Academic literature on the topic 'Calvarial Suture'
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Journal articles on the topic "Calvarial Suture"
1
Moursi, Amr M., Phillip L. Winnard, Alissa V. Winnard, John M. Rubenstrunk, and Mark P. Mooney. "Fibroblast Growth Factor 2 Induces Increased Calvarial Osteoblast Proliferation and Cranial Suture Fusion." Cleft Palate-Craniofacial Journal 39, no. 5 (September 2002): 487–96. http://dx.doi.org/10.1597/1545-1569_2002_039_0487_fgfiic_2.0.co_2.
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Objective: Craniosynostosis has been associated with fibroblast growth factors (FGFs) and their receptors. The purpose of this study was to quantitatively determine the effect of FGF2 on rat calvarial osteoblasts and a rat cranial suture formation model. Design: Fetal rat calvarial osteoblasts were cultured with and without FGF2. Cell attachment and proliferation was determined by alamarBlue dye assay and cell morphology by toluidine-blue staining. In rat calvarial organ culture, postnatal day 15 rat calvariae with dura mater were placed in serum-free media with and without FGF2. A unique quantitative analysis of suture fusion was developed by obtaining measurements of suture bridging in histological serial sections at progressive stages of fusion. Results: Attachment for cells treated with FGF2 was similar to control. In contrast, proliferation was higher for cells treated with FGF2 while maintaining an osteoblastic morphology. After 5 days in organ culture, FGF2-treated posterior frontal sutures showed a dramatic increase in fusion, compared with untreated controls. This increased fusion was maintained throughout days 7 and 10 in culture. Also, fusion was enhanced on the dural side of the suture, as is normally observed in vivo, and the normal tissue architecture was maintained. Conclusions: These results indicate that FGF2 can promote rat osteoblast attachment and normal cell morphology as well as induce cell proliferation. In calvarial organ culture, FGF2 treatment produced an enhanced suture fusion. These results provide further support for a critical role for FGF2 in cranial suture development. These studies also present a new quantitative approach to evaluating the effect of suture-perturbing growth factors on cranial suture fusion.
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Kim, H. J., D. P. Rice, P. J. Kettunen, and I. Thesleff. "FGF-, BMP- and Shh-mediated signalling pathways in the regulation of cranial suture morphogenesis and calvarial bone development." Development 125, no. 7 (April 1, 1998): 1241–51. http://dx.doi.org/10.1242/dev.125.7.1241.
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The development of calvarial bones is tightly co-ordinated with the growth of the brain and needs harmonious interactions between different tissues within the calvarial sutures. Premature fusion of cranial sutures, known as craniosynostosis, presumably involves disturbance of these interactions. Mutations in the homeobox gene Msx2 as well as the FGF receptors cause human craniosynostosis syndromes. Our histological analysis of mouse calvarial development demonstrated morphological differences in the sagittal suture between embryonic and postnatal stages. In vitro culture of mouse calvaria showed that embryonic, but not postnatal, dura mater regulated suture patency. We next analysed by in situ hybridisation the expression of several genes, which are known to act in conserved signalling pathways, in the sagittal suture during embryonic (E15-E18) and postnatal stages (P1-P6). Msx1 and Msx2 were expressed in the sutural mesenchyme and the dura mater. FGFR2(BEK), as well as Bmp2 and Bmp4, were intensely expressed in the osteogenic fronts and Bmp4 also in the mesenchyme of the sagittal suture and in the dura mater. Fgf9 was expressed throughout the calvarial mesenchyme, the dura mater, the developing bones and the overlying skin, but Fgf4 was not detected in these tissues. Interestingly, Shh and Ptc started to be expressed in patched pattern along the osteogenic fronts at the end of embryonic development and, at this time, the expression of Bmp4 and sequentially those of Msx2 and Bmp2 were reduced, and they also acquired patched expression patterns. The expression of Msx2 in the dura mater disappeared after birth. <P> FGF and BMP signalling pathways were further examined in vitro, in E15 mouse calvarial explants. Interestingly, beads soaked in FGF4 accelerated sutural closure when placed on the osteogenic fronts, but had no such effect when placed on the mid-sutural mesenchyme. BMP4 beads caused an increase in tissue volume both when placed on the osteogenic fronts and on the mid-sutural area, but did not effect suture closure. BMP4 induced the expression of both Msx1 and Msx2 genes in sutural tissue, while FGF4 induced only Msx1. We suggest that the local application of FGF on the osteogenic fronts accelerating suture closure in vitro, mimics the pathogenesis of human craniosynostosis syndromes in which mutations in the FGF receptor genes apparently cause constitutive activation of the receptors. Taken together, our data suggest that conserved signalling pathways regulate tissue interactions during suture morphogenesis and intramembranous bone formation of the calvaria and that morphogenesis of mouse sagittal suture is controlled by different molecular mechanisms during the embryonic and postnatal stages. Signals from the dura mater may regulate the maintenance of sutural patency prenatally, whereas signals in the osteogenic fronts dominate after birth.
