A TECHNIQUE FOR MEASURING LINEAR BONE GROWTH DURING SHORT TIME INTERVALS IN CATTLE

1981 ◽  
Vol 61 (4) ◽  
pp. 1049-1053
Author(s):  
W. C. GRAHAM ◽  
M. A. PRICE
Keyword(s):  
Growth Plate ◽  
Ultraviolet Light ◽  
Present Experiment ◽  
Bone Growth ◽  
Age Groups ◽  
Epiphyseal Growth Plate ◽  
Time Intervals ◽  
Bone Length ◽  
Green Fluorescent ◽  
Short Time

A technique is described for meausuring increases in bone length during defined periods before slaughter in cattle. It consists of jugular infusions of oxytetracycline at specified time intervals. Oxytetracycline identifies the sites of ossification in growing bones at the time of infusion by leaving a label which can be seen as a yellow-green fluorescent line under ultraviolet light. By applying a series of labels at known time intervals, the amount and rate of bone growth at any particular site during those time intervals can be determined. In the present experiment the distal epiphyseal growth plate in the radiuses of young cows (five 2-yr-olds, five 3-yr-olds and four 4-yr-olds) were studied. The increase in bone length at that site for the three age groups was found to be 0.0732, 0.0205 and 0.0000 mm/day respectively.

scholarly journals Expression of vascular endothelial growth factor in the growth plate is stimulated by estradiol and increases during pubertal development

2010 ◽  
Vol 205 (1) ◽  
pp. 61-68 ◽  
Author(s):  
Joyce Emons ◽  
Andrei S Chagin ◽  
Torun Malmlöf ◽  
Magnus Lekman ◽  
Åsa Tivesten ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Growth Plate ◽  
Bone Growth ◽  
Pubertal Development ◽  
Mrna Levels ◽  
Vascular Endothelial ◽  
Epiphyseal Growth Plate ◽  
Vegf Expression ◽  
Endothelial Growth Factor

Longitudinal bone growth is regulated in the growth plate. At the end of puberty, growth velocity diminishes and eventually ceases with the fusion of the growth plate through mechanisms that are not yet completely understood. Vascular endothelial growth factor (VEGF) has an important role in angiogenesis, but also in chondrocyte differentiation, chondrocyte survival, and the final stages of endochondral ossification. Estrogens have been shown to up-regulate VEGF expression in the uterus and bone of rats. In this study, we investigated the relation between estrogens and VEGF production in growth plate chondrocytes both in vivo and in vitro. The expression of VEGF protein was down-regulated upon ovariectomy and was restored upon estradiol (E2) supplementation in rat growth plates. In cultured rat chondrocyte cell line RCJ3.1C5.18, E2 dose dependently stimulated 121 and 189 kDa isoforms of VEGF, but not the 164 kDa isoform. Finally, VEGF expression was observed at both protein and mRNA levels in human growth plate specimens. The protein level increased during pubertal development, supporting a link between estrogens and local VEGF production in the growth plate. We conclude that estrogens regulate VEGF expression in the epiphyseal growth plate, although the precise role of VEGF in estrogen-mediated growth plate fusion remains to be clarified.

Direct administration of testosterone increases rat tibial epiphyseal growth plate width

1989 ◽  
Vol 121 (3) ◽  
pp. 401-405 ◽  
Author(s):  
Song Guang Ren ◽  
Saul Malozowski ◽  
Prosper Sanchez ◽  
Donald E. Sweet ◽  
D. Lynn Loriaux ◽  
...  
Keyword(s):  
Growth Plate ◽  
Bone Growth ◽  
Serum Testosterone ◽  
Male Rats ◽  
Testosterone Enanthate ◽  
Epiphyseal Growth Plate ◽  
Igf I ◽  
Direct Administration ◽  
Tibial Epiphyseal ◽  
Plate Width

