scholarly journals Parathyroid hormone induces formation of new cancellous bone with substantial mechanical strength at a site where it had disappeared in old rats

2002 ◽  
pp. 431-438 ◽  
Author(s):  
H Oxlund ◽  
M Dalstra ◽  
C Ejersted ◽  
TT Andreassen

OBJECTIVE: The present study addresses the question--can PTH induce formation of trabeculae in areas where cancellous bone has disappeared? Two-year-old male rats were chosen, because in this aged animal model the distal femurs have almost no cancellous bone, and the marrow cavity has reached a substantial dimension. DESIGN: The rats were injected for 56 days with either PTH(1-34), 15 nmol/kg/day (62.5 microg/kg/day), or vehicle. METHODS: Transverse specimens, 2-mm high, were cut from the distal femoral metaphysis. Marrow cavity diameters and cancellous bone trabeculae were analysed by a micro-computerized tomography scanner. The cancellous bone within the cortical and endocortical rim of each specimen was submitted to a biomechanical compression test. Furthermore, the cancellous bone was studied by dynamic tetracycline labelling and histomorphometry. RESULTS: In the vehicle-injected group the trabecular bone volume was 0% (0-1.4), median (range). All PTH-injected rats had trabeculae in the distal metaphysis and the trabecular bone volume (6.7% (2.3-12.0)) was markedly increased (P<0.003). The median trabecular thickness was increased (P<0.003) in the PTH-injected rats (118 microm (104-125)) compared with the vehicle group (0 microm (0-71)). The compressive stress was increased (P<0.003) in the PTH-injected group (0.7 MPa (0.1-2.1)) compared with the vehicle-injected group (0 MPa (0-0.4)). The histomorphometry revealed that only 3 animals of the 10 in the vehicle-injected group had trabeculae in the distal femoral metaphysis. All PTH-injected animals (12 of 12) had continuous trabecular bone network in the marrow cavity. CONCLUSION: Intermittent PTH treatment induced marked formation of new cancellous bone trabeculae with substantial mechanical strength, at a site where it had disappeared in old rats.

1988 ◽  
Vol 255 (2) ◽  
pp. R243-R247 ◽  
Author(s):  
L. Vico ◽  
D. Chappard ◽  
S. Palle ◽  
A. V. Bakulin ◽  
V. E. Novikov ◽  
...  

Seven male rats were exposed to 7 days of weightlessness in the Soviet mission COSMOS 1667 and compared with seven control rats by bone histomorphometric methods. In proximal tibial metaphysis, the trabecular bone volume was markedly reduced in flight animals. Trabeculae were decreased in number and thickness; this probably leads to alteration of bone mechanical properties. Formation activity (reflected by measurements of osteoid seams) was decreased at trabecular and endosteal levels. Resorption activity (estimated by count of osteoclast number and active resorption surfaces using a histoenzymologic method) remained unchanged. The imbalance between these cellular activities appears to be responsible for the loss of trabecular bone mass. In proximal femoral metaphysis, measurements were performed in an area located under the muscular insertions. The trabecular bone volume, despite a slight decrease in flight rats, was not significantly different from that of control rats. Furthermore, osteoclastic and osteoid parameters were unchanged. Differential responses between these two long bones need additional investigations. In thoracic and lumbar vertebrae no detectable change in bone mass and bone resorption parameters was found.


2010 ◽  
Vol 25 (11) ◽  
pp. 2311-2319 ◽  
Author(s):  
Pornpimol Rianthavorn ◽  
Robert B. Ettenger ◽  
Isidro B. Salusky ◽  
Beatriz D. Kuizon

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Jingyan Fu ◽  
Matthew Goldsmith ◽  
Sequoia D. Crooks ◽  
Sean F. Condon ◽  
Martin Morris ◽  
...  

