Epi- and metaphyseal morphology in the long bones of BDIX/Han rats

1996 ◽  
Vol 30 (1) ◽  
pp. 35-41 ◽  
Author(s):  
C. Stark ◽  
B. Kahrmann ◽  
E. Walzel
Keyword(s):  
Growth Plate ◽  
Long Bones ◽  
Adult Rats ◽  
Growth Plates ◽  
The Matrix ◽  
Different Strains ◽  
Regressive Changes

Development and morphology of the epiphyses of the long bones were investigated in 93 adult rats of 7 different strains (BDIX/Han, BDE/Han, BN/Han, DA/Han, LEW/Han, AVN/IpcV/Wistar/Rehbrücke, Shoe: WIST) from the age of 14 weeks up to the age of 78 weeks. Strain-related differences were found in the development of the secondary centre of ossification, which was retarded in the BDIX/Han rats. Furthermore, closure of the growth plate started earlier in the BDIX/Han rats. In addition various regressive changes were detected in the growth plates of long bones of all rats, but not of the ribs. The frequency and extent of these changes varied between individuals and strains. Degeneration of the matrix and necrosis were already observed at 14 weeks of age.

Weight loading young chicks inhibits bone elongation and promotes growth plate ossification and vascularization

2005 ◽  
Vol 98 (6) ◽  
pp. 2381-2389 ◽  
Author(s):  
A. Reich ◽  
N. Jaffe ◽  
A. Tong ◽  
I. Lavelin ◽  
O. Genina ◽  
...  
Keyword(s):  
Blood Vessels ◽  
Growth Plate ◽  
Developmental Process ◽  
Mechanical Strain ◽  
Cell Counting ◽  
Mechanical Stimuli ◽  
Growth Plates ◽  
Average Width ◽  
The Matrix ◽  
Weight Loading

The mechanical stimuli resulting from weight loading play an important role in mature bone remodeling. However, the effect of weight loading on the developmental process in young bones is less well understood. In this work, chicks were loaded with bags weighing 10% of their body weight during their rapid growth phase. The increased load reduced the length and diameter of the long bones. The average width of the bag-loaded group's growth plates was 75 ± 4% that of the controls, and the plates showed increased mineralization. Northern blot analysis, in situ hybridization, and longitudinal cell counting of mechanically loaded growth plates showed narrowed expression zones of collagen types II and X compared with controls, with no differences between the relative proportions of those areas. An increase in osteopontin (OPN) expression with loading was most pronounced at the bone-cartilage interface. This extended expression overlapped with tartarate-resistant acid phosphatase staining and with the front of the mineralized matrix in the chondro-osseous junction. Moreover, weight loading enhanced the penetration of blood vessels into the growth plates and enhanced the gene expression of the matrix metalloproteinases MMP9 and MMP13 in those growth plates. On the basis of these results, we speculate that the mechanical strain on the chondrocytes in the growth plate causes overexpression of OPN, MMP9, and MMP13. The MMPs enable penetration of the blood vessels, which carry osteoclasts and osteoblasts. OPN recruits the osteoclasts to the cartilage-bone border, thus accelerating cartilage resorption in this zone and subsequent ossification which, in turn, contributes to the observed phenotype of narrower growth plate and shorter bones.

scholarly journals Sox5 and Sox6 are needed to develop and maintain source, columnar, and hypertrophic chondrocytes in the cartilage growth plate

2004 ◽  
Vol 164 (5) ◽  
pp. 747-758 ◽  
Author(s):  
Patrick Smits ◽  
Peter Dy ◽  
Srijeet Mitra ◽  
Véronique Lefebvre
Keyword(s):  
Growth Plate ◽  
Terminal Differentiation ◽  
Mouse Embryos ◽  
Null Alleles ◽  
Chondrocyte Differentiation ◽  
Long Bones ◽  
Cartilage Growth ◽  
Growth Plates ◽  
Cellular Source ◽  
Cartilage Growth Plate

Sox5 and Sox6 encode Sry-related transcription factors that redundantly promote early chondroblast differentiation. Using mouse embryos with three or four null alleles of Sox5 and Sox6, we show that they are also essential and redundant in major steps of growth plate chondrocyte differentiation. Sox5 and Sox6 promote the development of a highly proliferating pool of chondroblasts between the epiphyses and metaphyses of future long bones. This pool is the likely cellular source of growth plates. Sox5 and Sox6 permit formation of growth plate columnar zones by keeping chondroblasts proliferating and by delaying chondrocyte prehypertrophy. They allow induction of chondrocyte hypertrophy and permit formation of prehypertrophic and hypertrophic zones by delaying chondrocyte terminal differentiation induced by ossification fronts. They act, at least in part, by down-regulating Ihh signaling, Fgfr3, and Runx2 and by up-regulating Bmp6. In conclusion, Sox5 and Sox6 are needed for the establishment of multilayered growth plates, and thereby for proper and timely development of endochondral bones.

