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Prenatal Diagnosis and Screening for Aneuploidy
Published in Vincenzo Berghella, Obstetric Evidence Based Guidelines, 2022
Sarah Harris, Angie Jelin, Neeta Vora
Characteristic facies, cardiovascular defects in 85%, most are VSD. Cleft of secondary palate, may be submucous cleft or velopharyngeal incompetence. Nasal reflux in infants. Transient neonatal hypocalcemia. Hypotonia. Immune system dysfunction. Postnatal growth delay. Developmental delay, learning disability, and psychological problems, especially in adolescence. Hypernasal speech.
Central Nervous System and Facial Development
Published in Mary C. Peavey, Sarah K. Dotters-Katz, Ultrasound of Mouse Fetal Development and Human Correlates, 2021
Mary C. Peavey, Sarah K. Dotters-Katz
The development of the face in both humans and mice is an intricate process. The roof of the mouth is formed by the palate, which serves to separate the nasal and oral cavities. For both humans and mice, the palate is formed from both the primary and the secondary palates. The primary palate is the most anterior part of the palate, while the secondary palate – which creates the majority of the palate – forms by a process of fusion of two paired palatal shelves, which are derived from the maxillary processes (2,3).
Clefts and craniofacial
Published in Tor Wo Chiu, Stone’s Plastic Surgery Facts, 2018
Secondary palate consists of the hard palate behind the incisive foramen and soft palate, and clefts represent failure of the lateral palatine processes to fuse with each other and the nasal septum/vomer.
Extracellular Matrix Remodeling During Palate Development
Published in Organogenesis, 2020
Xia Wang, Chunman Li, Zeyao Zhu, Li Yuan, Wood Yee Chan, Ou Sha
The morphogenesis of the mammalian secondary palate begins with the outgrow of two palatal shelves from the maxillary processes on both sides of the tongue on an embryonic day (E) 12.1 The two vertically oriented palatal shelves soon elevate horizontally and opposite each other on E 14–15.1 Then, the palatal shelves epithelia disintegrate in the midline and their mesenchymal compartment fuse completely to form an intact palatal roof.1 Cells in the palatal shelves originate from three sources of embryonic tissue/structures: the superficial palatal epithelium is derived from the embryonic ectoderm, the underlying palatal mesenchyme mainly from the neural crest.1,2 Supporting these cells is the infrastructure composed by complex extracellular matrix network.
The biochemistry, signalling and disease relevance of RYK and other WNT-binding receptor tyrosine kinases
Published in Growth Factors, 2018
James P. Roy, Michael M. Halford, Steven A. Stacker
Mammalian models are pivotal for elucidating the biological function of human genes. The initial characterization of Ryk-knockout mice revealed phenotypes including craniofacial and skeletal defects along with embryonic lethality (Halford et al., 2000). Homozygote Ryk-deficient mice die on their day of birth and the embryos display growth retardation, a cleft secondary palate and malformed limbs, facial bones and cranial vault (Figure 3). However, Ryk+/− mice have no identified phenotypes or reduction in life expectancy (Halford et al., 2000). Since then further studies have identified a range of other phenotypes in Ryk-deficient mice in particular within the nervous system such as aberrant axonal guidance (Keeble et al., 2006) and exencephaly (Macheda et al., 2012) (Figure 3), demonstrating a diversity of RYK-dependent developmental processes which have been reviewed previously (Halford et al., 2015). Two developmental phenotypes common to WNT-binding RTK knockout mice are defects of the inner ear/cochlea and neural tube (Figure 3), demonstrating defective non-canonical signalling. Mice lacking wild-type PTK7 or ROR receptors also show defects in the cardiovascular and respiratory systems (Figure 3). This raises the possibility of Ryk-deficient mice also having phenotypes in these organ systems. An impediment to further study encountered with knockout mice of each WNT-binding RTK is their perinatal death (Figure 3).
Global, regional and national burden of orofacial clefts from 1990 to 2019: an analysis of the Global Burden of Disease Study 2019
Published in Annals of Medicine, 2023
Dawei Wang, Boyu Zhang, Qi Zhang, Yiping Wu
The aetiology of orofacial clefts is complex, relating to different embryological origins and times of development [6,7]. The failure of the formation of the primary palate leads to a cleft lip, while a cleft palate arises from the failed formation of the secondary palate [4]. The cause of orofacial clefts can be considered as the interaction between genetic alterations and environmental factors [8,9]. Recently, many candidate genes and loci have been demonstrated to be associated with the occurrence of orofacial clefts [10–12]. The environmental factors, including smoking, alcohol consumption, dietary and vitamin deficiencies, parental age, environmental toxins and socioeconomic status, may also affect the presence of orofacial clefts [13–17].