Department of Anatomy, Laboratory of Neuromodulation of Experimental Pain, University of São Paulo, Av Lineu Prestes 2415, ICB III, São Paulo, 05508-000, Brazil.
Department of Physiology, Laboratory of Cellular Neurobiology, University of São Paulo, Av Lineu Prestes 1524, ICB I, São Paulo, 05508-000, Brazil.
Lasers Med Sci. 2021 Aug;36(6):1297-1305. doi: 10.1007/s10103-021-03246-9. Epub 2021 Jan 15.
The aim of this work was to investigate the involvement of substance P (SP), osteopontin (OPN), and satellite glial cells (SGC) on photobiomodulation-induced (PBM) antinociceptive effect in an experimental model of dentin hypersensitivity (DH). Rats ingested isotonic drink (ID, pH 2.87) for 45 consecutive days and after this period received PBM irradiation at λ660 nm or λ808 nm (1 J, 3.5 J/cm, 100 mW, 10 s, 0.028 cm, continuous wave, 3 consecutive daily sessions), and were evaluated for nociceptive behavior 24, 48, 72 h, and 14 days after laser treatments. ID ingestion induced an increase on thermal sensitivity of DH characteristics in rats that was completely reversed by PBM treatment at both 660 and 808 nm. Immunohistochemical analysis revealed increased SP expression at both dentin-pulp complex (DPC) and trigeminal ganglia (TG) of DH-rats which did not occur in PBM groups by PBM treatment. Also, the increase of glial fibrillary acidic protein (GFAP) observed in the TG of DH-rats was also reversed by PBM treatment. Finally, PBM at both 660 and 808 nm increased OPN expression in the dentin-pulp complex of DH-rats after 14 days of PBM treatment. All in all, this data demonstrates that PBM reverses nociception in a DH experimental model by inhibiting neurogenic inflammation and inducing a regenerative response.
本研究旨在探讨在牙本质敏感（DH）的实验模型中，P 物质（SP）、骨桥蛋白（OPN）和卫星胶质细胞（SGC）在光生物调节（PBM）诱导的镇痛作用中的作用。大鼠连续 45 天摄入等渗饮料（ID，pH2.87），在此期间接受 λ660nm 或 λ808nm 的 PBM 照射（1J、3.5J/cm、100mW、10s、0.028cm、连续波、3 次连续每日治疗），并在激光治疗后 24、48、72 小时和 14 天评估疼痛行为。ID 摄入使 DH 大鼠的热敏感性增加，这种增加在 660nm 和 808nm 的 PBM 处理下完全逆转。免疫组织化学分析显示，DH 大鼠牙本质牙髓复合体（DPC）和三叉神经节（TG）中 SP 表达增加，而 PBM 处理组则未发生这种情况。此外，DH 大鼠 TG 中观察到的神经胶质纤维酸性蛋白（GFAP）的增加也被 PBM 处理所逆转。最后，在 PBM 治疗 14 天后，660nm 和 808nm 的 PBM 均增加了 DH 大鼠牙本质牙髓复合体中 OPN 的表达。总之，这些数据表明，PBM 通过抑制神经源性炎症和诱导再生反应来逆转 DH 实验模型中的疼痛。
