MICROCHEMICAL ANALYSIS OF HUMAN TIBIAL GROWTH CARTILAGE IN VARIOUS FORMS OF DWARFISM

1972 ◽  
Vol 69 (4) ◽  
pp. 659-688 ◽  
Author(s):  
V. Stanescu ◽  
R. Stanescu ◽  
J. A. Szirmai
Keyword(s):  
Growth Plate ◽  
Chondroitin Sulphate ◽  
Epiphyseal Plate ◽  
Molecular Characteristics ◽  
Growth Disorders ◽  
Normal Children ◽  
Collagen Concentration ◽  
Vitamin D Resistant Rickets ◽  
Pooled Samples ◽  
Tibial Epiphyseal

ABSTRACT Microchemical determinations of glycosaminoglycans and collagen were preformed in isolated histological zones from sections of tibial epiphyseal plate biopsies obtained from children with growth disorders (pituitary dwarfism, congenital myxoedema, Turner's syndrome, Noonan's syndrome, mucopolysaccharidosis type VI, vitamin D resistant rickets and achondroplasia). Alternate sections were used for histochemical localization of glycosaminoglycans and proteins. The values were compared with those found in comparable zones of the growth plate from normal children of the same age. The chondroitin sulphate concentration (% of defatted dry wt.) in the normal epiphyseal plate increased from the resting zone towards the proliferating/hypertrophic zone; collagen exhibited a reverse trend. In some of the pathological biopsies the concentration of chondroitin sulphate was slightly decreased whereas that of collagen was slightly increased. A marked increase in the collagen concentration was found in achondroplasia. The solubility profiles of the cetylpyridinium complexes of the chondroitin sulphate fraction showed three main peaks with slight but characteristic differences in the various zones of the normal cartilage plate. Significant shifts in the proportion of these peaks were observed in several pathological biopsies, indicating possible deviations from the normal molecular characteristics of the chondroitin sulphate. Analysis of the main chondroitin sulphate fraction, obtained from pooled samples of normal tibial growth plate after fractionation on the macroscale, indicated that all three peaks contained both chondroitin-4 sulphate and chondroitin-6 sulphate and that they probably differed in their molecular weight.

Traumatic Premature Closure of the Distal Tibial Epiphyseal Plate

1967 ◽  
Vol 38 (1-4) ◽  
pp. 520-531 ◽  
Author(s):  
A. Langenskiöld
Keyword(s):  
Epiphyseal Plate ◽  
Premature Closure ◽  
Tibial Epiphyseal

Human placental lactogen inhibits growth without changing serum levels of IGF-1 in rats: an apparent specific action of the hormone

1992 ◽  
Vol 127 (2) ◽  
pp. 146-151 ◽  
Author(s):  
Mimi H Chiang ◽  
Charles S Nicoll
Keyword(s):  
Epiphyseal Plate ◽  
Skeletal Growth ◽  
Female Rats ◽  
Placental Lactogen ◽  
Total Serum ◽  
Inhibitory Effects ◽  
Growth Inhibitory ◽  
Growth Promoting ◽  
Tibial Epiphyseal ◽  
Plate Width

Previous work in our laboratory has shown that the internal environment of rats has reduced growth-promoting activity during the second half of gestation and this condition is associated with resistance to the anabolic effects of GH. The placenta appears to be responsible for this condition but injections of estradiol plus progesterone into virgin females did not mimic it. Accordingly, it seemed worthwhile to test the effects of a placental lactogen (PL) for possible growth inhibitory effects. In the present study the effects of human (h)PL on skeletal growth in young female rats and on the growth of embryonic tissue transplants under their kidney capsules were investigated. Human (h) and bovine (b) GH, and ovine prolactin (oPRL) were also tested to determine whether the results obtained with hPL were specific. Twice daily subcutaneous injections of a high dose of hPL (10mg/day), but not of oPRL (5 mg/day) for 7 days inhibited both host tail growth and tibial epiphyseal plate width, and growth of whole 10-day embryo transplants. Injections of hGH at 1 mg/day for 8 days significantly increased host skeletal growth and growth of 12-day embryonic head transplants; at the same dose, neither bGH nor oPRL affected growth of the embryonic heads or of the host tibial epiphyseal plate width, but the bGH increased host tail growth. By contrast, the 1 mg/day dose of hPL significantly reduced the host's tibial epiphyseal plate width, tail growth, and transplant growth; lower doses of hPL (10 and 100 μg/day) were also inhibitory. Although all the hormone treatments increased total serum IGF-1 levels in the females, none of them had a significant effect when compared to saline injected control animals. Thus, the growth-inhibitory effects of hPL treatment appear to be specific to that hormone and they are not mediated by depression of serum IGF-1 levels. If these effects of hPL are mimicked by one or more of the rodent PLs, then the reduced growth-promoting activity and resistance to GH action that occurs in pregnant rats could be due to the rat PLs. These results indicate that in addition to having glucose-sparing effects in the mother, PLs could promote fetal growth by inhibiting growth of maternal tissues, which would thus spare other metabolites, such as amino acids and vitamins, for the conceptus.

