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Rat Calvaria (rat + calvaria)
Selected AbstractsTGF-,1 alone and in combination with calcium hydroxide is synergistic to TGF-,1 production by osteoblasts in vitroINTERNATIONAL ENDODONTIC JOURNAL, Issue 5 2000A. Jaunberzins Abstract Aim To examine the effects of calcium hydroxide (Ca(OH)2), transforming growth factor-beta (TGF-,1), and Ca(OH)2/TGF-,1 coadministration on TGF-,1 and interleukin-6 (IL-6) synthesis by early (subculture 1) and late (subculture 5) osteoblast cultures. Methodology Early and late cultures were established using bone cells harvested from 21-day-old fetal rat calvaria. Cell cultures of both early and late osteoblasts were divided into four groups: group 1, control; group 2, cells challenged with Ca(OH)2; group 3, cells challenged with TGF-,1; and group 4, cells challenged with Ca(OH)2 and TGF-,1 in combination. TGF-,1 and IL-6 levels for all groups were determined using ELISA methodology. Results anova and Tukey HS analyses revealed that osteoblasts of groups 3 and 4 significantly increased (P < 0.001) TGF-,1 synthesis in both early and late cultures of osteoblasts. IL-6 was not detected in any of the groups considered in this study. Conclusions Exogenous TGF-,1 has an autocrine effect on cell cultures of osteoblasts. Administration of TGF-,1 alone or in combination with Ca(OH)2 increases the synthesis of TGF-,1 in osteoblast cultures. Ca(OH)2 and TGF-,1 are compatible when placed in a culture of osteoblasts. Ca(OH)2 provides a favourable environment for the anabolic effects of TGF-,1. [source] GATA-3 transduces survival signals in osteoblasts through upregulation of bcl-xL gene expression,JOURNAL OF BONE AND MINERAL RESEARCH, Issue 10 2010Ruei-Ming Chen Abstract GATA-3, a transcription factor, participates in regulating cell development, proliferation, and death. This study was aimed at evaluating the roles of GATA-3 in protecting osteoblasts against oxidative stress,induced apoptotic insults and their possible mechanisms. Pretreatment with nitric oxide (NO) for 24 hours protected osteoblasts, prepared from neonatal rat calvaria, against oxidative stress,induced apoptotic insults. Such protection involved enhancement of Bcl-XL messenger (m)RNA and protein syntheses and the translocation of this antiapoptotic protein from the cytoplasm to mitochondria. GATA-3 was detected in rat osteoblasts, and GATA-3-specific DNA-binding elements exist in the promoter region of the bcl-xL gene. NO preconditioning attenuated oxidative stress,caused suppression of GATA-3 mRNA and protein synthesis and the translocation of this transcription factor from the cytoplasm to nuclei. Application of GATA-3 small interfering (si)RNA into osteoblasts decreased the levels of this transcription factor and simultaneously inhibited Bcl-XL mRNA synthesis. Pretreatment with NO lowered the oxidative stress,caused alteration in the binding of GATA-3 to its specific DNA motifs. Oxidative stress,inhibited Runx2 mRNA expression, but NO preconditioning decreased such inhibition. NO pretreatment time-dependently enhanced the association of GATA-3 with Runx2. Knocking down the translation of GATA-3 using RNA interference significantly decreased the protection of NO preconditioning against oxidative stress,induced alterations of cell morphologies, DNA fragmentation, and cell apoptosis. In comparison, overexpression of GATA-3 could promote NO preconditioning,involved Bcl-XL expression and cell survival. Therefore, this study shows that GATA-3 plays critical roles in mediating survival signals in osteoblasts, possibly through upregulating bcl-xL gene expression. © 2010 American Society for Bone and Mineral Research. [source] Environmental Toxicants May Modulate Osteoblast Differentiation by a Mechanism Involving the Aryl Hydrocarbon Receptor,,JOURNAL OF BONE AND MINERAL RESEARCH, Issue 10 2007Elizabeth P Ryan Abstract The AHR mediates many of the toxicological effects of aromatic hydrocarbons. We show that AHR expression in osteoblasts parallels the induction of early bone-specific genes involved in maturation. The AHR may not only mediate the effects of toxicants, but with an as yet unidentified ligand, be involved in the differentiation pathways of osteoblasts. Introduction: Metabolic bone diseases arise as a result of an imbalance in bone cell activities. Recent evidence suggests that environmental toxicants may be contributing factors altering these activities. One candidate molecule implicated in mediating the toxic effects of exogenous compounds