Document Detail


Accelerated bone formation and increased osteoblast number contribute to the abnormal tooth germ development in parathyroid hormone-related protein knockout mice.
MedLine Citation:
PMID:  15542035     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Our previous study showed that tooth germs at late embryonic stage [later than embryonic day 17.5 (E17.5)] and neonatal homozygous parathyroid hormone-related protein (PTHrP)-knockout mice are compressed or penetrated by the surrounding alveolar bone tissue. In vivo and in vitro studies have shown that the development of the tooth germ proper is not disturbed, but insufficient alveolar bone resorption, due to the decreased number and hypofunction of osteoclasts, is the main cause of this abnormality. In addition to the insufficient alveolar bone resorption, progressive bone formation toward tooth germs was observed in homozygous mice, suggesting that accelerated bone formation also contributes to this abnormality. To further investigate this, homozygous mice at E14.0 and E15.5, when alveolar bone is forming, were used for histochemical and bone histomorphometric analyses. In contrast to the late embryonic stage, the alveolar bone did not yet compress developing tooth germs in homozygous mice on E14.0, but a larger amount of bone tissue was seen compared to wild-type littermates. Histomorphometric analysis of bone at E14.0 revealed that the osteoblast numbers and surfaces in the mandibles and in the bone collar of femora of homozygous mice were significantly higher than those of wild-type mice. However, unlike our previous study showing the osteoclast surface on E18.5 in homozygous mice to be significantly lower than that of wild-type mice, this study at E14.0 showed no significant difference between the two genotypes. To evaluate the amount of calcification around tooth germs, 3D images of mandibles were reconstructed from the calcein-labeled sections of the wild-type and mutant mice. Labeling was performed at E14.0, and the mice were sacrificed 1 h after the calcein injection to minimize the effect of bone resorption. Comparison of the 3D images revealed that the labeled surface was larger around developing tooth germs in homozygous mouse than in wild-type mouse. On day E15.5, osteoblasts approached the enamel organ of homozygous mice but this was not observed in wild-type mice. In this study, we report a systemic increase in osteoblast number and accelerated bone formation in homozygous PTHrP-knockout mice, both of which contribute to the abnormal tooth development.
Authors:
Y Kitahara; N Suda; T Terashima; O Baba; K Mekaapiruk; V E Hammond; Y Takano; K Ohyama
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Bone     Volume:  35     ISSN:  8756-3282     ISO Abbreviation:  Bone     Publication Date:  2004 Nov 
Date Detail:
Created Date:  2004-11-15     Completed Date:  2005-09-06     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8504048     Medline TA:  Bone     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1100-6     Citation Subset:  IM    
Affiliation:
Maxillofacial Orthognathics, Department of Maxillofacial Reconstruction and Function, Division of Maxillofacial/Neck Reconstruction, Graduate School, Tokyo Medical and Dental University, Tokyo 113-8549, Japan. y-kitahara.mort@tmd.ac.jp
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MeSH Terms
Descriptor/Qualifier:
Acid Phosphatase / metabolism
Alkaline Phosphatase / metabolism
Animals
Calcinosis / enzymology,  metabolism,  pathology
Chondrocytes / pathology
Femur / chemistry,  enzymology,  pathology
Histocytochemistry
Isoenzymes / metabolism
Mandible / chemistry,  enzymology,  pathology
Mice
Mice, Inbred C57BL
Mice, Knockout
Osteoblasts / chemistry,  enzymology,  pathology*
Osteoclasts / enzymology
Osteogenesis / genetics*
Parathyroid Hormone-Related Protein / genetics*,  metabolism
Tooth Germ / chemistry,  embryology,  pathology*
Chemical
Reg. No./Substance:
0/Isoenzymes; 0/Parathyroid Hormone-Related Protein; EC 3.1.3.-/tartrate-resistant acid phosphatase; EC 3.1.3.1/Alkaline Phosphatase; EC 3.1.3.2/Acid Phosphatase

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