scholarly journals Autoradiographic Studies of the Utilization of Ca45 by the Chick Embryo

1958 ◽  
Vol 4 (2) ◽  
pp. 163-168 ◽  
Author(s):  
Perry M. Johnston
Keyword(s):  
Chick Embryo ◽  
Bone Formation ◽  
Bone Matrix ◽  
Endochondral Bone Formation ◽  
Paraffin Sections ◽  
Endochondral Bone ◽  
Tissue Sections ◽  
Isotope Concentration ◽  
Neutral Formalin

Calcium-45 was injected into the dense albumen of fertile hen's eggs, to the extent of 25 µc. per egg. The eggs were incubated under standard conditions and three or more embryos removed daily and fixed in 10 per cent neutral formalin. Stripping-film autoradiograms were prepared from paraffin sections of the tibiofibulae. Exposure varied with the isotope concentration. The tissue sections with their autoradiograms in place were stained with dilute Giemsa, while other sections were stained with hematoxylin-azure-eosin and by von Kossa to demonstrate bone salt. At about 9 days, Ca45 is found in the cartilage template both intra- and extracellularly. Between 9 and 11 days, a primary diaphyseal lamella is deposited which is largely acellular. The lamella is eroded by capillaries from the periosteum and a resorption center is established in the cartilage. New lamellae of bone are deposited centrifugally in an imbricated pattern. Bone matrix formation precedes calcification by about 1 to ½ days, and calcification in a particular lamella is not uniform. Endochondral bone formation is described, as well as calcification of the epiphyseal/diaphyseal cartilage. Calcium-45 occurs intracellularly in the osteocyte during bone formation.

scholarly journals Demineralized bone matrix-induced endochondral bone formation in pigs

1991 ◽  
Vol 62 (12) ◽  
pp. 1179-1181
Author(s):  
Mika MYOJO ◽  
Seiji KUSUHARA ◽  
Go NOGUCHI ◽  
Takashi NAKAOYAMA
Keyword(s):  
Bone Formation ◽  
Demineralized Bone Matrix ◽  
Bone Matrix ◽  
Endochondral Bone Formation ◽  
Endochondral Bone ◽  
Demineralized Bone

scholarly journals Bone phenotypes in rheumatology – there is more to bone than just bone

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Christian S. Thudium ◽  
Signe Holm Nielsen ◽  
Samra Sardar ◽  
Ali Mobasheri ◽  
Willem Evert van Spil ◽  
...  
Keyword(s):  
Bone Formation ◽  
Skeletal Development ◽  
Bone Matrix ◽  
Matrix Composition ◽  
Endochondral Bone Formation ◽  
Common Denominator ◽  
Endochondral Bone ◽  
Pathological Conditions ◽  
Simple Change ◽  
Rheumatological Diseases

AbstractOsteoarthritis, rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis, all have one clear common denominator; an altered turnover of bone. However, this may be more complex than a simple change in bone matrix and mineral turnover. While these diseases share a common tissue axis, their manifestations in the area of pathology are highly diverse, ranging from sclerosis to erosion of bone in different regions. The management of these diseases will benefit from a deeper understanding of the local versus systemic effects, the relation to the equilibrium of the bone balance (i.e., bone formation versus bone resorption), and the physiological and pathophysiological phenotypes of the cells involved (e.g., osteoblasts, osteoclasts, osteocytes and chondrocytes). For example, the process of endochondral bone formation in chondrocytes occurs exists during skeletal development and healthy conditions, but also in pathological conditions. This review focuses on the complex molecular and cellular taxonomy of bone in the context of rheumatological diseases that alter bone matrix composition and maintenance, giving rise to different bone turnover phenotypes, and how biomarkers (biochemical markers) can be applied to potentially describe specific bone phenotypic tissue profiles.

scholarly journals Ovotransferrin and ovotransferrin receptor expression during chondrogenesis and endochondral bone formation in developing chick embryo

1994 ◽  
Vol 124 (4) ◽  
pp. 579-588 ◽  
Author(s):  
C Gentili ◽  
R Doliana ◽  
P Bet ◽  
G Campanile ◽  
A Colombatti ◽  
...  
Keyword(s):  
Chick Embryo ◽  
Bone Formation ◽  
Blot Analysis ◽  
Receptor Expression ◽  
Hypertrophic Chondrocytes ◽  
Endochondral Bone Formation ◽  
Metabolic Labeling ◽  
Matrix Assembly ◽  
Endochondral Bone ◽  
Low Level