AbstractAnimals in space exploration studies serve both as a model for human physiology and as a means to understand the physiological effects of microgravity. To quantify the microgravity-induced changes to bone health in animals, we systematically searched Medline, Embase, Web of Science, BIOSIS, and NASA Technical reports. We selected 40 papers focusing on the bone health of 95 rats, 61 mice, and 9 rhesus monkeys from 22 space missions. The percentage difference from ground control in rodents was –24.1% [Confidence interval: −43.4, −4.9] for trabecular bone volume fraction and –5.9% [−8.0, −3.8] for the cortical area. In primates, trabecular bone volume fraction was lower by –25.2% [−35.6, −14.7] in spaceflight animals compared to GC. Bone formation indices in rodent trabecular and cortical bone were significantly lower in microgravity. In contrast, osteoclast numbers were not affected in rats and were variably affected in mice. Thus, microgravity induces bone deficits in rodents and primates likely through the suppression of bone formation.


Cells ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 2200
Author(s):  
Weirong Xing ◽  
Sheila Pourteymoor ◽  
Gustavo A. Gomez ◽  
Yian Chen ◽  
Subburaman Mohan

We previously showed that conditional disruption of the Phd2 gene in chondrocytes led to a massive increase in long bone trabecular bone mass. Loss of Phd2 gene expression or inhibition of PHD2 activity by a specific inhibitor resulted in a several-fold compensatory increase in Phd3 expression in chondrocytes. To determine if expression of PHD3 plays a role in endochondral bone formation, we conditionally disrupted the Phd3 gene in chondrocytes by crossing Phd3 floxed (Phd3flox/flox) mice with Col2α1-Cre mice. Loss of Phd3 expression in the chondrocytes of Cre+; Phd3flox/flox conditional knockout (cKO) mice was confirmed by real time PCR. At 16 weeks of age, neither body weight nor body length was significantly different in the Phd3 cKO mice compared to Cre−; Phd3flox/flox wild-type (WT) mice. Areal BMD measurements of total body as well as femur, tibia, and lumbar skeletal sites were not significantly different between the cKO and WT mice at 16 weeks of age. Micro-CT measurements revealed significant gender differences in the trabecular bone volume adjusted for tissue volume at the secondary spongiosa of the femur and the tibia for both genotypes, but no genotype difference was found for any of the trabecular bone measurements of either the femur or the tibia. Trabecular bone volume of distal femur epiphysis was not different between cKO and WT mice. Histology analyses revealed Phd3 cKO mice exhibited a comparable chondrocyte differentiation and proliferation, as evidenced by no changes in cartilage thickness and area in the cKO mice as compared to WT littermates. Consistent with the in vivo data, lentiviral shRNA-mediated knockdown of Phd3 expression in chondrocytes did not affect the expression of markers of chondrocyte differentiation (Col2, Col10, Acan, Sox9). Our study found that Phd2 but not Phd3 expressed in chondrocytes regulates endochondral bone formation, and the compensatory increase in Phd3 expression in the chondrocytes of Phd2 cKO mice is not the cause for increased trabecular bone mass in Phd2 cKO mice.


1984 ◽  
Vol 29 (3) ◽  
pp. 171-175 ◽  
Author(s):  
B. E. C. Nordin ◽  
J. Aaron ◽  
R. Speed ◽  
R. M. Francis ◽  
N. Makins

Trabecular bone volume, forming surface and percent surface resorption have been determined in iliac crest samples obtained post mortem from 43 young men and 49 elderly men and in biopsies obtained from 22 males with spinal osteoporosis. The mean bone volume was significantly lower in the old than in the young controls and significantly lower again in the osteoporotic cases. Forming surfaces were significantly lower in the old than the young controls but were not different as between old controls and cases of osteoporosis. Percent surface resorption was the same in young and old controls but significantly increased in the osteoporotics. Multiple regression analysis showed that trabecular bone volume was a significant positive function of forming surface and a significant inverse function of fractional surface resorption. Age-related (simple) osteoporosis in men appears to be due to reduced bone formation whereas pathological (accelerated) osteoporosis is due to increased bone resorption.


Bone ◽  
2013 ◽  
Vol 53 (1) ◽  
pp. 221-230 ◽  
Author(s):  
Christine Gaudin-Audrain ◽  
Nigel Irwin ◽  
Sity Mansur ◽  
Peter R. Flatt ◽  
Bernard Thorens ◽  
...  

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