Effect of low‐intensity pulsed ultrasound on orofacial sensory disturbance following inferior alveolar nerve injury: Role of neurotrophin‐3 signaling. (8th July 2021)

• Record Type: Journal Article
• Authors: Tsuchimochi, Akane; Endo, Chitose; Motoyoshi, Mitsuru; Tamura, Miki; Hitomi, Suzuro; Hayashi, Yoshinori; Shinoda, Masamichi
• Is Part Of: European journal of oral sciences. Volume 129:Number 5(2021)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2021-07-08
• Subjects: hypesthesia -- neurotrophin‐3 -- trigeminal ganglion -- Schwann cells; Dentistry -- Periodicals; Oral medicine -- Periodicals; 617.6005
• DOI: 10.1111/eos.12810
• Languages: English
• ISSNs: 0909-8836

Abstract

Abstract: Percutaneous treatment of low‐intensity pulsed ultrasound (LIPUS) to the site of inferior alveolar nerve (IAN) transection promotes functional regeneration, but the detailed mechanism is unknown. We examined the involvement of neurotrophin‐3 (NT‐3), which primarily binds with tropomyosin receptor kinase C (TrkC), in functional transected IAN regeneration following LIPUS treatment in rats. Daily LIPUS treatment to the transected IAN was performed, and the mechanical sensitivity of the facial skin was measured for 14 d. On day 5 after IAN transection, the expression of NT‐3 in the transected IAN and TrkC‐positive trigeminal ganglion neurons were immunohistochemically examined. Further, the effect of TrkC neutralization on the acceleration of facial mechanosensory disturbance restoration due to LIPUS treatment was analyzed. LIPUS treatment to the site of IAN transection significantly facilitated functional recovery from sensory disturbance on facial skin. Schwann cells in the transected IAN expressed NT‐3, and LIPUS treatment increased the amount of NT‐3. The facilitated recovery from the mechanosensory disturbance by continuous LIPUS treatment was inhibited by the ongoing TrkC neutralization at the IAN transection site. These results suggest that LIPUS treatment accelerates the recovery of orofacial mechanosensory function following IAN transection through the enhancement of NT‐3 signaling in the transected IAN.