: An anatomical site in the oral cavity can be used to trigger the jaw opening reflex in patients with pseudobulbar palsy who have difficulty opening the mouth. The site is located at the midpoint between the palatoglossal arch and pterygomandibular fold and medial to the retromolar pad. However, previous findings on the nerves innervating this particular area are inconsistent. Therefore, in this study, we carefully investigated the sensory nerves that innervate the area near the trigger point of the jaw opening reflex. Materials and methods: For the morphological investigation of sensory innervation in this area, in this study we exposed the cranial nerves in 26 halves of cadaver head and observed their distribution in soft tissue. Results: In all cases, several nerve fibers diverged anteroinferiorly from the lingual nerve located between its junction with the chorda tympani nerve and the junction with the communicating branch of the submandibular ganglion. These nerve fibers, thought to be the facial branches of the lingual nerve, innervated the mucosa in the vicinity of the palatoglossal arch, retromolar pad, and the lingual gingiva of the last molar which were near to the trigger point of the jaw opening reflex. Conclusion: The results suggest that the sensory nerve that induces the jaw opening reflex appears to be the branches to isthmus of fauces diverged from the lingual nerve.