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PubMed1985

Prenatal stress and increased fluctuating asymmetry in the parietal bones of neonatal rats.

Recent studies have reported increased fluctuating dental and long bone asymmetry in neonates as a function of prenatal stress. The present study was designed to assess the effects of prenatal stress on a third calcium-dependent system, membranous bone. Pregnant rats were exposed to cold, heat, or noise from conception through parturition. Bilateral parietal bone lengths were measured in the term neonates. Levels of fluctuating asymmetry were found to be significantly increased (p less than .001) in all three stressed groups compared to unstressed controls. Results support the concept of a generalized stress response, and suggestions are offered for human osteological application.

Animals↗
PubMed1995

Parietal bone non-secreting solitary myeloma (plasmacytoma) with spread to the epidural space and scalp. Case report.

A case of solitary osteolytic lesion in the parietal bone in an otherwise asymptomatic patient is reported. Skull radiographs showed a radio-lucent lesion with well-defined margins without sclerotic reaction, CT scan demonstrated a mass that markedly enhanced extending from the epidural to the subcutaneous space of the parietal region. The patient underwent surgery and tumor was completely excised. Pathological examination showed tumor to be a plasmacytoma synthesizing kappa chains. Postoperatively the patient received radiotherapy. Four years after treatment there was no sign of local recurrence on CT can and of progression of multiple myeloma on clinical and laboratory studies. Our recommended treatment is that of a complete surgical excision followed by radiation to dose levels of 45-50 Gy. The patients should be followed carefully because of either local recurrence or possible progression to multiple myeloma. Radiotherapy and chemotherapy should started when signs of progression or other significant disease manifestations occur.

Aged↗
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↗
PubMed1995

The number of tartrate-resistant acid phosphatase-positive osteoclasts on neonatal mouse parietal bones is decreased when prostaglandin synthesis is inhibited and increased in response to prostaglandin E2, parathyroid hormone, and 1,25 dihydroxyvitamin D3.

The culture of parietal bones from 4-day old mice in indomethacin (Ind) for 1 day caused a large reduction in the number of tartrate-resistant acid phosphatase positive osteoclasts (TRAP + OC) relative to both control bones and to freshly isolated bones. This reduction did not occur if prostaglandin E2 (PGE2) was present. When 5-bromo-2'-deoxyuridine (BDU) was injected into 4-day old mice, newly formed TRAP + OC nuclei became labeled 1 day later; these bones were then cultured with Ind for 1 day. TRAP + OC and newly labeled TRAP+OC nuclei were commensurately decreased in number. This suggests an active down-regulation rather than merely the inhibition of new TRAP+OC formation. Incubation of bones with Ind and either PGE2, parathyroid hormone, or 1,25 dihydroxyvitamin D3 for 6 hours following a 1-day preincubation in Ind, resulted in an increase in TRAP + OC compared with Ind alone. Using BDU labeling in vitro and in vivo, we show that this increase in number of TRAP+OC is not the result of cell proliferation, but rather differentiation of postmitotic precursors.

Acid Phosphatase↗
PubMed2005

Cavernous hemangioma of the parietal bone. A case report.

Intraosseous cavernous hemangiomas are a rare finding in the calvarium. It is a benign tumors arising from the intrinsic vasculature of the bone. We report one case observed in a 31 year-old female, presented with a progressive left parietal mass. A plain X-ray of the skull and cranial CT-scan showed a osteolytic lesion in the left parietal bone. Surgery consisted of total resection of the lesion and cranioplasty. The postoperative course was uneventful. Histological study revealed a cavernous hemangioma of the diploe. In view of this observation and the literature review, clinical; radiological and therapeutic aspect of this rare entity are discussed.

Adult↗
PubMed1991

Mechanism of regulation of prostaglandin production by parathyroid hormone, interleukin-1, and cortisol in cultured mouse parietal bones.

