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Journal articles on the topic "Suture fusion"

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Boyajian, Michael K., Hanny Al-Samkari, Dennis C. Nguyen, Sybill Naidoo, and Albert S. Woo. "Partial Suture Fusion in Nonsyndromic Single-Suture Craniosynostosis." Cleft Palate-Craniofacial Journal 57, no. 4 (February 4, 2020): 499–505. http://dx.doi.org/10.1177/1055665620902299.

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Introduction: Partial synostosis of cranial sutures has been shown to have clinical and diagnostic significance. However, there is limited published information about how suture fusion progresses over time. In this study, we evaluate patients with nonsyndromic single-suture synostosis. We aim to define the incidence of partial versus complete suture fusion and whether a correlation exists between the degree of suture fusion and age. Methods: Two hundred fifty-four patients with nonsyndromic single-suture synostosis were evaluated. Preoperative computed tomography (CT) scans were rendered in 3-dimensions, all sutures were visualized and assessed for patency or fusion, and length of fusion was measured. Findings were grouped according to suture type (sagittal, coronal, metopic, or lambdoid), the degree of fusion (full, >50%, or <50%), and patient age at time of CT scan (0-90, 91-180, 181-360, or >360 days). Data were analyzed to correlate patient age versus the degree of suture fusion. Results: For all patients, 72% had complete and 28% had partial synostosis. Ratios of full to partial fusion for each suture type were as follows: sagittal 97:36, coronal 35:22, metopic 46:4, and lambdoid 4:10. The sagittal, coronal, and metopic groups demonstrated greater probabilities of complete suture fusion as patient age increases ( P = .021, P < .001, P = .001, respectively). This trend was also noted when all sutures were considered together by age-group ( P < .001). Conclusion: We note a partial suture fusion rate of 28.3%. Our analysis shows a correlation between the extent of suture synostosis and patient age. Finally, we demonstrate that different sutures display different patterns of partial and complete fusion.
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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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Bradley, James P., Jamie P. Levine, Christopher Blewett, Thomas Krummel, Joseph G. Mccarthy, and Michael T. Longaker. "Studies in Cranial Suture Biology: In Vitro Cranial Suture Fusion." Cleft Palate-Craniofacial Journal 33, no. 2 (March 1996): 150–56. http://dx.doi.org/10.1597/1545-1569_1996_033_0150_sicsbv_2.3.co_2.

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The biology underlying craniosynostosis remains unknown. Previous studies have shown that the underlying dura mater, not the suture itself, signals a suture to fuse. The purpose of this study was to develop an in vitro model for cranial-suture fusion that would still allow for suture-dura interaction, but without the influence of tensional forces transmitted from the cranial base. This was accomplished by demonstrating that the posterior frontal mouse cranial suture, known to be the only cranial suture that fuses in vivo, fuses when plated with its dura in an organ-culture system. In such an organ-culture system, the sutures are free from both the influence of dural forces transmitted from the cranial base and from hormonal influences only available in a perfused system. For the cranial-suture fusion in vitro model study, the sagittal sutures (controls that remain patent in vivo) and posterior frontal sutures (that fuse in vivo) with the underlying dura were excised from 24-day-old euthanized mice, cut into 5 × 4 × 2-mm specimens, and cultured in a chemically defined, serum-free media. One hundred sutures were harvested at the day of sacrifice, then every 2 days thereafter until 30 days in culture, stained with H & E, and analyzed. A subsequent cranial-suture without dura in vitro study was performed in a similar fashion to the first study, but only the calvariae with the posterior frontal or sagittal sutures (without the underlying dura) were cultured. Results from the cranial-suture fusion in vitro model study showed that all sagittal sutures placed in organ culture with the underlying dura remained patent. More importantly, the posterior frontal sutures with the underlying dura, which were plated-down as patent at 24 days of age, demonstrated fusion after various growth periods in organ culture. In vitro posterior frontal mouse-suture fusion occurred in an anterior-to-posterior direction but in a delayed fashion, 4 to 7 days later than in vivo posterior frontal mouse-suture fusion. In contrast, the subsequent cranial-suture without dura in vitro study showed patency of all sutures, including the posterior frontal suture. These data from in vitro experiments indicate that: (1) mouse calvariae, sutures, and the underlying dura survive and grow in organ-culture systems for 30 days; (2) the local dura, free from external influences transmitted from the cranial base and hormones from distant sites, influences the cells of its overlying suture to cause fusion; and (3) without dura influence, all in vitro cranial sutures remained patent. By first identifying the factors involved in dural-suture signaling and then regulating these factors and their receptors, the biologic basis of suture fusion and craniosynostosis may be unraveled and used in the future to manipulate pathologic (premature) suture fusion.
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Cyprus, Garrett N., Jefferson W. Overlin, Rafael A. Vega, Ann M. Ritter, and René Olivares-Navarrete. "Spatial regulation of gene expression in nonsyndromic sagittal craniosynostosis." Journal of Neurosurgery: Pediatrics 22, no. 6 (December 2018): 620–26. http://dx.doi.org/10.3171/2018.6.peds18229.

