• The korean journal of orthodontics
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• v.34 no.2 s.103
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• pp.143-152
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• 2004

It has not been elucidated whether the initiation of condylar development of the mandible is related with the periosteum of the mandible, or if it derives from a separate programmed blastema not related with the mandible. Also, although the mandibular condylar cartilage is known to promote growth, few studies have dealt with molecular-biologic mechanisms such as the expression of specific genes according to the differentiation of the mandibular condyle. To elucidate the unique cellular characteristics, development, and differentiation process of the mandibular condyle, an examination of expressions of genes characteristic of cartilage and bone were carried out using RT-PCR and mRNA in situ hybridization. 1. Type? collagen mRNA was detected with type II collagen mRNA in the differentiation and growth process of the cartilage of the mandibular condyle. TypeII collagen mRNA was demonstrated in the whole resting md upper part of the poliferative zone, whereas type II collagen mRNA was observed in the resting, proliferative and upper hypertrophic cartilage zone of the mandibular condyle. 2. The condylar cartilage rapidly increased in size due to the accumulation of hypertrophic chondrocytes as characterized by the expression of type II collagen mRNA during postnatal development. 3. BMP-4 mRNA was present in the anlage of the future condylar process and also in the ossifying mandibular body. 4. IHH mRNA was limited exclusively to the lower part of the proliferative zone and the upper part of the hypertrophic cartilage zone during condylar development. These findings were different from those in the growth-plate cartilage of the long bone, indicating a characteristic feature of the differentiation of the chondrocytes in the condylar cartilage present in prenatal and postnatal development. Furthermore, it was also suggested that chondroblasts of condylar cartilage rapidly differentiate into hypertrophic chondrocytes with increased functional Load force such as muscle activity and mastication.

• Journal of Periodontal and Implant Science
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• v.28 no.4
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• pp.703-721
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• 1998

In order to observe the effects of Nicotine and NNK on cultured human gingival fibroblast, several factors were examined including mutagenicity, the number of cells attached culture plate surface through MTT test, the abundance of collagen & collagenase in mRNA level and collagenolytic activity in extracellular matrix. The results were as follows; 1. Regardless of the co-existence of S9, Nicotine did not show the mutagenicity by itself and NNK by itself showd the same result; However, dose related mutagenicity was shown in NNK with S9. 2. The number of fibroblasts attached cultured plate surface was measured by MTT procedure. The number of cells in Non-smokers increased at all time periods as compared to those of smoker. 3. Non-smoker's fibroblast treated by NNK or Nicotine was dosedependently dosedependently decreased in the number of cells when compared to untreated control. In higher dose, Nicotine showed the cellular toxicity, but NNK did not. 4. No change in the abundance of mRNA for pro${\alpha}1$ and pro${\alpha}2$ was shown in Nicotine treated group but in gingival fibroblasts following treatment with NNK, the abundance of mRNA for pro${\alpha}1$, but not pro${\alpha}2$ collagen was decreased. 5. The abundance of mRNA for collagenase was decreased when NNK was treated but no change occurred in Nicotine treated group. 6. The effect of NNK and Nicotine in collagenolytic activity showed that, collagenase activity exclusively react to type I collagen, was increased in both group, but gelatinase exclusively react to type IV collagen was not influenced at all. Collagenase activity of smoker's fibroblast was also increased as much as Nicotine and NNK group. The findings suggest that both of Nicotine and NNK lead gingival fibroblast to decrease in the abundance of collagen. And it seems to be that Nicotine and NNK have independent pathway toward the gingival fibroblast.

• The korean journal of orthodontics
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• v.38 no.3
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• pp.187-201
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• 2008

Objective: The aim of this study was to determine whether cortical punching stimulates the expression of matrix metalloproteinase-1, -8, and -13 in orthodontic tooth movement in rats. Methods: A total of 32 male sprague-dawley rats at 15 weeks old were divided into two groups of 16 rats each, to form the tooth movement with cortical punching (TMC) group and tooth movement only (TM) group. A total of 20 gm of orthodontic force was applied to rat incisors to cause experimental tooth movement. Cortical punching was performed on the palatal side near the central incisor with a 1.0 mm width microscrew in the TMC group. The duration of tooth movement was 1, 4, 7, and 14 days. Results: Measurements of the mRNA expression were selected as the means to determine the identification of expression of MMP-1, -8, and -13. In the TMC group, the expression of collagen type I was greater than that of the TM group from day 4 to day 14. Expression of TIMP-1 in the TM group was greater than that of the TMC group in the pressure side of PDL and alveolar bone cell at day 4. In the TMC group, TIMP-1 was expressed at the osteoclast, but not at the tooth surface of the TM group at day 14, Maximum induction of the mRNA of MMP-1 was observed on day 4 in the TMC group, but it was observed on day 7 in the TM group. MMP-8 mRNA of the TMC group was twice greater than that of the TM group at f days. In the TMC group, maximum induction of MMP-13 mRNA was observed on day 1. Conclusions: These findings suggested that cortical punching can stimulate remodeling of PDL and alveolar bone connective tissues during experimental orthodontic tooth movement in rats.

