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Biomedical subjects

W S Jee

Publications and source records attributed to W S Jee.

At least 145 records · Page 8Linked to original sources
PubMed1988

Skeletal tissue responses to thermal injury: an experimental study.

Skeletal changes occurring secondary to burn injuries were studied in an experimental animal model for thermal injury. One hindlimb of female Sprague-Dawley rats (200-250g) was subjected to a standardized thermal injury; the other hindlimb was left untreated. Control animals received no experimental treatment. Effects on skeletal architecture were studied at the proximal tibial metaphysis and tibial diaphysis using static histomorphometry. Bone formation dynamics were studied from a series of bone fluorochrome labels administered before the experiment began, early (days 8, 9) postburn treatment (PBT) and late PBT (days 17, 18). Animals were sacrificed on day 21 PBT. In proximal tibial metaphyses of burn-treated limbs, trabecular bone area (TBA) and trabecular number in all regions except the primary spongiosa, were significantly reduced. TBA was also decreased, but not significantly in nontreated limbs. Longitudinal growth rate, growth plate thickness and growth cartilage cell production rate are greater in burn-treated than in nonburned and control bones. Burn-treated diaphyses showed extensive woven bone formation at periosteal surfaces, and corresponding increases of bone areas and periosteal perimeters. Endocortical surfaces showed only typical occasional resorption areas. No intracortical changes were observed. Mineral appositional rate (MAR) and bone formation rate (BFR) at endocortical surfaces were markedly depressed after thermal injury, significant changes were noted in both limbs of treated animals. Among burned limbs, the early PBT label was absent from all specimens, indicating a virtual shutdown of osteoblast activity and recruitment. Similarly in nonburned limb bone, the label was absent from 50% of the specimens; in those bones in which the label was present, label lengths, appositional and bone formation rates were significantly reduced relative to the control specimens. Comparison of average bone formation dynamics for the total PBT interval indicates that MAR and BFR in burned treated tibiae were reduced to approximately 25% of control values. MAR and BFR from the nonburned side of treated animals were significantly reduced as well, to about 55% of control values. These data indicate that the principal metaphyseal effects of thermal injury are stimulation of growth cartilage proliferation, and depression of ossification and osteoblast activity. In diaphyses, thermal injury causes extensive local periosteal woven bone proliferation and a dramatic depression of endosteal bone formation. The latter effect, while more severe locally, is also evident systemically.

Animals↗
PubMed1988

Microdistribution and local dosimetry of 226Ra in trabecular bone of the beagle.

Sections of lumbar vertebral bodies of young adult beagle dogs have been analyzed autoradiographically to characterize and quantify the local distribution of 226Ra by means of a scanning microscope photometer. The animals received a single injection of 355 kBq/kg body weight and were serially sacrificed at 5 to 1381 days postinjection. Hotspot concentrations decreased from about 51 kBq/g bone at 5 days to 20 kBq/g at 1381 days postinjection. The diffuse concentration changed from 8.3 to 1.9 kBq/g. The mean 226Ra concentration in the trabecular areas scanned was initially higher and at the end of the observation period lower than the average calculated for the whole lumbar vertebral column. Density and area of, and fraction of bone activity in, hotspots virtually remained constant. With time hotspots tended to become translocated into bone volume. Mean dose rates to lining cells from both hotspots and diffuse labels decreased from about 210 mGy/d at early postinjection times to 105 mGy/d. This corresponds to 2.5 to 1.1 times the average skeletal dose rate. A discussion of the level of irradiation in terms of hit frequencies shows that osteoblasts in the initial phase of hotspot formation receive about 60 hits to their nucleus for the duration of bone formation. After about 6 months, however, the 226Ra concentration in new bone and the corresponding hit frequency appears to be low enough that interference with bone formation is unlikely. Morphometric measurements showed that abnormal bone accretion and thickening of trabeculae occurred. This was interpreted as an imbalance between bone formation and resorption. Both formation and resorption seem to be substantially lowered compared to control animals.

Animals↗
PubMed1987

The bone lining cell: a distinct phenotype?

It is argued that the flat cells that line nonremodeling endosteal bone surfaces are a distinct phenotype. These cells have a distinct morphology and they most likely have important functional roles in skeletal physiology, metabolism, and remodeling. For these reasons this cell seems deserving of a proper name. The name bone lining cell seems to have gained some acceptance but there will be continued confusion as long as skeletologists use this same term to generically describe cells that line bone surfaces, regardless of their actual identity.

