Cortical bone growth and maturational changes in dwarf rats induced by recombinant human growth hormone

1996 ◽  
Vol 270 (1) ◽  
pp. E51-E59 ◽  
Author(s):  
D. A. Martinez ◽  
M. W. Orth ◽  
K. E. Carr ◽  
R. Vanderby ◽  
A. C. Vailas
Keyword(s):  
Growth Hormone ◽  
Bone Formation ◽  
Cortical Bone ◽  
Rapid Growth ◽  
Crystal Size ◽  
Bone Growth ◽  
Recombinant Human Growth Hormone ◽  
Bone Collagen ◽  
Bone Maturation ◽  
Hydroxyapatite Crystal

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.

Cortical bone maturation in young hypophysectomized rats

1991 ◽  
Vol 260 (5) ◽  
pp. E690-E694
Author(s):  
D. A. Martinez ◽  
A. C. Vailas ◽  
R. E. Grindeland
Keyword(s):  
Cortical Bone ◽  
Bone Growth ◽  
Bone Collagen ◽  
Control Group ◽  
Cross Link ◽  
Mineral Density ◽  
Bone Maturation ◽  
Collagen Concentration ◽  
Hypophysectomized Rats ◽  
Link Formation

Cortical bone growth and maturation were studied in young growing rats (62 days) that were hypophysectomized. After 10 days, femur bones were obtained for morphological and biochemical analysis of the middiaphysis. Hypophysectomy significantly decreased (42%) normal body growth demonstrated by reductions in body weight. Bone morphology data indicate that hypophysectomy significantly inhibits the circumferential growth of the middiaphysis as well as region-specific thickness compared with the control group. The effects of hypophysectomy on cortical bone mineral composition and density were significantly greater in the hypophysectomized rats. Bone density and total mineral density were significantly greater, 17% and 24%, respectively, in the hypophysectomized group compared with control animals. Bone collagen maturation, measured by the amount of the mature collagen cross-link hydroxylysylpyridinoline, in the hypophysectomized animals was significantly greater (130%). Also, collagen concentration and content per unit volume were significantly greater, 24% and 70%, respectively, in the hypophysectomized group. Our findings suggest that "normal" growth and maturation of cortical bone in rapidly growing animals is dependent upon the modulation of pituitary hormones. These data also suggest that an increased rate of mature collagen cross-link formation may be modified by the turnover rate of collagen and other matrix constituents. In addition, hormonal mechanisms associated with a suppression of bone growth may enhance the probability of mature collagen cross-link formation.

scholarly journals Enhancement of bone formation in rabbits by recombinant human growth hormone

1993 ◽  
Vol 64 (5) ◽  
pp. 562-566 ◽  
Author(s):  
Anders Ehrnberg ◽  
Otte Brosjö ◽  
Peter Låftman ◽  
Olle Nilsson ◽  
Lennart Strömberg
Keyword(s):  
Growth Hormone ◽  
Bone Formation ◽  
Human Growth Hormone ◽  
Recombinant Human Growth Hormone ◽  
Human Growth

Simulated resistance training, but not alendronate, increases cortical bone formation and suppresses sclerostin during disuse

2012 ◽  
Vol 112 (5) ◽  
pp. 918-925 ◽  
Author(s):  
B. R. Macias ◽  
J. M. Swift ◽  
M. I. Nilsson ◽  
H. A. Hogan ◽  
S. D. Bouse ◽  
...  
Keyword(s):  
Resistance Training ◽  
Bone Formation ◽  
Cortical Bone ◽  
Bone Growth ◽  
Formation Rate ◽  
Bone Geometry ◽  
Muscle Contractions ◽  
Hindlimb Unloading ◽  
Sprague Dawley ◽  
Cross Sectional

Mechanical loading modulates the osteocyte-derived protein sclerostin, a potent inhibitor of bone formation. We hypothesized that simulated resistance training (SRT), combined with alendronate (ALEN) treatment, during hindlimb unloading (HU) would most effectively mitigate disuse-induced decrements in cortical bone geometry and formation rate (BFR). Sixty male, Sprague-Dawley rats (6-mo-old) were randomly assigned to either cage control (CC), HU, HU plus either ALEN (HU+ALEN), or SRT (HU+SRT), or combined ALEN and SRT (HU+SRT/ALEN) for 28 days. Computed tomography scans on days − 1 and 28 were taken at the middiaphyseal tibia. HU+SRT and HU+SRT/ALEN rats were subjected to muscle contractions once every 3 days during HU (4 sets of 5 repetitions; 1,000 ms isometric + 1,000 ms eccentric). The HU+ALEN and HU+SRT/ALEN rats received 10 μg/kg ALEN 3 times/wk. Compared with the CC animals, HU suppressed the normal slow growth-induced increases of cortical bone mineral content, cortical bone area, and polar cross-sectional moment of inertia; however, SRT during HU restored cortical bone growth. HU suppressed middiaphyseal tibia periosteal BFR by 56% vs. CC ( P < 0.05). However, SRT during HU restored BFR at both periosteal (to 2.6-fold higher than CC) and endocortical (14-fold higher than CC) surfaces ( P < 0.01). ALEN attenuated the SRT-induced BFR gains during HU. The proportion of sclerostin-positive osteocytes in cortical bone was significantly higher (+121% vs. CC) in the HU group; SRT during HU effectively suppressed the higher proportion of sclerostin-positive osteocytes. In conclusion, a minimum number of high-intensity muscle contractions, performed during disuse, restores cortical BFR and suppress unloading-induced increases in sclerostin-positive osteocytes.

