EXPERIMENTAL TOOTH MOVEMENT-INDUCED GLIAL ACTIVATION AND MICROGLIAL MODULATION CAN ATTENUATE ORTHODOTIC PAIN

摘要

Microglia and astrocyte in the central nervous system are known to respond to peripheral injury and release cytokines that induce pain. If an orthodontic force that generates inflammatory-like response is applied to the tooth, microglia may respond to the tooth movement causing pain. Several analgesics are used to control pain during orthodontic treatment; however, most of them also are known to inhibit tooth movement. Minocyclin is known to disrupt the activation of microglia selectively to attenuate and delay pain while minimizing effects on the peripheral system. In this pilot study, we hypothesized that lasting nociception induced by experimental tooth movement will lead to glial activation at the medulla and glial inactivation by minocycline medication will show anti-nociceptive activity. Thirty adult rats divided equally between minocycline treatment and controls were sacrificed after 3, 5, 7 and 14 days after experimental tooth movement for immunohistochmestry of OX-42 (microgilia activation), glial fibrillary acidic protein (GFAP; astrocyte activation) and c-fos double immunostaining. There was a significant increase in both microglia and astrocyte activity after tooth movement. Minocycline application resulted in significant reduction of microglia, astrocyte and c-fos activity associated with tooth movement. These findings suggest that microglia are potential contributors for the delay in pain observed during orthodontic treatment. Furthermore, minocycline may be a new innovative pre-emptive analgesic that selectively blocks long-lasting pain and effectively contributes to reduced pain and/or discomfort during orthodontic treatment.