Abstract. Local injection of hormones into the tibial epiphyseal growth plate offers a possible model to answer whether sex steroids can affect bone growth directly. To answer this question, we injected different doses of testosterone enanthate (4, 40, 120 and 400 μg/100 g of rat weight) once into the tibial epiphyseal growth plate of castrated 35-day-old male rats. The contralateral tibia was injected with sesame oil and served as control. All animals were sacrificed at age 42 days. Tibias were removed for measurement of epiphyseal growth plate width and blood was collected for measurement of serum IGF-I and testosterone. The lower doses of testosterone enanthate (4, 40 and 120 μg/100 g) did not produce any significant change in epiphyseal growth plate width. Testosterone at the largest dose tested (400 μg/100 g) increased epiphyseal growth plate width by about 15% compared to control (p < 0.01). At this dose, serum testosterone was not increased, suggesting that the effect on epiphyseal growth plate width was not due to higher systemic testosterone concentrations. No differences in IGF-I levels were observed among the groups. We conclude that direct administration of testosterone enanthate at a dose of 400 μg/100 g into the rat tibial epiphyseal growth plate can increase epiphyseal growth plate width.

scholarly journals Locally produced estrogen promotes fetal rat metatarsal bone growth; an effect mediated through increased chondrocyte proliferation and decreased apoptosis

2006 ◽  
Vol 188 (2) ◽  
pp. 193-203 ◽  
Author(s):  
A S Chagin ◽  
D Chrysis ◽  
M Takigawa ◽  
E M Ritzen ◽  
L Sävendahl
Keyword(s):  
Growth Plate ◽  
Bone Growth ◽  
Longitudinal Growth ◽  
Epiphyseal Growth Plate ◽  
Chondrocyte Proliferation ◽  
Growth Plate Cartilage ◽  
Ici 182,780 ◽  
Metatarsal Bones ◽  
Fetal Rat ◽  
Estrogen Synthesis

The importance of estrogens for the regulation of longitudinal bone growth is unequivocal. However, any local effect of estrogens in growth plate cartilage has been debated. Recently, several enzymes essential for estrogen synthesis were shown to be expressed in rat growth plate chondrocytes. Local production of 17β-estradiol (E2) has also been demonstrated in rat costal chondrocytes. We aimed to determine the functional role of locally produced estrogen in growth plate cartilage. The human chondrocyte-like cell line HCS-2/8 was used to study estrogen effects on cell proliferation (3H-labeled thymidine uptake) and apoptosis (cell death detection ELISA kit). Chondrocyte production of E2 was measured by RIA and organ cultures of fetal rat metatarsal bones were used to study the effects of estrogen on longitudinal growth rate. We found that significant amounts of E2 were produced by HCS-2/8 chondrocytes (64.1 ± 5.3 fmol/3 days/106cells). The aromatase inhibitor letrozole (1 μM) and the pure estrogen receptor antagonist ICI 182,780 (10 μM) inhibited proliferation of HCS-2/8 chondrocytes by 20% (P<0.01) and almost 50% (P<0.001), respectively. Treatment with ICI 182,780 (10 μM) increased apoptosis by 228% (P<0.05). Co-treatment with either caspase-3 or pan-caspase inhibitors completely blocked ICI 182,780-induced apoptosis (P<0.001 vs ICI 182,780 only). Moreover, both ICI 182,780 (10 μM) and letrozole (1 μM) decreased longitudinal growth of fetal rat metatarsal bones after 7 days of culture (P<0.01). In conclusion, our data clearly show that chondrocytes endogenously produce E2 and that locally produced estrogen stimulates chondrocyte proliferation and protects from spontaneous apoptosis. In addition, longitudinal growth is promoted by estrogens locally produced within the epiphyseal growth plate.

scholarly journals Skeletal Toxicity of Coplanar Polychlorinated Biphenyl Congener 126 in the Rat Is Aryl Hydrocarbon Receptor Dependent

2020 ◽  
Vol 175 (1) ◽  
pp. 113-125 ◽  
Author(s):  
Ashlee E Williams ◽  
James Watt ◽  
Larry W Robertson ◽  
Gopi Gadupudi ◽  
Michele L Osborn ◽  
...  
Keyword(s):  
Growth Plate ◽  
Bone Growth ◽  
Polychlorinated Biphenyl ◽  
Corn Oil ◽  
Specific Effect ◽  
Tissue Growth ◽  
Bone Formation Rate ◽  
Bone Length ◽  
Dynamic Histomorphometry ◽  
Pcb 126

