• Restorative Dentistry and Endodontics
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• v.41 no.3
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• pp.202-209
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• 2016

Objectives: The purpose of this study was to investigate the involvement of TRPA1 in the cinnamaldehyde-induced pulpal blood flow (PBF) change in the feline dental pulp. Materials and Methods: Mandibles of eight cats were immobilized and PBF was monitored with a laser Doppler flowmetry at the mandibular canine tooth. To evaluate the effect of cinnamaldehyde on PBF, cinnamaldehyde was injected into the pulp through the lingual artery at a constant rate for 60 seconds. As a control, a mixture of 70% ethanol and 30% dimethyl sulfoxide (DMSO, vehicle) was used. To evaluate the involvement of transient receptor potential ankyrin 1 (TRPA1) in PBF change, AP18, a specific TRPA1 antagonist, was applied into the pulp through the Class V dentinal cavity followed by cinnamaldehyde-administration 3 minutes later. The paired variables of experimental data were statistically analyzed using paired t-test. A p value of less than 0.05 was considered as statistically significant. Results: Administration of cinnamaldehyde (0.5 mg/kg, intra-arterial [i.a.]) induced significant increases in PBF (p < 0.05). While administration of a TRPA1 antagonist, AP18 (2.5 - 3.0 mM, into the dentinal cavity [i.c.]) caused insignificant change of PBF (p > 0.05), administration of cinnamaldehyde (0.5 mg/kg, i.a.) following the application of AP18 (2.5 - 3.0 mM, i.c.) resulted in an attenuation of PBF increase from the control level (p < 0.05). As a result, a TRPA1 antagonist, AP18 effectively inhibited the vasodilative effect of cinnamaldehyde (p < 0.05). Conclusions: The result of the present study provided a functional evidence that TRPA1 is involved in the mechanism of cinnamaldehyde-induced vasodilation in the feline dental pulp.

• Korean Journal of Veterinary Research
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• v.50 no.4
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• pp.303-310
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• 2010

Demand on specialized feline dentistry has increased over the years, partly due to growing feline population in Korea. Despite the notable increase in the population, not much researches has been conducted on oral disease for stray cats. Thus this research was conducted on 81 adult stray cats from Gwangju in Korea (42 males and 39 females) with average weight of 3.4 kg and also focused on occurrence of periodontal disease (plaque and calculus), feline odontoclastic resorptive lesion (FORL), stomatitis and tooth anomaly. Formation of dental plaque and calculus were abundant on maxilla than mandible, especially distributed much on 4th premolar teeth and 1st molar teeth. After thorough examination of oral cavity, 33 stray cats (40.7%) were found to have oral disease. Eighteen stray cats (22.2%) had tooth fracture which was evident on cuspid and missing teeth were present on 2nd premolar tooth of maxilla and 2nd incisor of mandible amongst 20 stray cats (24.7%). FORL was present on cuspids and 2nd premolar tooth of maxilla among 10 stray cats (12.3%). Stomatitis was involved with FORL, missing tooth, and tooth fracture. Therefore, it was determined that stomatitis, FORL, and periodontal disease were closely associated.

• Restorative Dentistry and Endodontics
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• v.21 no.1
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• pp.375-384
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• 1996

The purpose of this study was to investigate the functional involvement of sympathetic nerve in the control of the microcirculation in the dental pulp with the aim of elucidation of the involvement of neuropeptides and sympathetic nerve in neurogenic inflammation. Experiments were done on the 7 cats anesthetised with sodium pentobarbital, and sympathetic nerve to the' dental pulp was stimulated electrically (10 Hz, 4 V, 1.5 ms, 3.5 mins). Ana-adrenoceptor antagonist phentolamine and a neuropeptide Y antagonist D-myo-inositol-1,2,6-trisphosphate (PP56) were injected close intra-arterially into the dental pulp without changing the systemic blood pressure. The probe of laser Doppler flowmeter was placed on the buccal surface of ipsilateral canine teeth to the stimulation, and pulpal blood flow was measured. Stimulation of the sympathetic nerve decreased pulpal blood flow by $55.24{\pm}7.74\;%$ (mean${\pm}$SEM, n = 13). Stimulation of the sympathetic nerve following the injection of the ${\alpha}$-adrenoceptor antagonist phentolamine ($0.1{\mu}g$/kg) caused decrease of pulpal blood flow by $14.35{\pm}3.43%$ (mean${\pm}$SEM, n=5). Phentolamine attenuated the sympathetic nerve-induced pulpal blood flow decrease by $74.02{\pm}9.32%$ (mean${\pm}$SEM) Stimulation of the sympathetic nerve following the injection of the neuropeptide Y antagonist PP56 (2.3 mg/kg) caused decrease of pulpal blood flow by $30.64{\pm}7.92%$ (mean${\pm}$SEM, n=6). PP56 attenuated the sympathetic nerve-induced pulpal blood flow decrease by $44.37{\pm}11.01%$ (mean${\pm}$SEM). These data provide evidences of the co-contribution of nerepinephrine and neuropeptide Y on the sympathetic nerve-induced vasoconstriction in the feline dental pulp. In addition, they show functional evidences that sympathetic nerve plays an active role in controlling the microcirculation of the dental pulp.

