Synergistic Effect of Parathyroid Hormone and Growth Hormone on Trabecular and Cortical Bone Formation in Hypophysectomized Rats

2010 ◽  
Vol 73 (4) ◽  
pp. 248-257 ◽  
Author(s):  
Maria Sarah N. Guevarra ◽  
James K. Yeh ◽  
Mariano Castro Magana ◽  
John F. Aloia
1992 ◽  
Vol 18 (1) ◽  
pp. 19-30 ◽  
Author(s):  
P. M. Schiltz ◽  
S. Mohan ◽  
T. Ohta ◽  
D. Glass ◽  
D. J. Baylink

1999 ◽  
Vol 14 (3) ◽  
pp. 439-448 ◽  
Author(s):  
Yanfei Ma ◽  
Webster S. S. Jee ◽  
Zhongzhi Yuan ◽  
Wei Wei ◽  
Hongka Chen ◽  
...  

1996 ◽  
Vol 270 (1) ◽  
pp. E51-E59 ◽  
Author(s):  
D. A. Martinez ◽  
M. W. Orth ◽  
K. E. Carr ◽  
R. Vanderby ◽  
A. C. Vailas

The growth hormone (GH)-deficient dwarf rat was used to investigate recombinant human (rh) GH-induced bone formation and to determine whether rhGH facilitates simultaneous increases in bone formation and bone maturation during rapid growth. Twenty dwarf rats, 37 days of age, were randomly assigned to dwarf plus rhGH (GH; n = 10) and dwarf plus vehicle (n = 10) groups. The GH group received 1.25 mg rhGH/kg body wt two times daily for 14 days. Biochemical, morphological, and X-ray diffraction measurements were performed on the femur middiaphysis. rhGH stimulated new bone growth in the GH group, as demonstrated by significant increases (P < 0.05) in longitudinal bone length (6%), middiaphyseal cross-sectional area (20%), and the amount of newly accreted bone collagen (28%) in the total pool of middiaphyseal bone collagen. Cortical bone density, mean hydroxyapatite crystal size, and the calcium and collagen contents (microgram/mm3) were significantly smaller in the GH group (P < 0.05). Our findings suggest that the processes regulating new collagen accretion, bone collagen maturation, and mean hydroxyapatite crystal size may be independently regulated during rapid growth.


2018 ◽  
Author(s):  
Christina Vrahnas ◽  
Pascal R Buenzli ◽  
Thomas A Pearson ◽  
Brenda L Pennypacker ◽  
Mark J Tobin ◽  
...  

AbstractAlthough cortical bone strength depends on optimal bone composition, the influences of standard therapeutic agents for osteoporosis on bone mineral accrual in cortical bone are not understood. This study compared effects on cortical bone composition of two current therapeutic approaches for osteoporosis: the anti-resorptive bisphosphonate alendronate (ALN), and anabolic intermittent parathyroid hormone (PTH). The experimental anti-resorptive cathepsin K inhibitor, odanacatib (ODN) which inhibits resorption without inhibiting bone formation, was also tested.To determine effects of these agents on Haversian remodeling and mineral accrual, we compared ALN (100μg/kg/2xweek), PTH(1-34) (15μg/kg, 5x/week) and ODN (7.5μM/day) administered for 10 months commencing 6 months after ovariectomy (OVX) in skeletally mature rabbits by histomorphometry. We used synchrotron-based Fourier-transform infrared microspectroscopy (sFTIRM), coupled to fluorochrome labelling, to measure maturation of the cortical matrix in situ at both endocortical and intracortical sites of bone formation.PTH and ODN, but not ALN, treatment increased bone toughness, and PTH treatment stimulated bone formation, not only on endocortical and periosteal bone, but also in intracortical pores. In Sham and OVX rabbits, normal matrix maturation was observed at both endocortical and intracortical sites including: mineral accrual (increasing mineral:matrix), carbonate substitution (carbonate:mineral) and collagen molecular compaction (amide I:II) in situ in endocortical and intracortical bone. ALN treatment reduced bone formation on these surfaces. In ALN-treated bone, while intracortical bone matured normally, endocortical bone did not show a significant increase in mineral:matrix. ODN treatment resulted in slower mineral accrual and limited carbonate substitution. While PTH-treatment did not modify matrix maturation in endocortical bone, the initial stages of mineral accrual were slower in intracortical bone.In conclusion, these three classes of therapy have differing effects on both bone formation, and the process of bone matrix maturation. ALN suppresses bone formation, and the normal process of matrix maturation in endocortical bone. ODN does not suppress bone formation, but limits mineral accrual. PTH stimulates bone formation, and the matrix formed matures normally in endocortical bone. The ability of PTH treatment to stimulate bone formation in intracortical bone may provide a novel additional mechanism by which PTH increases bone strength.


Bone ◽  
1999 ◽  
Vol 24 (5) ◽  
pp. 491-497 ◽  
Author(s):  
G Prakasam ◽  
J.K Yeh ◽  
M.-M Chen ◽  
M Castro-Magana ◽  
C.T Liang ◽  
...  

2009 ◽  
Vol 10 (7) ◽  
pp. 1057-1067 ◽  
Author(s):  
Troels T. Andreassen ◽  
Peter H. Jørgensen ◽  
Hans Oxlund ◽  
Allan Flyvbjerg ◽  
Hans Ørskov

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