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Results for “Growth plate”

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At least 19 recordsLinked to original sources
PubMed1979

Stimulation of cartilage zones of the calf costochondral growth plate in vitro by growth hormone dependent rat plasma somatomedin activity.

The actions of rat plasma somatomedin activity dependent on growth hormone were investigated in vitro on separated zones of cartilage from the calf costochondral junction. Plasma somatomedin maximally stimulated the uptake of[3H]thymidine into cartilage cells of the proliferating region. Cartilage deeper in the growth plate possessed the highest uptake of [35S]sulphate which was also stimulated by somatomedin. Somatomedin, therefore, appears to promote both cell replication and matrix synthesis throughout the growth plate cartilage although the two processes were greatest in different cartilage regions. Growth hormone or tri-iodothyronine did not directly alter the uptake of either isotope into the growth plate cartilage.

Animals↗
PubMed1979

The fine structure of the proximal growth plate of the avian tibia.

The ultrastructure of the proximal tibial growth plate of the 7 weeks old chicken has been described. Little ultrastructural difference could be ascertained between growth plates examined from normal white leghorn and commercial broiler chickens. The growth plate may be divided into five zones: interstitial, proliferating, prehypertrophic, hypertrophic, and degenerating hypertrophic. These zones reflect a maturation of chondrocytes, beginning with a stage of high mitotic and cytoplasmic activity passing through a stage of active secretion of matrical components (prehypertrophic and hypertrophic) and ending with degeneration of the cells and calcification of the matrix. Mineralization of the matrix appears to be initiated within matrical dense bodies, as in the mammal. Single hydroxyapatite crystals are first encountered about 0.1 mm proximal (i.e. towards the knee) to the limit of metaphyseal blood vessel ingrowth, while dense calcification is observed 0.1 mm distal to the tips of these metaphyseal vessels. The diameter of microfibrillary collagen in the growth plate matrix ranges from approximately 9 nm in the proximal zones to 19 nm in the distal zones. Many of the fibrils in the distal zones have a more or less distinct periodicity. Other major elements of the growth plate matrix are the ruthenium red-stained syncytial aggregates of mucopolysaccharides which are probably derived from the granules within the large intracellular Golgi vesicles. These findings have led the author to conclude that, while light microscopy indicates that avian and mammalian growth plates have very different structures, electron microscopy finds many similarities, suggesting that the physiological control mechanisms in these two vertebrate classes have much in common.

Animals↗
PubMed1979

Skeletal changes during prolonged external irradiation: alterations in marrow, growth plate and osteoclast populations.

This report describes hematologic and skeletal changes in young mice subjected to continuous external whole body irradiation (45 rads/day) for 4 days to 12 weeks. Irradiation caused a rapid depletion of hematopoietic stem cells, marrow aplasia and pancytopenia, all of which persisted during the period of irradiation but resolved afterward. In spite of suppressed cellular proliferation and disarray of cartilage cell columns in metaphyseal plates, linear bone growth appeared to continue at physiologic rates. Histologic and morphometric studies provided no evidence of impaired osteoblast function, but the presence of thickended trabeculae beneath the growth plate and of cartilagenous islands within cortical shafts of long bones indicated that bone remodeling was deficient. Direct osteoclast counts demonstrated that marrow aplasia was followed by a progressive decline that could not be reversed by parathormone injections or infusions with mature macrophages and lymphocytes but that resolved once the bone marrow recovered following cessation of irradiation. Therefore, the altered bone remodeling probably resulted from radiation injury to osteoclast precursors in the hematopoietic compartment.

Animals↗
PubMedDate not supplied

The mechanical strength of the growth plate under the influence of sex hormones.

As sex hormones are considered to play a role in the etiology of the slipped upper femoral epiphysis, the influence of sex hormones on the mechanical strength of the epiphyseal plate was investigated in 310 female and 70 male rats. Ovariectomy weakened the strength of the growth plate while orchiectomy strengthened it. Estrogen given after ovariectomy, markedly strengthened the plate. Histologic examination revealed that the width of the growth plate was narrower in the mechanically stronger group. Hydroxyproline content increased and hexosamine content decreased in the epiphyseal plates of the mechanically stronger group. These observations confirm the view that sex hormones, especially estrogen, regulate the mechanical, morphologic, and biochemical functions of the growth plate.

Animals↗
PubMed1979

Identification of phosphopeptides and gamma-carboxyglutamic acid-containing peptides in epiphyseal growth plate cartilage.

Uncalcified cartilage from the epiphyseal portion of bovine scapulae, both distant and adjacent to the epiphyseal growth plate, and the calcified cartilage of the epiphyseal growth plate itself were analyzed for the presence of O-phosphoserine [Ser(P)], O-phosphothreonine [Thr(P)] and gamma-carboxyglutamic acid (G1a). Only trace amounts of these Ca2+-binding amino acids or the peptides containing them were found in the unmineralized tissues. In contrast, whole calcified cartilage, and especially the most mineralized fraction obtained by density centrifugation, contained considerable amounts of all three amino acids. Essentially all of the G1a and the majority of the Ser(P) and Thr(P) were present in non-collagenous, non-diffusible proteins extractable in EDTA at near-neutral pH.

