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At least 19 recordsLinked to original sources
PubMed1990

Morphological relationships between osteoclasts and bone resorption surfaces on mouse parietal bones.

Parietal bones from mice 1-20 weeks of age were histochemically stained for detection of acid-phosphatase activity and then observed by the light microscope to evaluate the distribution and shape of osteoclasts on the inner surface of their bones. After microscopic examination, the same bones were macerated by NaOCl to both remove organic materials and expose the mineralized surface. The inner surface was then examined by scanning electron microscopy and the observations were compared with the light micrographs of the areas where osteoclasts were located. The bone resorption areas were identified as well-demarcated rough areas, and corresponded to the areas where osteoclasts were distributed. In young mice, osteoclasts observed in the bone resorption areas, which were composed of accumulations of irregular concavities, were mainly polygonal or round in shape. In adult mice, elongated osteoclasts with longer or shorter cytoplasmic processes were predominant; the bone concavities were also elongated and gathered in a flame-like pattern. The findings suggest that osteoclasts change shape according to their resorptive activities and that the activities differ between growing bones and those where growth has ceased, probably in relation to the modeling and remodeling of the bone.

Acid Phosphatase↗
PubMed1992

Stimulative effects of cadmium on bone resorption in neonatal parietal bone resorption.

Effects of cadmium on bone resorption were investigated using neonatal mouse parietal bone culture system. Cadmium at 0.5 microM and above stimulated hydroxyproline release as well as 45Ca release. As cadmium-stimulated bone resorption was inhibited by calcitonin, bone resorption induced by cadmium is osteoclast-mediated bone resorption. CI-1, collagenase inhibitor, depressed cadmium-stimulated bone resorption in a dose-dependent manner. Osteoblasts are also involved in cadmium-induced bone resorption. Indomethacin-inhibited cadmium-stimulated bone resorption and cadmium-treated bones released prostaglandin E2 to a greater extent than untreated bones. Cadmium-stimulated bone resorption was shown to be dependent on the production of prostaglandin E2. 3-Isobutyl-1-methylxanthine potentiated cadmium-stimulated bone resorption and verapamil depressed it. It is possible that an increase in levels of cAMP and calcium ion in bone cells is involved in cadmium-induced bone resorption. From these results, cadmium was found to stimulate osteoclast-mediated bone resorption which is dependent on prostaglandin E2. Second messengers in cadmium-induced bone resorption may be cAMP and calcium ion.

Animals↗
PubMed1989

[Ultrastructural studies of initial calcification of mouse fetal parietal bone in vitro].

The parietal bone fragment (1.5 mm square) extracted from murine fetal calvaria (periosteum was removed) in the latter stage of gestation was cultured in alpha-MEM containing 10% fetal bovine serum over 10-day period, and the initial calcification site was subsequently examined utilizing both electron microscopy and histochemical methods. At the initial calcification site, the so-called "matrix vesicle" (width 100 nm), derived from osteoblasts which induce matrix formation, and the larger vesicular structures (width 100-600 nm) which originated from degenerated or dead cells were observed. Additionally dead osteoblast-like cells phagocytosing bone crystals participated in bone nodul formation. In the border region between the degenerated or disrupted cells and the functioning cells, multilamellar structures (mainly composed of phospholipids) were frequently observed. Concurrently it was concluded that there is a possibility of partial deposition of calcium salts on the surface of the above mentioned cells under some circumstances. Through selective decalcification, it was determined that bone trabecule was formed by fusion of respective bone noduli and degraded collagen fibrils which filled the intervening spaces. From the above results, it was evident that both the matrix vesicles derived from functioning osteoblast, and the vesicular structures derived from the degenerated or dead cells concurrently phagocytosing spicules and collagen fibrils were involved in the initial calcification process of the membranous bone in vitro.

Animals↗
PubMed1990

Simultaneous assessment of bone resorption and formation in cultures of 22-day fetal rat parietal bones: effects of parathyroid hormone and prostaglandin E2.

