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Pregnancy Timeline by SemestersFetal liver is producing blood cellsHead may position into pelvisBrain convolutions beginFull TermWhite fat begins to be madeWhite fat begins to be madeHead may position into pelvisImmune system beginningImmune system beginningPeriod of rapid brain growthBrain convolutions beginLungs begin to produce surfactantSensory brain waves begin to activateSensory brain waves begin to activateInner Ear Bones HardenBone marrow starts making blood cellsBone marrow starts making blood cellsBrown fat surrounds lymphatic systemFetal sexual organs visibleFinger and toe prints appearFinger and toe prints appearHeartbeat can be detectedHeartbeat can be detectedBasic Brain Structure in PlaceThe Appearance of SomitesFirst Detectable Brain WavesA Four Chambered HeartBeginning Cerebral HemispheresFemale Reproductive SystemEnd of Embryonic PeriodEnd of Embryonic PeriodFirst Thin Layer of Skin AppearsThird TrimesterSecond TrimesterFirst TrimesterFertilizationDevelopmental Timeline
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Home | Pregnancy Timeline | News Alerts |News Archive March 7, 2014

 

Apert syndrome is caused by errors in bone formation with one outcome being
the fusing of skull sutures, the soft tissue that exists between bones in the skull.

Image Credit: www.thefetus.net.






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3-D imaging reveals how Apert Syndrome develops

Apert Syndrome can cause the bones in the fetal skull to fuse together, a mutation causing mid-facial deformities, a variety of neural malformations and impaired brain growth.

Three dimensional images of two different mouse models of Apert Syndrome, show that cranial deformation begins before birth and continues worsening with growth.

Apert Syndrome is caused by mutations in the gene FGFR2 — a growth factor that typically produces a protein functioning in cell division, which regulates cell growth and maturation, helps in the formation of blood vessels, wound healing, and in general embryo development.


With certain mutations, the FGFR2 gene causes the bones in the skull to fuse together in the fetus. These mutations cause mid-facial deformities, a variety of neural, limb and tissue malformations and may lead to cognitive impairment.


Understanding the growth pattern of the head in an individual, the ability to anticipate where the bones will fuse and grow next, and using simulations "could contribute to improved patient-centered outcomes either through changes in surgical approach, or through more realistic modeling and expectation of surgical outcome," the researchers said in the Feb. 28, 2014 issue of BMC Developmental Biology.

Joan T. Richtsmeier, Distinguished Professor of Anthropology, Penn State, and her team looked at two sets of mice, each having a different mutation that causes Apert Syndrome in humans and causing similar cranial problems in the mice. They checked bone formation and the fusing of sutures, soft tissue that usually exists between bones n the skull, in the mice at 17.5 days after conception and at birth -- 19 to 21 days after conception.


"It would be difficult, actually impossible, to observe and score the exact processes and timing of abnormal suture closure in humans as the disease is usually diagnosed after suture closure has occurred.

"With these mice, we can do this at the anatomical level by visualizing the sutures prenatally using micro-computed tomography -- 3-D X-rays -- or at the mechanistic level by using immunohistochemistry, or other approaches to see what the cells are doing as the sutures close."

Joan T. Richtsmeier, Distinguished Professor of Anthropology, Pennsylvania State University


Early fusion of bones of the skull and of face makes it impossible for the head to grow in the typical fashion. Researchers found that the changed growth pattern contributed significantly to continuing skull deformation and facial deformation increasing over time.


"Currently, the only option for people with Apert syndrome is rather significant reconstructive surgery, sometimes successive planned surgeries that occur throughout infancy and childhood and into adulthood.

"These surgeries are needed to restore function to some cranial structures, perhaps allowing for brain expansion in some situations; and in general, provide more typical cranial features."

Joan T. Richtsmeier


Using 3-D imaging, the researchers were able to estimate how the changes in the growth patterns caused by either of the two different mutations produced both head and facial deformities.

"If what we found in mice is analogous to the processes at work in humans with Apert syndrome, then we need to decide whether or not a surgical approach - that we know is necessary - is also sufficient," said Richtsmeier. "If it is not, in some cases, then we need to be working towards therapies that can replace or further improve surgical outcomes."

Abstract (provisional)
Differences in cranial morphology arise due to changes in fundamental cell processes like migration, proliferation, differentiation and cell death driven by genetic programs. Signaling between fibroblast growth factors (FGFs) and their receptors (FGFRs) affect these processes during head development and mutations in FGFRs result in congenital diseases including FGFR-related craniosynostosis syndromes. Current research in model organisms focuses primarily on how these mutations change cell function local to sutures under the hypothesis that prematurely closing cranial sutures contribute to skull dysmorphogenesis. Though these studies have provided fundamentally important information contributing to the understanding of craniosynostosis conditions, knowledge of changes in cell function local to the sutures leave estimates of change in overall three-dimensional cranial morphology largely unexplained. Here we investigate growth of the skull in two inbred mouse models each carrying one of two gain-of-function mutations in FGFR2 on neighboring amino acids (S252W and P253R) that in humans cause Apert syndrome, one of the most severe FGFR-related craniosynostosis syndromes. We examine late embryonic skull development and suture patency in Fgfr2 Apert syndrome mice between embryonic day 17.5 and birth, and quantify the effects of these mutations on three-dimensional skull morphology, suture patency and growth.

Other Penn State researchers on this project include Susan M. Motch Perrine, post doctoral research assistant, and Neus Martínez-Abadías, former post doctoral fellow, now at Center for Genomic Regulation, Barcelona, Spain. Other researchers include Theodore M. Cole III, associate teaching professor, University of Missouri-Kansas City School of Medicine; Kristina Aldridge, former post doctoral fellow at Penn State and currently assistant professor, University of Missouri-Columbia; and Ethylin Wang Jabs, professor, Icahn School of Medicine at Mount Sinai.

The National Institute of Dental and Craniofacial Research, the American Recovery and Reinvestment Act and the National Science Foundation partially funded this work.