This Article
Right arrow Full Text (PDF)
Right arrow Letters to the Editor: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when Letters to the Editor are posted
Right arrow Alert me if a correction is posted
Services
Right arrow E-mail this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My File Cabinet
Right arrow Download to citation manager
Right arrowReprints and Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Breur, G. J.
Right arrow Articles by Wilsman, N. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Breur, G. J.
Right arrow Articles by Wilsman, N. J.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us   Add to Technorati  
What's this?

The Journal of Bone and Joint Surgery, Vol 74, Issue 4 516-528, Copyright © 1992 by Journal of Bone and Joint Surgery, Inc


JOURNAL CONTENTS

Cellular basis of decreased rate of longitudinal growth of bone in pseudoachondroplastic dogs

GJ Breur, CE Farnum, GA Padgett and NJ Wilsman
Department of Comparative Biosciences, School of Veterinary Medicine, University of Wisconsin, Madison.

Regulation of growth of long bones occurs in cartilage growth plates, where proliferation of chondrocytes, matrix synthesis, and an increase in vertical height in the direction of growth all contribute to the final length of a bone. In this study, we tested the hypothesis that an increase in chondrocytic vertical height is a major variable that accounts for the decreased rate of growth of long bones in Scottish deerhound dogs that had pseudoachondroplasia. The diagnosis of pseudoachondroplasia is based, primarily, on the demonstration of alternating electron-dense and electron-lucent lamellae with a periodicity of 100 to 150 nanometers in dilated rough endoplasmic reticulum. These ultrastructural changes are similar to those seen in humans who have pseudoachondroplasia. In Scottish deerhounds that have the disease, growth of bone is approximately 65 per cent of that in normal animals. There were striking differences in the diameters of proliferating and hypertrophic chondrocytes in pseudoachondroplastic animals compared with normal animals. Specifically, the horizontal diameter of proliferating chondrocytes was 22.7 micrometers in normal animals and 11.3 micrometers in pseudoachondroplastic animals. The vertical diameter of proliferating chondrocytes was 4.8 and 7.6 micrometers in normal and pseudoachondroplastic animals. In the distal 100 micrometers of the hypertrophic zone, the mean horizontal diameter of hypertrophic chondrocytes was 29.6 and 19.1 micrometers and the mean vertical diameter was 22.8 and 18.6 micrometers in normal and pseudoachondroplastic animals. All these differences were statistically significant. The changes in vertical height resulted in a significant difference in the incremental difference in vertical height between chondrocytes from the proliferative and hypertrophic zones in normal animals (18.0 micrometers per chondrocyte) and pseudoachondroplastic animals (11.0 micrometers per chondrocyte). Each chondrocyte in the abnormal plates achieved only 61 per cent of the incremental difference of chondrocytes in normal plates. The mean cellular volume of chondrocytes in the hypertrophic zone was 13,050 cubic micrometers in the normal animals and 10,740 cubic micrometers in the pseudoachondroplastic animals. This difference was not statistically significant. These results are discussed in relation to current theories of the role of the shape and change in volume of chondrocytes in the regulation of longitudinal growth of bone.(ABSTRACT TRUNCATED AT 400 WORDS)
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Technorati Technorati    What's this?


This article has been cited by other articles:


Home page
J. Biol. Chem.Home page
M. Schmitz, A. Becker, A. Schmitz, C. Weirich, M. Paulsson, F. Zaucke, and R. Dinser
Disruption of Extracellular Matrix Structure May Cause Pseudoachondroplasia Phenotypes in the Absence of Impaired Cartilage Oligomeric Matrix Protein Secretion
J. Biol. Chem., October 27, 2006; 281(43): 32587 - 32595.
[Abstract] [Full Text] [PDF]


Home page
J. Am. Soc. Nephrol.Home page
E. CARBAJO, J. M. LÓPEZ, F. SANTOS, F. A. ORDÓÑEZ, P. NIÑO, and J. RODRÍGUEZ
Histologic and Dynamic Changes Induced by Chronic Metabolic Acidosis in the Rat Growth Plate
J. Am. Soc. Nephrol., June 1, 2001; 12(6): 1228 - 1234.
[Abstract] [Full Text]


Home page
J. Am. Soc. Nephrol.Home page
A. COBO, J. LÓPEZ, E. CARBAJO, F. SANTOS, J. ALVAREZ, M. FERNÁNDEZ, and A. WERUAGA
Growth Plate Cartilage Formation and Resorption Are Differentially Depressed in Growth Retarded Uremic Rats
J. Am. Soc. Nephrol., May 1, 1999; 10(5): 971 - 979.
[Abstract] [Full Text]