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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 secondary palate begins development at 11.5 dpc as with the palatal shelf outgrowths arising from the oral surface of the maxillary processes, followed by vertical growth which forms the palatal shelves (8). At 13.5 dpc the palatal shelves can are now distinct forms along the anterior-posterior axis. Of note, the most critical coordination of events occur from 14.0 to 15.5 dpc in the mouse fetus. Elevation of the palatal shelves occurs in the short time frame from 14–14.5 dpc, followed by contact of the palatal shelves at 15.0 dpc. After meeting in the midline, the palatal shelves will completion of fusion of the palate by 15.5 dpc (8,9); these above actions correlate to palatogenesis events beginning in the sixth week of gestation with completion of palatal fusion by 12 weeks (8).
Anatomy and Embryology of the Mouth and Dentition
Published in John C Watkinson, Raymond W Clarke, Terry M Jones, Vinidh Paleri, Nicholas White, Tim Woolford, Head & Neck Surgery Plastic Surgery, 2018
As is evident from the description above, palate formation is a complicated process. The palatal shelves must grow to the appropriate size; the palatal shelves must elevate at the appropriate time on both sides; the medial edge epithelia of the palatal shelves must adhere to form a midline epithelial seam: the midline epithelial seam must degenerate to allow for the establishment of mesenchymal continuity across the midline. Any interference or mistiming of these processes may contribute towards the formation of a cleft palate. Clefts of the palate, like those of the lip, are multifactorial malformations, involving both genetic (polygenic) and environmental factors. Recent research on palatogenesis has concentrated on two main events: palatal shelf elevation and the initial stage of fusion of the shelves.
Three-dimensional (3D) cell culture studies: a review of the field of toxicology
Published in Drug and Chemical Toxicology, 2023
Seda İpek, Aylin Üstündağ, Benay Can Eke
3D organoid models can also be used to study developmental toxicity due to their ability to emulate the morphology of developing tissue in vitro. In vitro organoids can capture key embryo morphogenesis events during the epithelial–mesenchymal transition and tissue fusion, which are common themes during embryonic development. In this respect, Belair et al. (2018) established an organoid model to investigate several cleft palate teratogens identified from rodent models as well as pharmacological inhibitors targeting known palatogenesis and epithelial morphogenesis pathways. The results showed that of the 12 potential teratogens associated with cleft palate, three was found to disrupt the organoid fusion depending on epithelial morphogenesis, while some were cytotoxic to fuzing organoids.
Extracellular Matrix Remodeling During Palate Development
Published in Organogenesis, 2020
Xia Wang, Chunman Li, Zeyao Zhu, Li Yuan, Wood Yee Chan, Ou Sha
Collagens are the major components of ECM in connective tissues. There are 28 distinct collagens composed of α1, α2, α3 subunits combination and classified into fibrillar collagens (Collagen I–III, V, and XI) and non-fibrillar forms (Collagen VI, IX, IV, etc.).5,19 Fibrillar collagens form strong and stable fibrils and organize the fibrils into three-dimensional network, for example, Collagen I fibrils for bones and Collagen II fibrils for cartilages.5 Non-fibrillar forms of collagens include Fibril-Associated Collagens and basement collagens. Fibril-Associated Collagens, such as Collagen IX, associate with collagen fibrils and bind them together to form thicker collagen fibers. Basement collagens are sheet-forming collagens such as Collagen IV, which form the two-dimensional network for all basal laminae.5,19 A variety of collagens are highly expressed in the palate and dynamically remodeled during palatogenesis (Tables 1 and 2).