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Wilkinson, C. Corbett, Cesar A. Serrano, Brooke M. French, Sarah J. Graber, Emily Schmidt-Beuchat, Lígia Batista-Silverman, Noah P. Hubbell, and Nicholas V. Stence. "Fusion patterns of minor lateral calvarial sutures on volume-rendered CT reconstructions." Journal of Neurosurgery: Pediatrics 26, no. 2 (August 2020): 200–210. http://dx.doi.org/10.3171/2020.2.peds1952.
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OBJECTIVESeveral years ago, the authors treated an infant with sagittal and bilateral parietomastoid suture fusion. This made them curious about the normal course of fusion of “minor” lateral sutures (sphenoparietal, squamosal, parietomastoid). Accordingly, they investigated fusion of these sutures on 3D volume-rendered head CT reconstructions in a series of pediatric trauma patients.METHODSThe authors reviewed all volume-rendered head CT reconstructions obtained from 2010 through mid-2012 at Children’s Hospital Colorado in trauma patients aged 0–21 years. Each sphenoparietal, squamosal, and parietomastoid suture was graded as open, partially fused, or fused. In several individuals, one or more lateral sutures were fused atypically. In these patients, the cephalic index (CI) and cranial vault asymmetry index (CVAI) were calculated. In a separately reported study utilizing the same reconstructions, 21 subjects had fusion of the sagittal suture. Minor lateral sutures were assessed, including these 21 individuals, excluding them, and considering them as a separate subgroup.RESULTSAfter exclusions, 331 scans were reviewed. Typically, the earliest length of the minor lateral sutures to begin fusion was the anterior squamosal suture, often by 2 years of age. The next suture to begin fusion—and first to complete it—was the sphenoparietal. The last suture to begin and complete fusion was the parietomastoid. Six subjects (1.8%) had posterior (without anterior) fusion of one or more squamosal sutures. Six subjects (1.8%) had fusion or near-complete fusion of one squamosal and/or parietomastoid suture when the corresponding opposite suture was open or nearly open. The mean CI and CVAI values in these subjects and in age- and sex-matched controls were normal and not significantly different. No individuals had a fused parietomastoid suture with open squamosal and/or sphenoparietal sutures.CONCLUSIONSFusion and partial fusion of the sphenoparietal, squamosal, and parietomastoid sutures is common in children and adolescents. It usually does not represent craniosynostosis and does not require cranial surgery. The anterior squamosal suture is often the earliest length of these sutures to fuse. Fusion then spreads anteriorly to the sphenoparietal suture and posteriorly to the parietomastoid. The sphenoparietal suture is generally the earliest minor lateral suture to complete fusion, and the parietomastoid is the last. Atypical patterns of fusion include posterior (without anterior) squamosal suture fusion and asymmetrical squamosal and/or parietomastoid suture fusion. However, these atypical fusion patterns may not lead to atypical head shapes or a need for surgery.
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Wilkinson, C. Corbett, Nicholas V. Stence, Cesar A. Serrano, Sarah J. Graber, Lígia Batista-Silverman, Emily Schmidt-Beuchat, and Brooke M. French. "Fusion patterns of major calvarial sutures on volume-rendered CT reconstructions." Journal of Neurosurgery: Pediatrics 25, no. 5 (May 2020): 519–28. http://dx.doi.org/10.3171/2019.11.peds1953.
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OBJECTIVERecently, the authors investigated the normal course of fusion of minor lateral calvarial sutures on “3D” volume-rendered head CT reconstructions in pediatric trauma patients. While evaluating these reconstructions, they found many more fused sagittal sutures than expected given the currently accepted prevalence of sagittal craniosynostosis. In the present study, using the same set of head CT reconstructions, they investigated the course of fusion of the sagittal as well as the lambdoid, coronal, and metopic sutures.METHODSThey reviewed all volume-rendered head CT reconstructions performed in the period from 2010 through mid-2012 at Children’s Hospital Colorado for trauma patients aged 0–21 years. Each sagittal, lambdoid, coronal, or metopic suture was graded as open, partially fused, or fused. The cephalic index (CI) was calculated for subjects with fused and partially fused sagittal sutures.RESULTSAfter exclusions, 331 scans were reviewed. Twenty-one subjects (6%) had fusion or partial fusion of the sagittal suture. Four of the 21 also had fusion of the medial lambdoid and/or coronal sutures. In the 17 subjects (5%) with sagittal suture fusion and no medial fusion of adjacent sutures, the mean CI was 77.6. None of the 21 subjects had been previously diagnosed with craniosynostosis. Other than in the 21 subjects already mentioned, no other sagittal or lambdoid sutures were fused at all. Nor were other coronal sutures fused medially. Coronal sutures were commonly fused inferiorly early during the 2nd decade of life, and fusion progressed superiorly and medially as subjects became older; none were completely fused by 18 years of age. Fusion of the metopic suture was first seen at 3 months of life; fusion was often not complete until after 2 years.CONCLUSIONSThe sagittal and lambdoid sutures do not usually begin to fuse before 18 years of age. However, more sagittal sutures are fused before age 18 than expected given the currently accepted prevalence of craniosynostosis. This finding is of unknown significance, but likely many of them do not need surgery. The coronal suture often begins to fuse inferiorly early in the 2nd decade of life but does not usually complete fusion before 18 years of age. The metopic suture often starts to fuse by 3 months of age, but it may not completely fuse until after 2 years of age.