Abstract Epidemiological evidence links polychlorinated biphenyls (PCBs) to skeletal toxicity, however mechanisms whereby PCBs affect bone are poorly studied. In this study, coplanar PCB 126 (5 μmol/kg) or corn oil vehicle was administered to N = 5 and 6 male and female, wild type (WT) or AhR −/− rats via intraperitoneal injection. Animals were sacrificed after 4 weeks. Bone length was measured; bone morphology was assessed by microcomputed tomography and dynamic histomorphometry. Reduced bone length was the only genotype-specific effect and only observed in males (p &lt; .05). WT rats exposed to PCB 126 had reduced serum calcium, and smaller bones with reduced tibial length, cortical area, and medullary area relative to vehicle controls (p &lt; .05). Reduced bone formation rate observed in dynamic histomorphometry was consistent with inhibition of endosteal and periosteal bone growth. The effects of PCB 126 were abolished in AhR −/− rats. Gene expression in bone marrow and shaft were assessed by RNA sequencing. Approximately 75% of the PCB-regulated genes appeared AhR dependent with 89 genes significantly (p &lt; .05) regulated by both PCB 126 and knockout of the AhR gene. Novel targets significantly induced by PCB 126 included Indian hedgehog (Ihh) and connective tissue growth factor (Ctgf/Ccn2), which regulate chondrocyte proliferation and differentiation in the bone growth plate and cell-matrix interactions. These data suggest the toxic effects of PCB 126 on bone are mediated by AhR, which has direct effects on the growth plate and indirect actions related to endocrine disruption. These studies clarify important mechanisms underlying skeletal toxicity of dioxin-like PCBs and highlight potential therapeutic targets.

Spaceflight and age affect tibial epiphyseal growth plate histomorphometry

1992 ◽  
Vol 73 (2) ◽  
pp. S19-S25 ◽  
Author(s):  
D. Montufar-Solis ◽  
P. J. Duke ◽  
G. Durnova
Keyword(s):  
Growth Plate ◽  
Bone Growth ◽  
Ultrastructural Level ◽  
Cell Number ◽  
Epiphyseal Growth Plate ◽  
Growth Plates ◽  
Proliferative Zone ◽  
Old Rats ◽  
Modifying Effect ◽  
Matrix Organization

Growth plate histomorphometry of rats flown aboard the Soviet biosatellite COSMOS 2044, a 14-day spaceflight, was compared with that of control groups. In growth plates of flight animals, there was a significant increase in cell number per column and height of the proliferative zone and a reduction in height and cell number in the hypertrophy/calcification zone. No significant differences were found in matrix organization at the ultrastructural level of flight animals, indicating that although spaceflight continues to affect bone growth of 15-wk-old rats, extracellular matrix is not altered in the same manner as seen previously in younger animals. All groups showed growth plate characteristics attributed to aging: lack of calcification zone, reduced hypertrophy zone, and unraveling of collagen fibrils. Tail-suspended controls did not differ from other controls in any of the parameters measured. Our results suggest that growth plates of older rats are less responsive to unloading by spaceflight or suspension than those of younger rats and provide new evidence about the modifying effect of spaceflight on the growth plate.

scholarly journals STAT1 mediates the increased apoptosis and reduced chondrocyte proliferation in mice overexpressing FGF2

Development ◽  
2001 ◽  
Vol 128 (11) ◽  
pp. 2119-2129 ◽  
Author(s):  
Malika Sahni ◽  
Regina Raz ◽  
J. Douglas Coffin ◽  
David Levy ◽  
Claudio Basilico
Keyword(s):  
Growth Plate ◽  
Bone Growth ◽  
Fgf Signaling ◽  
Intramembranous Ossification ◽  
Epiphyseal Growth Plate ◽  
Growth Plate Chondrocytes ◽  
Chondrocyte Proliferation ◽  
Transgenic Mouse Line ◽  
Proliferative Zone ◽  
Significant Correction