1-Carboxyglutamic Acid↗
PubMed2023

Osteolectin increases bone elongation and body length by promoting growth plate chondrocyte proliferation.

Osteolectin is a recently identified osteogenic growth factor that binds to Integrin α11 (encoded by Itga11), promoting Wnt pathway activation and osteogenic differentiation by bone marrow stromal cells. While Osteolectin and Itga11 are not required for the formation of the skeleton during fetal development, they are required for the maintenance of adult bone mass. Genome-wide association studies in humans reported a single-nucleotide variant (rs182722517) 16 kb downstream of Osteolectin associated with reduced height and plasma Osteolectin levels. In this study, we tested whether Osteolectin promotes bone elongation and found that Osteolectin-deficient mice have shorter bones than those of sex-matched littermate controls. Integrin α11 deficiency in limb mesenchymal progenitors or chondrocytes reduced growth plate chondrocyte proliferation and bone elongation. Recombinant Osteolectin injections increased femur length in juvenile mice. Human bone marrow stromal cells edited to contain the rs182722517 variant produced less Osteolectin and underwent less osteogenic differentiation than that of control cells. These studies identify Osteolectin/Integrin α11 as a regulator of bone elongation and body length in mice and humans.

Adult↗
PubMed1975

The influence of corticosteriods on the normal and papain-treated epiphysial growth plate in the rabbit.

Children undergoing continuous corticosteroid therapy become stunted in height. The mechanism of this inhibition of natural growth has been investigated in the lower femoral epiphysial growth plate of young rabbits on daily corticosteroid. The growth plate became narrow: fewer cells in the germinative zone gave rise to short widely-spaced chondrocyte columns, each with a reduced number of mature and hypertrophic cells; the pattern of trabecular bone in the metaphysis was also disturbed. After even small doses these changes develop very rapidly, and therefore impose a threat to the growth of children receiving treatment with corticosteroids.

Adrenal Cortex Hormones↗
PubMed1979

Kniest dysplasia. A histochemical study of the growth plate.

Chondro-osseous tissue from four patients with the Kniest dysplasia was studied histochemically using a new plastic embedding technique. Extensive vacuolar changes were observed p--1 throughout the endochondral growth plate and adjacent resting cartilage. These changes occurred within the cartilage matrix and also in the lacunae of degenerating chrondrocytes. The septa of the lesions contained chondroitin sulfate, but little keratan sulfate or collagen. Resting cartilage not adjacent to the growth plate stained irregularly and showed few of the vacuolar lesions, and chondrocytes were enlarged and contained cytoplasic inclusions, but no vacuolar material. Thus, there appears to be a sequence of events initiated by cellular accumulation of a substance and progressing to cellular and matrix degeneration.

Adolescent↗
PubMed1976

In vitro epiphyseal-plate growth in various constant electrical fields.

An in vitro epiphyseal-plate model was subjected to various electrical fields. At a voltage gradient of 1500 volts per centimeter, a consistent, highly significant acceleration of growth of the epiphyseal plate occurred as measured from photomacrographs and as indicated by incorporation of 45Ca, 35S, and 3H-thymidine. The growth acceleration was due to voltage gradients and not to current flow. Although the mechanism of action of the electrical field is not known, it is obvious that the voltage gradient, either directly or indirectly, incites a physiological response of the growth-plate chondrocyte.

Animals↗
PubMed1977

Defects in the cartilaginous growth plates of brachymorphic mice.

Homozygous brachymorphic (bm/bm) mice are characterized by disproportionately short stature. Newborn bm/bm epiphyseal cartilages are shorter than normal although the cells in the different zones of growth are relatively well organized. The extracellular matrix reacts poorly with stains specific for sulfated glycosaminoglycans. The ultrastructural appearance of the cartilage matrix indicates normal collagen fibrils; however, proteoglycan aggregate granules are smaller than normal and are present in reduced numbers, particularly in the columnar and hypertrophic zones of the growth plate. In addition, a prominent network of fine filaments, which are extractable in 4 M guanidine hydrochloride, are present in the bm/bm cartilage matrix. These findings suggest that a defect affecting the proteoglycan component of cartilage occurs in bm/bm mice.

Animals↗
PubMed1979

Diastropic dwarfism: a histochemical and ultrastructural study of the endochondral growth plate.

