کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
3115574 | 1582675 | 2016 | 8 صفحه PDF | دانلود رایگان |
• Microglia and astrocytes may play roles in pain transmission during tooth movement.
• Minocycline administration selectively inhibited microglial and c-Fos expression.
• Minocycline has the potential to control pain during orthodontic treatment.
IntroductionOrthodontic tooth movement causes pain to a patient. Glial cells are nonneuronal cells in the central nervous system and are implicated in various types of pain. In this study, we assessed glial activation responses after experimental tooth movement using immunocytochemical detection of anti-CD11b (OX42) and glial fibrillary acidic protein immunoreactivity to illustrate the microglial and astrocytes response, respectively. In addition, the effect of minocycline in reducing pain during tooth movement was also investigated.MethodsFifty-five Sprague Dawley rats with and without administration of minocycline after 1, 3, 5, 7, and 14 days (n = 5, for each) of tooth movement were used. Immunohistochemistry for microglia (OX42) and astrocyte (glial fibrillary acidic protein) were performed at the medullary dorsal horn (trigeminal subnucleus caudalis). Three-dimensional quantitative analysis was performed with a confocal fluorescence microscope and a software program.ResultsThere was a significant increase in the OX42 and glial fibrillary acidic protein immunoreactivity in response to tooth movement in the medullary dorsal horn. Furthermore, systematic administration of minocycline, a selective inhibitor of microglial activation, significantly attenuated the nociceptive c-Fos expression in the medullary dorsal horn that was induced by experimental tooth movement.ConclusionsThese data indicate the possible importance of microglial activation in the development of orthodontic pain. This is also the first report on the systematic application of minocycline.
Journal: American Journal of Orthodontics and Dentofacial Orthopedics - Volume 149, Issue 6, June 2016, Pages 881–888