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OBJECTIVECranial suture patterning and development are highly regulated processes that are not entirely understood. While studies have investigated the differential gene expression for different sutures, little is known about gene expression changes during suture fusion. The aim of this study was to examine gene expression in patent, fusing, and fused regions along sagittal suture specimens in nonsyndromic craniosynostosis patients.METHODSSagittal sutures were collected from 7 patients (average age 4.5 months) who underwent minimally invasive craniotomies at the Children’s Hospital of Richmond at VCU under IRB approval. The sutures were analyzed using micro-CT to evaluate patency. The areas were classified as open, fusing, or fused and were harvested, and mRNA was isolated. Gene expression for bone-related proteins, osteogenic and angiogenic factors, transforming growth factor–β (TGF-β) superfamily, and Wnt signaling was analyzed using quantitative polymerase chain reaction and compared with normal sutures collected from fetal demise tissue (control).RESULTSMicro-CT demonstrated that there are variable areas of closure along the length of the sagittal suture. When comparing control samples to surgical samples, there was a significant difference in genes for Wnt signaling, TGF-β, angiogenic and osteogenic factors, bone remodeling, and nuclear rigidity in mRNA isolated from the fusing and fused areas of the sagittal suture compared with patent areas (p < 0.05).CONCLUSIONSIn nonsyndromic sagittal craniosynostosis, the affected suture has variable areas of being open, fusing, and fused. These specific areas have different mRNA expression. The results suggest that BMP-2, FGFR3, and several other signaling pathways play a significant role in the regulation of suture fusion as well as in the maintenance of patency in the normal suture.
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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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Chim, Harvey, Sunil Manjila, Alan R. Cohen, and Arun K. Gosain. "Molecular signaling in pathogenesis of craniosynostosis: the role of fibroblast growth factor and transforming growth factor–β." Neurosurgical Focus 31, no. 2 (August 2011): E7. http://dx.doi.org/10.3171/2011.5.focus1197.

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The interplay of signals between dura mater, suture mesenchyme, and brain is essential in determining the fate of cranial sutures and the pathogenesis of premature suture fusion leading to craniosynostosis. At the forefront of research into suture fusion is the role of fibroblast growth factor and transforming growth factor–β, which have been found to be critical in the cell-signaling cascade involved in aberrant suture fusion. In this review, the authors discuss recent and ongoing research into the role of fibroblast growth factor and transforming growth factor–β in the etiopathogenesis of craniosynostosis.
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Regelsberger, Jan, Tobias Schmidt, Björn Busse, Julia Herzen, Michael Tsokos, Michael Amling, and Felix Beckmann. "Synchrotron–microcomputed tomography studies of normal and pathological cranial sutures: further insight." Journal of Neurosurgery: Pediatrics 5, no. 3 (March 2010): 238–42. http://dx.doi.org/10.3171/2009.10.peds09138.

