• The korean journal of orthodontics
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• v.33 no.5 s.100
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• pp.391-398
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• 2003

Distraction osteogenesis is a well-estabilished procedure of membraneous bone formation and has been used to correct craniofacial deformities in dentofacial orthopedic-surgery area for decades. In this articale, distraction osteogenesis is used for treatment of facial asymmetry. The patient underwent procedures to lengthen the mandibular ramus and body. After distraction, orthodontic treatment was done for ooclusal settling.

• Journal of the korean academy of Pediatric Dentistry
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• v.26 no.4
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• pp.652-663
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• 1999

Craniosynostosis, the premature fusion of cranial sutures, presumably involves disturbance of the interactions between different tissues within the cranial sutures. Interestingly, point mutaions in the genes encoding for the fibroblast growth factor receptors(FGFRs), especially FGFR2, cause various types of human craniosynostosis syndromes. To elucidate the function of these genes in the early morphogenesis of mouse cranial sutures, we first analyzed by in situ hybridization the expression of FGFR2(BEK) and osteopontin, an early marker of osteogenic differentiation, in the sagittal suture of calvaria during embryonic(E15-E18) and postnatal stage(P1-P3). FGFR2(BEK) was intensely expressed in the osteogenic fronts, whose cells undergo differentiation into osteoprogenitor cells that ultimately lay down the bone matrix. Osteopontin was expressed throughout the parietal bones excluding the osteogenic fronts, the periphery of the parietal bones. To further examine the role of FGF-mediated FGFR signaling in cranial suture, we did in vitro experiments in E15.5 mouse calvarial explants. Interestingly, implantation of FGF2 soaked beads onto both the osteogenic fronts and mid-mesenchyme of sagittal suture after 36 hours organ culture resulted in the increase of the tissue thickness and cell number around FGF2 beads, moreover FGF4-soaked beads implanted onto the osteogenic fronts stimulated suture closure due to an accelerated bone growth, compared to FGF4 beads placed onto mid-mesenchyme of sagittal suture and BSA control beads. In addition FGF2 induced the ectopic expression of osteopontin and Msx1 genes. Taken together, these data indicate that FGF-mediated FGFR signaling has a important role in regulating the cranial bone growth and maintenance of cranial suture, and suggest that FGF-mediated FGFR signaling is involved in regulating the balance between the cell proliferation and differentiation through inducing the expression of osteopontin and Msx1 genes.

• Applied Microscopy
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• v.31 no.3
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• pp.287-305
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• 2001

To investigate a role of cartilage canals in osteogenesis and growth of the vertebrae, in human fetuses ranging from 50 mm to 260 mm crown rump length were studied by electron microscopy. The initial appearance of cartilage canals of the vertebral body was observed at 60 mm fetus. In 80 mm fetus, primary ossification center in the vertebral body was first noted. The vertebral body showed calcified chondrocytes surrounded by a tone of hypertrophied chondrocytes and deep canals which terminated in calcified matrix. Most hypertrophied chondrocytes in the centrum showed in various stage of degeneration in disorderly arrangement. At the blind end of deep canal, osteogenic cells, osteoblasts and chondroclasts were observed. Resorption of unmineralized cartilage septa was undertaken by perivascular cells within cartilage canals. The ruffled border of the chondroclast was restricted to resorption site of calcified cartilagenous matrix. The periosteal bone formation was followed by the appearance of primary center of the centrum at 120 mm fetus. The osteoblasts of the perichondrium started to lay down a thin membranous bony lamella on the outer surface of the osseous trabeculae of the centrum. The processes of bone formation in the vertebral bodies were found to possess morphological similarities to that occurring at secondary center of the epiphysis of a long bone. These results indicate that the connective tissue cells within the cartilage canals proliferate and differentiate into osteoblasts at the site of endochondral ossification of the vertebrae.

• The korean journal of orthodontics
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• v.26 no.2 s.55
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• pp.187-196
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• 1996

Underlying malocclusions and dentofacial deformities are often related to variations in the craniofacial development. Type I and type II collagens are considered the major collagens of bone and cartilage respectively. Monitoring the patterns of those protein expressions during development will Provide a basis for the understanding of normal and abnormal growths. This study was undertaken to investigate the morphogenetic changes and the expression patterns of type I and II collagen proteins involved in the developing mandible of human embryos and fetuses. 50 embryos and fetuses were studied with Hematoxylin and Eosin, Alcian, blue-PAS, Masson Trichrome, md Immunohistochemical stains. The results were as follows : 1. A 13.5 mm embryo showed the stomatodeum with dental lamina, maxillary and mandibular processes. Meckel's cartilage appeared in the mandibular arch of a 20.5 mm embryo. New bone formation was bilaterally initiated at the outer side of middle portion of Meckel's cartilage of 22-38 mm embryos. 2. Meckel'cartilage was resorbed at the 15th week fetus. The endochondral ossification was observed where there was direct replacement of cartilage by bone. Meckel'cartilage disappeared and membraneous ossification were observed at the 25th week. 3. Before the appearance of Meckel's cartilage, the expression of type I collagen was moderate at the odontogenic epithelium of maxillary & mandibular process, but mild for the expression of type II collagen. 4. During the appearance of Meckel's cartilage and new bone formation, the immunoactivity of type II collagen was more expressed than type I collagen at the Meckel's cartilage and new bone. 5. During intrarmembranous bone formation, the expression of type II collagen was rare in the bony trabeculae. There was a switch for the expression of collagens from type II to type I during the appearance of Meckel's cartilage.