Ovotransferrin expression during chick embryo tibia development has been investigated in vivo by immunocytochemistry and in situ hybridization. Ovotransferrin was first observed in the 7 day cartilaginous rudiment. At later stages, the factor was localized in the articular zone of the bone epiphysis and in the bone diaphysis where it was concentrated in hypertrophic cartilage, in zones of cartilage erosion and in the osteoid at the chondro-bone junction. When the localization of the ovotransferrin receptors was investigated, it was observed that chondrocytes at all stages of differentiation express a low level of the oviduct (tissue) specific receptor. Interestingly, high levels of the receptor were detectable in the 13-d old tibia in the diaphysis collar of stacked-osteoprogenitor cells and in the layer of derived osteoblasts. High levels of oviduct receptor were also observed in the primordia of the menisci. Metabolic labeling of proteins secreted by cultured chondrocytes and osteoblasts and Northern blot analysis of RNA extracted from the same cells confirmed and completed the above information. Ovotransferrin was expressed by in vitro differentiating chondrocytes in the early phase of the culture and, at least when culture conditions allowed extracellular matrix assembly, also by hypertrophic chondrocytes and derived osteoblast-like cells. Osteoblasts directly obtained from bone chips produced ovotransferrin only at the time of culture mineralization. By Western blot analysis, oviduct receptor proteins were detected at a very low level in extract from differentiating and hypertrophic chondrocytes and at a higher level in extract from hypertrophic chondrocytes undergoing differentiation to osteoblast-like cells and from mineralizing osteoblasts. Based on these results, the existence of autocrine and paracrine loops involving ovotransferrin and its receptor during chondrogenesis and endochondral bone formation is discussed.

scholarly journals The culture microenvironment of juvenile idiopathic arthritis synovial fibroblasts is favorable for endochondral bone formation through BMP4 and repressed by chondrocytes

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Megan M. Simonds ◽  
Amanda R. Schlefman ◽  
Suzanne M. McCahan ◽  
Kathleen E. Sullivan ◽  
Carlos D. Rose ◽  
...  
Keyword(s):  
Juvenile Idiopathic Arthritis ◽  
Bone Formation ◽  
Synovial Fibroblasts ◽  
Conditioned Media ◽  
Endochondral Bone Formation ◽  
Endochondral Bone ◽  
Member Gene ◽  
Bmp Antagonist ◽  
Fibroblast Like Synoviocytes ◽  
Tgfβ Superfamily

Abstract Background We examined influences of conditioned media from chondrocytes (Ch) on juvenile idiopathic arthritis synovial fibroblasts (JFLS) and potential for JFLS to undergo endochondral bone formation (EBF). Methods Primary cells from three control fibroblast-like synoviocytes (CFLS) and three JFLS were cultured in Ch-conditioned media and compared with untreated fibroblast-like synoviocytes (FLS). RNA was analyzed by ClariomS microarray. FLS cells cultured in conditioned media were exposed to either TGFBR1 inhibitor LY3200882 or exogenous BMP4 and compared with FLS cultured in conditioned media from Ch (JFLS-Ch). Media supernatants were analyzed by ELISA. Results In culture, JFLS downregulate BMP2 and its receptor BMPR1a while upregulating BMP antagonists (NOG and CHRD) and express genes (MMP9, PCNA, MMP12) and proteins (COL2, COLX, COMP) associated with chondrocytes. Important TGFβ superfamily member gene expression (TGFBI, MMP9, COL1A1, SOX6, and MMP2) is downregulated when JFLS are cultured in Ch-conditioned media. COL2, COLX and COMP protein expression decreases in JFLS-Ch. BMP antagonist protein (NOG, CHRD, GREM, and FST) secretion is significantly increased in JFLS-Ch. Protein phosphorylation increases in JFLS-Ch exposed to exogenous BMP4, and chondrocyte-like phenotype is restored in BMP4 presence, evidenced by increased secretion of COL2 and COLX. Inhibition of TGFBR1 in JFLS-Ch results in overexpression of COL2. Conclusions JFLS are chondrocyte-like, and Ch-conditioned media can abrogate this phenotype. The addition of exogenous BMP4 causes JFLS-Ch to restore this chondrocyte-like phenotype, suggesting that JFLS create a microenvironment favorable for endochondral bone formation, thereby contributing to joint growth disturbances in juvenile idiopathic arthritis.

