scholarly journals Osteogenic response under the periosteum by magnesium implantation in rat tibia

Author(s):  
Kenji ODASHIMA ◽  
Yoshinaka SHIMIZU ◽  
Yuya SANO ◽  
Akiko YAMAMOTO ◽  
Toshiji MUKAI ◽  
...  
1972 ◽  
Vol 70 (4) ◽  
pp. 676-682 ◽  
Author(s):  
Cipora Streifler ◽  
Arie Orenstein ◽  
Arieh Harell

ABSTRACT The influence of thyrocalcitonin (TCT) on the enzymes alkaline phosphatase and inorganic pyrophosphatase in rat bone, kidney and intestine was studied. The rats were injected with TCT every hour for 4 hours. They were divided into groups and were sacrificed 1 h after the first, second, third and fourth injection respectively. The plasma calcium was found to be reduced. Enzyme studies showed that: a) in tibia metaphysis homogenates alkaline phosphatase increased in response to TCT, to 198, 175, 154 and 183 per cent of the non-injected rats after 1, 2, 3, and 4 injections, respectively; inorganic pyrophosphatase was elevated to 356, 209, 221, 425 per cent after the same TCT injections. b) In kidney homogenates alkaline phosphatase was reduced to 75, 53, 79, 68 per cent of the non-injected rats after 1, 2, 3 and four doses, respectively; inorganic pyrophosphatase was reduced to 78, 56, 77 and 71 per cent after the same injections of TCT. c) In the jejunum, alkaline phosphatase was found to be 88.5, 71, 91 and 115 per cent of the untreated rats after 1, 2, 3 and 4 injections, respectively; pyrophosphatase in this tissue was found to be 105, 102, 102 and 113 per cent of the normal under the above conditions. The results indicate: 1. TCT causes increases in alkaline phosphatase and inorganic pyrophosphatase activities in bone. The increase of pyrophosphatase is significantly more marked than the increase of alkaline phosphatase; 2. in kidney tissue, the action of TCT on these two enzymes is slower and their activities are equally reduced; 3. in the jejunum no significant effect of TCT on the activity of these two enzymes was observed.


2004 ◽  
Vol 286 (4) ◽  
pp. F739-F748 ◽  
Author(s):  
Angela J. Brewer ◽  
Lucie Canaff ◽  
Geoffrey N. Hendy ◽  
Harriet S. Tenenhouse

Mutations in the PHEX gene are responsible for X-linked hypophosphatemia, a renal phosphate-wasting disorder associated with defective skeletal mineralization. PHEX is predominantly expressed in bones and teeth and in the parathyroid gland of patients with chronic renal failure and tertiary hyperparathyroidism. The purpose of the present study was to examine the effects of renal insufficiency and 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] on the regulation of PHEX expression in rat tibia and parathyroid gland. In rats fed a high-phosphate (Pi) diet, ⅚ nephrectomy elicited a significant increase in the serum parathyroid hormone (PTH) concentration that was associated with a significant increase in the abundance of PHEX mRNA and protein in the tibia and a significant increase in PHEX mRNA in the parathyroid gland. In contrast, 1,25(OH)2D3 administration to intact rats fed a control diet elicited a significant decrease in the serum PTH concentration that was accompanied by a significant decrease in PHEX mRNA and protein abundance in the tibia and a significant decrease in PHEX mRNA in the parathyroid gland. In addition, the increases in serum PTH levels and PHEX mRNA in the tibia and parathyroid gland in ⅚ nephrectomized rats fed a high-Pi diet were blunted by 1,25(OH)2D3. Serum PTH concentration was positively and significantly correlated with tibial PHEX mRNA and protein abundance. In summary, we demonstrate that PHEX expression in the tibia and parathyroid gland is increased by chronic renal insufficiency and decreased by 1,25(OH)2D3 administration and suggest that PTH status may play an important role in mediating these changes in PHEX expression.


Engineering ◽  
2021 ◽  
Author(s):  
Hao Zhu ◽  
Håvard Jostein Haugen ◽  
Giuseppe Perale ◽  
Janne Elin Reseland ◽  
Liebert Parreiras Nogueira ◽  
...  

1981 ◽  
Vol &NA; (160) ◽  
pp. 290???294 ◽  
Author(s):  
CLYDE B. KERNEK ◽  
ALONZA PERRY
Keyword(s):  

2014 ◽  
Vol 29 (2) ◽  
pp. e241-e246 ◽  
Author(s):  
Heli Rushinek ◽  
Michael Alterman ◽  
Amir Laviv ◽  
Ervin I. Weiss ◽  
Michael Friedman ◽  
...  

2001 ◽  
Vol 11 (s1) ◽  
pp. S137-S142 ◽  
Author(s):  
Wendy M. Kohrt

The osteogenic response to mechanical stress is blunted with aging. It has been postulated that this decline in responsiveness is related to (a) a limited ability to engender the strain necessary to reach the bone modeling threshold, due to decreased muscle mass and strength, and/or (b) a decline in certain hormones or growth factors that may interact with mechanical signals to change the sensitivity of bone cells to strain. There is reason to believe that both of these factors contribute to the reduced ability to increase bone mass through exercise with advancing age. Weight-bearing endurance exercise and resistance exercise have both been found to increase bone mass in older women and men. However, exercise training studies involving older individuals have generally resulted in increased bone mineral density only when the exercise is quite vigorous. There is also evidence that the osteogenic response to mechanical loading is enhanced by estrogens. Whether age-related changes in other factors (e.g., other hormones, growth factors, cytokines) also contribute to the reduced responsiveness of the aged skeleton to mechanical loading remains to be investigated.


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