Unregulated FGF receptor signaling results in bone malformations that affect both endochondral and intramembranous ossification, and is the basis for several genetic forms of human dwarfism. FGF signaling inhibits chondrocyte proliferation and we have previously shown that the transcription factor STAT1 mediates the growth inhibitory effect of FGF in vitro. We provide genetic evidence that STAT1 is a modulator of the negative regulation of bone growth by FGF in vivo. We crossed Stat1−/− mice with a transgenic mouse line overexpressing human FGF2 (TgFGF). TgFGF mice exhibit phenotypes characterized by chondrodysplasia and macrocephaly, which affect endochondral and intramembranous ossification. We found that the chondrodysplasic phenotype of these mice results both from reduced proliferation and increased apoptosis of growth plate chondrocytes. Loss of STAT1 function in TgFGF mice led to a significant correction of the chondrodysplasic phenotype, but did not affect the skull malformations. The reduced proliferation of TgFGF growth plate chondrocytes, as well as their excessive apoptosis, were restored to near-normal levels in the absence of STAT1 function. Unregulated FGF signaling in TgFGF mice also induced apoptosis in calvarial osteoblasts that was not, however, corrected by the absence of STAT1. Detailed analysis of Stat1−/− growth plates uncovered a transient phenotype, characterized by an expansion of the proliferative zone and by acceleration of longitudinal bone growth, that attenuated as the animals grew older. These results document an essential role for STAT1 in FGF-mediated regulation of cell growth that is specific to the epiphyseal growth plate.

scholarly journals Effect on knee disarticulation on bone growth in immature rabbits

1997 ◽  
Vol 21 (3) ◽  
pp. 189-194
Author(s):  
S. Alsancak ◽  
B. Erdemli ◽  
Z. Korkusuz
Keyword(s):  
Growth Plate ◽  
Research Laboratory ◽  
Bone Growth ◽  
Skin Flap ◽  
Epiphyseal Growth Plate ◽  
Flap Technique ◽  
The University ◽  
Knee Disarticulation

This study was designed by the University of Ankara Experimental and Research Laboratory for animals in 1997. In the study an anteroposterior skin flap technique was used for 20 knee disarticulation amputations and also in 20 trans-femoral amputations on immature rabbits, in order to investigate their effects on the femoral epiphyseal growth plate. The femurs of the rabbits were observed radiographically for 8 weeks. It was observed that the femurs tended to grow at a slower rate compared to the normal contralateral femur. These studies showed that the disarticulated limb femurs grew 0.68cm shorter on average compared to the contralateral femurs and the femurs in the trans-femoral amputated limbs 3.58cm shorter on average compared to the contralateral ones. These results were found to be statistically significant.

scholarly journals GPR30 Estrogen Receptor Expression in the Growth Plate Declines as Puberty Progresses

2007 ◽  
Vol 92 (12) ◽  
pp. 4873-4877 ◽  
Author(s):  
Andrei S. Chagin ◽  
Lars Sävendahl
Keyword(s):  
Growth Plate ◽  
Bone Growth ◽  
Receptor Expression ◽  
Skeletal Maturation ◽  
Tall Stature ◽  
Leg Length ◽  
Epiphyseal Growth Plate ◽  
Growth Plates ◽  
Longitudinal Bone Growth ◽  
Proliferative Zone

Abstract Objective: Our objective was to study whether GPR30 is expressed in the epiphyseal growth plate and its potential role as a modulator of pubertal growth. Background: Estrogens play a crucial role in the regulation of skeletal maturation and longitudinal bone growth. We have previously shown that both estrogen receptors (ERs) α and β are expressed in the human epiphyseal growth plate. Recently, a membrane-bound ER referred to as GPR30 was discovered, but the role played by this receptor in the regulation of longitudinal bone growth is not yet known. Patients/Methods: Biopsies were collected from the tibial growth plates of 14 boys and seven girls that underwent epiphyseal surgery to arrest longitudinal bone growth. The patients were in different stages of puberty and suffered from inequality in leg length or extreme tall stature. Paraffin-embedded sections of the growth plates were used to detect expression of the GPR30 protein. Results: The highest level of GPR30 expression was observed in hypertrophic chondrocytes, although cells with positive immunostaining were also detected in the resting zone. In contrast, no immunoreactivity was found in the proliferative zone. During pubertal progression there was a clear decline in the level of GPR30 expression in both boys and girls. Conclusions: The novel ER GPR30 is expressed in the human growth plate, and the level of expression declines during pubertal progression. Although a relationship between GPR30 expression and age may underlie the observed pubertal decline in the GPR30 level, our observations suggest that this receptor could be involved in the modulation of longitudinal bone growth during puberty.

