• Applied Microscopy
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• v.24 no.1
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• pp.59-76
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• 1994

Fine structure of the distal femoral epiphysis of growing mouse was studied by electron microscopy. The first morphological evidence of developing secondary center of ossification in the distal femoral epiphysis was found at newborn mouse. Ossification center was in the form of multiple foci of calcification and its cells were represented by remnant of degenerated cells within large lacunae that were separated by mineralized cartilaginous septa. Endochondral ossification beneath the articular cartilage proceeded in a less orderly manner than metaphyseal endochondral ossification. Columns of hypertrophied chondrocytes were not distinctly parallel to intercellular mineralized septa in all direction. Hypertrophied chondrocytes in the inner zone of the epiphseal center of ossification showed disintegrated. Resorption of mineralized cartilaginous septa was undertaken by perivascular cells and multinucleated chondroclasts. Resorption of the calcified cartilage was restricted to the region of ruffled border of the chondroclast. Growth along the metaphyseal side of the epiphyseal center of ossification was different from that along the articular surface. As the secondary center expanded toward the metaphyseal side, many vascular buds penetrated unmineralized cartilaginous septa and invaded viable chondrocytes. Many hypertrophied chondrocytes bodering the metaphyseal side of bone center remained viable after they became embedded in mineralized cartilaginous septa. This result suggested that the hypertrophied.

• 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.35 no.5 s.112
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• pp.351-360
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• 2005

This study aimed to investigate the effects of indomethacin on distribution and expression of COX-2 and IGF-1 in the mandibular condyle ofi growing dogs and to examine the number of chondroclasts around the mineralization zone indomethacin inhibits prostatlandin $E_2$ production in the tissue by inhibiting synthesis of cyclooxygenase 2. Prostaglandin $E_2$ stimulates insulin-like growth factor synthesis. Insulin-like growth factor stimulates growth of mandibular condylar cartilage. Eight mongrel dogs. aged 13-14 weeks, were divided into 4 groups. Group 1 and group 2 were administered indomethacin 2 mg/Kg/day orally two times a day for 7 days and 14 days respectively. Group 3 were administered indomethacin 8mg/Kg/day orally 2 times a day for 14 days, and 4he control group were administered a placebo. The mandibular condyle heads were sectioned in $5{\mu}m$ thickness The specimens were stained with H-E staining. COX-2 immunohistochemical staining and IGF-1 immunohistochemical staining and examined under microscope. After TRAP staining, the number of chondroclasts were calculated The observed results were as follows: Indomethacin inhibited expression and distribution of COX-2 and IGF-1 on the proliferative zone of condylar cartillage. Indomethacin decreased the number of chondroclastes on the mineralization zone by a time-dependent manner (P<0.05). Indomethacin inhibited expression and distribution of IGF-I by a dose and time-dependent manner. These results show that indomethacin inhibited expression and distribution of COX-2 and IGF-1 on the proliferative zone of condylar cartilage and decreased the number of chondroclasts and suggests that when indomethacin is administered for a long time, condyle growth could be delayed.