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Object Both CT and high-frequency ultrasound have been shown to be reliable diagnostic tools used to differentiate normal cranial sutures from suture synostosis. In nonsynostotic plagiocephaly, overlapping of the bony plates and the so-called “sticky suture” is still controversial and is believed to represent a pathological fusion process. Synchrotron–microcomputed tomography (SRmCT) studies were undertaken to determine whether positional head deformities can be assumed to be true suture pathologies. Methods Morphological features and growth development of 6 normal cranial sutures between the ages of 3 and 12 months were analyzed histologically. Additionally 6 pathological sutures, including sagittal synostosis and nonsynostotic plagiocephaly (NSP), were compared with the group of normal sutures by histological and SRmCT studies. Synchrotron-microcomputed tomography is a special synchrotron radiation source with a high photon flux providing a monochromatic x-ray beam with a very high spatial resolution. Morphological characteristics of the different suture types were evaluated and bone density alongside the sutures was measured to compare the osseous structure of the adjacent bony plates of normal and pathological sutures. Results Histologically jointlike osseous edges of the normal sutures were seen in the 1st month of life and interlocking at the age of approximately 12 months. During this 1st year, bone thickness increases and suture width decreases. The SRmCT studies showed that: 1) sutures and adjacent bones in NSP are comparable to normal sutures in terms of their morphological aspects; 2) bone densities in the adjacent bony plates of NSP and normal sutures are not different; 3) thickening of the diploe with ridging of the bone in sagittal synostosis is associated with significantly higher bone density; 4) synostotic sutures are only partially fused but vary in their extent; and 5) nonfused sections in sagittal synostosis behave like normal sutures without any signs of pathological bone formation. Conclusions Sutures in patients with NSP were found without any morphological irregularities or different osseous structures alongside those compared with normal sutures. Thus, a true suture pathology or osseous change of the adjacent bony plates is highly unlikely in NSP. Even though the number of specimens is limited in this series, cranial suture fusion seems to start at one undetermined point and spread along the suture, whereas other parts of the same suture are not involved according to morphological aspects and bone density measurements of the adjacent bones. This theory may represent a dynamic fusion process completed over time but just starting too early.
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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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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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Poisson, Elyane, James J. Sciote, Richard Koepsel, Gregory M. Cooper, Lynne A. Opperman, and Mark P. Mooney. "Transforming Growth Factor-β Isoform Expression in the Perisutural Tissues of Craniosynostotic Rabbits." Cleft Palate-Craniofacial Journal 41, no. 4 (July 2004): 392–402. http://dx.doi.org/10.1597/02-140.1.

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Objective To describe the expression patterns of the various transforming growth factor-β (Tgf-β) isoforms, known to be involved in suture development, in the perisutural tissues of rabbits with naturally occurring craniosynostosis and relate such differential expression to the pathogenesis of premature suture fusion. Method Twenty-one coronal sutures were harvested from six wild-type control New Zealand White rabbits and five rabbits with familial coronal suture synostosis at 25 days of age for histomorphometric and immunohistochemical analyses. Tgf-β isoform immunoreactivity was assessed using indirect immunoperoxidase procedures with specific antibodies. Results Synostosed sutures had significantly (p < .01) greater bone area and relatively more osteoblasts and osteocytes in the osteogenic fronts, compared with wild-type sutures. Tgf-β isoform immunoreactivity showed differential staining patterns between wild-type and synostosed perisutural tissues. In wild-type sutures, Tgf-β1 and Tgf-β3 immunoreactivity was significantly (p < .001) greater than Tgf-β2 staining in all perisutural tissues. In synostosed sutures, the opposite pattern was observed, with Tgf-β2 immunoreactivity significantly (p < .001) greater than Tgf-β1 and Tgf-β3 in the osteogenic fronts, dura mater, and periosteum. Conclusions Findings from this study suggest that an overexpression of Tgf-β2, either in isolation or in association with an underexpression of Tgf-β1 and Tgf-β3, may be related to premature suture fusion (craniosynostosis) in this pathological rabbit model. These abnormal expression patterns may be involved in premature suture fusion either through increased cell proliferation, decreased apoptosis of the osteoblasts or both at the osteogenic fronts.
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Dissertations / Theses on the topic "Suture fusion"