Growth and Mitotic Rate of the Proximal Tibial Epiphyseal Plate in Hypophysectomized Rats Given Estradiol and Human Growth Hormone

1975 ◽  
Vol 16 (344_suppl) ◽  
pp. 69-74 ◽  
Author(s):  
Per-Olof Gustafsson ◽  
Håkan Kasström ◽  
Lars Lindberg ◽  
Sten-Erik Olsson
Keyword(s):  
Growth Hormone ◽  
Human Growth Hormone ◽  
Human Growth ◽  
Mitotic Rate ◽  
Epiphyseal Plate ◽  
Hypophysectomized Rats ◽  
Tibial Epiphyseal

scholarly journals Serum Levels of 20-Kilodalton Human Growth Hormone (GH) Are Parallel Those of 22-Kilodalton Human GH in Normal and Short Children

1999 ◽  
Vol 84 (1) ◽  
pp. 98-104 ◽  
Author(s):  
Mayumi Ishikawa ◽  
Susumu Yokoya ◽  
Katsuhiko Tachibana ◽  
Yukihiro Hasegawa ◽  
Toshiaki Yasuda ◽  
...  
Keyword(s):  
Body Mass Index ◽  
Short Stature ◽  
Physiological Role ◽  
Growth Disorders ◽  
Turner's Syndrome ◽  
Turner’S Syndrome ◽  
Nocturnal Sleep ◽  
Normal Children ◽  
Significant Difference ◽  
The Mean

Twenty-kilodalton human GH (20K), which is one of the human GH (hGH) variants, is thought to be produced by alternative premessenger ribonucleic acid splicing. However, its physiological role is still unclear due to the lack of a specific assay. We have measured serum 20K and 22-kDa hGH (22K) by specific ELISAs to investigate the physiological role of 20K in children. The subjects were 162 normal children, aged 1 month to 20 yr; 12 patients with GH deficiency (GHD), aged 11 months to 13 yr; 57 children with non-GHD short stature, aged 2–17 yr; and 13 girls with Turner’s syndrome, aged 5 months to 15 yr. Samples were collected at random from normal children and were collected after hGH provocative tests and 3-h nocturnal sleep from GHD, non-GHD short stature, and Turner’s syndrome children. The mean basal serum concentrations of 22K and 20K were 2.4 ± 2.8 ng/mL and 152.3 ± 184.0 pg/mL in normal boys and 2.5 ± 3.1 ng/mL and 130.6 ± 171.5 pg/mL in normal girls, respectively. The percentages of 20K (%20K) were 5.8 ± 2.1% and 6.0 ± 3.2% in 83 normal boys and 79 normal girls, respectively. There was no significant difference in %20K either among ages or between the prepubertal stage and the pubertal stage in normal boys and girls. The mean %20K values in basal samples of provocative tests in 12 patients with GHD, non-GHD short stature, and Turner’s syndrome were 6.5 ± 2.4%, 6.5 ± 3.8%, and 5.9 ± 3.2%, respectively. There was no significant difference in %20K among normal children and these growth disorders, and there was no significant difference in %20K throughout the hGH provocative tests and 3-h nocturnal sleep in these growth disorders. There was also no significant correlation between the percentage of 20K and the height sd score or body mass index in either normal children or subjects with these growth disorders. In conclusion, the %20K is constant, regardless of age, sex, puberty, height sd score, body mass index, and GH secretion status. The regulation of serum 20K levels remains to be established.

Ultrastructure of the tibial epiphyseal growth plate in microphthalmic (mi/mi) mice

1989 ◽  
Vol 34 (2) ◽  
pp. 77-84 ◽  
Author(s):  
D. Paxinos-Maroudas ◽  
R.N. Powell ◽  
G.M. Newcomb
Keyword(s):  
Growth Plate ◽  
Epiphyseal Growth Plate ◽  
Tibial Epiphyseal

scholarly journals Genes with Specificity for Expression in the Round Cell Layer of the Growth Plate are Enriched in GWAS of Human Height

2021 ◽  
Author(s):  
Nora E. Renthal ◽  
Priyanka Nakka ◽  
John M. Baronas ◽  
Henry M. Kronenberg ◽  
Joel N. Hirschhorn
Keyword(s):  
Growth Plate ◽  
Cell Layer ◽  
Skeletal Growth ◽  
Gwas Data ◽  
Growth Disorders ◽  
Genome Wide Association Studies ◽  
Round Cell ◽  
P Values ◽  
Gene Set ◽  
Human Height

ABSTRACTHuman adult height reflects the outcome of childhood skeletal growth. Growth plate (epiphyseal) chondrocytes are key determinants of height. As epiphyseal chondrocytes mature and proliferate, they pass through three developmental stages, which are organized into three distinct layers in the growth plate: 1) resting (round), 2) proliferative (flat), and 3) hypertrophic. Recent genome-wide association studies (GWAS) of human height identified numerous associated loci, which are enriched for genes expressed in growth plate chondrocytes. However, it remains unclear which specific genes expressed in which layers of the growth plate regulate skeletal growth and human height.To connect the genetics of height and growth plate biology, we analyzed GWAS data through the lens of gene expression in the three dissected layers of murine newborn tibial growth plate. For each gene, we derived a specificity score for each growth plate layer and regressed these scores against gene-level p-values from recent height GWAS data. We found that specificity for expression in the round cell layer, which contains chondrocytes early in maturation, is significantly associated with height GWAS p-values (p=8.5×10−9); this association remains after conditioning on specificity for the other cell layers. The association also remains after conditioning on membership in an “OMIM gene set” (genes known to cause monogenic skeletal growth disorders, p<9.7×10−6). We replicated the association in RNA-seq data from maturing chondrocytes sampled at early and late time points during differentiation in vitro: we found that expression early in differentiation is significantly associated with p-values from height GWAS (p=6.1×10−10) and that this association remains after conditioning on expression at 10 days in culture and on the OMIM gene set (p<0.006). These findings newly implicate genes highlighted by GWAS of height and specifically expressed in the round cell layer as being potentially important regulators of skeletal biology.

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