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4 "Neurogenic inflammation"
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Case Report
Vital tooth with periapical lesion: spontaneous healing after conservative treatment
Hyun-Joo Kim, Seung-Jong Lee, Il-Young Jung, Sung-Ho Park
Restor Dent Endod 2012;37(2):123-126.   Published online May 18, 2012
DOI: https://doi.org/10.5395/rde.2012.37.2.123
AbstractAbstract PDFPubReaderePub

It is often presumed that apical periodontitis follows total pulp necrosis, and consequently root canal treatment is commonly performed. Periapical lesion development is usually caused by bacteria and its byproduct which irritate pulp, develop pulpitis, and result in necrosis through an irreversible process. Afterwards, apical periodontitis occurs. This phenomenon is observed as an apical radiolucency in radiographic view. However, this unusual case presents a spontaneous healing of periapical lesion, which has developed without pulp necrosis in a vital tooth, through conservative treatment.

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Original Articles
Effect of local anesthesia on pulpal blood flow in mechanically stimulated teeth
Wan-Sik Chu, Seung-Ho Park, Dong-Kuk Ahn, Sung Kyo Kim
J Korean Acad Conserv Dent 2006;31(4):257-262.   Published online January 14, 2006
DOI: https://doi.org/10.5395/JKACD.2006.31.4.257
AbstractAbstract PDFPubReaderePub
Abstract

The aims of the study were to evaluate the effect of epinephrine-containing local anesthetics on pulpal blood flow (PBF) and to investigate its effect on cavity preparation-induced PBF change. PBF was recorded using a laser Doppler flowmeter (Perimed Co., Sweden) from canines of nine cats under general anesthesia before and after injection of local anesthetics and after cavity preparation. 2% lidocaine hydrochloride with 1 : 100,000 epinephrine was administered by local infiltration given apical to the mandibular canine at the vestibular area and the same volume of isotonic saline was injected on the contralateral tooth as a control. A round carbide bur was operated at slow speed with isotonic saline flushing to grind spherical cavities with increasing depth through the enamel and into the dentin on both teeth. The obtained data was analyzed with paired t-test.

Cavity preparation caused significant increase of PBF (n = 9, p < 0.05). Local infiltration of lidocaine with epinephrine resulted in decreases of PBF (n = 9, p < 0.05), whereas there was no significant change of PBF with the physiologic saline as a control. Cavity preparation on tooth anesthetized with lidocaine with epinephrine caused significantly less increase of PBF than in control tooth (p < 0.05).

Therefore, the result of the present study demonstrates that local infiltration of 2% lidocaine with 1 : 100,000 epinephrine effectively reduces PBF increase caused by cavity preparation.

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REGULATION OF PULPAL MICROCIRCULATION BY CALCITONIN GENE-RELATED PEPTIDE
Sung-Kyo Kim, Young-Kyung Kim, Myoung-Uk Jin
J Korean Acad Conserv Dent 2005;30(6):470-476.   Published online January 14, 2005
DOI: https://doi.org/10.5395/JKACD.2005.30.6.470
AbstractAbstract PDFPubReaderePub
Abstract

The purpose of this study was to investigate the function of calcitonin gene-related peptide (CGRP) in regulatory mechanism of pulpal microcirculation with the aim of elucidating neurogenic inflammation.

Experiments were performed on twelve cats under general anesthesia. CGRP was administered through the femoral vein to see the systemic influence and through the external carotid artery to see the local effect. Sympathetic nerve to the dental pulp was stimulated electrically and pulpal blood flow (PBF) was measured with a laser Doppler flowmeter on the canine teeth to the drug administration. The paired variables of control and experimental data were compared by paired t-test and differences with p < 0.05 were considered statistically significant.

Systemic administration of CGRP (0.3 μg/kg) exerted decreases in systemic blood pressure and caused changes in PBF with an initial increase followed by decrease and a more marked second increase and decrease.

Close intra-arterial (i.a.) injection of CGRP (0.03 μ/kg) resulted in slight PBF increase. The effect of CGRP resulted in no significant increase in PBF in the presence of CGRP8-37.

The electrical stimulation of the sympathetic nerve alone resulted in PBF decreases. The i.a. administration of CGRP following the electrical stimulation of the sympathetic nerve compensated the decreased PBF. Therefore, CGRP effectively blocked the sympathetic nerve stimulation-induced PBF decrease.

Results of the present study have provided evidences that even though the local vasodilatory function of CGRP are weak, CGRP is effectively involved in blocking the vasoconstriction caused by sympathetic nerve stimulation in the feline dental pulp.

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Local application of NK1 receptor antagonists and pulpal blood flow in cat
Young-Kyung Kim, Wan-Sik Chu, Ho-Jeong Lee, Dong-Kuk Ahn, Hyun-Mi Yoo, Sung-Kyo Kim
J Korean Acad Conserv Dent 2004;29(3):239-248.   Published online May 31, 2004
DOI: https://doi.org/10.5395/JKACD.2004.29.3.239
AbstractAbstract PDFPubReaderePub

The purpose of this study was to investigate the influence of NK1 receptor antagonists on the pulpal blood flow (PBF) when applied iontophoretically through the dentinal cavity of the teeth in order to understand whether iontophoretically applied NK1 receptor antagonists can control the pulpal inflammation.

Eleven cats were anesthetized with alpha-chloralose and urethane, and substance P (SP) was administered to the dental pulp through the catheterized lingual artery in doses that caused PBF change without the influence of systemic blood pressure. NK1 receptor antagonists were applied iontophoretically to the prepared dentinal cavity of ipsilateral canine teeth of the drug administration, and PBF was monitored. Data were analyzed statistically with paired t-test.

PBF increase after iontophoretic application of the NK1 receptor antagonists followed by the intra-arterial administration of SP was significantly less than PBF increase after iontophoretic application of the 0.9% saline followed by the intra-arterial administration of SP as a control (p < 0.05).

Iontophoretic application of the NK1 receptor antagonists (0.2~3.4 mM) following the intra-arterial administration of SP resulted in less increase of PBF than the iontophoretic application of the 0.9% saline following the intra-arterial administration of SP as a control (p < 0.05).

Therefore, the results of the present study provide evidences that the iontophoretic application is an effective method to deliver drugs to the dental pulp, and that iontophoretically applied NK1 receptor antagonists block SP-induced vasodilation effectively. The above results show the possibility that the iontophoretical application of NK1 receptor antagonists can control the neurogenic inflammation in the dental pulp.

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