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Perlyn, Chad A., Gillian Morriss-Kay, Tron Darvann, Marissa Tenenbaum, and David M. Ornitz. "Model for the Pharmacologic Treatment of Crouzon Syndrome." Neurosurgery 59, no. 1 (July 1, 2006): 210–15. http://dx.doi.org/10.1227/01.neu.0000224323.53866.1e.
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Abstract OBJECTIVE Crouzon syndrome is caused by mutations in FGFR2 leading to constitutive activation of receptors in the absence of ligand binding. The syndrome is characterized by premature fusion of the cranial sutures that leads to abnormal skull shape, restricted brain growth, and increased intracranial pressure. Surgical remodeling of the cranial vault is currently used to treat affected infants. The purpose of this study was to develop a pharmacologic strategy using tyrosine kinase inhibition as a novel treatment for craniosynostotic syndromes caused by constitutive FGFR activation. METHODS Characterization of cranial suture fusion in Fgfr2C342Y/+ mutant mice, which carry the most common Crouzon mutation, was performed using MicroCT analysis from embryogenesis through maturation. Whole calvarial cultures from wild-type and Fgfr2C342Y/+ mice were then established and calvaria cultured for 2 weeks in the presence of DMSO control or PD173074, an FGFR tyrosine kinase inhibitor. Paraffin sections were prepared to show suture morphology and calcium deposition. RESULTS In untreated Fgfr2C342Y/+ cultures, the coronal suture fused bilaterally with loss of overlap between the frontal bone and parietal bone. Calvaria treated with PD173074 (2 (M) showed patency of the coronal suture and were without evidence of any synostosis. CONCLUSION: We report the successful use of PD173074 to prevent in-vitro suture fusion in a model for Crouzon syndrome. Further studies are underway to develop an in-vivo treatment protocol as a novel therapeutic modality for FGFR associated craniosynostotic syndromes.
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Moursi, Amr M., Phillip L. Winnard, Doug Fryer, and Mark P. Mooney. "Delivery of Transforming Growth Factor-β2-Perturbing Antibody in a Collagen Vehicle Inhibits Cranial Suture Fusion in Calvarial Organ Culture." Cleft Palate-Craniofacial Journal 40, no. 3 (May 2003): 225–32. http://dx.doi.org/10.1597/1545-1569_2003_040_0225_dotgfa_2.0.co_2.
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Objective To determine whether antibody perturbation of Tgf-β, delivered in a collagen gel, could inhibit cranial suture fusion. Design Attachment and proliferation of osteoblasts cultured on a collagen gel with or without anti-Tgf-β2 antibody were determined by AlamarBlue dye assay and cell morphology by toluidine-blue staining. In rat calvarial organ culture, collagen gel with and without anti-Tgf-β2 antibody was injected subperiosteally over the posterior frontal suture of postnatal day 15 rat calvariae. A quantitative analysis of suture fusion was used to measure suture bridging in histological serial sections at various time points. Results Attachment and proliferation for cells cultured on collagen gel with anti-Tgf-β2 antibody were similar to collagen gel controls. Although proliferation was lower than on tissue culture plastic, cells treated with anti-Tgf-β2 antibody maintained an osteoblastic morphology. After 7, 10, and 15 days in organ culture, anti-Tgf-β2 antibody treatment caused a reduction in the percent bridging of posterior frontal sutures, compared with controls. Sutures exposed to anti-Tgf-β2 antibody and fibroblast growth factor-2 concurrently did not show an inhibition of bony bridging. Conclusions These results support previous reports suggesting a role for Tgf-β2 in cranial suture fusion. In cell culture the collagen gel, both with and without anti-Tgf-β2 antibody, promoted similar osteoblast attachment, proliferation, and osteoblastic morphology. In organ culture anti-Tgf-β2 antibody was delivered in a bioactive state via a collagen gel to inhibit cranial suture fusion. Also, the results suggest that the inductive effect of fibroblast growth factor-2 is not dependent on Tgf-β2 activity. Together, these results provide further support for the role of Tgf-β2 in cranial suture fusion.
