| It goes to prove that primary sensory neurons not only serve afferent and efferent functions, but also are sensitized after persistent noxious stimulation. Substance P ( SP ) and calcitonin gene related peptide ( CGRP ), which participate in sensitization, afferent and efferent activities, are important neuropeptides in primary sensory neurons.The occlusal trauma results in dental hypersensitiveness and pulpitis. The main pathologic changes of dental hypersensitiveness and pulpitis are the pulp hyperemia at early stage, and the inflammation, degeneration and necrosis of dental pulp at late stage. Upon pathologic studies, Investigators deduced that the pathogenesis was the defect of pulp circulation due to occlusal trauma. General viewpoint approved that depression of excessive occlusal force on blood vessel, such as periodontal and periapical blood vessel, contributed to the defect of pulp circulation. However, the new theories about microcirculation show that retrograde liberation of vasoactive neuropeptides from nerve endings play an important role in the regulation of microcirculation. After noxious stimulation, the primary nociceptive neurons release a great deal SP and CGRP to peripheral tissue by axon reflex. These neurotransmitters participate in peripheral nociception, inflammation, immune and reparation. Our previous experiment revealed the expression of SP immunoreactive fibres changed in dental pulp following occlusal trauma. It is well known that CGRP and SP have vigorously vasoactive function, which can lead vasodilation and exudation. They play an important part in pulp hyperemia, pulp microcirculatory disturbance and the pathogenesis of pulpitis. The changes of neuropeptides during occlusal trauma suggest that pulp microcirculatory disturbance and inflammation may be the result of pulp sensory nerve modulation. To date, No study to elucidate the relationshipbetween the changes of pulp neuropeptides and the variation of pulp microcirculation following occlusal trauma.Through direct nerve damage in apical area, change of stress or tissue damage, occlusal trauma stimulated nerve endings and evoked chronic pain in deeper orofacial region. Chronic orofacial pain, as a common disease, is difficult to cure. Thus, to investigate the mechanism of chronic orofacial pain is importance. However, previous studies about orofacial pain mainly involve central conduction and pain regulation of acute orofacial pain. The hot point on chronic orofacial pain still focused on etiology, treatment and psychology of chronic pain derived from temporomandibular joint ( TMJ ) and its related muscle. The knowledge of pain mechanism, particular primary sensory neurons sensitization, central conduction and mediated mechanism of chronic orofacial pain is very poor. In contrast, the one focus of neuroscience research has being been the mechanism of chronic pain. It has been determined that peripheral terminals of primary nociceptive neurons release neurotransmitter to tissues responding to noxious stimulation, simultaneously, the afferent nerve excite, and the central endings of primary nociceptive neurons release neurotransmitter and neuromodulator, transmitting the pain signal to central nerve. The phenotype of primary sensory neurons changes because of chronic pain. Expression of pain-induced neurotransmitter and receptor population, which few express or no express at normal condition, increase significantly, leading the sensitivity of neurons increase, SP and glutamate acid (Glu), the most important pain-induced neurotransmitter, and their receptor expression is the main mechanism of chronic pain. Therefore, expression increase of SP, Glu and their receptors is looked upon as a marker of high excitement of neurons. To identify whether the sensitization of primary nerve center occurs after occlusal trauma, and to analysis the mechanism of chronic orofacial pain, Testing the changes of SP, Glu and their receptors in primary nerve center will be important.PNs and NaN, both sodium channels, are no...
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