Recrystallization in Ultra-Fine Grain Structures of AA3104 Alloy Processed by ECAP and HPT

2012 ◽  
Vol 715-716 ◽  
pp. 346-353
Author(s):  
H. Paul ◽  
T. Baudin ◽  
K. Kudłacz ◽  
A. Morawiec
Keyword(s):  
High Pressure Torsion ◽  
Deformation Mode ◽  
Second Phase ◽  
Orientation Measurement ◽  
Angular Pressing ◽  
Second Phase Particles ◽  
Average Grain Size ◽  
The Matrix ◽  
Electron Microscopes ◽  
Different Strains

The objective of this study was to determine the effect of deformation mode on recrystallization behavior of severely deformed material. Commercial purity AA3104 aluminum alloy was deformed via high pressure torsion and equal channel angular pressing to different strains and then annealed to obtain the state of partial recrystallization. The microstructure and the crystallographic texture were analysed using scanning and transmission electron microscopes equipped with orientation measurement facilities. The nucleation of new grains was observed in bulk recrystallized samples and during in-situ recrystallization in the transmission microscope. Irrespective of the applied deformation mode, a large non-deformable second phase particles strongly influenced strengthening of the matrix through deformation zones around them. It is known that relatively high stored energy stimulates the nucleation of new grains during the recrystalization. In most of the observed cases, the growth of recrystallized grains occurred by the coalescence of neighboring subcells. This process usually led to nearly homogeneous equiaxed grains of similar size. The diameter of grains in the vicinity of large second phase particles was only occasionally significantly larger than the average grain size. Large grains were most often observed in places far from the particles. TEM orientation mapping from highly deformed zones around particles showed that orientations of new grains were not random and only strictly defined groups of orientations were observed.

scholarly journals Cam morphology in young male football players mostly develops before proximal femoral growth plate closure: a prospective study with 5-yearfollow-up

2018 ◽  
Vol 53 (9) ◽  
pp. 532-538 ◽  
Author(s):  
Pim van Klij ◽  
Marinus P Heijboer ◽  
Abida Z Ginai ◽  
Jan A N Verhaar ◽  
Jan H Waarsing ◽  
...  
Keyword(s):  
Growth Plate ◽  
Alpha Angle ◽  
Football Players ◽  
Growth Plates ◽  
Time Points ◽  
Open Growth Plate ◽  
Morphology Development ◽  
Open Growth ◽  
Cam Morphology

ObjectivesCam morphology is not completely understood. The aim of this study was threefold: (1) to investigate if cam morphology development is associated with growth plate status; (2) to examine whether cam morphology continues to develop after growth plate closure; and (3) to qualitatively describe cam morphology development over 5-year follow-up.MethodsAcademy male football players (n=49) participated in this prospective 5-year follow-up study (baseline 12–19 years old). Anteroposterior and frog-leg lateral views were obtained at baseline (142 hips), 2.5-year (126 hips) and 5-year follow-up (98 hips). Cam morphology on these time points was defined as: (A) visual scores of the anterior head-neck junction, classified as: (1) normal, (2) flattening, and (3) prominence; and (B) alpha angle ≥60°. Proximal femoral growth plates were classified as open or closed. Cam morphology development was defined as every increase in visual score and/or increase in alpha angle from <60° to ≥60°, between two time points. This resulted in 224 measurements for cam morphology development analysis.ResultsCam morphology development was significantly associated with open growth plates based on visual score (OR: 10.03, 95% CI 3.49 to 28.84, p<0.001) and alpha angle (OR: 2.85, 95% CI 1.18 to 6.88, p=0.020). With both definitions combined, cam developed in 104 of 142 hips during follow-up. Of these 104 hips, cam developed in 86 hips (82.7%) with open growth plate and in 18 hips (17.3%) with a closed growth plate. Cam morphology developed from 12 to 13 years of age until growth plate closure around 18 years.ConclusionCam morphology of the hip is more likely to develop with an open growth plate.

scholarly journals Exposure to the RXR agonist SR11237 in early life causes disturbed skeletal morphogenesis in a rat model

2019 ◽  
Author(s):  
Holly Dupuis ◽  
Michael Andrew Pest ◽  
Ermina Hadzic ◽  
Thin Xuan Vo ◽  
Daniel B. Hardy ◽  
...  
Keyword(s):  
Growth Plate ◽  
Bone Growth ◽  
Long Bone ◽  
Tunel Staining ◽  
Long Bones ◽  
Micro Computed Tomography ◽  
Computed Tomography Scanning ◽  
Calcified Tissue ◽  
Trap Staining ◽  
Tomography Scanning

