• Journal of Life Science
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• v.10 no.4
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• pp.408-421
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• 2000

We tried to establish the culture method of the chondrocyte isolated from the epiphyseal cartilage and to investigate morphological changes of chondrocyte cultured with enzyme-digested costal cartilage, the perichondrium and experimentally damaged meniscus of rabbit. De novo chondrocyte pellets were prepared from epiphyseal plates by culturing isolated epiphyseal chondrocytes from 4 week. old rabbits. We morphologically assessed the cartilage formation of the chondrocyte culture with enzyme-digested costal carilage, the perichondrial culture, the cultured chondrocytes transplants into experimentally damaged meniscus of rabbits, the perichondrial culture, the cultured chondrocytes transplants into experimentally damaged meniscus of rabbit. In the 24 days, the epiphyseal chondrocytes maintained the typical phenotypes of the partial nodular cell formation. The 30 days cryopreserved chondrocytes showed abnormal and irregular shape. In the type II collagen added culture, the chondrocytes showed expanded rough endoplasmic reticulum and small and large round-like vesicles of processes. In the type IV collagen added culture, the chondrocytes showed large perinuclear vaculoes and abundant well-developed rough endoplasmic reticulum of processes. In the culture with enzyme- digested costal cartilage and the perichondrial culture, the chondrocytes showed a few swelling rough endoplasmic reticulum and vacuoles. The cultured epiphyseal chondrocytes maintained typical phenotype and the chondrocytes were grown faster and maintained more typical phenotype in the type II and IV collagen added culture. The transformed chondrocytes secreted abundant extracellular matrix in the type II collagen added culture, and showed processes in the type IV collagen added culture. The perichondrial chondrocytes were grown faster and their implants were able to transplant. The cultured chondrocytes transplanted into experimentally damaged meniscus were adapted between the meniscus tissues. And the immunocyto-chemical reaction of the type II collagen of the chondrocytes were found to be maintained. The chondrocytes cultured cartilage. The chondrocytes secreted abundantly. The cultured chondrocytes transplanted into experimentally damaged meniscus changed immature cells into enlarged mature cells with extracellular secretion.

• Applied Microscopy
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• v.26 no.2
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• pp.197-206
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• 1996

cis-Dichlorodiammineplatinum (II) (cis-Platin) inhibits the proliferation and growth of the tumor cells by way of inhibiting DNA and protein synthesis of the cancer cells. Although cis-Platin is very effective antitumor drug, it also produces many other side effects. Thus the author has studied the effects of cis-Platin on the proximal epiphyseal plate in the tibia of the rat. The results were as follows: In the chondrocyte of the proliferative zone, sacculated, and fragmented cisternae of rough endoplasmic reticulum, some mitochondria with disorganized mitochondrial cristae and distorted procollagens were observed, and in the matrix some large matrix granules and dispersed collagen fibrils were revealed on the 1st, 3rd day and 1st week group of cis-Platin treated rats. In the chondrocyte of the proliferative zone of cis-Platin treated rats on the 2nd and 3rd week group, parallely arranged rough endoplasmic reticulum and many procollagens were shown, and in the matrix a number of large matrix granules and many small matrical granules as well as collagen fibrils were revealed. Consequently it is suggested that though cis-Platin induces the degenerative changes of the chondrocyte resulting in components of the cartilagenous matrix, these toxic effects are regressed with time.

• Molecules and Cells
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• v.43 no.8
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• pp.739-748
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• 2020

Stringent regulation of the chondrocyte cell cycle is required for endochondral bone formation. During the longitudinal growth of long bones, mesenchymal stem cells condense and differentiate into chondrocytes. Epiphyseal chondrocytes sequentially differentiate to form growth-plate cartilage, which is subsequently replaced with bone. Although the importance of nuclear factor 1C (Nfic) in hard tissue formation has been extensively studied, knowledge regarding its biological roles and molecular mechanisms in this process remains insufficient. Herein, we demonstrated that Nfic deficiency affects femoral growth-plate formation. Chondrocyte proliferation was downregulated and the number of apoptotic cell was increased in the growth plates of Nfic^-/- mice. Further, the expression of the cell cycle inhibitor p21 was upregulated in the primary chondrocytes of Nfic^-/- mice, whereas that of cyclin D1 was downregulated. Our findings suggest that Nfic may contribute to postnatal chondrocyte proliferation by inhibiting p21 expression and by increasing the stability of cyclin D1 protein.

• Maxillofacial Plastic and Reconstructive Surgery
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• v.18 no.3
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• pp.411-427
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• 1996

The purpose of this study was to observe the healing process and the distribution of fibronectin in injured condylar cartilage and bone by using LM and SEM. In order to perform this study, 40 male rat, weighing about 250g were selected. Under general anesthesia with Pentobarbital sodium, condylar cartilage and neck bone were resected. Then, the wound was irrigated with saline and closed with 5-0 chromic catgut and 4-0 silk by layer-to-layer suturing. The experimental rats were sacrificed by perfusion with 3% paraformaldehyde at 1st and 4th week after operation. The condylar process and surrounding tissues were cut, demineralized, dehydrated and embedded in paraffin. The histological observation of the specimens in LM level was performed after H-E stain and Azan stain. For localization of fibronectin, immunostaining was achieved by the avidin-biotin complex method. To study the change on condylar surface, the specimens were dehydrated, dried, gold coated and were observed with a scanning electron microscope(Hitachi S-2300). The results were as follows ; 1. The cartilage group and the bone group were repaired with epiphyseal cartilage layer on the cut surface as the normal control group. 2. The cut surface was repaired more quickly in the cartilage group than in the bone group. 3. Chondrocytes, diferentiated during healing, were stained strongly to anti-fibronectin, and fibronectin was supposed to participatein chondrocyte differentiation and cartilagenous matrix formation. 4. Fibronectin was distributed more in the new bone than in the old bone, and the osteoblasts surrounding it were also stained strongly. Fibronectin was supposed to participate in new bone matrix formation. 5. Fibronectin is supposed to be associated with the differentiation, migration and adhesion of chondrocyte and osteoblast and to participate in endochondral bone formation.

