Spatiotemporal Expression of Sclerostin in Odontoblasts during Embryonic Mouse Tooth Morphogenesis

被引:15
作者
Naka, Takahiro [1 ]
Yokose, Satoshi [1 ]
机构
[1] Ohu Univ, Sch Dent, Dept Conservat Dent, Div Restorat Dent, Fukushima 9638611, Japan
关键词
Development; immunohistochemistry; mouse; odontoblasts; SOST/sclerostin; tooth; BONE-FORMATION; DENTAL-PULP; CELL-DIFFERENTIATION; NEURAL CREST; SOST GENE; WNT; INHIBITION; PROTEIN; DEFICIENCY; EPITHELIUM;
D O I
10.1016/j.joen.2010.11.025
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
Introduction: Sclerostin is the product of the SOST gene. Loss-of-function mutations in the SOST gene result in a high bone mass phenotype, thus confirming that sclerostin is a negative regulator of bone mass. SOST knockdown in humans also causes oral and dental malformations. However, the relationship between sclerostin and tooth development is unclear. Methods: Using immunohistochemical techniques, we investigated sclerostin expression during fetal mouse tooth development and adult mouse tooth morphogenesis. Results: Sclerostin was expressed in the secretory odontoblasts located along the ameloblasts of fetal mouse tooth germ and adult incisor. Sclerostin expression was also observed in the fetal and adult osteocytes in the jaw bone. Conclusion: These results suggest that sclerostin, one of the important regulatory factors of differentiated odontoblast function, may usable in vital pulp therapy. (J Endod 2011;37:340-345)
引用
收藏
页码:340 / 345
页数:6
相关论文
共 32 条
[1]   Characterization and gene expression of high conductance calcium-activated potassium channels displaying mechanosensitivity in human odontoblasts [J].
Allard, B ;
Couble, ML ;
Magloire, H ;
Bleicher, F .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (33) :25556-25561
[2]   A generalized skeletal hyperostosis in two siblings caused by a novel mutation in the SOST gene [J].
Balemans, W ;
Cleiren, E ;
Siebers, U ;
Horst, J ;
Van Hul, W .
BONE, 2005, 36 (06) :943-947
[3]   Increased bone density in sclerosteosis is due to the deficiency of a novel secreted protein (SOST) [J].
Balemans, W ;
Ebeling, M ;
Patel, N ;
Van Hul, E ;
Olson, P ;
Dioszegi, M ;
Lacza, C ;
Wuyts, W ;
Van den Ende, J ;
Willems, P ;
Paes-Alves, AF ;
Hill, S ;
Bueno, M ;
Ramos, FJ ;
Tacconi, P ;
Dikkers, FG ;
Stratakis, C ;
Lindpaintner, K ;
Vickery, B ;
Foernzler, D ;
Van Hul, W .
HUMAN MOLECULAR GENETICS, 2001, 10 (05) :537-543
[4]  
Bei M, 1998, DEVELOPMENT, V125, P4325
[5]   SYNDROME OF THE MONTH - SCLEROSTEOSIS [J].
BEIGHTON, P .
JOURNAL OF MEDICAL GENETICS, 1988, 25 (03) :200-203
[6]   SOST/sclerostin, an osteocyte-derived negative regulator of bone formation [J].
Bezooijen, RL ;
ten Dijke, P ;
Papapoulos, SE ;
Löwik, CWGM .
CYTOKINE & GROWTH FACTOR REVIEWS, 2005, 16 (03) :319-327
[7]   Bone dysplasia sclerosteosis results from loss of the SOST gene product, a novel cystine knot-containing protein [J].
Brunkow, ME ;
Gardner, JC ;
Van Ness, J ;
Paeper, BW ;
Kovacevich, BR ;
Proll, S ;
Skonier, JE ;
Zhao, L ;
Sabo, PJ ;
Fu, YH ;
Alisch, RS ;
Gillett, L ;
Colbert, T ;
Tacconi, P ;
Galas, D ;
Hamersma, H ;
Beighton, P ;
Mulligan, JT .
AMERICAN JOURNAL OF HUMAN GENETICS, 2001, 68 (03) :577-589
[8]   Runx2 and dental development [J].
Camilleri, Simon ;
McDonald, Fraser .
EUROPEAN JOURNAL OF ORAL SCIENCES, 2006, 114 (05) :361-373
[9]  
Chai Y, 2000, DEVELOPMENT, V127, P1671
[10]   Bone density ligand, sclerostin, directly interacts with LRP5 but not LRP5G171V to modulate Wnt activity [J].
Ellies, Debra L. ;
Viviano, Beth ;
McCarthy, John ;
Rey, Jean-Philippe ;
Itasaki, Nobue ;
Saunders, Scott ;
Krumlauf, Robb .
JOURNAL OF BONE AND MINERAL RESEARCH, 2006, 21 (11) :1738-1749