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Connerney, Jeannette J. "Balance between Formation of Twist1 Homodimer and Heterodimer Regulate Suture Fusion." Fogler Library, University of Maine, 2007. http://www.library.umaine.edu/theses/pdf/ConnerneyJJ2007.pdf.

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Hughes, Christopher. "A finite element modelling strategy for suture anchor devices." Thesis, Brunel University, 2014. http://bura.brunel.ac.uk/handle/2438/11553.

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Suture or bone anchors are used to reattach a tendon or ligament after it has been torn away from the bone. Anchors provide secure attachments to bone during trauma or reconstructive surgery, holding the ligament or tendon in place and potentially allowing greater mobility during recovery. Computer modelling techniques are used to investigate both established bone anchor technology, such as threaded implants, and emerging technologies such as cement augmentation or sonic-fusion. Sonic fusion is an ultrasound-assisted anchoring method which has recently been introduced in low load maxillofacial applications, and is expected to be used in other low load applications such as hallux valgus alignment procedures and suture attachment. Threaded anchors were examined using two Finite Element (FE) models of human cancellous bone, representing both “normal” and “weaker” bone. Simulation and analysis revealed the critical nature of modelling the microstructure of bone. Changing the direction of loading in the model leads to significant changes in the response of the construct, and this cannot be represented in continuum models, or in physical models using artificial cancellous bone. Rapid prototyping (RP) using 3d printing was used for validation of the FE models. While this method has previously been implemented to create physical bone models, testing an assembly model and comparing it to FE results for inclined loading had not been attempted. RP models were created of the threaded anchor in both “normal” and “weaker” bone, and a sonic fusion model in the normal bone was also created. These models were then subjected to mechanical testing. Results produced from the simulation correlated with the physical results. The importance of a cortical layer was re-confirmed. At the apparent densities simulated, engagement with the cortical layer increases pull-out force dramatically. Engaging the anchor even with a thin cortical layer can produce a significant improvement to pull-out strength. Novel sonic fusion FE models were created from a CT scan of animal bone, and the geometry for both the sonic-fusion pin and bone were taken from the CT scan. Computer generated geometry was used to build pin concepts of varying shapes. It was shown that if good engagement is made with bone, as in the case of all of the concepts created, then sonic fusion can produce a good holding power - comparable with that of a threaded anchor. The results showed that sonic-fusion requires less drill penetration into the bone, meaning less of the inherent bone structure is removed – vital for patients with poor bone quality. Bone cement models were investigated. Bone augmentation models were created, and the addition of cement demonstrated an improvement in anchor holding power. The research showed that there are benefits to using FEA as a tool to evaluate the mechanical aspects of cement distribution. The results proved the hypothesis that augmentation will likely increase the holding power of anchor, and its distribution will affect pull-out significantly. This work has created a method for modelling and evaluating both established and novel bone anchor technology in CT bone geometry, a procedure which could be expanded to other bone implants. It has been validated using the innovative approach of rapid prototyping.
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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.

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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/.

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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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Johnson, David. "A comprehensive screen of genes implicated in craniosynostosis." Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.365877.

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Leitch, Victoria Dawn. "Changing the face of craniosynostosis: the role of RBP4 in osteogenesis and suture fusion." Thesis, 2011. http://hdl.handle.net/2440/78604.