• Restorative Dentistry and Endodontics
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• v.21 no.1
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• pp.366-374
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• 1996

The purpose of this study was to investigate whether D-myo-inositol-l,2,6-trisphosphate (PP56) can effectively antagonize vasoconstriction caused by neuropeptide Y in the dental pulp, and to understand involvement of neuropeptide Y in the regulation of microcirculation in the dental pulp with the aim of elucidating neurogenic inflammation. Experiments were performed on 7 cats anesthetised with sodium pentobarbital, and neuropeptide Y and a neuropeptide Y antagonist PP56 were injected close intra-arterially into the dental pulp. The probe of laser Doppler flowmeter was placed on the buccal surface of ipsilateral canine teeth to the drug administration and pulpal blood flow was measured. Intra-arterial injection of neuropeptide Y (1.3-$2.0\;{\mu}g$/kg) resulted in pulpal blood flow decrease of $37.73{\pm}5.73%$(mean${\pm}$SEM) (n=9). Intra-arterial injection of PP56(0.3 mg/kg) alone changed pulpal blood flow little by 1.03 % reduction. The effect of neuropeptide Y in the presence of PP56 resulted in significantly less decreases in pulpal blood flow ranging from $27.17{\pm}5.37$ to $16.63{\pm}3.48%$ from control as compared with neuropeptide Y alone(n = 13). In effect, PP56 attenuated pulpal blood flow caused by neuropeptide Y. Results of the present study have provided evidences that a non-peptide PP56 is capable of antagonizing vasoconstriction caused by neuropeptide Y in the feline dental pulp. In addition, they show functional evidences that neuropeptide Y plays an active role in modulating the microcirculation of the dental pulp.

• The korean journal of orthodontics
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• v.14 no.2
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• pp.187-202
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• 1984

There are evidences that exogenous electric currents are capable of enhancing bone formation and resolution, and that the conversion of the bioelectric response to biochemical activity provides the directional component of orthodontic tooth movement. In addition, evidence has implicated cyclic nucleotides in alveolar bone cellular activation mechanism during orthodontic tooth movement. In view of these evidences, this study was performed to investigate the effects of exogenous electric currents on cyclic nuclotide levels in feline alveolar bone and the possible clinical application of electric currents as an additional orthodontic tool. In the first study, three groups of three adult cats were subjected to application of a constant direct current of $10{\pm}2$ microamperes to gingival tissue near maxillary canine noninvasively for 1, 3, and 7 days respectively. In the second study, three groups of three adult cats each were treated by an electric-orthodontic procedure for 1, 3, and 7 days respectively. The left maxillary (control) canine received an orthodontic force of 80gm alone at time of initiation, while the right maxillary (experimental) canine received combined force-electric stimulation (80gm of force and $10{\pm}2$ microamperes of a constant D.C. currents). Alveola, bone samples were obtain from the mesial (tension and/or cathode) and the distal (compression and/or anode) sites surrounding maxillary canines as well as from contralateral control sites. The samples were extracted, boiled, homogenized, and the supernatants were assayed for cyclic nucleotides (cAMP, cGMP) by a radioimmunoassay method. And also the amount of tooth movement was measured in the second study. On the basis of this study, the following conclusions can be drawn: 1. The fluctuation pattern of cyclic nucleotide levels in alveolar bone treated by exogenous electric currents was similar to that treated by orthodontic force. 2. The cAMP levels in alveolar bone of electrically treated teeth significantly elevated above the control values. And of electrically treated teeth, the values of the anode sites were higher than those of the cathode sites. 9. The cGMP levels in alveolar bone of electrically treated teeth elevated above the control values at the initiation phase of treatment, but dropped below the control values at time of termination. And of electrically treated teeth, the values of the cathode sites were higher than those of the anode sites. 4. The rate of tooth movement in teeth . treated by force-electric combination increased with the length of treatment as compared to that treated by mechanical force alone.

• Restorative Dentistry and Endodontics
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• v.30 no.6
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• pp.470-476
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• 2005

The purpose of this Study was to invest)gate the function or 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 $(0.3{\mu}g/ka)$ exerted decreases in systemic blood pressure and caused changes in PBF with an initial increase i311owed by decrease and a move marked second increase and decrease. Close intra-arterial (i.a.) injection of CCRP $(0.03{\mu}g/kg)$ resulted in slight PBF increase. The effect of CGRP resulted in no significant increase in PBF in the presence of $CGRP_{8-37}$. The electrical stimulation of the sympathetic nerve alone resulted in PBF decreases. The j.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, CCRP is effectively involved in blocking the vasoconstriction caused by sympathetic nerve stimulation in the feline dental pulp.