scholarly journals In vivo and in vitro Chondrocyte Metabolism in Relationship to the Developemnt of Tibial Dyschondroplasia in Broiler Chickens

1993 ◽  
Author(s):  
Roland M. Leach ◽  
Mark Pines ◽  
Carol V. Gay ◽  
Shmuel Hurwitz
Keyword(s):  
In Situ Hybridization ◽  
Growth Plate ◽  
Bone Growth ◽  
Future Research ◽  
Epiphyseal Growth Plate ◽  
Growth Plate Chondrocytes ◽  
Tibial Dyschondroplasia ◽  
Sequence Of Events

Skeletal deformities are a significant financial and welfare problem for the world poultry industry. Tibial dyschondroplasia (TD) is the most prevalent skeletal abnormality found in young broilers, turkeys and ducks. Tibial dyschondroplasia results from a perturbation of the sequence of events in the epiphyseal growth plate, the tissue responsible for longitudinal bone growth. The purpose of this investigation was to test the hypothesis that TD was the result of a failure of growth plate chondrocytes to differentiate and express the chemotactic molecules required for cartilage vascularization. In this investigation in situ hybridization and immunocytochemical techniques were used to study chondrocyte gene products associated with cartilage maturation and vascularization such as osteopontin, osteonectin, type X collagen, and alkaline phosphatase. All markers were present in the growth plate tissue anter or to the TD lesion but were greatly diminished in the TD lesion. Thus, rather than not acquiring the markers for hypertrophy, it appears that the growth plate chondrocytes reach a certain stage of hypertrophy and then de-differentiate into cells which resemble chondrocytes in the prehypertrophic zone. Similar patterns were observed in all TD tissues examined whether the lesions were spontaneous or induced by dietary treatments or genetic selection. The decrease in gene expression can at least be partially explained by the fact that many of the dysplastic chondrocytes show classic signs of apoptosis. These results provide an explanation for the observation that a variety of genes show reduced expression in the TD lesion when examined by in situ hybridization. This would suggest that future research should focus on the earliest detectable stages in the development of TD and examine endocrine and autocrine factors which cause chondrocytes to de-differentiate and undergo premature apoptosis.

Effects of Hypophysectomy on the Occurrence and Calcifiability of Matrix Vesicles in the Epiphyseal Growth Plate of Immature Rats

1980 ◽  
Vol 38 ◽  
pp. 578-579
Author(s):  
S. I. Coleman ◽  
W. J. Dougherty
Keyword(s):  
Growth Plate ◽  
Matrix Vesicles ◽  
Epiphyseal Growth Plate ◽  
Hard Tissue ◽  
Hormonal Factors ◽  
Post Surgery ◽  
Mineral Deposition ◽  
Thin Sectioning ◽  
Integral Role ◽  
Cellular Secretion

In the cellular secretion theory of mineral deposition, extracellular matrix vesicles are believed to play an integral role in hard tissue mineralization (1). Membrane limited matrix vesicles arise from the plasma membrane of epiphyseal chondrocytes and tooth odontoblasts by a budding process (2, 3). Nutritional and hormonal factors have been postulated to play essential roles in mineral deposition and apparently have a direct effect on matrix vesicles of calcifying cartilage as concluded by Anderson and Sajdera (4). Immature (75-85 gm) Long-Evans hooded rats were hypophysectomized by the parapharyngeal approach and maintained fourteen (14) days post-surgery. At this time, the animals were anesthetized and perfusion fixed in cacodylate buffered 2.5% glutaraldehyde. The proximal tibias were quickly dissected out and split sagittally. One half was used for light microscopy (LM) and the other for electron microscopy (EM). The halves used for EM were cut into blocks approximately 1×3 mm. The tissue blocks were prepared for ultra-thin sectioning and transmission EM. The tissue was oriented so as to section through the epiphyseal growth plate from the zone of proliferating cartilage on down through the hypertrophic zone and into the initial trabecular bone. Sections were studied stained (double heavy metal) and unstained.

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