• The Journal of Korean Academy of Prosthodontics
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• v.8 no.1
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• pp.48-55
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• 1968

1958년(年) Fullmer와 $Lillie^9$에 의(依)하여 최초(最初)로 보고(報告)된 Oxytalan 섬유(纖維)는 산(酸)에 내성(耐性)이 강(强)한 섬유(纖維)로 치근막(齒根膜)에 많이 출현(出現)하고 기계적(機械的) 자극(刺戟)에 의(依)하여 배열(配列), 주행(走行) 및 수적(數的)인 변화(變化)를 가져온다. 저자(著者)는 교정력(矯正力)을 이용(利用)하여 치아(齒牙)를 이동(移動) 시킨후(後) 치근막내(齒根膜內) Oxytalan섬유(纖維)의 수(數), 주행(走行) 및 형태(形態)의 변화(變化)를 실험적(實驗的)으로 관찰(觀察)한바 있어 이를 보고(報告)하는 바이다. 본연구(本硏究)에 사용(使用)된 실험동물(實驗動物)로는 체중(體重) 60gram내외(內外)의 자성백서(雌性白鼠) 15마리를 택(澤)하였다. 각동물(各動物)은 Ether마취후(麻醉後) 교정용(矯正用) 고무줄편(片)을 상악우측(上顎右側) 제1구치(第一臼齒)와 제2구치(第二臼齒) 사이에 삽입(揷入)하여 24, 48, 72시간(時間) 간격(間隔)으로 관찰(觀察)하였다. 동물(動物)을 도살후(屠殺後) 상악골(上顎骨)을 적출(摘出)하여 10%중성(中性) 호루마린에 고정후(固定後) 3%의산(蟻酸)으로 탈회(脫灰)하였다. 파라핀 포매후(包埋後) 근원심적(近遠心的)으로 $4{\sim}6{\mu}$의 절편(切片)을 만들어 Hematoxylin-eosin 및 Aldehyde fuchsin염색(染色)을 시행(施行)하여 경험(鏡險)한 결과(結果)는 하기(下記)와 같다. 1. 치아이동후(齒牙移動後) 교원성섬유(膠原性纖維) 및 Oxytalan섬유(纖維)들의 배열(配列)에 있어 뚜렷한 차이(差異)를 보였다. 2. 치아이동후(齒牙移動後) 사주섬유(斜走纖維)는 염박측(壓迫側)에서는 치아장축(齒牙長軸)에 수직(垂直)되게, 견인측(牽引側)에서는 평행(平行)되게 주행(走行)하고 있었다. 3. 48시간군(時間群)에서 세포증식(細胞增殖)이 심(甚)하였다. 4. Oxytalan섬유(纖維)는 치아(齒牙)들에 교정력(矯正力)을 가(加)한후(後) 견인(牽引) 염박(壓迫) 양측(兩側) 공(共)히 수(數)가 증가(增加)하였다. 5. 염박측(壓迫側)에서 Oxytalan섬유(纖維)는 속(束)을 형성(形成)하며 치아장축(齒牙長軸)에 평행(平行)되게 주행(走行)하였다. 6.견인측(牽引側)에서는 하나 또는 두세개의 섬유(纖維)들이 산발적(散發的)으로 치아장축(齒牙長軸)에 평행(平行)되게 하였다. 7. Oxytalan섬유(纖維)의 수(數)는 염박측(壓迫側)에서 보다 견인측(牽引側)에서 더 변화(變化)가 많았다.

• Journal of the korean academy of Pediatric Dentistry
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• v.30 no.4
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• pp.643-653
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• 2003

Fibroblast growth factor (FGF) / FGF receptor (FGFR) mediated signaling is required for skeletogenesis in cluding intramembranous and endochondral ossifications Runx2 ($Cbfa1/Pebp2{\alpha}A/AML3$) is an essential transcription factor for osteoblast differentiation and bone formation. Murine calvaria and mandible are concurrently undergoing both intramembranous bone and cartilage formations in the early developmental stage. However the mechanism by which these cartilage formations are regulated remains unclear. To elucidate the effect of FGF signaling on development of cranial sutural cartilage and Meckel's cartilage and to understand the role of Runx2 in these process, we have done both in vivo and in vitro experiments. Alcian blue staining showed that cartilage formation in sagittal suture begins from embryonic stage 16 (E16), Meckel's cartilage formation in mandible from E12. We analyzed by in situ hybridization the characteristics of cartilage cells that type II collagen, not type X collagen, was expressed in sagittal sutural cartilage and Meckel's cartilage. In addition, Runx2 was not expressed in Meckel's cartilage as well as sagittal sutural cartilage, except specific expression pattern only surrounding both cartilages. FGF signaling pathway was further examined in vitro. Beads soaked in FGF2 placed on the sagittal suture and mandible inhibited both sutural and Meckel's cartilage formations. We next examined whether Runx2 gene lies in FGF siganling pathway during regulation of cartilage formation. Beads soaked in FGF2 on sagittal suture induced Runx2 gene expression. These results suggest that FGF signaling inhibits formations of sagittal sutural and Meckel's cartilages, also propose that FGF siganling is involved in the proliferation and differentiation of chondroblasts through regulating the transcription factor Runx2.