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Vastardis, H., J. B. Mulliken, and J. Glowacki. "Unilateral Coronal Synostosis: A Histomorphometric Study." Cleft Palate-Craniofacial Journal 41, no. 4 (July 2004): 439–46. http://dx.doi.org/10.1597/03-012.1.
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Objective This histomorphometric study compared the open and prematurely fused side of the coronal suture in subjects with unilateral coronal synostosis (UCS). Methods Sutures and parasutural bone were obtained from seven subjects with nonsyndromic UCS during operative correction at 3 to 24 months of age. Histological and cellular analyses were performed for the affected and open sutures. Specimens were examined by light and polarizing microscopy. Sutural patterns, osseous morphology, calvarial thickness, tartrate-resistant acid phosphatase (TRAP)-positive cells, and marrow spaces were evaluated histomorphologically, qualitatively, and semiquantitatively. Histomorphometry was performed to determine total projected area of marrow space as a percentage of unit area, total number of TRAP-positive cells per specimen, and perisutural cranial thickness. Results Polarizing microscopy showed that affected sutures were composed of more lamellar bone than the normal sutures. By light microscopy, the clinically fused sutures were 1.7-fold thicker (p < .02), had twofold larger marrow spaces (p < .0006), and contained sixfold more TRAP-positive osteoclasts in marrow spaces near the suture (p < .04) than the normal sutures. Quantitative analysis of the normal sutures revealed that calvarial thickness was greater with age and that there was an inverse correlation between medullary area and age. For the affected sutures, there was also an age-related increase in calvarial thickness. There were also trends for age-related declines in numbers of osteoclasts in both open and affected sides. Conclusions These results question the hypothesis that defective osteoclastic activity is pivotal in the pathogenesis of UCS and support the hypothesis that this condition results from abnormally active bony remodeling.
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Rice, D. P., T. Aberg, Y. Chan, Z. Tang, P. J. Kettunen, L. Pakarinen, R. E. Maxson, and I. Thesleff. "Integration of FGF and TWIST in calvarial bone and suture development." Development 127, no. 9 (May 1, 2000): 1845–55. http://dx.doi.org/10.1242/dev.127.9.1845.
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Mutations in the FGFR1-FGFR3 and TWIST genes are known to cause craniosynostosis, the former by constitutive activation and the latter by haploinsufficiency. Although clinically achieving the same end result, the premature fusion of the calvarial bones, it is not known whether these genes lie in the same or independent pathways during calvarial bone development and later in suture closure. We have previously shown that Fgfr2c is expressed at the osteogenic fronts of the developing calvarial bones and that, when FGF is applied via beads to the osteogenic fronts, suture closure is accelerated (Kim, H.-J., Rice, D. P. C., Kettunen, P. J. and Thesleff, I. (1998) Development 125, 1241–1251). In order to investigate further the role of FGF signalling during mouse calvarial bone and suture development, we have performed detailed expression analysis of the splicing variants of Fgfr1-Fgfr3 and Fgfr4, as well as their potential ligand Fgf2. The IIIc splice variants of Fgfr1-Fgfr3 as well as the IIIb variant of Fgfr2 being expressed by differentiating osteoblasts at the osteogenic fronts (E15). In comparison to Fgf9, Fgf2 showed a more restricted expression pattern being primarily expressed in the sutural mesenchyme between the osteogenic fronts. We also carried out a detailed expression analysis of the helix-loop-helix factors (HLH) Twist and Id1 during calvaria and suture development (E10-P6). Twist and Id1 were expressed by early preosteoblasts, in patterns that overlapped those of the FGF ligands, but as these cells differentiated their expression dramatically decreased. Signalling pathways were further studied in vitro, in E15 mouse calvarial explants. Beads soaked in FGF2 induced Twist and inhibited Bsp, a marker of functioning osteoblasts. Meanwhile, BMP2 upregulated Id1. Id1 is a dominant negative HLH thought to inhibit basic HLH such as Twist. In Drosophila, the FGF receptor FR1 is known to be downstream of Twist. We demonstrated that in Twist(+/)(−) mice, FGFR2 protein expression was altered. We propose a model of osteoblast differentiation integrating Twist and FGF in the same pathway, in which FGF acts both at early and late stages. Disruption of this pathway may lead to craniosynostosis.