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Craniosynostosis is the premature fusion of cranial sutures and results in the compensatory malformation of the skull to accommodate the rapid growth of the brain during early childhood. This PhD thesis aims to look at the molecular mechanisms at play during this premature fusion; in particular it follows on from a recent microarray study of craniosynostosis tissue conducted in this laboratory. This study showed a 37x down regulation of RBP4 in fused sutures in humans. RBP4 is a retinol binding protein whose function is to transport retinol in the blood to target tissue, where it is metabolised to retinoic acid. This is of interest as retinoic acid is known to have an influence on bone growth. In this PhD project we have used animal and cell culture models to assess the levels of RBP4 during suture fusion and osteogenesis and its possible role in this process. Expression of Rbp4, Stra6 and other markers of osteogenesis were assessed using quantitive PCR in a mouse model of Saethre-Chotzen craniosynostosis syndrome (Twist1⁺/⁻). This demonstrated an initial correlation between suture fusion and Rbp4 down regulation as well as an inverse relationship between Rbp4 and Stra6 expression. However, sutures that did not fuse and parietal bone also displayed downregulation of Rbp4 at later timepoints. Histology showed that this might be related to parietal bone thickening. Multiple cell culture models were trialed, but proved unsuitable for RBP4 studies in osteogenesis. The commonly used mouse pre-osteoblastic cell line, MC3T3-E1, mineralised but did not express Rbp4. Primary coronal suture cells were isolated from mice, which expressed Rbp4, but failed to mineralise. Subsequently, primary cell cultures from human sutures were tested in osteogenesis assays and showed a decrease in RBP4 levels during mineralisation. Immunocytochemistry was used to determine the localisation of RBP4 in suture cells compared to Huh7 cells, a liver carcinoma cell line with known secretion of RBP4. Results showed that RBP4 is localised to the endoplasmic reticulum in suture cells, differing to the localization seen in Huh7 cells. Western blot analysis also demonstrated that unlike liver cells, human suture cells do not secrete detectable levels of RBP4. Finally, functional studies to analyse the role of RBP4 in osteogenesis using a lentiviral delivery system for over expression of RBP4 showed no effect on the ability of human suture cells to mineralise. A high level of overexpression was achieved however there were issues with infection efficiency which may have affected the outcome of these experiments. These studies demonstrate some unique characteristics of RBP4 in suture cells and extend its role beyond a simple serum transporter of retinol. In addition to a role in suture fusion, these results could be a reflection of a broader function of RBP4 in normal bone growth and osteogenesis.
Thesis (Ph.D.) -- University of Adelaide, School of Paediatrics and Reproductive Health, 2011
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Sutor, Sarah [Verfasser]. "The GTPase assay as a highly sensitive model system for characterization of human cannabinoid receptors and their ligands : Gαi2 co-expression and fusion studies and the impact of RGS proteins / vorgelegt von Sarah Sutor geb. Geiger." 2010. http://d-nb.info/1008575704/34.

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Books on the topic "Suture fusion"

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Hsieh, Hannah, Lauren Thornton, and Glenn Mann. Craniosynostosis and Anesthetic Management for Cranial Vault Remodeling. Edited by David E. Traul and Irene P. Osborn. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190850036.003.0015.

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Craniosynostosis is a congenital malformation involving premature fusion of one or more skull sutures restricting normal growth of the cranium. The sequelae of premature cranial suture fusion are not only cosmetic and may cause elevated intracranial pressure in children. Treatment for craniosynostosis is surgical, and the perioperative management often entails a multidisciplinary team consisting of neurosurgery, plastic surgery, anesthesiology, and critical care. Although the optimal age of repair remains controversial, it is suggested that intervention is best performed prior to 12 months of age. The anesthetic challenges for these complex surgeries include difficult airway management, significant blood loss, long surgical duration, and pain control in children of young age.
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Karlberg, Helena. Craniosynostosis Repair. Edited by Erin S. Williams, Olutoyin A. Olutoye, Catherine P. Seipel, and Titilopemi A. O. Aina. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190678333.003.0023.