Animals↗
PubMed1987

Bone age and remodeling: a mathematical treatise.

Remodeling of an element of mineralized bone is described by specifying the probability per unit time of being replaced as a function of age of the element. The functional dependence of this probability is called the "law of remodeling." The properties of this stochastic law of remodeling are discussed in terms of random, selective, and redundant remodeling. A relationship between the law of remodeling and the mean bone tissue age is derived. It is shown how the probability density of bone age for individual elements of bone depends on the law of remodeling. The mathematical formalism is exemplified by assuming a specific parametric form of the law. A procedure for experimentally determining the law is suggested based on tracing the resorption of single fluorescent labels. Finally, the extension of the model to a real skeleton with regional differences in turnover rates is discussed.

Age Determination by Skeleton↗
PubMed1987

The role of bone cells in increasing metaphyseal hard tissue in rapidly growing rats treated with prostaglandin E2.

The skeletal effects of graded doses of prostaglandin E2 (PGE2) given to weanling Sprague-Dawley rats for 3 weeks were investigated to elucidate the role of bone cells in increasing hard tissue mass. Decalcified (3 micron) sections were quantified in the light microscope by point hit and intersect counting using a Merz grid. Hard tissue mass (bone and calcified cartilage) and osteoblast, osteoclast and osteoprogenitor cell numbers were counted in metaphyseal tissue bands 0.24, 0.48, 0.72, 1.20, 1.68, 2.16, 2.64, 3.12, 3.60 and 4.08 mm from the growth plate metaphyseal junction. Changes were different and more marked in the secondary spongiosa than the primary spongiosa of the proximal tibial metaphysis of treated rats. In the primary spongiosa of rats treated with 3 or 6 mg PGE2/kg/d (1) an increase in bone and hard tissue masses and (2) a decrease in osteoclasts, osteoprogenitor cell numbers and surface to volume ratio was observed. In the secondary spongiosa (lower metaphysis) of rats treated with 2 same dose levels (1) an increase in bone mass, calcified cartilage cores, and hard tissue mass and perimeter, an elevation of osteoprogenitor cell and osteoblast numbers, a depression of osteoclast, osteoclast nuclei numbers and surface to volume ratio and new sites of intramembranous ossification (woven bone formation) originating from the cortico-endosteal envelope was observed. In this growing rat skeletal model, we showed that PGE2 increases metaphyseal calcified tissue mass by depressing hard tissue resorption and stimulating the replication and differentiation of osteoblast precursors to form new foci of woven bone.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Assessment of cortical and trabecular bone distribution in the beagle skeleton by neutron activation analysis.

The distribution of bone calcium between morphologically identifiable cortical and trabecular bone obtained by dissection and quantitated by neutron activation analysis (NAA) is described. The skeleton of a female beagle dog was dissected into approximately 400 pieces and assayed for 49Ca produced in the University of California, Irvine TRIGA reactor. For each of the skeletal sections, we give the initial weight of the alcohol-fixed tissue, which includes cortical bone, trabecular bone, marrow, and cartilage, and a final tissue weight after the marrow and trabecular bone have been dissected away; total section and cortical section calcium weights are reported. The level of detail is represented, for example, by the vertebrae, which were divided into three parts (body, spine, and transverse processes) and by the long bones, which were divided into 10-12 parts such that characterization of the epiphysis, metaphysis, and diaphysis was accomplished. The median percentage cortical calcium values for cervical, thoracic, and lumbar vertebrae were 82%, 56%, and 66%, respectively; however, variation within these groups and among individual vertebral sections was about a factor of 2. For long bones, the median percentage cortical calcium varied from 90-100% in the midshaft to below 50% in the proximal and distal sections. The final calculated cortical tissue-to-calcium mass ratio (TCR) varied from about 4.5 for midshafts of the long bones to about 9 for thoracic vertebral bodies and indicated that the mineral fraction of cortical bone is not constant throughout the skeleton. The ratio of cortical to trabecular calcium in the skeleton was 79.6:20.4.

Activation Analysis↗
PubMed1986

Effect of 16,16-dimethyl prostaglandin E2 methyl ester on weanling rat skeleton: daily and systemic administration.