• The Korean Journal of Oral and Maxillofacial Pathology
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• v.42 no.5
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• pp.145-152
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• 2018

A 57 years old female complained of severe pain on the right temporomandibular joint (TMJ) area. Her right condyle had been partly resected under surgical operation 13 years ago due to condyle hypertrophy, thereafter she felt dull pain on TMJ area and recently the lesion became severely swelled and painful leading to cancer phobia. The present radiological views showed slightly enlarged and sclerosed condyle with increased radiopacity, but its articular sliding function was almost disable during mouth opening. The patient's TMJ lesion was carefully managed with conservative physiotherapy and pain treatment. The microsection of condyle head obtained from the previous operation was re-evaluated histologically, and it was finally diagnosed as osteochondrosis dissecans (OCD), exhibiting hyperplastic proliferation of cartilage in condyle head and marked vascular dilatation in epiphyseal zone. This abnormal cartilage tissue was distinguishable from normal cartilage tissue found in the peripheral cartilaginous cap of the same microsection. The involved cartilage cap showed thick hypertrophic chondrocyte zone with horizontal and vertical clefts accompanying diffuse hyaline degeneration. The superficial fibrous zone of cartilage cap was thickened and frequently peeled off, while lower hypertrophic zone of cartilage cap was highly cellular and proliferative. Consequently, the endochondral ossification became aberrant and resulted pre-mature apoptosis of many hypertrophic chondrocytes, followed by diffuse and mild inflammatory reaction in the underlying marrow tissue. Therefore, it was suggested that this hypertrophic condyle lesion, OCD, be differentiated depending on radiological and histological features from ordinary condyle hyperplasia, osteochondroma, and osteoarthritis, and that the pathological confirmation of OCD may provide a reliable modality for dental and medical treatment of chronic and painful TMJ lesion.

• Applied Microscopy
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• v.27 no.3
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• pp.225-234
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• 1997

Vincristine, a kind of anticancerous drugs, interferes with development of microtubles and synthesis of nucleic acid and proteins in cells, and destructs cytoplasmic membrane so that mitosis of cancer cells is inhibited. Unfortunately these anticancerous effects by vioneristime are not limited to specific cancer cells, so several side effects are produced. This study was performed to explore the effects of vincristine on the fine structure of cytoplasmic organelles and cartilagenous matrix in proximal epiphyseal plate of the tibia in rat. The results were as follows: 1. Cisternae of rough endoplasmic reticulum (RER) were fragmented and sacculated, and membrane-bound ribocomes of RER were detached at 3 and 6 hours after vincristine treatment. Severely dilated, fagmented and sacculated cisternae of RER were found at 12 hours after vincristine treatment, and at 24 hours after vincristine treatment a few cisternae were framented and sacculated. At 72 hours after vincristine treatment cisternae of RER were parallely well arraged. 2. Golgi complex was atrophied at 3, 6, and 12 hours after vincristine treatment, while at 72 hours after vincristine treatment the cisternae of Golgi complex were made of 5-6 layers. 3. Mitochondria with disorganized mitochondrial cristae and outer membrane-losed mitochondria were found at 3 hours after vincristine treatment. At 6 and 12 hours after vincristine treatment mitochondria had possessed disorganized cristae, and a few mitochondria with disorganized cristae were. observed at 24 hours after vincristine treatment. While at 72 hours after vincristine treatment mitochondria were shown distinct cristae and double membranes. 4. Phagosome were begun to observe at 3 hourse after vincristine treatment, and at 24 hourse after vincristine treatment many phagosomes were found, while at 72 hours after vincristine treatment a few phagosomes were observed. 5. In the cartilagenous matrix large-sized matrix granules were decreased and collagen fibrils were dispersed at 3, 6, and 12 hours after vincristine treatment, while at 72 hours after vincristine treatment many large-sized matrix granules and numerous matrix it is suggested that although vincristine may induce the degenerative changes of the chondrocyte, resulting in changes of components of the cartilagenous matirx, these toxic effects may be regressed with time.

• The Journal of Korean Medicine
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• v.33 no.2
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• pp.1-10
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• 2012

Objectives: This study was aimed to investigate the effect of Bojungikgitang-gagambang (BJIG) on longitudinal bone growth in rats. Methods: The BJIG treated group (300 mg/kg) and the control group (vehicle) were administered orally twice daily for 4 days. To investigate the effects of BJIG we measured body weight gain. The bone growth effect was analyzed by measuring between fluorescent lines marked with tetracycline, which plays the role of fluorescent dye on the surface of the tibia. Tetracycline was intraperitoneally injected. The height of growth plates in the epiphyseal plate was measured. The expression of bone morphogenetic protein-2 (BMP-2) and insuline-like growth factor-1 (IGF-1) was investigated by immunohistochemistry. Results: BJIG caused a significant acceleration of longitudinal bone growth of $349.7{\pm}15.9{\mu}m/day$ compared to control ($319.8{\pm}21.4{\mu}m/day$). The height of overall growth plate was not significantly more compared to the control, but the size of cells in the proliferative zone and hypertrophic zone were. In the immunohistochemistry, BMP-2 and IGF-1 were expressed markedly in the proliferative or hypertrophic zone, respectively. Conclusions: BJIG stimulated the chondrocyte hypertrophy and chondrogenesis in the growth plate and directly increased the longitudinal tibia length of rats.