| Pain is almost inevitable and, for the patient, the most unpleasant reaction to orthodontic therapy. It begins a few hours after application of an orthodontic force and lasts for approximately several days. In the past, changes of nerve fibers in the periodontium were paid attention separately during experimental tooth movement. However, little attention was put in the primary sensory neuron and its central terminals. Primary sensory neurons, whose cell bodies located in the trigeminal ganglion (TG), transmit orofacial nociceptive information to central neurons. Their central processes terminate on trigeminal subnucleus caudalis (Vc), whose impulses are conveyed to the somatosensory cortex, in which Vc plays an important role in convergence and transmission of the orofacial nociceptive information, as well as modulation. Therefore, to investigate the plastic changes of those neurons will help us to understand the mechanism of orthodontic pain.Calcitoningene-related peptide ( CGRP) is the most important pain-induced neurotransmitter; therefore, the increasing expression of CGRP is looked upon as a marker of high excitement of neurons. To identify whether the sensitization of primary sensory neurons occurs after experimental tooth movement and to analyse the mechanism of orthodontic pain, testing the changes of CGRP in primary nerve center will be important.In recent years, it has become clear that nerve growth factor (NGF) plays an important role in the function of nociceptive perception in the adult. The sensitivity of the peripheral nociceptive system appears to be under regulation by NGF. In inflammatory conditions, increased NGF produced in target tissues retrograde transport to TG and lead to changes in gene expression leading to long lasting plastic changes in neuron function. To date, few studies show the changesof NGF protein and its high-affinity receptor, TrkA, in PDL during the experimental tooth movement.According to these hints, following experiments are designed to explain the above mentioned problems.1. The changes of CGRP in primary sensory neurons during the experimental tooth movement in the rat.Objective: To investigate the changes of CGRP in the TG and its peripheral and central terminals. To study the effect of the experiment tooth movement on sensitization, conduction of primary sensory neurons and the central mechanism of orthodontic pain.Methods: Model of the experimental tooth movement was established by insertion of a separating elastic between the upper first and second molars to mimic clinical orthodontic tooth movement and immunohistochemical of CGRP in the PDL, pulp and Vc was carried out. The expressions of CGRP mRNA in TG were tested by RT-PCR technology. Results:(1) The number of CGRP-containing nerve fibers decreased significantly in PDL and pulp at 6 hours after tooth movement, but increased at the 3 days; the maximum density of CGRP immunoreactivity was found at the 1 week after tooth movement and returned to the control level at 2 week.(2) Comparing to the control side, the number of CGRP- immunoreactive neurons in TG decreased in the experimental side after 6 hours of the experimental tooth movement, but increased at the 3 day, 1 week.( 3 ) Comparing to control group, the gene expression of CGRP mRNA duringthe experimental tooth movement was upregulated to a different extent and in a time- dependent manner. Expression of CGRP mRNA increased after 24 hours of the experimental tooth movement, reached the highest at 3 days and return to normal at 2 weekes.(4) The number of CGRP-containing nerve fibers decreased significantly in experimental side of Vc at 6, 24 hours after tooth movement. The density of CGRP immunoreactivity in experimental side was more than control side at 1 week after tooth movement and returned to the control level at 2 week.Conclution: During the experimental tooth movement, synthesis of CGRP in primary sensory neurons increases, and the release of CGRP from its peripheral and central nerve endings also increase. These resul...
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