Force-Induced Craniosynostosis in the Murine Sagittal Suture

Oppenheimer, Adam J.; Rhee, Samuel T.; Goldstein, Steven A.; Buchman, Steven R.

doi:10.1097/prs.0b013e3181bf806c

Cited by 32 publications

(26 citation statements)

References 49 publications

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“…metopic and sagittal). Recently, an in vitro model of force-induced sagittal craniosynostosis has corroborated the importance of intrauterine constraint in the initiation of midline craniosynostosis (Oppenheimer et al 2009). Advanced maternal age (35 years and older) and birth weight (> 4000 g) are additional environmental components of sagittal NSC (Boulet et al 2008).…”

Section: Introductionmentioning

confidence: 93%

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New insights into the relationship between suture closure and craniofacial dysmorphology in sagittal nonsyndromic craniosynostosis

et al. 2010

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Premature closure of the sagittal suture occurs as an isolated (nonsyndromic) birth defect or as a syndromic anomaly in combination with other congenital dysmorphologies. The genetic causes of sagittal nonsyndromic craniosynostosis (NSC) remain unknown. Although variation of the dysmorphic (scaphocephaly) skull shape of sagittal NSC cases has been acknowledged, this variation has not been quantitatively studied three-dimensionally (3D). We have analyzed the computed tomography skull images of 43 infants (aged 0.9–9 months) with sagittal NSC using anatomical landmarks and semilandmarks to quantify and characterize the within-sample phenotypic variation. Suture closure patterns were defined by dividing the sagittal suture into three sections (anterior, central, posterior) and coding each section as ‘closed’ or ‘fused’. Principal components analysis of the Procrustes shape coordinates representing the skull shape of 43 cases of NSC did not separate individuals by sex, chronological age, or dental stages of the deciduous maxillary first molar. However, analysis of suture closure pattern allowed separation of these data. The central section of the sagittal suture appears to be the first to fuse. Then, at least two different developmental paths towards complete fusion of the sagittal suture exist; either the anterior section or the posterior section is the second to fuse. Results indicate that according to the sequence of sagittal suture closure patterns, different craniofacial complex shapes are observed. The relationship between craniofacial shape and suture closure indicates not only which suture fused prematurely (in our case the sagittal suture), but also the pattern of the suture closure. Whether these patterns indicate differences in etiology cannot be determined with our data and requires analysis of longitudinal data, most appropriately of animal models where prenatal conditions can be monitored.

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Section: Introductionmentioning

confidence: 93%

“…metopic and sagittal). Recently, an in vitro model of force‐induced sagittal craniosynostosis has corroborated the importance of intrauterine constraint in the initiation of midline craniosynostosis (Oppenheimer et al. 2009).…”

Section: Introductionmentioning

confidence: 95%

New insights into the relationship between suture closure and craniofacial dysmorphology in sagittal nonsyndromic craniosynostosis

et al. 2010

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“…Also, Oppenheimer et al . has demonstrated that cyclical forces led to premature fusion of sagittal sutures 25 but the effect of changes in the stiffness of the cranial suture tissues in bone formation has yet to be investigated. Since bone generation is mediated by signalling mechanisms that include stimuli from the surrounding environment, pathological changes in the physiology of the sutures of children with craniosynostosis may be associated with changes in the stimuli provided by the extracellular environment that impairs the functional capacity of cells within the sutures to sense and respond to these stimuli.…”

Section: Introductionmentioning

confidence: 99%

Identification of stiffness-induced signalling mechanisms in cells from patent and fused sutures associated with craniosynostosis

Barreto

González-Vázquez

Cameron

et al. 2017

Sci Rep

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Craniosynostosis is a bone developmental disease where premature ossification of the cranial sutures occurs leading to fused sutures. While biomechanical forces have been implicated in craniosynostosis, evidence of the effect of microenvironmental stiffness changes in the osteogenic commitment of cells from the sutures is lacking. Our aim was to identify the differential genetic expression and osteogenic capability between cells from patent and fused sutures of children with craniosynostosis and whether these differences are driven by changes in the stiffness of the microenvironment. Cells from both sutures demonstrated enhanced mineralisation with increasing substrate stiffness showing that stiffness is a stimulus capable of triggering the accelerated osteogenic commitment of the cells from patent to fused stages. The differences in the mechanoresponse of these cells were further investigated with a PCR array showing stiffness-dependent upregulation of genes mediating growth and bone development (TSHZ2, IGF1), involved in the breakdown of extracellular matrix (MMP9), mediating the activation of inflammation (IL1β) and controlling osteogenic differentiation (WIF1, BMP6, NOX1) in cells from fused sutures. In summary, this study indicates that stiffer substrates lead to greater osteogenic commitment and accelerated bone formation, suggesting that stiffening of the extracellular environment may trigger the premature ossification of the sutures.

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“…These growth alterations appear to occur both by tension and compression (Sun et al, 2004;Herring, 2008). However, compression has also been suggested to cause cessation of growth at the calvarial sutures (Oppenheimer et al, 2009). Cartilage is much less relatively affected by muscle loads compared to sutures and periodontal ligaments (Bjork and Skieller, 1983), and in humans the masticatory muscle phenotype is associated with variations in the vertical growth of the face, but not with sagittal growth (Rowlerson et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Masticatory HyperMuscularity is not Related to Reduced Cranial Volume in Myostatin‐Knockout Mice

Cray

Kneib

Vecchione

et al. 2011

The Anatomical Record

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It has been suggested recently that masticatory muscle size reduction in humans resulted in greater encephalization through decreased compressive forces on the cranial vault. Following this logic, if masticatory muscle size were increased, then a reduction in brain growth should also occur. The present study was designed to test this hypothesis using a myostatin (GDF-8) knockout mouse model. Myostatin is a negative regulator of skeletal muscle growth, and individuals lacking this gene show significant hypermuscularity. Sixty-two (32 wild-type and 30 GDF-8 −/− knockout), 1, 28, 56 and 180 day old CD-1 mice were used. Body and masseter muscle weights were collected following dissection and standardized lateral and dorsoventral cephalographs were obtained. Cephalometric landmarks were identified on the radiographs and cranial volume was calculated. Mean differences were assessed using a two-way ANOVA. KO mice had significantly greater body and masseter weights beginning at 28 days compared to WT controls. No significant differences in cranial volumes were noted between KO and WT. Muscle weight was not significantly correlated with cranial volume in 1, 28, or 180 day old mice. Muscle weights exhibited a positive correlation with cranial volume at 56 days. Results demonstrate that masticatory hypermuscularity is not associated with reduced cranial volume. In contrast, there is abundant data demonstrating the opposite, brain growth determines cranial vault growth and masticatory apparatus only affects ectocranial morphology. The results presented here do not support the hypothesis that a reduction in masticatory musculature relaxed compressive forces on the cranial vault allowing for greater encephalization.

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Force-Induced Craniosynostosis in the Murine Sagittal Suture

Cited by 32 publications

References 49 publications

New insights into the relationship between suture closure and craniofacial dysmorphology in sagittal nonsyndromic craniosynostosis

New insights into the relationship between suture closure and craniofacial dysmorphology in sagittal nonsyndromic craniosynostosis

Identification of stiffness-induced signalling mechanisms in cells from patent and fused sutures associated with craniosynostosis

Masticatory HyperMuscularity is not Related to Reduced Cranial Volume in Myostatin‐Knockout Mice

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