scholarly journals Endochondral calcification by hypertrophic chondrocytes in the Meckel's cartilage grafted into the isogenic mouse spleen.

1990 ◽  
Vol 53 (2) ◽  
pp. 187-192 ◽  
Author(s):  
Kiyoto ISHIZEKI ◽  
Naoki FUJIWARA ◽  
Mitsutaka SUGAWARA ◽  
Tokio NAWA
2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Hong Zhang ◽  
Xiaopeng Zhao ◽  
Zhiguang Zhang ◽  
Weiwei Chen ◽  
Xinli Zhang

The purpose of this study is to investigate the spacial expression pattern and functional significance of three key transcription factors related to bone and cartilage formation, namely, Sox9, Runx2, and Osterix in cartilages during the late development of mouse mandible. Immunohistochemical examinations of Sox9, Runx2, and Osterix were conducted in the mandibular cartilages of the 15 neonatal C57BL/6N mice. In secondary cartilages, both Sox9 and Runx2 were weakly expressed in the polymorphic cell zone, strongly expressed in the flattened cell zone and throughout the entire hypertrophic cell zone. Similarly, both transcriptional factors were weakly expressed in the uncalcified Meckel’s cartilage while strongly expressed in the rostral cartilage. Meanwhile, Osterix was at an extremely low level in cells of the flattened cell zone and the upper hypertrophic cell zone in secondary cartilages. Surprisingly, Osterix was intensely expressed in hypertrophic chondrocytes in the center of the uncalcified Meckel’s cartilage while moderately expressed in part of hypertrophic chondrocytes in the rostral process. Consequently, it is suggested that Sox9 is a main and unique positive regulator in the hypertrophic differentiation process of mandibular secondary cartilages, in addition to Runx2. Furthermore, Osterix is likely responsible for phenotypic conversion of Meckel’s chondrocytes during its degeneration.


1995 ◽  
Vol 170 (2) ◽  
pp. 387-396 ◽  
Author(s):  
Kun Sung Chung ◽  
Howard H. Park ◽  
Kang Ting ◽  
Hiroko Takita ◽  
Suneel S. Apte ◽  
...  

2011 ◽  
Vol 218 (5) ◽  
pp. 517-533 ◽  
Author(s):  
Tamaki Yokohama-Tamaki ◽  
Takashi Maeda ◽  
Tetsuya S. Tanaka ◽  
Shunichi Shibata

2020 ◽  
pp. 002203452096011
Author(s):  
M. Farahat ◽  
G.A.S. Kazi ◽  
E.S. Hara ◽  
T. Matsumoto

During orofacial tissue development, the anterior and posterior regions of the Meckel’s cartilage undergo mineralization, while the middle region undergoes degeneration. Despite the interesting and particular phenomena, the mechanisms that regulate the different fates of Meckel’s cartilage, including the effects of biomechanical cues, are still unclear. Therefore, the purpose of this study was to systematically investigate the course of Meckel’s cartilage during embryonic development from a biomechanical perspective. Histomorphological and biomechanical (stiffness) changes in the Meckel’s cartilage were analyzed from embryonic day 12 to postnatal day 0. The results revealed remarkable changes in the morphology and size of chondrocytes, as well as the occurrence of chondrocyte burst in the vicinity of the mineralization site, an often-seen phenomenon preceding endochondral ossification. To understand the effect of biomechanical cues on Meckel’s cartilage fate, a mechanically tuned 3-dimensional hydrogel culture system was used. At the anterior region, a moderately soft environment (10-kPa hydrogel) promoted chondrocyte burst and ossification. On the contrary, at the middle region, a more rigid environment (40-kPa hydrogel) enhanced cartilage degradation by inducing a higher expression of MMP-1 and MMP-13. These results indicate that differences in the biomechanical properties of the surrounding environment are essential factors that distinctly guide the mineralization and degradation of Meckel’s cartilage and would be valuable tools for modulating in vitro cartilage and bone tissue engineering.


Development ◽  
2020 ◽  
Vol 147 (11) ◽  
pp. dev190488 ◽  
Author(s):  
Ceilidh Marchant ◽  
Peter Anderson ◽  
Quenten Schwarz ◽  
Sophie Wiszniak

2012 ◽  
Vol 295 (5) ◽  
pp. 734-741 ◽  
Author(s):  
Rong-Tao Yang ◽  
Chi Zhang ◽  
Yong Liu ◽  
Hai-Hua Zhou ◽  
Zu-Bing Li

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