• Clinical and Experimental Pediatrics
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• v.46 no.6
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• pp.606-609
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• 2003

Goltz syndrome(focal dermal hypoplasia) is a rare disorder characterized by ectodermal and mesodermal dysplasia described in 1962 by Goltz. In Korea, one case of Goltz syndrome was reported in 1994. The inheritance mode is mostly X-linked dominant. Skin abnormality is the most common manifestation including hypoplasia of the dermis. Skeletal involvement such as syndactyly, polydactyly, scoliosis, kyphosis and spina bifida occulta may be present, also ocular and dental abnormalities are reported. Radiologic findings are the osteopathy and striation of the long bone. We experienced a case of Goltz syndrome in a 9-year old female who was presented with right side hypotrophy, focal dermal hypoplasia, ocular(anidria, microcornea), dental(oligodontia, amelogenesis) and skeletal(syndactyly) abnormalities. Skin biopsy was performed and showed decreased expression of type I collagen gene with Northern blotting.

• Polymer(Korea)
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• v.29 no.5
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• pp.501-507
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• 2005

Small intestinal submucosa (SIS) had been widely used as a biomaterial without immune rejection responses. SIS sponges prepared by crosslinking with 1-ethyl-3-(3-dimethylaminopropyl) carbodiimide hydrochloride (EDC). SIS powders dissolved in $3\%(v/v)$ acetic acid aqueous solution for 48hrs and freeze-dried. EDC solution ($H_2O$ : ethanol = 5 : 95) as a crosslink agent was used in concentration of 100mM. In vitro, rat-BMSCs seeded in SIS sponges and induced the osteogenesis for 28 days. We have characterized the osteogenic potential of rat-BMSCs in SIS sponges by alkaline phosphatase activity(ALP), n assay, SEM and RT-PCR for osteogenic phenotype. In SEM, all morphology of SIS sponges was regular and showed interconnected pore structure. By RT-PCR analysis, we observed type I collagen expression. These results demonstrate osteogenic differentiation of rat-BMSCs. In conclusion, we confirmed that the morphology of surface, cross-section, and side of SIS sponges were highly porous with good interconnections between each pores, which can support the surface of cell growth, proliferation, and differentiation. This result indicates that SIS sponge is useful for osteogenesis of BMSCs.

• The korean journal of orthodontics
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• v.33 no.6 s.101
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• pp.485-497
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• 2003

The form and function of the craniofacial structure critically depend on genetic information. With recent advances in the molecular technology, genes that are important for normal growth and morphogenesis of the craniofacial skeleton are being rapidly uncovered, shaping up modem craniofacial biology. One of them is fibroblast growth factor receptor 2 (FGFR2). Specific point mutations in the. FGFR2 gene have been linked to Apert syndrome, which is characterized by premature closure of cranial sutures and craniofacial anomalies as well as limb deformities. To study pathogenic mechanisms underlying craniosynostosis phenotype of Apert syndrome, we used a transgenic approach; an FGFR2 minigene construct containing an Apert mutation (a point mutation that substitute proline at the position 253 to arginine; P253R) was introduced into fertilized mouse germ cells by DNA microinjection. The injected cells were then allowed to develop into transgenic mice. We used a bone-specific promoter (a DNA fragment from the type I collagen gene) to confine the expression of mutant FGFR2 gene to the bone tissue, and asked whether expression of mutant FGFR2 in bone is sufficient to cause the craniosynostosis phenotype in mice. Initial characterization of these mice shows prematurely closed cranial sutures with facial deformities expected from Apert patients. We also demonstrate that the transgene produces mutant FGFR2 protein with increased functional activities. Having this useful mouse model, we now can ask questions regarding the role of FGFR2 in normal and abnormal development of cranial bones and sutures.