Bovine PTH-(1-34) (PTH), human recombinant interleukin-1 alpha (IL-1), and cortisol were tested for their effects on bone resorption, prostaglandin (PG) production, and PG endoperoxide synthase (PGH synthase or cyclooxygenase) mRNA levels in cultured mouse parietal bones. Cultures were treated with PTH and IL-1 in the presence and absence of cortisol and arachidonic acid (AA). We found that both PTH and IL-1 stimulated the release of PGE2 and 6-keto-PGF1 alpha (the stable metabolite of PGI2). Stimulation of each metabolite by IL-1 at 0.6-60 pM was 2- to 118-fold, and that by PTH at 24 pM to 24 nM was 3- to 53-fold. Thus, IL-1 was 40-fold more potent than PTH in stimulating PG release. Moreover, IL-1 showed 2- to 3-fold greater efficacy than PTH in stimulating PGE2 release. However, IL-1 was only 4-fold more potent and no more effective than PTH in stimulating 45Ca release. IL-1 (60 pM) and PTH (2.4 nM) stimulation of PGE2 production showed a similar time course, with a lag phase of 0.75-1.5 h. Cortisol (1-100 nM) reduced basal PGE2 production and calcium release. The absolute amounts of PG produced in response to PTH and IL-1 were reduced in the presence of cortisol, but in the presence of AA the relative increases were still from 2.5- to 26-fold compared with levels in cultures treated with cortisol alone. Cortisol reduced the stimulation of 45Ca release by IL-1, but not by PTH. AA (10(-5) M) amplified PG production in response to PTH and IL-1, but not 45Ca release. In bones labeled with [3H]AA, IL-1 and PTH increased [3H]PGE2 and [3H]6-keto-PGF1 alpha release, as measured by HPLC and TLC. IL-1 slightly increased [3H]AA release, but PTH did not. Cortisol decreased [3H]AA release. To test for an effect on PG production at the level of PGH synthase, mRNA levels were measured. mRNA was increased by both PTH and IL-1 to a similar extent despite the greater effect of IL-1 on PGE2 production. Cortisol did not change PGH synthase mRNA levels and did not block the stimulation by PTH or IL-1. We conclude that IL-1 is a more potent stimulator of PG production and bone resorption than PTH. Stimulation of PG production by both PTH and IL-1 is mediated at least in part by increasing PGH synthase, but IL-1 may have an additional effect on AA release.

Animals↗
PubMed1991

Glucocorticoids inhibit fibronectin synthesis and messenger ribonucleic acid levels in cultured fetal rat parietal bones.

The effects of corticosterone on fibronectin production, bone growth, and morphology were examined in a mineralizing organ culture system derived from 20-day-old fetal rat parietal bones. During 4 days of culture, 1-1000 nM corticosterone had no significant effect on the increase in dry weight or on DNA content, but 100 and 1000 nM corticosterone did inhibit the increase in calcium content. Light microscopic examination of the 4-day cultures demonstrated a glucocorticoid-induced change in osteoblast shape and organization along the mineralizing front of the bone. A dose-dependent inhibition of fibronectin secretion into the medium was determined by enzyme-linked immunosorbent assay. In control cultures, fibronectin production was 0.105 +/- 0.005 microgram/ml.bone at 24 h and 0.397 +/- 0.037 microgram/ml.bone during the 72- to 96-h interval. The maximal inhibition of fibronectin secretion was 45% at 24 h and 70% at 96 h with 1000 nM corticosterone. Both immunofluorescent visualization of fibronectin staining in the tissue and a Western blot of fibronectin in the tissue showed a decrease in fibronectin levels. At 24 and 96 h, a dose- and time-dependent decrease in fibronectin mRNA transcripts was found. At 24 and 96 h, 1000 nM corticosterone produced a decrease of 42% and 62%, respectively, in fibronectin mRNA levels. Our findings show that glucocorticoids inhibit fibronectin production in developing bone. The decrease in fibronectin synthesis may contribute to altered osteoblast organization and function during bone formation.

Animals↗
PubMedDate not supplied

Morphological study of recombinant human transforming growth factor beta 1-induced intramembranous ossification in neonatal rat parietal bone.

Recombinant human transforming growth factor beta 1 (rhu TGF beta 1) was injected singly or repeatedly for 3-12 days into the periosteum of the right side parietal bone of neonatal rats under the period of bone growth, and the time course of histological changes of the bone was observed by light and electron microscopy and by enzyme histochemistry. The repeated injections of rhu TGF beta 1 at 200 ng/day increased the thickness of the bone tissue on the treated side, which was about twice the nontreated side value after 12-day injections. On the dermal side, preosteoblasts in the periosteum increased in an early stage of treatment, and thereafter, differentiation into osteoblasts, increase of bone matrix, bone marrow cavity formation, and increase of osteoclasts within the bone marrow cavities were observed. Activation of osteoblasts on the dura mater side was also seen. The single injection of rhu TGF beta 1 at 200 ng resulted only in increased osteoprogenitor cell layers and bone matrix formation in an early stage, and the thickness of the osteoprogenitor cell layers and bone tissue at 12 days after single injection was comparable to the values on the nontreated side. At 1 microgram, however, the osteoblasts were activated, and the osteoprogenitor cell layers and bone matrix formation were markedly increased. At 12 days, the bone tissue thickness on the treated side was about twice the nontreated side value, as in the repeated treatment groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

Material properties of the inner and outer cortical tables of the human parietal bone.