We have developed a method that allows us to measure bone resorption and formation simultaneously in the parietal bones from 22-day fetal rat calvaria. Parietal bones labeled with 45Ca, by injection of the mother, were cultured for 72 h with parathyroid hormone (PTH, bovine 1-34, 1.56 nM) or prostaglandin E2 (PGE2, 100 nM), in the presence or absence of indomethacin (Indo, 1 microM) or corticosterone (Cort, 1 microM). Two hours prior to the end of the culture, the bones were pulsed with [3H]-proline or [3H]-thymidine. Resorption was assessed as the percent of 45Ca released into the medium. Incorporation of [3H]-proline into collagenase digestible protein (CDP) and of [3H]-thymidine into DNA (TDR) were measured to assess collagen and DNA synthesis, respectively. Basal %45Ca release was 16 +/- 1% and was significantly decreased by Indo and Cort. Cort decreased TDR and CDP while Indo did not. PTH and PGE2 significantly increased %45Ca release, and this was not blocked by Indo. However, in the presence of Cort, only PTH increased %45Ca release while PGE2 did not. PGE2 increased TDR under all culture conditions while PTH increased TDR only in the presence of Cort. While PTH and PGE2 had the same effects on bone resorption, they had different effects on CDP. PGE2 increased CDP in the presence of Indo or Cort but PTH did not. Thus, this model allows us to study bone resorption, collagen synthesis, and DNA synthesis simultaneously. We have also shown that PTH and PGE2 differ in their sensitivity to inhibition of resorption by Cort and in their effects on bone formation.

Animals↗
PubMed1992

Parietal bone mobility in the anesthetized cat.

To quantify parietal bone motion in reference to the medial sagittal suture, a newly developed instrument was attached to the surgically exposed skull of anesthetized adult cats. The instrument differentiated between lateral and rotational parietal bone movements around the fulcrum of the suture. Bone movement was produced by external forces applied to the skull and by changes in intracranial pressure associated with induced hypercapnia, intravenous injections of norepinephrine, and controlled injections of artificial cerebrospinal fluid into the lateral cerebral ventricle. Responses varied considerably among test animals. Generally, lateral head compression caused sagittal suture closure, small inward rotation of the parietal bones, increased intraventricular pressure, transient apnea, and unstable systemic arterial blood pressure. Graded increases in intracranial volume produced stepped increases in pressure, lateral expansion at the sagittal suture, and outward rotation of the parietal bones. We attribute variations in animal response largely to differences in intracranial and suture compliance among them. Cranial suture compliance may be an important factor in defining total cranial compliance.

Animals↗
PubMed1991

Cortisol modulates the actions of interleukin-1 alpha on bone formation, resorption, and prostaglandin production in cultured mouse parietal bones.

Previous studies have shown that both interleukin-1 (IL-1) and glucocorticoids inhibit collagen synthesis in bone organ and cell cultures. In this study we examined their interactions in cultured neonatal mouse parietal bones. IL-1 alpha stimulated [3H]thymidine incorporation. Cortisol decreased thymidine incorporation, but did not block the effect of IL-1. Both cortisol and IL-1 alpha decreased the incorporation of [3H]proline into collagenase-digestible protein (CDP) and reduced alpha 1(I)procollagen mRNA levels at 72 h. Noncollagen protein (NCP) labeling was increased by IL-1 and decreased by cortisol. In the presence of cortisol, IL-1 alpha (6 pM) increased CDP as well as NCP labeling. The increase in CDP labeling was paralleled by an increase in alpha 1(I)procollagen mRNA, suggesting a pretranslational site for the cortisol-IL-1 alpha interaction. In the same bones, cortisol consistently blocked IL-1 alpha-stimulated 45Ca release and prostaglandin E2 (PGE2) production. The ability of IL-1 alpha to increase CDP in the presence of cortisol was the same in the presence or absence of indomethacin, an inhibitor of PGE2 synthesis, or aphidicholin (30 microM), an inhibitor of DNA synthesis, indicating that the reversal was neither PG mediated nor dependent on cell proliferation. In conclusion, our results demonstrate that IL-1 inhibits collagen, but not NCP or DNA, synthesis and that cortisol inhibits IL-1 alpha-induced bone resorption and PGE2 production and reverses its inhibitory effect on collagen synthesis in cultured neonatal mouse calvariae.

Animals↗
PubMed1991

Effect of 1,25-dihydroxyvitamin D3 on prostaglandin E2 production in cultured mouse parietal bones.