The effects of 0, 0.3, 1.0, and 3.0 mg of 16,16-dimethyl prostaglandin E2 methyl ester (Di-M-PGE2) per kilogram per day administered subcutaneously for 21 days to fluorescent-labeled weanling rats were studied, by single-photon absorptiometric and static and dynamic histomorphometric techniques, to determine possible alterations in growth and mineralized tissue mass and their mechanisms of response. Specimens of femurs, proximal tibia, and tibial shaft were analyzed. Di-M-PGE2 caused a reduction in bone elongation and a dramatic accumulation in metaphyseal trabecular hard tissue mass. At high doses, the growth cartilage exhibited reduced thickness and degenerative cell size and cell production rate. The increased metaphyseal trabecular hard tissue mass was restricted to the secondary spongiosa region and was observed at all dose levels. The metaphysis was further characterized by an increase in bone and calcified cartilage cores, a marked elevation in osteoblast and osteoclast numbers, in osteoblast-to-osteoclast ratios, and in ratios of differentiated cells to osteoprogenitor cells. These findings were consistent with the interpretations that Di-M-PGE2 depressed bone elongation by delaying the division and maturation of growth plate chondrocytes; stimulated the differentiation of osteoblasts and osteoclasts, thus generating more differentiated bone cells but suppressing their activities; and increased metaphyseal trabecular hard tissue by creating an imbalance in osteoblasts over osteoclasts and suppressing hard tissue resorption.

16,16-Dimethylprostaglandin E2↗
PubMed1986

Humoral and ionic regulation of osteoclast acidity.

Regulation of the acidity of osteoclasts was determined in situ on the endocranial surfaces of mouse calvaria using acridine orange, a fluorescent weak base. Osteoclasts could be identified by large size, multiple nuclei, relatively small numbers of cells, and the way and the extent to which they took up the dye. Nonosteoclastic cells were stained mainly in their nuclei and occasionally in a few lysosomes surrounding their nuclei, which were uniformly single in nonosteoclasts. Nuclei in osteoclasts were also stained, but the staining of the nuclei was partially masked by the intensity and completeness of the staining of the cytoplasm. In some cells the cytoplasmic staining appeared to be in discrete granules, giving the cytoplasm a bright, frothy appearance. This fluorescence was present in both treated and untreated cells and aided in identifying the osteoclasts. Acridine orange fluorescence at 624 nm intensity, and hence, osteoclast acidity, was increased by parathyroid hormone and prostaglandin E2. Parathyroid hormone-induced increases in acidity were inhibited by calcitonin, cortisol, sodium fluoride, and prostaglandin E2. Furthermore, osteoclast acidity was dependent largely or partially on maintenance of K+ and Na+ gradients, patent Na+ channels, chloride-bicarbonate exchange, and H+, K+-ATPase. These findings demonstrate that osteoclasts become acidified by mechanisms similar to those occurring in gastric parietal cells.

Acridine Orange↗
PubMed1986

Immobilization-associated osteoporosis in primates.

The progressive osteopenic changes in tibial compact bone in adult male monkeys (Macaca nemestrina) were examined histologically during chronic studies of immobilization. The animals were restrained in a semirecumbent position, which reduces normally occurring stresses in the lower extremities and results in bone mass loss. The longest immobilization studies were of 7 months duration. Losses of haversian bone tended to occur predominantly in the proximal tibia and were characterized by increased activation with excessive depth of penetration of osteoclastic activity. There was no apparent regulation of the size and orientation of resorption cavities. Rapid bone loss seen during 10 weeks of immobilization appeared to be due to unrestrained osteoclastic activity without controls and regulation, which are characteristic of adaptive systems. The general pattern of loss persisted throughout 7 months of immobilization. Clear-cut evidence of a formation phase in haversian bone was seen only after 2 months of reambulation. During this period osteoblasts accumulated within resorption cavities, and there was matrix apposition. Within 6 months of recovery there was increased bone turnover, and resorption cavities with diameters of 500-1500 micron were filled partially with new bone; the mean wall thickness of new bone was 2 to 3 times larger than normal. In addition there were numerous remodeling sites that were of normal size and orientation. Trabecular bone was lost during immobilization, and it is probable that losses of large trabecular plates are not replaced, and consequently original bone volume in the cross section is not recovered. In this immobilization model we observed bone resorption occurring for long periods without apparent interruption.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

The effects of prostaglandin E2 in growing rats: increased metaphyseal hard tissue and cortico-endosteal bone formation.