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Craniosynostosis is the fusion of one or more cranial sutures; such fusion occurs due to multiple factors and typically occurs in utero. Depending on the sutures involved, the infant can have significant abnormalities in skull shape. The structural abnormality is corrected surgically, frequently after a series of operations starting from infancy and occurring even late in childhood, depending on the sutures that are fused. During these surgeries, an infant can lose substantial volumes of blood, increasing the risk of hypovolemia and venous air embolism. It is imperative for the pediatric anesthesiologist to employ various modalities to minimize blood loss and also recognize clinical signs indicating the need for transfusion.
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Book chapters on the topic "Suture fusion"

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Koppel, David, and Jaime Grant. "Modern Management of Craniosynostosis." In Oral and Maxillofacial Surgery for the Clinician, 1813–41. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-15-1346-6_79.

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AbstractThis chapter aims to outline to the reader the various forms of craniosynostosis (premature fusion of cranial sutures) and their management. It covers the pertinent aspects important in the assessment and management of these patients and provides an overview of the surgical procedures available, the indications for these and a guide as to how, and when, to implement them.
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White, Nicholas. "Assessment of patients with craniosynostosis." In Oxford Textbook of Plastic and Reconstructive Surgery, edited by Hiroshi Nishikawa, Felicity V. Mehendale, and David C. G. Sainsbury, 697–704. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780199682874.003.0183.

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The term craniosynostosis denotes the pathological partial or complete absence of one or more cranial sutures which manifests as abnormal skull growth. Although it is often referred to as premature fusion this is misleading as only the metopic suture fuses in the normal physiological state. The remaining sutures change and mature in macroscopic and microscopic form during growth but remain present. This chapter discusses the assessment of patients with craniosynostosis.
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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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Duncan, Christian, and Hiroshi Nishikawa. "Non-syndromic craniosynostosis." In Oxford Textbook of Plastic and Reconstructive Surgery, edited by Hiroshi Nishikawa, Felicity V. Mehendale, and David C. G. Sainsbury, 705–12. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780199682874.003.0184.

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Craniosynostosis is defined as the premature fusion of a skull suture and has an incidence of approximately 1:2000 live births. Historically, craniosynostosis was subdivided into primary and secondary synostosis. Further subclassifications included syndromic/non-syndromic and single/multisuture. Multisuture synostoses also give rise to characteristic head shapes, which, with experience, are readily identifiable by experienced clinicians using clinical examination alone. While in the past, single-suture craniosynostosis was classified as ‘non-syndromic’, advances in genetic analysis has shown that this may not be the case in a proportion of these cases, just as some multisuture presentations may also be non-syndromic. This particularly applies to unicoronal craniosynostosis along with some metopic and bicoronal synostosis. Given the higher rate of syndromic association in these patients, along with the tendency to require late surgery for facial scoliosis in unicoronal and unilambdoid patients, this cohort should be regarded as a more complex subset.
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Kimbel, William H., Yoel Rak, Donald C. Johanson, Ralph L. Holloway, and Michael S. Yuan. "Recovery and Reconstruction of A.L. 444-2." In The Skull of Australopithecus afarensis. Oxford University Press, 2004. http://dx.doi.org/10.1093/oso/9780195157062.003.0005.