1,25-Dihydroxyvitamin D3 [1,25-(OH)2D3] was tested for its effects on prostaglandin E2 (PGE2) production and bone resorption in cultured mouse parietal bones. We found that at 24 h 1,25-(OH)2D3 increased 45Ca release but did not affect PGE2 production. However, at 48 h 1,25-(OH)2D3 produced a dose-related increase in PGE2 production. PGE2 production was increased with 1,25-(OH)2D3 at 10(-10)-10(-8) M, and 45Ca release was increased with 1,25-(OH)2D3 at 10(-11)-10(-8) M. The effects of 1,25-(OH)2D3 on PGE2 production persisted in the presence of cortisol (10(-8) M), and the effects were greater in the presence of arachidonic acid (10(-5) M) or fetal bovine serum (10%). Human interleukin-1 alpha (IL-1, 1 ng/ml) and bovine parathyroid hormone-(1-34) (PTH, 10 ng/ml) increased PGE2 production earlier and to a greater extent than 1,25-(OH)2D3. The PGE2 response to IL-1 and PTH was not affected by 1,25-(OH)2D3 at 24 h, but at 48 h 1,25-(OH)2D3 (10(-8) M) increased the PGE2 response to both IL-1 and PTH. The stimulation of 45Ca release at 48 h by high concentrations of 1,25-(OH)2D3, PTH, or IL-1 was similar, and there was no evidence for an additive effect. To test for an effect of 1,25-(OH)2D3 on endogenous IL-1 production, experiments were performed in the presence of an IL-1 receptor antagonist (IL-1Ra, 1000 ng/ml), which has been found to block selectively IL-1 effects on bone resorption and PG production.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

In vitro mineralization of fetal rat parietal bones in defined serum-free medium: effect of beta-glycerol phosphate.

We have developed a bone organ culture system that mineralizes in vitro. Fetal rat parietal bones (20 days old) were cultured in a chemically defined serum-free medium containing physiological 3 mM phosphate. During 5 days in culture, calcium content increased from 26 to 55 micrograms and dry weight increased from 137 to 194 micrograms. After 2 days in vivo, the calcium content of the parietal bone showed a comparable increase to 49 micrograms and dry weight increased to 183 micrograms. During culture, the mineralized bone area in thick sections increased from 11 to 23%, which paralleled the doubling in calcium content. Fluorescent calcein labeling during the 5 day culture period demonstrated that calcification occurs in an ordered pattern. Protein synthesis was assessed by measuring incorporation of [3H]proline into collagenase-digestible protein (CDP) and noncollagen protein (NCP). The percentage collagen synthesis decreased from 17.5% at 0 time to 5.0% at 2 days and then increased to 9.4% at 5 days of culture. Varying the inorganic phosphate concentration in the medium or adding beta-glycerol phosphate was found to affect mineralization. After 5 days in culture, bones treated with 1 mM phosphate exhibited a large region of unmineralized osteoid with only a 23% increase in calcium content compared with 112% in control (3 mM phosphate) bones and a 28% increase in dry weight compared with a 40% increase in control. Treatment for 5 days with 6 mM phosphate or 1, 3, or 10 mM beta-glycerol phosphate had no significant effect on dry weight compared to control bones. However, bone calcium content increased significantly from 55 +/- 5 micrograms in control cultures to 105 +/- 7 with 6 mM phosphate, 74 +/- 6 with 3 mM beta-glycerol phosphate, and 75 +/- 5 micrograms with 10 mM beta-glycerol phosphate. Calcified area measured by histomorphometry was also significantly greater than in control bones, but this was mainly due to ectopic calcification in the periosteum, representing from 23 to 74% of the total increase in calcified matrix in bones cultured with 6 mM phosphate or 1-10 mM beta-glycerol phosphate. Ultrastructural analysis demonstrated that ectopic calcification was associated with cell death and debris. Therefore, calcification with beta-glycerol phosphate and high concentrations of inorganic phosphate differed from mineralization in vivo or in bones cultured with a physiologically concentration of phosphate.

Calcium↗
PubMed1991

A unique case of congenital bilateral absence of parietal bones in a neonate.

The remains of an unidentified female neonate were discovered in a field in central Missouri. Examination revealed bilateral absence of the parietal bones. A search of the literature describing similar defects suggests that the present case represents a unique condition, described here for the first time.

Female↗
PubMed1989

Benign osteoblastoma of the parietal bone: case report.

A case of benign osteoblastoma of the parietal bone is presented. Attention is drawn first to the rarity of this tumor and second to the fact that the radiological and histopathological features of the tumor reported here lead us to suspect the presence of regressive features in its evolution.

Adult↗
PubMed1990

Effect of partial removal of frontal or parietal bone on concentrations of mRNAs coding for preprocholecystokinin and preprosomatostatin in rat neocortex.