Even though the cranial vault functions as protection for the brain and as a support structure for facial and masticatory functions, little is known about its mechanical properties or their variations. The cranial vault bone is interesting because of its maintenance in spite of low functional strains, and because calvarial bone cells are often used in cell culture studies. We measured thickness, density, and ash weight, and ultrasonically determined elastic properties throughout the cortices of 10 human parietal bones. The results are unique for studies of the cranial vault because: 1) measurements focused specifically on the cortical components, 2) the orientations of the axes of maximum stiffness were determined before measurement of elastic properties, and 3) two related measurements (bone density and percent ash weight) were compared. Results showed that the periosteal cortical plate (outer table) and the endosteal cortical plate (inner table) had significant differences in material properties. The outer table was on average thicker, denser, and stiffer than the inner table, which had a higher ash weight percentage. Within each table there were significant differences in thicknesses, ash weight percentages, and E(2)/E(3) anisotropies among sites. Few sites on either table had significant orientations of the axes of maximum stiffness. Despite this apparent randomness in orientation, almost all sites exhibited anisotropies equivalent to other parts of the skeleton.

Aged↗
PubMed1988

Parathyroid hormone modulates transforming growth factor beta activity and binding in osteoblast-enriched cell cultures from fetal rat parietal bone.

Transforming growth factor beta (TGF-beta) is produced by bone cells, is abundant in bone matrix, and regulates bone cell biochemical processes. In osteoblast-enriched fetal rat parietal bone cell cultures, low TGF-beta doses increase DNA synthesis, whereas higher levels are less mitogenic, stimulate collagen production, and decrease alkaline phosphatase activity. Parathyroid hormone by itself has minimal effects on these processes, but it opposes the effects of TGF-beta and alters TGF-beta binding to its receptors in osteoblast-enriched cultures. Some functions ascribed to parathyroid hormone in bone may therefore result from alterations in TGF-beta activity, suggesting that the local effects of TGF-beta in bone are under systemic hormonal control.

Animals↗
PubMed1988

Further biochemical and molecular characterization of primary rat parietal bone cell cultures.

Primary bone cell cultures are used widely to examine the regulation of bone metabolism by growth factors and hormones. Characterization of this model system is now being conducted at the molecular level to define modulation of gene expression. Cells were obtained from rat parietal bone by sequential collagenase digestions. Cell populations were evaluated for bone-related products, including collagen isoform expression and mRNA levels, alkaline phosphatase activity, and osteocalcin production. Serum-deprived, confluent cultures of the first and second collagenase-released populations produced a lower percentage of total protein as collagen than the third, fourth, and fifth populations, while co-culturing the third through fifth populations resulted in the highest level. Collagen typing on SDS-polyacrylamide gels revealed an abundance of mature type I collagen in all cell populations; type III collagen synthesis was undetectable by this method. This is in contrast to the presence of cytoplasmic mRNA for both type I and type III collagen in all cell populations, suggesting post-transcriptional modulation of type III collagen synthesis. The expression of alkaline phosphatase and osteocalcin was highest in cultures of later released cells, indicating that these cell populations display phenotypic characteristics associated with cells of the osteoblast lineage.

Alkaline Phosphatase↗
PubMed1996

Osteoclasts are not the major source of interleukin-6 in mouse parietal bones.

Interleukin-6 (IL-6) is produced by bone cells and has been shown to stimulate the proliferation of osteoclast progenitors. Which cells in bone produce IL-6 is controversial. This article tests the hypothesis that tartrate-resistant acid phosphatase-positive osteoclasts (TRAP + OC) in neonatal mouse parietal bones are the major source of IL-6. Bones were preincubated with indomethacin to decrease the number of TRAP + OC and the amount of IL-6 produced. Incubation with parathyroid hormone or prostaglandin E2 increased the number of TRAP + OC and the amount of IL-6 produced. Calcitonin and 17 beta-estradiol inhibited this increase in TRAP + OC but had no effect on IL-6 production. 1,25-dihydroxy-vitamin D3 also stimulated an increase in TRAP + OC number but did not cause increased IL-6 production. Both the endocranial and ectocranial membranes of these bones produced large amounts of IL-6. TRAP activity in extracts of endocranial membranes was 14-fold that of the ectocranial membrane and, histochemically, some TRAP + cells could be detected here. However, the ectocranial membranes produced more IL-6 than the endocranial membranes. We conclude that TRAP + OC are not a major source of IL-6 in this system.

Acid Phosphatase↗