is the aryl hydrocarbon receptor (AHR). Materials and Methods: Osteoblasts isolated from neonatal rat calvaria were analyzed for AHR expression by quantitative PCR, Western blot, and immunohistochemistry. In addition, AHR activation was evaluated by electromobility gel shift assay and fluorescence microscopy. Results: Our findings showed AHR expression in mature osteoblasts in vivo. The pattern of AHR expression peaks after alkaline phosphatase and before induction of osteocalcin. We first show that AHR functions as a transactivating receptor in osteoblasts, as evidenced by its ligand-dependent migration to the nucleus and its association with known dioxin response elements. AHR activation by 2,3,7,8-tetrachlorodibenzo -p -dioxin (TCDD) mediated the induction of cytochrome p450 1A1 and cycloxygenase-2 protein levels. This effect could be inhibited by the potent AHR antagonist, 3,4 methoxynitroflavone. Furthermore, lead treatment of osteoblasts upregulates the expression of AHR mRNA and protein levels, supporting a novel mechanism whereby lead in the skeleton may increase the sensitivity of bone cells to toxicant exposure. Conclusions: These data imply that the AHR mediates the effects of aromatic toxicants on bone and that AHR expression is regulated during osteoblast differentiation. [source] Differential Expression of Estrogen Receptor-Related Receptor , and Estrogen Receptors , and , in Osteoblasts In Vivo and In Vitro,JOURNAL OF BONE AND MINERAL RESEARCH, Issue 8 2002Edith Bonnelye Abstract The orphan nuclear estrogen receptor-related receptor (ERR) , is expressed by osteoblastic cells, is known to transactivate at least one osteoblast-associated gene osteopontin (OPN) and plays a functional role in osteoprogenitor cell proliferation and differentiation. To dissect further the role of ERR-, in bone formation, we compared its expression to that of the estrogen receptor (ER) , and ER-, in rat calvaria (RC) and fetal tibia in vivo and in RC and rat bone marrow (RBM) cells in vitro. We found that ERR-, is highly and widely expressed in most, if not all, cells in RC cell cultures from early proliferation stages through mineralized nodule formation; ER-, was localized similarly but at lower levels and ER-,, although present, was barely detectable. These patterns of expression in vitro correlated with what we observed in vivo in sections of 21-day fetal RC, in which ERR-, appeared to be more highly expressed than either of the ERs. Interestingly, ERR-, also is highly expressed in RBM cells, while ER-, and ER-, mRNA is expressed, but at lower levels. Moreover, we found that ERR-,, ER-,, and ER-, were all expressed in osteoblasts in fetal and adult tibia whereas they were expressed differentially in calvaria in vivo in subsets of osteoblasts, supporting the hypothesis that ERR-, may interact with one or both of the ERs in those osteoblasts in which they are coexpressed and that all three receptors may be required for bone formation but at different times and for different functions. [source] Bone healing in critical-size defects treated with platelet-rich plasma: a histologic and histometric study in rat calvariaJOURNAL OF PERIODONTAL RESEARCH, Issue 2 2008M. R. Messora Background and Objective:, The purpose of this study was to analyze histologically the influence of autologous platelet-rich plasma on bone healing in surgically created critical-size defects in rat calvaria. Material and Methods:, Thirty-two rats were divided into two groups: the control group (group C) and the platelet-rich plasma group. An 8-mm-diameter critical-size defect was created in the calvarium of each animal. In group C the defect was filled by a blood clot only. In the platelet-rich plasma group, 0.35 mL of platelet-rich plasma was placed in the defect and covered by 0.35 mL of platelet-poor plasma. Both groups were divided into subgroups (n = 8) and killed at either 4 or 12 wk postoperatively. Histometric (using image-analysis software) and histologic analyses were performed. The amount of new bone formed was calculated as a percentage of the total area of the original defect. Percentage data were transformed into arccosine for statistical analysis (analysis of variance, Tukey, p < 0.05). Results:, No defect completely regenerated with bone. The platelet-rich plasma group had a statistically greater amount of bone formation than group C at both 4 wk (17.68% vs. 7.20%, respectively) and 12 wk (24.69% vs. 11.65%, respectively) postoperatively. Conclusion:, Within the limits of this study, it can be concluded that