Chondro-osseous tissue from five patients with diastropic dwarfism was studied by histologic, histochemical, and electron microscopic methods. The major abnormalities observed were: 1) irregular distribution of chondrocytes undergoing degeneration in the resting cartilage; 2) abnormal distribution of collagens in the resting cartilage; 3) a spectrum of fibrous matrix lesions in the resting cartilage which ranged from focal areas of aggregated collagen fibrils to large cystic lesions in which intracartilagenous ossification occurred; and 4) shortened, irregular cellular columns within the growth plate which were occasionally disrupted by matrix lesions extending from the resting cartilage. These alterations in chondro-osseous morphology have not been observed in any of the other skeletal dysplasias examined to date and appear to be pathognomonic for this disorder.

Adolescent↗
PubMed1978

The effects of ethylene-1-hydroxy-1, 1-diphosphonate on cellular transformation and organic matrix of the epiphyseal growth plate of the rat--a light microscopic and ultrastructural study.

Ethylene-1-hydroxy-1, 1-diphosphonate (EHDP) was administered intraperitoneally to one-day-old rats. In the first experiment, each animal was given 4 injections of EHDP distributed over two consecutive days and corresponding to a total amount of EHDP of 100 mg/kg bwt/day. The animals were sacrificed 12 hours after the last injection. In the second experiment, each animal was given 3 injections, each containing 50 mg of EHDP/kg bwt, with an interval of 6 hours and were thereafter left to survive for 4 days. Animals in the first experiment showed in comparison to normal controls an increased width of the hypertrophic zone; lack of calcified septa within the zone of provisional calcification; persistent atypical chondrocytes in the calcification zone and a large number of matrix vesicles lacking in crystals. The ground substance showed an accumulation of fine precipitates apparently representing undegraded aggregates of proteoglycan macromolecules. Animals in the second experiment formed a new apparently normal epiphyseal growth plate, while the "old" epiphyseal cartilage formed under the influence of EHDP remained largely unresorbed within the metaphysis. Besides the previously described inhibitory effects of diphosphonates on the crystallization of matrix vesicles and the growth of hydroxyapatite crystals, EHDP, at the doses used, was found to have a profound inhibitory effect on the differentiation and migration of the epiphyseal chondrocytes as well as on the degradation of proteoglycan macromolecules. The observed inhibition of vascular invasion appears to be related to inhibition of enzyme degradation of the ground substance, as evidenced by the observation of extracellular lysosomelike bodies in the erosion zone.

Animals↗
PubMed1979

Morphology of the perforating cartilage canals in the proximal tibial growth plate of the chick.

Perforating canals arise exclusively from junctional canals just above the reserve zone and they do not branch after entering the proliferative zone. They are uniformly spaced and arranged in parallel array. The cartilage canals terminate near the beginning of the zone of hypertrophic cartilage cells. Vascular components within the perforating canals consist of a central arteriole surrounded by enlarged, interconnected capillaries which are individually in contact with the adjacent cartilage matrix. TEM shows that the capillary endothelium is extremely attenuated, possesses numerous fenestrations and lacks a continuous basement membrane. The central arteriole is enlarged through the midpart of the canal and then narrows to communicate with the capillaries near the bottom of the canal. The large capillaries ascend from their point of origin and recombine near the top of the growth plate to exit as a single venule. The vascular arrangement therefore describes a system in which the outgoing blood runs in close proximity, but counter to, the incoming blood. This vascular arrangement within the perforating cartilage canal would most likely allow the zone of maturing cartilage cells to receive the highest concentration of nutrients.

Animals↗
PubMed1978

Ca2+ transport by chondrocyte mitochondria of the epiphyseal growth plate.

In a study of the Ca2+ kinetics of mitochondria of chick epiphyseal chondrocytes, the rate of Ca2+ uptake was linear up to a medium Ca2+ concentration of 30 mum. The half maximal transport rate occurred at 34 mum Ca2+. The Ca2+ uptake rate, expressed as a function of time, was 35 nmoles/mg protein/min; the presence of Mg2+ had little effect on Ca2+ accumulation. While these kinetic parameters did not differ significantly from mitochondria of cells of nonmineralizing tissues, the respiratory characteristics of the chondrocyte organelles exhibited functional differences. Thus, up to 350 nmoles Ca2+/mg protein, chondrocyte mitochondria performed coupled oxidative phosphorylation. Calcium uptake was energy supported, while Ca2+ binding was low. Addition of respiratory inhibitors and uncouplers to these mitochondria resulted in a rapid loss of more than 80% of the total Ca2+. The Ca/Pi ratio of the extrudate was very similar to the ratio of the ions in cartilage septum fluid. In the most mineralized zones of the epiphyseal plate, there was little change in the state 4 respiratory rate, but nonspecific Ca2+ binding was elevated and a high percentage of the total Ca2+ was in a nonextrudable form. The results indicate that in cells preparing for mineralization, much of the total mitochondrial Ca2+ is in a form that can be transported to the calcification front. In cells close to the calcification front, nonextrudable Ca2+ may form calcium phosphate granules described by other investigators.

Animals↗