Growth Hormone Stimulates Cortical Bone Formation in Immature Hypophysectomized Rats

1992 ◽  
Vol 18 (1) ◽  
pp. 19-30 ◽  
Author(s):  
P. M. Schiltz ◽  
S. Mohan ◽  
T. Ohta ◽  
D. Glass ◽  
D. J. Baylink
Keyword(s):  
Growth Hormone ◽  
Bone Formation ◽  
Cortical Bone ◽  
Hypophysectomized Rats

scholarly journals A four year dose-response study of recombinant human growth hormone treatment of growth hormone deficient children: effects on growth, bone growth and bone mineralization

2000 ◽  
pp. 42-46 ◽  
Author(s):  
G Radetti ◽  
F Buzi ◽  
C Paganini ◽  
C Martelli ◽  
S Adami
Keyword(s):  
Growth Hormone ◽  
Bone Growth ◽  
Bone Mineralization ◽  
Recombinant Human Growth Hormone ◽  
Human Growth ◽  
Bone Age ◽  
Hormone Treatment ◽  
Height Velocity ◽  
Mineral Density ◽  
Group A

To evaluate the effects of two regimens of recombinant human GH (rhGH) on growth, bone growth and bone mineralization in GH deficient children, we studied two groups (A and B), each including 16 GH deficient children matched for sex, age, body mass index, height, height velocity and bone age/chronological age ratio (BA/CA). Group A was treated with a weekly rhGH dose of 1IU/kg and group B with 0.5IU/kg. After four years of therapy, we evaluated the auxological outcome, bone morphometry (metacarpal index: MI) and bone mineralization by quantitative roentgen microdensitometry at the middle region of the II metacarpal and ultra-distal radius. Height increased significantly in both groups, being significantly higher in group A after four years of therapy, while BA/CA remained similar in the two groups. Bone growth (measured by the MI), and bone mineral density at the metacarpal (mostly trabecular bone) and at the ultra-distal radial (mostly cortical bone) site did not differ in the two groups, nor did these three parameters differ from normal controls. In conclusion, after four years a greater height gain was achieved by the higher dose of rhGH compared with the conventional dose, but there were no differences in bone growth and mineralization.

scholarly journals IL-23 receptor deficiency results in lower bone mass via indirect regulation of bone formation

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Wida Razawy ◽  
Celso H. Alves ◽  
Marijke Koedam ◽  
Patrick S. Asmawidjaja ◽  
Adriana M. C. Mus ◽  
...  
Keyword(s):  
Bone Formation ◽  
Bone Mass ◽  
Cortical Bone ◽  
Bone Growth ◽  
Osteoclast Differentiation ◽  
Bone Homeostasis ◽  
Littermate Control ◽  
Cortical Bone Mass

AbstractThe IL-23 receptor (IL-23R) signaling pathway has pleiotropic effects on the differentiation of osteoclasts and osteoblasts, since it can inhibit or stimulate these processes via different pathways. However, the potential role of this pathway in the regulation of bone homeostasis remains elusive. Therefore, we studied the role of IL-23R signaling in physiological bone remodeling using IL-23R deficient mice. Using µCT, we demonstrate that 7-week-old IL-23R−/− mice have similar bone mass as age matched littermate control mice. In contrast, 12-week-old IL-23R−/− mice have significantly lower trabecular and cortical bone mass, shorter femurs and more fragile bones. At the age of 26 weeks, there were no differences in trabecular bone mass and femur length, but most of cortical bone mass parameters remain significantly lower in IL-23R−/− mice. In vitro osteoclast differentiation and resorption capacity of 7- and 12-week-old IL-23R−/− mice are similar to WT. However, serum levels of the bone formation marker, PINP, are significantly lower in 12-week-old IL-23R−/− mice, but similar to WT at 7 and 26 weeks. Interestingly, Il23r gene expression was not detected in in vitro cultured osteoblasts, suggesting an indirect effect of IL-23R. In conclusion, IL-23R deficiency results in temporal and long-term changes in bone growth via regulation of bone formation.

Effects of growth hormone and testosterone on cortical bone formation and bone density in aged orchiectomized rats

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