The Effects of Vitamin D Deficiency on Histomorphometry and Strength of Rat Vertebrae

Author(s):  
Kathy Chou ◽  
Grace Kim ◽  
Marjolein C. H. van der Meulen

Vitamin D3 is integral to both bone remodeling and calcium homeostasis [1]. With vitamin D deficiency, rickets develops during growth and osteomalacia results in adulthood [2]; in both cases, mineralization is altered and bones are more prone to fracture. Although the degenerative effects of vitamin D deficiency on trabecular architecture have been studied, investigations examining both compromised tissue material properties and mechanical properties in the vertebrae of growing animals are scarce. Therefore, the objective of this study was to investigate cancellous bone architecture and mechanical property changes caused by altered mineralization through vitamin D deficiency in growing rats.

Bone ◽  
2020 ◽  
Vol 136 ◽  
pp. 115322
Author(s):  
Elizabeth L. Lin ◽  
Gary S. Gottesman ◽  
William H. McAlister ◽  
Vinieth N. Bijanki ◽  
Karen E. Mack ◽  
...  

2000 ◽  
Vol 21 (9) ◽  
pp. 296-302
Author(s):  
Terence A. Joiner ◽  
Carol Foster ◽  
Thomas Shope

1975 ◽  
Vol 3 (2) ◽  
pp. 105-110 ◽  
Author(s):  
W. H. Opie ◽  
C. J. B. Muller ◽  
H. Kamfer

1999 ◽  
Vol 20 (4) ◽  
pp. 283-286 ◽  
Author(s):  
S. Uysal ◽  
A.G. Kalayci ◽  
K. Baysal

PEDIATRICS ◽  
1977 ◽  
Vol 60 (5) ◽  
pp. 761-761
Author(s):  
Sara B. Arnaud

Drs. Giangiacomo and Gleason are quite correct in their criticism that the number of patients with vitamin D deficiency rickets is too small for statistical comparison of the concentration of serum 25-hydroxyvitamin D (25-OH-D) in mild, moderate, and severe rickets. For this reason, we did not attempt this type of statistical comparison (Student's t test). The statistical analysis which supports our conclusion is the calculation of the regression between senim 25-OH-D, ng/ml and the stage of the disease, designated by arbitrary numbers 1, 2, and 3 for mild, moderate, and severe.


Neurology ◽  
2020 ◽  
Vol 95 (12) ◽  
pp. e1764-e1765
Author(s):  
Rita Monni ◽  
Francesca Beccaria ◽  
Flavio Boscaini ◽  
Benedetta Frassine ◽  
Giuseppe Capovilla

1980 ◽  
Vol 239 (4) ◽  
pp. G261-G265
Author(s):  
C. F. Cramer ◽  
J. McMillan

Growing rats even when vitamin D deficient became adapted to inorganic phosphorus (Pi) deficiency by increasing absorption and minimizing excretion. Feeding low-Pi diet for 3 wk reduced urinary Pi by 80% (P < 0.001), and urinary 32P by 50% (P < 0.001). Low-Pi regimen increased 32p absorption from a 32P-labeled meal by 50% (P < 0.001), even when the animals were vitamin D deficient or thyroparathyroidectomized. The marked increase in retention of 32P in phosphorus-deficient rats could not be accounted for by decreased endogenous intestinal excretion plus increased kidney reabsorption; increased intestinal absorption played a part. 32P absorption was significantly reduced (P < 0.001) by vitamin D deficiency in rats fed either control diet (.6%) Pi or low-Pi diet (0.03%). Endogenous intestinal or urinary excretion of 32P was unaltered by vitamin D deficiency. The evidence supports the hypothesis that there are two mechanisms for phosphorus adaptation: kidney retention not requiring vitamin D, and inreased intestinal absorption of Pi not requiring parathyroids, thyroids, or vitamin D.


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