AbstractLongitudinal bone growth occurs through endochondral ossification (EO), controlled by various signaling molecules. Retinoid X Receptor (RXR) is a nuclear receptor with important roles in cell death, development, and metabolism. However, little is known about its role in EO. In this study, the agonist SR11237 was used to evaluate RXR activation on EO.Rats given SR11237 from post-natal day 5 to 15 were harvested for micro-computed tomography scanning and histology. In parallel, newborn CD1 mouse tibiae were cultured with increasing concentrations of SR11237 for histological and whole mount evaluation.RXR agonist-treated rats were smaller than controls, and developed dysmorphia of the growth plate. Cells invading the calcified and dysmorphic growth plate appeared pre-hypertrophic in size and shape corresponding with P57 immunostaining. Additionally, SOX9 positive cells were found surrounding the calcified tissue. The epiphysis of SR11237 treated bones showed increased TRAP staining, and additional TUNEL staining at the osteo-chondral junction. MicroCT revealed morphological disorganization in the long bones of treated animals. Isolated mouse long bones treated with SR11237 grew significantly less than their DMSO controls.This study demonstrates that stimulation of the RXR receptor causes irregular ossification, premature closure of the growth plate, and disrupted long bone growth in rodent models.

scholarly journals Ultrastructural localization of the C-propeptide released from type II procollagen in fetal bovine growth plate cartilage.

1996 ◽  
Vol 44 (5) ◽  
pp. 433-443 ◽  
Author(s):  
E R Lee ◽  
C E Smith ◽  
R Poole
Keyword(s):  
Growth Plate ◽  
Ultrastructural Localization ◽  
Collagen Fibrils ◽  
Type Ii ◽  
Guanidinium Hydrochloride ◽  
High Affinity ◽  
Sds Page ◽  
The Matrix ◽  
Fetal Bovine ◽  
Mineralized Matrix

We used immunochemical and immunoelectron gold techniques to determine whether the C-propeptide previously identified in the matrix of endochondral cartilage (CPII) was still a part of the Type 11 procollagen molecule or had been released from it. Guanidinium hydrochloride extraction, followed by SDS-PAGE and Western blotting techniques and immunoelectron localization, revealed that predominantly only the released form (hereafter referred to as released CPII) was detected. The ultrastructural distribution of this CPII was examined with affinity-purified antibodies and with immunogold or immunoperoxidase localization techniques in the presence or absence of embedding resins. These methods yielded similar results. Although no significant amount of this CPII was retained in the matrix after guanidinium hydrochloride extraction, it was present in two recognizable sites under normal conditions, i.e., locally concentrated in a random association with collagen fibrils in the nonmineralized matrix and mainly concentrated in interfibrillar mineralizing sites in the mineralized matrix. These results suggest that the C-propeptide that has been released from Type II procollagen associates with collagen fibrils and then preferentially associates with mineralizing sites when these form in the endochondral cartilage. The significance of this preference for mineral is not known but may have something to do with its high affinity for hydroxyapatite.

scholarly journals Catch-Up Growth after Hypothyroidism Is Caused by Delayed Growth Plate Senescence

Endocrinology ◽  
2008 ◽  
Vol 149 (4) ◽  
pp. 1820-1828 ◽  
Author(s):  
Rose Marino ◽  
Anita Hegde ◽  
Kevin M. Barnes ◽  
Lenneke Schrier ◽  
Joyce A. Emons ◽  
...  
Keyword(s):  
Growth Rate ◽  
Growth Inhibition ◽  
Growth Plate ◽  
Bone Growth ◽  
Structural Characteristics ◽  
Linear Growth Rate ◽  
Growth Plate Chondrocytes ◽  
Growth Plates ◽  
Catch Up ◽  
Growth Inhibiting

Catch-up growth is defined as a linear growth rate greater than expected for age after a period of growth inhibition. We hypothesized that catch-up growth occurs because growth-inhibiting conditions conserve the limited proliferative capacity of growth plate chondrocytes, thus slowing the normal process of growth plate senescence. When the growth-inhibiting condition resolves, the growth plates are less senescent and therefore grow more rapidly than normal for age. To test this hypothesis, we administered propylthiouracil to newborn rats for 8 wk to induce hypothyroidism and then stopped the propylthiouracil to allow catch-up growth. In untreated controls, the growth plates underwent progressive, senescent changes in multiple functional and structural characteristics. We also identified genes that showed large changes in mRNA expression in growth plate and used these changes as molecular markers of senescence. In treated animals, after stopping propylthiouracil, these functional, structural, and molecular senescent changes were delayed, compared with controls. This delayed senescence included a delayed decline in longitudinal growth rate, resulting in catch-up growth. The findings demonstrate that growth inhibition due to hypothyroidism slows the developmental program of growth plate senescence, including the normal decline in the rate of longitudinal bone growth, thus accounting for catch-up growth.