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Hudgins, Roger J., Fernando D. Burstein, and William R. Boydston. "Total calvarial reconstruction for sagittal synostosis in older infants and children." Journal of Neurosurgery 78, no. 2 (February 1993): 199–204. http://dx.doi.org/10.3171/jns.1993.78.2.0199.
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✓ Premature closure of the sagittal suture is the most common form of craniosynostosis, but this condition occasionally goes unrecognized until the child is too old to undergo procedures that depend upon continued calvarial growth for success. As the entire calvaria is affected and thus misshapen by sagittal synostosis, late correction involves total calvarial reconstruction. The extensive nature of this undertaking has precluded its utilization despite the presence of significant deformities. Adapting the techniques and experience gained from craniofacial surgery, the authors performed total calvarial reconstruction on nine children with sagittal synostosis and subsequent scaphocephaly diagnosed after the age of 1 year. In each case the goals of shortening the anteroposterior length, widening the biparietal diameter, and reducing frontal and occipital deformities were met. Morbidity consisted of acute blood loss, postoperative hyponatremia, and in one case a residual skull defect. The rationale for this procedure and the techniques utilized are discussed.
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Reddy, Kesava, Harold Hoffman, and Derek Armstrong. "Delayed and Progressive Multiple Suture Craniosynostosis." Neurosurgery 26, no. 3 (March 1, 1990): 442–48. http://dx.doi.org/10.1227/00006123-199003000-00011.
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Abstract A considerable amount of information is available on various types of craniosynostoses. The patient exhibiting single suture synostosis that progresses to involve multiple sutures is distinctly uncommon, as is the patient exhibiting delayed synostosis involving all of the calvarial sutures. We report a group of 11 such patients with progressive and delayed holocalvarial synostosis. Most patients exhibited features of raised intracranial pressure or developmental delay, and in all patients symptoms were relieved after surgery. The diagnostic and therapeutic implications of this type of presentation in craniosynostosis are discussed.
Dissertations / Theses on the topic "Calvarial Suture"
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Coussens, Anna Kathleen. "Molecular regulation of calvarial suture morphogenesis and human craniofacial diversity." Thesis, Queensland University of Technology, 2007. https://eprints.qut.edu.au/16481/1/Anna_Coussens_Thesis.pdf.
Full textAbstract:
This body of work is concerned with the genetics of craniofacial morphology and specifically with that of the cranial sutures which form fibrous articulations between the calvarial bones. The premature fusion of these sutures, known as craniosynostosis, is a common developmental abnormality and has been extensively utilised here as a tool through which to study the genetics of suture morphogenesis and craniofacial diversity.
Investigations began with a search for polymorphisms associated with normal variation in human craniofacial characteristics. Denaturing High-Performance Liquid chromatography was used to identify polymorphisms in two genes causative for
craniosynostosis by analysing DNA from a large cohort of individuals from four
ethnogeographic populations. A single nucleotide polymorphism in fibroblast growth factor receptor 1 was identified as being associated with variation in the cephalic index, a common measure of cranial shape.
To further, and specifically, investigate the molecular processes of suture morphogenesis gene expression was compared between unfused and prematurely fusing/fused suture tissues isolated from patients with craniosynostosis. Two approaches, both utilising Affymetrix gene expression microarrays, were used to identify genes differentially expressed during premature suture fusion. The first was a novel method which utilised the observation that explant cells from both fused and unfused suture tissue, cultured in minimal medium, produce a gene expression profile characteristic of minimally differentiated osteoblastic cells. Consequently, gene expression was compared between prematurely fused suture tissues and their corresponding in vitro de-differentiated cells. In addition to those genes known to be involved in suture morphogenesis, a large number of novel genes were identified which were up-regulated in the differentiated in vivo state and are thus implicated in premature suture fusion and in vivo osteoblast differentiation.
The second microarray study involved an extensive analysis of 16 suture tissues and compared gene expression between unfused (n=9) and fusing/fused sutures (n=7).
Again, both known genes and a substantially large number of novel genes were identified as being differentially expressed. Some of these novel genes included retinol binding protein 4 (RBP4), glypican 3 (GPC3), C1q tumour necrosis factor 3 (C1QTNF3), and WNT inhibitory factor 1 (WIF1). The known functions of these genes are suggestive of potential roles in suture morphogenesis. Realtime quantitative RT PCR (QRT-PCR) was used to verify the differential expression patterns observed for 11 genes and Western blot analysis and confocal microscopy was used to investigate the protein expression for 3 genes of interest. RBP4 was found to be localised on the ectocranial surface of unfused sutures and in cells lining the osteogenic fronts while GPC3 was localised to suture mesenchyme of unfused sutures.