Partial removal of the frontal or parietal bone increased concentrations of mRNAs coding for preprocholecystokinin and preprosomatostatin in rat parietotemporal cortex by more than 170 and 67%, respectively, when measured 3 days after the operation. The increases were independent of the anaesthetic agent used during the operation and were transient with a maximum usually observed 3 days after the operation. They occurred not only in areas close to or under the removed bone part, but also in more distant areas. Thus, removal of the frontal bone also enhanced levels of preprocholecystokinin- and preprosomatostatin-mRNA in the parietotemporal and occipital cortex. mRNA concentrations were increased in the inner as well as outer layers of the cortex. The possible experimental and pathophysiological implications of the observed changes in gene expression of both neuropeptides in neocortical neurons are discussed.

Animals↗
PubMed1992

Ipriflavone inhibits osteoclast differentiation in parathyroid transplanted parietal bone of rats.

Ipriflavone, a synthetic isoflavone-derived flavonoid, was shown to have inhibitory effect on bone resorption. In order to study its mechanism of action directly on bone, 46 female Wistar rats were divided into six groups and medicated orally for 25 days as follows: groups 1 and 2 were given 1% carboxymethylcellulose solution (vehicle), groups 3, 4, 5, and 6 were administered ipriflavone at doses of 0.178, 0.356, 0.712, and 1.424 mmol/kg/day (suspended in vehicle), respectively. On the 22nd day, parathyroid glands, taken from donor rats, were transplanted in contact with the outer surface of the periosteum of both the right and the left parietal bones of rats from groups 2, 3, 4, 5, and 6. The group 1 rats underwent sham operation. Bone histomorphometry, performed on the ectocranial periosteum of parietal bones, showed that absolute erosion boundary, absolute eroded area, absolute erosion depth, number of tartrate-resistant acid phosphatase (TRAP)-positive polynucleated osteoclasts, and number of TRAP-positive mononucleated cells decreased in ipriflavone-treated rats compared with group 2 rats. The reduction was roughly proportional to the increase of drug dosage and reached statistical significance in rats of groups 5 and 6. The same parameters were extremely low in group 1 rats. Mineral apposition rate did not differ in any of the groups. Significant increase of serum calcium and significant decrease of serum phosphate were found in group 2 rats compared with group 1 rats, whereas no differences from controls were detected in ipriflavone-treated animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

An immunocytochemical method for studying the kinetics of osteoclast nuclei on intact mouse parietal bone.

An immunocytochemical method using an antibody against 5-bromo-2'-deoxyuridine has been applied to the study of the kinetics of osteoclast nuclei on intact mouse parietal bones. Osteoclasts containing tartrate-resistant acid phosphatase show nuclei that are positive for the thymidine analogue within 24 hours of injection into four-day old mice. Labelled osteoclast nuclei decline in number with a half-life of 1.3 days, compatible with a random mechanism of cell death rather than a fixed lifespan. This is shorter than has previously been reported and the possible reasons for this are suggested. The main advantages compared with autoradiography are the shortened processing time and the large number of osteoclasts that can be examined per parietal bone.

Animals↗
PubMed1990

Glucocorticoids stimulate resorption in fetal rat parietal bones in vitro.

The effect of glucocorticoids on bone resorption was examined in a serum-free mineralizing organ culture system derived from 20 day fetal rat parietal bones. Bone resorption was assessed by prelabeling the fetal rats in utero with 45Ca and determining the daily release of 45Ca into the medium of cultured bones. During the first 24 h of treatment a transient stimulation of bone resorption was found; 4.5 +/- 0.3% of the total 45Ca was released into the medium with 1 nM corticosterone and 4.1 +/- 0.2% with 10 nM corticosterone compared to 2.9 +/- 0.2% in control bones. Treatment with 1 and 10 nM dexamethasone for 24 h also showed an increase in 45Ca release compared to control bones. During the same time period 45Ca release was 6.9 +/- 1.4% with 10 nM parathyroid hormone. At later time points 100 and 1000 nM corticosterone inhibited 45Ca release, but 1 and 10 nM corticosterone values were similar to controls. At 24 h the number of osteoclasts per mm2 tissue in bone lacunae was significantly elevated with 1-100 nM corticosterone and 10 nM parathyroid hormone compared to control bones. In control bones 0.10 +/- 0.05 osteoclasts per mm2 of tissue were found, but 0.59 +/- 0.21 osteoclasts per mm2 were seen with 10 nM corticosterone and 1.50 +/- 0.34 with 10 nM parathyroid hormone. An additional assay of bone resorption, the release of lysosomal beta-glucuronidase into the medium was also elevated in glucocorticoid and parathyroid hormone-treated cultures.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