To assess the efficacy of PGE2 in inducing in vivo bone formation, graded doses of prostaglandins E2 were administered to 255 g rats. Histomorphometric analyses of selected sequential fluorescent-labeled bones of rats treated with 0, 0.3, 1.0, 3, or 6 mg PGE2/kg/d for 21 days showed that the doses PGE2 depressed longitudinal bone growth, increased growth cartilage thickness slightly, decreased degenerative cartilage cell size and cartilage cell production slightly, and increased proximal tibial metaphyseal hard-tissue mass markedly. Periosteal bone formation was depressed at the higher doses, and an early, slight depression in endosteal bone formation was also observed, along with a striking late increase in endosteal bone formation and in the formation of trabecular bone in the marrow cavity of the tibial shaft. The characteristics and magnitude of these responses were quite similar to those observed in our previous study of the effects of PGE2 on weanling rats except for the delayed increase in cortico-endosteal bone formation.

Animals↗
PubMed1985

Stimulation of carbonic anhydrase in osteoclasts by parathyroid hormone.

Changes in the acidity of osteoclasts were evaluated by direct measurement of the fluorescent intensity of osteoclasts exposed to acridine orange, a fluorescent weak base which becomes concentrated in acid-containing subcellular compartments. Parathyroid hormone (PTH) produced dose-dependent increases in fluorescent intensity; maximal increases in intensity occurred at doses between 3 and 10 micrograms PTH/ml of culture medium. Acetazolamide, a potent inhibitor of carbonic anhydrase, inhibited the increase in fluorescence induced by PTH, but this drug was less effective in reducing fluorescence in maximally than in submaximally stimulated osteoclasts, indicating that either more enzyme or more resistant enzyme was present in the PTH-stimulated cells. Because increased fluorescence of acridine orange is a sign of greater acidity, these results suggest that (1) PTH stimulates the acidity of osteoclasts, (2) carbonic anhydrase activity is necessary for maximum acidity, and (3) carbonic anhydrase is activated by PTH.

Acetazolamide↗
PubMed1985

Effects of N,N,N',N'-ethylenediaminetetramethylene phosphonic acid and 1-hydroxyethylidene-1,1-bisphosphonic acid on calcium absorption, plasma calcium, longitudinal bone growth, and bone histology in the growing rat.

Phosphonate compounds are of considerable interest because of their effects on biological mineralization and mineral metabolism. The effects of graded doses given parenterally or orally of N,N,N',N'-ethylenediamine tetramethylene phosphonic acid (EDITEMPA) on calcium absorption, plasma calcium, endochondral bone elongation, and osseous tissue histology of rats were determined. In some experiments 1-hydroxyethylidene-1,1-bisphosphonic acid (HEBP) was included for comparison. Given sc for 7 days, EDITEMPA caused dose-related decreases in net weight gain, intestinal calcium absorption, and longitudinal bone growth. There were also increases in total plasma calcium concentrations and excess osteoid accumulation in bone. When EDITEMPA was given po for 7, 28, or 90 days, few changes in osseous tissues were observed and then only at the highest dose (333 mg/kg/day). An equivalent dose of HEBP caused substantial changes in osseous tissues and calcium parameters.

Administration, Oral↗
PubMed1985

The effects of prostaglandin E2 in rapidly growing rats: depressed longitudinal and radial growth and increased metaphyseal hard tissue mass.

The effects of 0, 0.3, 1.0, 3.0, or 6.0 mg of prostaglandin E2 (PGE2)/kg/day administered subcutaneously for 3 weeks to triple fluorochrome-labeled weanling rats are reported. Microradiographs and undecalcified sections of proximal tibiae, tibial shafts, and seventh caudal vertebrae were evaluated by static and dynamic bone histomorphometry techniques. Significant changes were observed only at higher dose levels. Proximal tibial longitudinal growth rates were depressed in doses of 1, 3, or 6 mg PGE2/kg/day. Growth plate thickness and the size of hypertrophic cartilage cells were decreased in animals given 3 and 6 mg of PGE2/kg/day, but the calculated rate of cartilage cell production was unaffected. At doses of 6 mg PGE2/kg/day, periosteal bone apposition rates between Day -1 and Day +19 in both the tibial shafts and caudal vertebral cortices were depressed by less than 25%. Cortical bone mass and endosteal bone apposition rates in the tibial shaft and caudal vertebrae were unaffected. Hard tissue mass in the secondary spongiosa of the proximal tibial metaphysis increased dramatically (28%, 44%, and 60%, respectively) in rats treated with 1, 3, or 6 mg PGE2/kg/day. In addition, the secondary spongiosa contained numerous islands of woven trabecular bone along with an increased number of trabeculae. The study demonstrates that high doses of PGE2 stimulate new woven trabecular bone production and depress longitudinal and radial growth in rapidly growing rats.

1-Carboxyglutamic Acid↗