scholarly journals Intraflagellar transport is essential for endochondral bone formation

Development ◽  
2007 ◽  
Vol 134 (2) ◽  
pp. 307-316 ◽  
Author(s):  
C. J. Haycraft ◽  
Q. Zhang ◽  
B. Song ◽  
W. S. Jackson ◽  
P. J. Detloff ◽  
...  
Keyword(s):  
Bone Formation ◽  
Intraflagellar Transport ◽  
Endochondral Bone Formation ◽  
Endochondral Bone

scholarly journals Osteoblast‐Specific Loss of IGF1R Signaling Results in Impaired Endochondral Bone Formation During Fracture Healing

2015 ◽  
Vol 30 (9) ◽  
pp. 1572-1584 ◽  
Author(s):  
Tao Wang ◽  
Yongmei Wang ◽  
Alicia Menendez ◽  
Chak Fong ◽  
Muriel Babey ◽  
...  
Keyword(s):  
Bone Formation ◽  
Fracture Healing ◽  
Endochondral Bone Formation ◽  
Endochondral Bone ◽  
Specific Loss ◽  
Igf1r Signaling

scholarly journals Conditional Deletion of Prolyl Hydroxylase Domain-Containing Protein 2 (Phd2) Gene Reveals Its Essential Role in Chondrocyte Function and Endochondral Bone Formation

Endocrinology ◽  
2016 ◽  
Vol 157 (1) ◽  
pp. 127-140 ◽  
Author(s):  
Shaohong Cheng ◽  
Weirong Xing ◽  
Sheila Pourteymoor ◽  
Jan Schulte ◽  
Subburaman Mohan
Keyword(s):  
Bone Formation ◽  
Growth Plate ◽  
Prolyl Hydroxylase ◽  
Conditional Knockout ◽  
Hypertrophic Chondrocytes ◽  
Endochondral Bone Formation ◽  
Bone Surface ◽  
Endochondral Bone ◽  
Prolyl Hydroxylase Domain

Abstract The hypoxic growth plate cartilage requires hypoxia-inducible factor (HIF)-mediated pathways to maintain chondrocyte survival and differentiation. HIF proteins are tightly regulated by prolyl hydroxylase domain-containing protein 2 (Phd2)-mediated proteosomal degradation. We conditionally disrupted the Phd2 gene in chondrocytes by crossing Phd2 floxed mice with type 2 collagen-α1-Cre transgenic mice and found massive increases (>50%) in the trabecular bone mass of long bones and lumbar vertebra of the Phd2 conditional knockout (cKO) mice caused by significant increases in trabecular number and thickness and reductions in trabecular separation. Cortical thickness and tissue mineral density at the femoral middiaphysis of the cKO mice were also significantly increased. Dynamic histomorphometric analyses revealed increased longitudinal length and osteoid surface per bone surface in the primary spongiosa of the cKO mice, suggesting elevated conversion rate from hypertrophic chondrocytes to mineralized bone matrix as well as increased bone formation in the primary spongiosa. In the secondary spongiosa, bone formation measured by mineralizing surface per bone surface and mineral apposition rate were not changed, but resorption was slightly reduced. Increases in the mRNA levels of SRY (sex determining region Y)-box 9, osterix (Osx), type 2 collagen, aggrecan, alkaline phosphatase, bone sialoprotein, vascular endothelial growth factor, erythropoietin, and glycolytic enzymes in the growth plate of cKO mice were detected by quantitative RT-PCR. Immunohistochemistry revealed an increased HIF-1α protein level in the hypertrophic chondrocytes of cKO mice. Infection of chondrocytes isolated from Phd2 floxed mice with adenoviral Cre resulted in similar gene expression patterns as observed in the cKO growth plate chondrocytes. Our findings indicate that Phd2 suppresses endochondral bone formation, in part, via HIF-dependent mechanisms in mice.

Oxygen Tension Directs Chondrogenic Differentiation of Myelo-Monocytic Progenitors During Endochondral Bone Formation

2007 ◽  
Vol 13 (8) ◽  
pp. 2011-2019 ◽  
Author(s):  
Jessica Shafer ◽  
Alan R. Davis ◽  
Francis H. Gannon ◽  
Christine M. Fouletier-Dilling ◽  
Zawaunyka Lazard ◽  
...  
Keyword(s):  
Bone Formation ◽  
Oxygen Tension ◽  
Chondrogenic Differentiation ◽  
Endochondral Bone Formation ◽  
Endochondral Bone
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