scholarly journals Inner histopathologic changes and disproportionate zone volumes in foetal growth plates following gestational hypoglycaemia in rats

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Vivi F. H. Jensen ◽  
Anne-Marie Mølck ◽  
Ingrid B. Bøgh ◽  
Jette Nowak ◽  
Birgitte M. Viuff ◽  
...  
Keyword(s):  
Growth Plate ◽  
Bone Growth ◽  
Skeletal Development ◽  
Long Bone ◽  
Structural Protein ◽  
Pregnant Rats ◽  
Growth Plates ◽  
Chondrocyte Maturation ◽  
Foetal Growth ◽  
Histopathologic Changes

AbstractMaternal hypoglycaemia throughout gestation until gestation day (GD)20 delays foetal growth and skeletal development. While partially prevented by return to normoglycaemia after completed organogenesis (GD17), underlying mechanisms are not fully understood. Here, we investigated the pathogenesis of these changes and significance of maternal hypoglycaemia extending beyond organogenesis in non-diabetic rats. Pregnant rats received insulin-infusion until GD20 or GD17, with sacrifice on GD20. Hypoglycaemia throughout gestation increased maternal corticosterone levels, which correlated with foetal levels. Growth plates displayed central histopathologic changes comprising disrupted cellular organisation, hypertrophic chondrocytes, and decreased cellular density; expression of pro-angiogenic factors, HIF-1α and VEGF-A increased in surrounding areas. Disproportionately decreased growth plate zone volumes and lower expression of the structural protein MATN-3 were seen, while bone ossification parameters were normal. Ending maternal/foetal hypoglycaemia on GD17 reduced incidence and severity of histopathologic changes and with normal growth plate volume. Compromised foetal skeletal development following maternal hypoglycaemia throughout gestation is hypothesised to result from corticosterone-induced hypoxia in growth plates, where hypoxia disrupts chondrocyte maturation and growth plate structure and volume, decreasing long bone growth. Maternal/foetal hypoglycaemia lasting only until GD17 attenuated these changes, suggesting a pivotal role of glucose in growth plate development.

The fibroblast growth factor receptor, FGFR3, forms gradients of intact and degraded protein across the growth plate of developing bovine ribs

2002 ◽  
Vol 361 (2) ◽  
pp. 231-241 ◽  
Author(s):  
Sujata G. PANDIT ◽  
Prasanthi GOVINDRAJ ◽  
Joachim SASSE ◽  
Peter J. NEAME ◽  
John R. HASSELL
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Growth Plate ◽  
Point Mutations ◽  
Growth Factor Receptor ◽  
Fibroblast Growth ◽  
Fgf Receptor ◽  
Hypertrophic Zone ◽  
The Matrix ◽  
Maximum Expression

Point mutations in the human fibroblast growth factor (FGF) receptor 3 gene (Fgfr3) produce a constitutively active receptor, which disrupts chondrocyte differentiation in the growth plate and results in skeletal dysplasias with severe shortening of the limbs. Alternative splicing of the Fgfr3 transcript gives rise to two isoforms, IIIc and IIIb, which vary in their specificity for FGF ligands. We examined the expression of these FGFR3 isoforms in the bovine fetal rib growth plate to determine whether levels of FGFR3 expression are zone-related. Transcripts for both Fgfr3 isoforms are expressed in rib growth plate, with maximum expression in the hypertrophic region and the least expression in the reserve zone. Fgfr3 IIIc is the predominant isoform in the growth plate. Western-blot analysis revealed the presence of full-length FGFR3 (135kDa) for both isoforms in the reserve zone, a major 98kDa fragment in all zones and smaller fragments primarily in the hypertrophic zone. Immunostaining localized FGFR3 to the pericellular region of reserve chondrocytes and to the extracellular matrix in the hypertrophic zone. These results suggest that the transmembrane form of FGFR3 increasingly undergoes proteolytic cleavage towards the hypertrophic zone to produce an extracellular-domain fragment of FGFR3, which is present in large amounts in the matrix of hypertrophic cells. These findings suggest a proteolytic regulatory mechanism for FGFR3, whereby Fgfr3 fragments could control availability of FGF for the intact receptor, and by which proteolysis could inactivate the receptor.

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