China
Africa
Explore chapters and articles related to this topic
Clefts and craniofacial
Published in Tor Wo Chiu, Stone’s Plastic Surgery Facts, 2018
Cartilaginous components include Maxillary process – the mesenchyme undergoes intramembranous ossification to form the premaxilla, maxilla, zygoma and part of the temporal bone.Mandibular process – Meckel’s cartilage forms in the mesenchyme of the mandibular process, and most of it eventually regresses to leave only the parts that form the incus and malleus, anterior ligament of malleus and sphenomandibular ligament. The mandible forms by intramembranous ossification using Meckel’s cartilage as a template rather than by direct ossification of the cartilage.
Anatomy of the Skull Base and Infratemporal Fossa
Published in John C Watkinson, Raymond W Clarke, Christopher P Aldren, Doris-Eva Bamiou, Raymond W Clarke, Richard M Irving, Haytham Kubba, Shakeel R Saeed, Paediatrics, The Ear, Skull Base, 2018
The sphenomandibular ligament is a fibrous band joining the spine of the sphenoid to the lingula of the mandible. It is derived from the first branchial arch (Meckel’s) cartilage. Anteriorly, it blends into the interpterygoid fascia, which separates the lateral and medial pterygoid muscles, stretching forward as a sheet to be attached to the posterior edge of the lateral pterygoid plate.
M
Published in Anton Sebastian, A Dictionary of the History of Medicine, 2018
Meckel, Johan Friedrich, Jr (1781–1833) Professor of anatomy at Halle, regarded as one of the greatest comparative anatomists prior to Johan Muller. The diverticulum of the ileum resulting from the persistence of the yolk sac of the embryo (Meckel diverticulum) was discovered by him in 1809. The cartilage of the first brachial arch (Meckel cartilage) was described by him in 1805.
Epidermal growth factor signalling pathway in endochondral ossification: an evidence-based narrative review
Published in Annals of Medicine, 2022
L. Mangiavini, G. M. Peretti, B. Canciani, N. Maffulli
More recently, in vivo models have been analysed to confirm the essential role of the EGF pathway in bone growth. EGFR knockout mice were stillbirth or lived only up to 6–8 days, displaying epithelial alterations and dysfunctions in several tissues, such as lungs and intestine. Interestingly, up to one-third of those mice had cleft palates, from retardation in skeletal development [98,99]. In humans, the cleft palate has been associated with polymorphism in TGFA gene, encoding for TGF-α, thus linking this condition to the EGF pathway [100]. Palate growth requires a correct development of the mandibular Meckel’s cartilage, and palate explants of Egfr-\- mice showed a decrease in the dimensions of Meckel’s cartilage, with the presence of undifferentiated cells with lower content of proteoglycans, consistent with an EGF-dependent modulation of chondrogenesis [101]. MMPs, downstream targets of EGF, mediate this phenotype [101]. Moreover, in vitro culture of palate organoids with human MSCs from the umbilical cord demonstrated that EGF significantly promoted proliferation, further proving its involvement in osteogenesis [102]. EGF-like protein signalling has also been associated with other human conditions characterised by growth retardation and skeletal abnormalities from impaired endochondral ossification [103,104].