A comparison between each unfused suture (coronal, sagittal, metopic, and lambdoid) demonstrated that gene expression profiles are suture-specific which, based on the identification of differentially expressed genes, suggests possible molecular bases for the differential timing of normal fusion and the response of each suture to different craniosynostosis mutations. One observation of particular interest was the presence of cartilage in unfused lambdoid sutures, suggesting a role for chondrogenesis in posterior skull sutures which have generally been thought to develop by intramembranous ossification without a cartilage precursor.
Finally, the effects of common media supplements used in in vitro experiments to stimulate differentiation of calvarial suture-derived cells were investigated with respect to their ability to induce in vivo-like gene expression. The response to standard differentiation medium (ascorbic acid + β-glycerophosphate) with and without dexamethasone was measured by both mineralisation and matrix formation assays and QRT-PCR of genes identified in the above described microarray studies. Both media induced collagen matrix and bone nodule formation indicative of differentiating osteoblasts. However, the genes expression profiles induced by both media differed and neither recapitulated the levels and profiles of gene expression observed in vivo for cells isolated from both fused and unfused suture tissues. This study has implications for translating results from in vitro work to the in vivo situation. Significantly, the dedifferentiation microarray study identified differentially expressed genes whose products may be considered candidates as more appropriate osteogenic supplements that may be used during in vitro experiments to better induce in vivo-like osteoblast differentiation.
This study has made a substantial contribution to the identification of novel genes and pathways involved in controlling human suture morphogenesis and craniofacial diversity. The results from this research will stimulate new areas of inquiry which will one day aid in the development of better diagnostics and therapeutics for craniosynostosis, and other craniofacial and more general skeletal abnormalities.
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Coussens, Anna Kathleen. "Molecular regulation of calvarial suture morphogenesis and human craniofacial diversity." Queensland University of Technology, 2007. http://eprints.qut.edu.au/16481/.
Full textAbstract:
This body of work is concerned with the genetics of craniofacial morphology and specifically with that of the cranial sutures which form fibrous articulations between the calvarial bones. The premature fusion of these sutures, known as craniosynostosis, is a common developmental abnormality and has been extensively utilised here as a tool through which to study the genetics of suture morphogenesis and craniofacial diversity. Investigations began with a search for polymorphisms associated with normal variation in human craniofacial characteristics. Denaturing High-Performance Liquid chromatography was used to identify polymorphisms in two genes causative for craniosynostosis by analysing DNA from a large cohort of individuals from four ethnogeographic populations. A single nucleotide polymorphism in fibroblast growth factor receptor 1 was identified as being associated with variation in the cephalic index, a common measure of cranial shape. To further, and specifically, investigate the molecular processes of suture morphogenesis gene expression was compared between unfused and prematurely fusing/fused suture tissues isolated from patients with craniosynostosis. Two approaches, both utilising Affymetrix gene expression microarrays, were used to identify genes differentially expressed during premature suture fusion. The first was a novel method which utilised the observation that explant cells from both fused and unfused suture tissue, cultured in minimal medium, produce a gene expression profile characteristic of minimally differentiated osteoblastic cells. Consequently, gene expression was compared between prematurely fused suture tissues and their corresponding in vitro de-differentiated cells. In addition to those genes known to be involved in suture morphogenesis, a large number of novel genes were identified which were up-regulated in the differentiated in vivo state and are thus implicated in premature suture fusion and in vivo osteoblast differentiation. The second microarray study involved an extensive analysis of 16 suture tissues and compared gene expression between unfused (n=9) and fusing/fused sutures (n=7). Again, both known genes and a substantially large number of novel genes were identified as being differentially expressed. Some of these novel genes included retinol binding protein 4 (RBP4), glypican 3 (GPC3), C1q tumour necrosis factor 3 (C1QTNF3), and WNT inhibitory factor 1 (WIF1). The known functions of these genes are suggestive of potential roles in suture morphogenesis. Realtime quantitative RT PCR (QRT-PCR) was used to verify the differential expression patterns observed for 11 genes and Western blot analysis and confocal microscopy was used to investigate the protein expression for 3 genes of interest. RBP4 was found to be localised on the ectocranial surface of unfused sutures and in cells lining the osteogenic fronts while GPC3 was localised to suture mesenchyme of unfused sutures. A comparison between each unfused suture (coronal, sagittal, metopic, and lambdoid) demonstrated that gene expression profiles are suture-specific which, based on the identification of differentially expressed genes, suggests possible molecular bases for the differential timing of normal fusion and the response of each suture to different craniosynostosis mutations. One observation of particular interest was the presence of cartilage in unfused lambdoid sutures, suggesting a role for chondrogenesis in posterior skull sutures which have generally been thought to develop by intramembranous ossification without a cartilage precursor. Finally, the effects of common media supplements used in in vitro experiments to stimulate differentiation of calvarial suture-derived cells were investigated with respect to their ability to induce in vivo-like gene expression. The response to standard differentiation medium (ascorbic acid + β-glycerophosphate) with and without dexamethasone was measured by both mineralisation and matrix formation assays and QRT-PCR of genes identified in the above described microarray studies. Both media induced collagen matrix and bone nodule formation indicative of differentiating osteoblasts. However, the genes expression profiles induced by both media differed and neither recapitulated the levels and profiles of gene expression observed in vivo for cells isolated from both fused and unfused suture tissues. This study has implications for translating results from in vitro work to the in vivo situation. Significantly, the dedifferentiation microarray study identified differentially expressed genes whose products may be considered candidates as more appropriate osteogenic supplements that may be used during in vitro experiments to better induce in vivo-like osteoblast differentiation. This study has made a substantial contribution to the identification of novel genes and pathways involved in controlling human suture morphogenesis and craniofacial diversity. The results from this research will stimulate new areas of inquiry which will one day aid in the development of better diagnostics and therapeutics for craniosynostosis, and other craniofacial and more general skeletal abnormalities.
