• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.31 no.6
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• pp.515-525
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• 2005

Purpose of study: Lingual nerve damage can be caused by surgery or trauma such as physical irriatation, radiation, chemotherapy, infection and viral infection. Once nerve damage occurred, patients sometimes complain taste change and loss of taste along with serious disturbance of tongue. The purpose of this study was to evaluate the effects of unilateral lingual nerve transection on taste as well as on the maintenance of taste buds. Materials & Methods: Male Sprague-Dawley rats weighing 220-250g received unilateral transection of lingual nerve, subjected to the preference test for various taste solutions (0.1M NaCl, 0.1M sucrose, 0.01M QHCl, or 0.01M HCl) with two bottle test paradigm at 2, 4, 6, or 8 weeks after the operation. Tongue was fixed with 8% paraformaldehyde. After fixation, they were observed with scanning electron microscope(JSM-$840A^{(R)}$, JEOL, JAPAN) and counted the number of the dorsal surface of the fungiform papilla for changes of fungiform papilla. And, Fungiform papilla were obtained from coronal sections of the anterior tongue(cryosection). After cryosection, immunostaining with $G{\alpha}gust$(I-20)(Santa Cruz Biotechnology, USA), $PLC{\beta}2$(Q-15)(Santa Cruz Biotechnology, USA), and $T_1R_1$(Alpha Diagnostic International, USA) were done. Immunofluorescence of labeled taste bud cells was examined by confocal microscopy(F92-$300^{(R)}$, Olympus, JAPAN). Results: The preference score for salty and sweet tended to be higher in the operated rats with statistical significance, compared to the sham rats. Fungiform papilla counting were decreased after lingual nerve transaction. In 2 weeks, maximum differences occurred. Gustducin and $T_1R_1$ expressions of taste receptor in 2 and 4 weeks were decreased. $PLC{\beta}2$ were not expressed in both experimental and control group. Conclusion: This study demonstrated that the taste recognition for sweet and salty taste changed by week 2 and 4 after unilateral lingual nerve transection. However, regeneration related taste was occurred in the presence of preserving mesoneurial tissue and the time was 6 weeks. Our results demonstrated that unilateral lingual nerve damage caused morphological and numerical change of fungiform papilla. It should be noted in our study that lingual nerve transection resulted in not only morphological and numerical change but also functional change of fungiform papillae.

• Restorative Dentistry and Endodontics
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• v.34 no.3
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• pp.169-176
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• 2009

Diabetes Mellitus (DM) is a syndrome accompanied with the abnormal secretion or function of insulin, a hormone that plays a vital role in controlling the blood glucose level (BGL). Type land 2 DM are most common form and the prevalence of the latter is recently increasing, The aim of this article was to assess whet her Type 2 DM could act as a predisposing risk factor on the pulpo-periapical pathogenesis. Previous literature on the pathologic changes of blood vessels in DM was thoroughly reviewed. Furthermore, a histopathologic analysis of artificially-induced periapical specimens obtained from Type 2 diabetic and DM-resistant rats was compared. Histopathologic results demonstrate that the size of periapical bone destruction w as larger and the degree of pulpal inflammation was more severe in diabetic rats, indicating that Type 2 D M itself can be a predisposing risk factor that makes the host more susceptible to pulpal infection. The possible reasons may be that in diabetic state the lumen of pulpal blood vessels are thickened by atheromatous deposits, and microcirculation is hindered, The function of polymorphonuclear leukocyte is also impair ed and the migration of immune cells is blocked, leading to increased chance of pulpal infection. Also, lack of collateral circulation of pulpal blood vessels makes the pulp more susceptible to infection. These decrease the regeneration capacity of pulpal cells or tissues, delaying the healing process, Therefore, when restorative treatment is needed in Type 2 DM patients, dentists should minimize irritation to the pulpal tissue un der control of BGL.

• Journal of Veterinary Clinics
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• v.32 no.4
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• pp.295-300
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• 2015

The aim of the study was to assess the in vitro effect of 808-nm InGaAs diode laser on rabbit articular chondrocyte proliferation and sulphated glycosaminoglycan (sGAG) synthesis in alginate bead. Previous studies revealed either positive or negative stimulatory effects of laser on different types of cells. A 808-nm InGaAs diode laser at 1.0W power output was used to irradiate the rabbit chondrocytes in alginate beads with energy densities of $31J/cm^2$ (G 1) and $62J/cm^2$ (G 2) corresponding to the experimental groups for 10 seconds and 20 seconds, respectively at 24, 48, 72 and 96 hours after seeding. Control group was left untreated. MTT assay was performed at 1 week and 2 weeks after the $1^{st}$ laser irradiation in alginate beads. sGAG synthesis in alginate beads at 1 week and 2 weeks were determined by DMMB assay. Histological evaluation for cellular distribution and sGAG deposition around the cells were performed by alcian blue stain. MTT assay revealed no positive stimulatory effect in cell proliferation in alginate bead. DMMB assay results showed significantly increased sGAG production in G 2 chondrocytes at 2 weeks. Image analysis of alcian blue stained slides also showed significantly higher percentage of positive alcian blue stain in G 2 chondrocytes. This result suggests that 808-nm InGaAs diode laser with 1.0 W power output although cannot stimulate cell proliferation it can increase the cell secretion activity and sGAG deposition in alginate beads.