platelet-rich plasma placed in the defects and covered by platelet-poor plasma significantly enhanced bone healing in critical-size defects in rat calvaria. [source] Systemic tetracycline delays degradation of three different collagen membranes in rat calvariaCLINICAL ORAL IMPLANTS RESEARCH, Issue 2 2009Ofer Moses Abstract Objectives: The aim of this study was to quantitatively evaluate the effect of systemic tetracycline (TTC) on the degradation of three different collagen membranes. Materials and methods: Collagen membranes were cut into 5 mm diameter membrane discs and labeled with aminohexanoyl-biotin- N -hydroxy-succinimide ester. One membrane disc each of a non-cross-linked [BioGide® (BG)], glutaraldehyde cross-linked [BioMend Extend® (BM)], and ribose cross-linked [OssixÔ (OS)] was implanted on the calvaria of 40 Wistar rats. Another 10 biotinylated collagen membrane discs from each membrane type were processed for histologic observation and served as baseline; half of them (five from each group) were also treated with formic acid to inspect possible interference with biotinilazation of collagen by formic acid used during the decalcification process. A 10 mg/kg dose of TTC (50% of the minimal recommended antibacterial dose) to the experimental (20 animals) and saline to the control (20 animals) group was administered intramuscularly every 3 days. From each group, block sections were retrieved in half of the animals after 14 days and in the remaining after 28 days. Decalcified tissue histology was stained with streptavidin horseradish peroxidase. A computer-assisted program measured the membranes' collagen contents. Statistical analysis consisted of analysis of variance (ANOVA) with repeated measures. Results: No statistically significant differences in collagen contents were appreciated between biotinylated non-implanted membranes treated or not treated by formic acid. Systemic TTC had a different effect on the bio-degradation of the membranes: while it significantly decreased the resorption of two of the membranes (BG and BM), it had minimal influence on the ribose cross-linked membrane (OS). ANOVA with repeated measures, tests of within-subjects effects, showed a statistically significant difference between the membranes (P<0.001), within the membranes at the different time-points (P<0.001), a significant interaction between membranes and time and between the membranes and administered TTC (P<0.001). Test of between-subject effects revealed a statistically significant interaction with time and with TTC (P<0.001). Conclusions: Systemically administered TTC in sub-antibacterial doses may offer a possible treatment alternative to reduce bio-degradation and enhance bio-durability of certain collagen membranes. The findings of the present study could have clinical application in large non-self-contained bone defects, where prolonged membrane barrier functions are desirable. [source] Morphometric evaluation of the repair of critical-size defects using demineralized bovine bone and autogenous bone grafts in rat calvariaCLINICAL ORAL IMPLANTS RESEARCH, Issue 8 2008Rodrigo Cardoso de Oliveira Abstract Objective: To evaluate the repair of critical-size bone defects in rats treated with demineralized bovine bone (DBB) compared with autogenous bone (AB). Material and method: A bone defect of 8 mm in diameter was created in the calvaria of 50 Rattus norvegicus, treated either with DBB or AB. Sub-groups of five rats of each group were killed at 7, 14, 21, 30 and 90 days post-operatively, and the skulls were removed and processed histologically. Histological sections were stained with hematoxylin and eosin. Result: Histological analysis showed complete closure of the defects with new bone at 90 days in group AB, and substitution of the biomaterial by fibrotic connective tissue in the DBB group at 21 days. Morphometric analysis showed that DBB was rapidly absorbed at 14 days, with its volume density decreasing from 47%±0.8% at 7 days to 1.2%±0.41% at 14 days. Subsequently, volume densities of the connective tissue and neoformed bone increased from 51.1%±11.17% to 86.8%±7.92% and from 1.9%±1.13% to 12%±8.02%, respectively, for the same time interval. The volume density of AB particles did not change throughout the experimental periods, but the amount of new bone increased markedly between 7 and 90 days, from 4.5%±1.57% to 53.5%±6.42% (P<0.05). Conclusion: DBB did not provide complete repair of the defects, with significantly less new bone formation than in the AB group. [source] | ||||||||||