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Connor, Elaine Catharine. "The role of hedgehog signalling in calvarial bone and suture development." Thesis, King's College London (University of London), 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.424472.
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Pribadi, Clara Mentari Putri. "The Role of Epigenetic Modifiers, Kdm6a and Kdm6b, in Calvarial Suture Development and Craniosynostosis." Thesis, 2022. https://hdl.handle.net/2440/135946.
Full textAbstract:
The five flat bones of human calvaria are held together by fibrous sutures, which remain open during development to accommodate for the growing brain. However, excessive osteogenic differentiation of mesenchymal progenitor cells (MPC) within the sutures can lead to premature suture fusion or craniosynostosis. Saethre-Chotzen Syndrome (SCS) is a common form of craniosynostosis, caused by TWIST-1 gene mutation. Currently, the only treatment for craniosynostosis involves multiple invasive cranial surgeries, which could lead to serious complications. Thus, an attempt to identify a non-invasive therapy is paramount. The present thesis has shown that the expressions of histone demethylases, KDM6A and KDM6B, are upregulated in calvarial cells from SCS patients and from an SCS model of Twist-1 haploinsufficient (Twist-1del/+) mice. KDM6A and KDM6B have been shown previously to promote osteogenesis in MPC by removing their epigenetic target, the repressive mark of tri-methylated lysine 27 on histone 3 (H3K27me3), from the promoters of osteogenic genes. An established pre-clinical SCS mouse model was utilised to investigate the inhibition of Kdm6a and Kdm6b activity using the pharmacological inhibitor GSK-J4 on calvarial cell osteogenic potential. Furthermore, a suture mesenchyme-specific deletion of Kdm6a was established to assess the effects of Kdm6a loss, in the suture development of naturally fusing suture, the posterior interfrontal suture. The results demonstrate for the first time that GSK-J4 treatment inhibited the osteogenic potential of calvarial stromal cells in vitro and the bone formation of ex vivo explants of Twist-1del/+ calvaria, with minimal level of toxicity. ChIP analyses revealed that GSK-J4 treatment elevated the levels of the H3K27me3 mark on osteogenic genes leading to repression of their expression. In vivo studies showed that the local administration of GSKJ4 onto the calvaria of Twist-1del/+ prevented premature suture fusion and kept the sutures open throughout calvarial development (Shpargel et al. 2017). Thus, the inhibition of Kdm6a and Kdm6b activity by GSK-J4 could be a potential therapeutic strategy for preventing craniosynostosis in children with SCS. Furthermore, conditional knockout of Kdm6a prevented suture fusion of posterior interfrontal suture, suggesting that Kdm6a involvement could also contribute to non-syndromic craniosynostosis.Thesis (Ph.D.) -- University of Adelaide, Adelaide Medical School, 2022
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Sampaio, Cintia Figueiredo. "The effect of intermittent hydrostatic compression on calvarial development a dissertation submitted in partial fulfillment ... for the degree of Master's of Science Department Orthodontics and Pediatric Dentistry ... /." 2004. http://catalog.hathitrust.org/api/volumes/oclc/68962638.html.
Full textBook chapters on the topic "Calvarial Suture"
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Bang, Katrina E., Stephen J. Bordes, and R. Shane Tubbs. "Anatomy of the Sutures of the Calvaria." In The Sutures of the Skull, 43–52. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-72338-5_4.
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McKinney, Alexander M. "Normal Variations and Developmental Anatomy of the Calvarial Sutures and Fontanelles Above the Skull Base." In Atlas of Normal Imaging Variations of the Brain, Skull, and Craniocervical Vasculature, 815–58. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-39790-0_27.
