Density of a sample bovine cortical bone matrix and its solid constituent in various media

1981 ◽  
Vol 33 (1) ◽  
pp. 499-504 ◽  
Author(s):  
Sidney Lees ◽  
John D. Heeley
2006 ◽  
Vol 24 (7) ◽  
pp. 1454-1462 ◽  
Author(s):  
Yanchun Liu ◽  
Shama Ahmad ◽  
Xiao Zheng Shu ◽  
R. Kent Sanders ◽  
Sally Anne Kopesec ◽  
...  

2015 ◽  
Vol 30 (12) ◽  
pp. 2229-2238 ◽  
Author(s):  
Alan C Seifert ◽  
Cheng Li ◽  
Suzanne L Wehrli ◽  
Felix W Wehrli

2004 ◽  
Vol 427 ◽  
pp. S62-S66 ◽  
Author(s):  
Jizong Gao ◽  
David Knaack ◽  
Victor M Goldberg ◽  
Arnold I Caplan

1982 ◽  
Vol 99 (3) ◽  
pp. 199-207 ◽  
Author(s):  
Jos� B. Volpon ◽  
Camilo A. M. Xavier ◽  
Renato Pinto Con�alves

2011 ◽  
Vol 165 (3) ◽  
pp. 393-400 ◽  
Author(s):  
Thor Ueland ◽  
Tove Lekva ◽  
Kari Otterdal ◽  
Tuva B Dahl ◽  
Nicoleta Cristina Olarescu ◽  
...  

ObjectivePatients with adult onset GH deficiency (aoGHD) have secondary osteoporosis, which is reversed by long-term GH substitution. Transforming growth factor β1 (TGFβ1 or TGFB1) is abundant in bone tissue and could mediate some effects of GH/IGFs on bone. We investigated its regulation by GH/IGF1in vivoandin vitro.Design and methodsThe effects of GH substitution (9–12 months, placebo controlled) on circulating and cortical bone matrix contents of TGFβ1 were investigated in patients with aoGHD. The effects of GH/IGF1 on TGFβ1 secretion in osteoblasts (hFOB), adipocytes, and THP-1 macrophages as well as the effects on release from platelets were investigatedin vitro.ResultsIn vivoGH substitution increased TGFβ1 protein levels in cortical bone and serum.In vitro, GH/IGF1 stimulation induced a significant increase in TGFβ1 secretion in hFOB. In contrast, no major effect of GH/IGF1 on TGFβ1 was found in adipocytes and THP-1 macrophages. Finally, a minor modifying effect on SFLLRN-stimulated platelet release of TGFβ1 was observed in the presence of IGF1.ConclusionGH substitution increases TGFβ1in vivoandin vitro, and this effect could contribute to improved bone metabolism during such therapy, potentially reflecting direct effect of GH/IGF1 on bone cells.


Endocrinology ◽  
2015 ◽  
Vol 156 (9) ◽  
pp. 3203-3214 ◽  
Author(s):  
Michele V. Clarke ◽  
Patricia K. Russell ◽  
David M. Findlay ◽  
Stephen Sastra ◽  
Paul H. Anderson ◽  
...  

During lactation, the large transfer of calcium from the mother to the milk is primarily sourced from the maternal skeleton. To determine whether the calcitonin receptor (CTR) plays a physiological role to protect the skeleton from excessive resorption during lactation, we assessed the maternal skeleton of global CTR knockout (CTRKO) and littermate control mice at the end of lactation (postnatal day 21). Micro-computed tomography analyses showed no effect on trabecular or cortical bone in the distal femur and L1 vertebra of maternal global CTR deletion at the end of lactation in global CTRKO mice compared with that in control mice. Bone resorption, as assessed by osteoclast number and activity at the end of lactation, was unaffected by maternal CTR deletion. Cathepsin K, carbonic anhydrase 2, matrix metalloproteinase 13, and receptor activator of nuclear factor-κB ligand mRNA levels, however, were markedly elevated by 3- to 6.5-fold in whole bone of lactating global CTRKO females. Because these genes have been shown to be up-regulated in osteocytes during lactation when osteocytes resorb their surrounding bone matrix, together with their reported expression of the CTR, we determined the osteocyte lacunar area in cortical bone. After lactation, the top 20% of osteocyte lacunar area in global CTRKO mice was 10% larger than the top 20% in control mice. These data are consistent with an increased osteocytic osteolysis in global CTRKO mice during lactation, which is further supported by the increased serum calcium observed in global CTRKO mice after lactation. These results provide evidence for a physiological role for the CTR to protect the maternal skeleton during lactation by a direct action on osteocytes to inhibit osteolysis.


2018 ◽  
Author(s):  
Dylan Shearer ◽  
Madison O Mervis ◽  
Eugene Manley ◽  
Anita B Reddy ◽  
Andrea I Alford

AbstractThrombospondin-2-deficiency is associated with impaired matrix maturation in osteoblasts and cortical bone of growing mice. Here we addressed the possibility that lysyl oxidase (LOX) contributes to this phenotype. After overnight serum starvation, pro-LOX levels were elevated compared to wild-type in marrow-derived osteoblasts from male and female TSP2−/− mice. The liberated LOX pro-peptide (LOPP) was faintly visible in serum-starved cultures. When serum was maintained, pro-LOX content was not affected by TSP2 status, but relative LOPP levels were elevated in cultures from female TSP2−/− mice. Two isoforms of pro-LOX at 75 kDa and 50 kDa were detected in detergent soluble protein extracts of diaphyseal tissue from growing mice. In female mice, TSP2 status did not affect detergent soluble pro-LOX content or the relative contribution of each band to the total signal. Instead, levels of the 50 kDa band were reduced in female TSP1−/− samples. In male diaphyseal tissue, total pro-LOX content and the contribution each isoform made to the total signal was not affected by TSP1 or TSP2 status. We did not detect 32 kDa mature LOX in detergent soluble preparations of cells or whole bone tissue. Detergent insoluble hydroxyproline content was reduced in diaphyseal tissue obtained from female TSP1−/− and TSP2−/− mice. In male diaphyseal cortical samples, TSP2 but not TSP1 deficiency was associated with reduced insoluble hydroxyproline content. Our data suggest that the trimeric thrombospondins contribute to bone matrix quality via non-redundant mechanisms that are dependent on the unique tissue milieu of the male and female skeleton.


2016 ◽  
Vol 55 (2) ◽  
pp. 35-39
Author(s):  
Jovan Janić ◽  
◽  
Žaklina Mijović ◽  
Dragan Mihailović ◽  
Nikola Živković ◽  
...  

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