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The A.L. 444-2 skull was found on 26 February 1992, during a strategic paleontological survey of Kada Hadar Member sediments that are stratigraphically situated between BKT-1 and BKT-2 tephras, on the eastern edge of the Awash River’s Kada Hadar tributary. Yoel Rak discovered two fragments of hominin occipital bone (A.L. 444-1) at the base of a steep hill composed of Kada Hadar Member silts and clays capped by a weathered sandstone remnant. Subsequent examination of the upslope surface revealed additional hominin skull fragments (the temporal bones and maxillae) clustered together and partially exposed in a narrow gully that dissected the face of the hill. During the next seven days, probing and dry sieving of the gully infill and hillside colluvium over a 77 m2 area led to the recovery of fragments representing about 75%–80% of a single hominin skull. It was immediately apparent that the upslope finds duplicated the anatomical parts represented by the two A.L. 444-1 occipital fragments and therefore constituted a second hominin individual, cataloged as A.L. 444-2. In addition, the lambdoidal suture of the A.L. 444-1 occipital is completely unfused, suggesting subadult status, whereas fused cranial sutures and extreme dental occlusal wear indicate an advanced ontogenetic age for A.L. 444-2. In February–March 1993 the A.L. 444 hillside was excavated in an effort to locate missing parts of the A.L. 444-2 skull and to determine its precise stratigraphic provenance. No further remains of the hominin skull were encountered in situ, but a complete viverrid cranium and indeterminate fragments of large mammal bone with preservation and patina (mottled dark gray, white, and yellowish gray) identical to those of the hominin were excavated in an unstratified, cemented carbonate silt that exactly matches the matrix adhering to A.L. 444-2. We are confident that the hominin skull is from this sedimentary horizon. It is approximately 10.5 m stratigraphically below the BKT-2 tephra, which outcrops in the immediate vicinity of A.L. 444 Single-crystal laser fusion (SCLF) 40Ar/39Ar ages for BKT-2 and Kada Hadar Tuff (KHT) bracket the geological age of A.L. 444-2 between 2.94 and 3.18 Myr (Kimbel et al., 1994; Walter, 1994; Semaw et al., 1997).
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Carver, Ed, and Doug Johnson. "Maxillofacial, craniofacial, and cleft surgery." In Paediatric Anaesthesia, 387–98. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198755791.003.0019.

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Maxillofacial surgery in paediatrics ranges from straightforward oral surgery to complex reconstructive surgery of the maxilla and mandible in cases of congenital or acquired abnormality. Craniofacial surgery is undertaken in supra-regional units and involves a multidisciplinary team of maxillofacial, neuro, and plastic surgeons. Much of craniofacial surgery in paediatrics is for craniosynostosis (premature fusion of one or more sutures of the skull) and can involve significant blood loss. Cleft lip and palate surgery in the UK is undertaken in a small number of regional centres, mainly by plastic surgeons. Anaesthesia for these specialities requires clear understanding of the procedure to be undertaken and readiness for potential perioperative complications. All these areas of practice need a good knowledge of, and ability in, the management of the difficult airway.
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Quinlan, Sean M. "Sculpting Ideal Bodies." In Morbid Undercurrents, 149–75. Cornell University Press, 2021. http://dx.doi.org/10.7591/cornell/9781501758331.003.0007.

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This chapter recounts how one doctor and his fellow travelers sutured together medical knowledge, gender, and political ideals, not in the family realm but in the fraternal and egalitarian world of the anatomist's studio. It begins with the scientific study conducted by the physician and artist Jean-Galbert Salvage (1772–1813) on the anatomical structure of the so-called Borghese Gladiator. The chapter investigates the settings of his work — and the ideological, aesthetic, and gendered assumptions that guided him. Ever since the Gladiator was first dug up and installed at the Villa Borghese outside of Rome, art critics had hailed the figure as a paragon of male beauty, elegance, and anatomical precision. The chapter then explores how Salvage was fusing political ideals and medical language in France during the post-revolutionary years: namely, the continuing desire, within critical legislative and intellectual groups, to regenerate the French nation in its “physical and moral” totality. The chapter argues that Salvage molded his Gladiator specimens so that he might bridge medicine and the fine arts and thus localize the regenerated male ideal in the material body. Here, medicine served as an essential means for expressing and mediating ideological hopes, fears, and memories.
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