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Zhang, Qi Feng, Shu Juan Zou, Meng Chun Qi, Yang Xi Chen, and Zhi He Zhao. "Effect of a Single Period of Mechanical Strain on Gene Expression Patterns of Ets1 and Cbfa1 in Murine Calvarial Sutural Osteoblast-Like Cells." In Key Engineering Materials, 1105–8. Stafa: Trans Tech Publications Ltd., 2007. http://dx.doi.org/10.4028/0-87849-422-7.1105.
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Villanueva, Philip A., and Erin Graves. "Calvarial Vault Fractures." In Neurotrauma, 83–92. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780190936259.003.0010.
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Calvarial vault fractures are commonly encountered finding within the head injury problem. Calvarial or vault fractures may be either closed or open, and either linear, comminuted, or depressed. In closed fractures, the galea over the fracture is intact. With open fractures, the galea is torn and the fracture exposed. Linear fractures, as the name implies, are generally nonbranching, generally do not cross suture lines, and bone on both sides of the fracture remains co-planar. Depressed fractures refer to a difference in height between the fracture plates. Comminuted fractures are characterized by fragmentation of the bone plates, and these fragments may be co-planar or depressed. Because of their wide spectrum of severity, it is critical for testing physicians to recognize the various types, presentations, and diagnostic and therapeutic implications of these entities.
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Di Rocco, Federico, Pierre-Aurelien Beuriat, and Eric Arnaud. "Craniofaciosynostosis." In Oxford Textbook of Neurological Surgery, edited by Ramez W. Kirollos, Adel Helmy, Simon Thomson, and Peter J. A. Hutchinson, 993–98. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198746706.003.0086.
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Craniosynostosis is a condition in which there is a premature fusion of one or more sutures of the skull with a modification of cranial growth and an abnormal skull shape. The shape is specific to the suture involved so the diagnosis is essentially clinical. The genetic causes remain largely unknown. Molecular researches have identified several mutations. Complications can result to the deformation of the skull but also abnormal facial morphology. Cerebellar tonsillar prolapse, hydrocephalus, intracranial hypertension, insufficient eye protection, respiratory obstructions, and orthodontic problems are the most common. Several factors play a role in the surgical indications. The aim of the surgery is functional and cosmetic. Techniques have evolved from simple strip to total calvarial and supraorbital remodelling, osteogenic bone distraction, and endoscopic procedures. In all craniosynostosis, long-term follow-up is mandatory because there is a risk of secondary synostosis which exists independently from the originally affected suture.
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Ishii, Mamoru, Jingjing Sun, Man-Chun Ting, and Robert E. Maxson. "The Development of the Calvarial Bones and Sutures and the Pathophysiology of Craniosynostosis." In Current Topics in Developmental Biology, 131–56. Elsevier, 2015. http://dx.doi.org/10.1016/bs.ctdb.2015.07.004.
Full textConference papers on the topic "Calvarial Suture"
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Marchiori, Julia Gabriela Oliveira, Jennyfer Paulla Galdino Chaves, Maria Cecilia Closs Ono, and Adriana Keijiro Maeda. "Trigonocephaly associated with myelomeningocele in infant: Case report." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.040.
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Context: Trigonocephaly is a type of craniostenosis due to the early closure of the metopic suture. His diagnosis is eminently clinical, but imaging tests are essential. The recommended treatment is surgical and should preferably be performed at the age of 3 to 9 months. Association between craniosynostosis and neural tube defect (NTDs) is rare and was sometimes considered as mere coincidence. However, Martinez-Lage et al. hypothesize that there is a causal relationship between these malformations since myelomeningocele reduces intracranial pulse pressure, which stimulates the early closure of cranial sutures. For Graham et al. the restriction of fetal movements in NTD carriers predisposes to craniosynostosis, as they are likely to keep the skull fixed against the mother’s pelvic bones. Case report: Male patient, 11 months, with West Syndrome. He congenitally presented myelomeningocele, and this deformity was corrected on his first day of life. He subsequently developed a keel-shaped forehead, protrusion of metopic suture, and hypertelorism. The diagnosis of trigonocephaly was ratified by computed tomography of the skull with three-dimensional reconstruction. Surgery was performed at 11 months. The access chosen was coronal and there was a wide exposure of the calvarium. Then all the metopic suture was removed through a bifrontal craniotomy, which allowed the remodeling of the frontal bone. Conclusions: It is necessary to make a diagnosis and early treatment of both comorbidities since delays in the conduct can result in disastrous consequences. In addition, there is a need to conduct more research to elucidate the interrelationship between craniosynostosis and NTD.