• Journal of Life Science
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• v.21 no.2
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• pp.183-193
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• 2011

Migration and differentiation of mesenchymal stem cells are crucial for tissue regeneration in response to injury. Sphingosine-1-phosphate (S1P) is a bioactive lipid that regulates a variety of biological processes, including proliferation, survival, differentiation and motility. In the present study, we determined the role of S1P in migration and differentiation of human bone marrow-derived mesenchymal stem cells (BMSCs). S1P stimulated migration of BMSCs in a dose- and time-dependent manner, and pre-incubation of the cells with pertussis toxin completely abrogated S1P-induced migration, suggesting involvement of Gi-coupled receptors in S1P-induced cell migration. S1P elicited elevation of intracellular concentration of $Ca^{2+}$ ($[Ca^{2+}]_i$) and pretreatment with VPC23019, an antagonist of $S1P_1/S1P_3$, blocked S1P-induced migration and increase of $[Ca^{2+}]_i$. Small interfering RNA-mediated knockdown of endogenous $S1P_1$ attenuated S1P-induced migration of BMSCs. Furthermore, S1P treatment induced expression of $\alpha$-smooth muscle actin ($\alpha$-SMA), a smooth muscle marker, and pretreatment with VPC23019 abrogated S1P-induced $\alpha$-SMA expression. S1P induced phosphorylation of p38 mitogen-activated protein kinase (MAPK), and pretreatment of cells with SB202190, an inhibitor of p38 MAPK, or adenoviral overexpression of a dominant-negative mutant of the p38 MAPK blocked S1P-induced cell migration and $\alpha$-SMA expression. Taken together, these results suggest that S1P stimulates migration and smooth muscle differentiation of BMSCs through an $S1P_1$-p38 MAPK-dependent mechanism.

• Journal of Periodontal and Implant Science
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• v.32 no.3
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• pp.457-473
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• 2002

The purposes of this study is to evaluate the combination effects of TGF-${\beta}_1$ and PDGF-BB on the periodontal ligament cells to use as a regeneration promoting agent of periodontal tissue. Human periodontal ligament cells were prepared from the first premolar tooth extracted for the orthodontic treatment and were cultured in DMEM/100% FBS at the $37^{\circ}C$, 5% $CO_2$ incubator. Authors measured the DNA synthesis, total protein, collagen and noncollagenous protein synthesis according to the concentration of TGF-${\beta}_1$,(1,5ng/ml) and PDGF-BB (1,10 ng/ml) in combination. To explore further this delayed effect of TGF-${\beta}_1$, we preincubated human periodontal ligament cells with TGF-${\beta}_1$ for 4 or 24 hours before PDGF-BB stimulation. The results were as follows: The DNA synthetic activity was increased dose dependently by TGF-${\beta}_1$, PDGF-BB. The combination of TGF-${\beta}_1$ and PDGF-BB consistently enhanced the DNA synthetic activity to PDGF-BB alone. The ability of TGF-${\beta}_1$ to enhance DNA synthetic activity in PDGF-BB treated periodontal ligament cells was dose dependent. The maximum mitogenic effect was at the 5ng/ml of TGF-${\beta}_1$ and l0ng/ml of PDGF-BB. Preincubation of cell with TGF-${\beta}_1$ resulted in significantly greater response to PDGF-BB at all TGF-${\beta}_1$ concentration studied, and may be useful for clinical application in periodontal regenerative procedures. The total protein, collagen and noncollagen synthesis was increased dose pendently by TGF-${\beta}_1$, PDGF-BB. The % of collagen was slightly decreased according to the concentration of TGF-${\beta}_1$, PDGF-BB. The effect of TGF-${\beta}_1$, PDGF-BB were not specific for collagen synthesis since it also increased noncollagenous protein synthesis. This study demonstrates that PDGF-BB is major mitogens for human periodontal ligament cells in vitro, and supports a role for TGF-${\beta}_1$ as a regulation of the mitogenic and total protein formation to PDGF-BB in these cells.