Prenatal Growth Flashcards
Ectoderm
epidermix, nasal & oral mucosa, tooth enamel, lens, oragns of hearing/equilibrium
Endoderm
lining of posterior tongue, pharynx, tympanic cavity, respiratory tract, parts of thyroid
Mesenchyme
bones, muscles, & connective tissues of the head (and all other parts of the body)
head mesenchyme is from two sources:
paraxial mesoderm (somitomeres & somites)
neural crest (via surface ectoderm)
mesenchyme from neural crest
bones & connective tissues of face & anterior skull (vault + base)
mesenchyme from paraxial mesoderm
all skeletal mm., bones & connective tissues of posterior skull (vault + base)
Ossification pathways: intramembranous
mesenchymal tissue located just below the dermis transforms directly into bone
lateral
ossification pathways: endochondral
mesenchyme forms a hyaline cartilage model; the cartilage is then replaced by bone tissue
medial
palatogenesis
inferior views of medial nasal prominences merging together to form primary hard palate (premaxilla)
medial nasal prominences give rise to: premaxilla and upper incisors
inferior view of lateral palatine processes merging to form secondary hard palate
Cleft lip &/or anterior cleft palate
results from mesenchyme deficiences; failure of tissues to merge; vascular defects; etc. in maxillary prominences & median nasal prominences
maybe uni or bilateral
posterior cleft palate (aka isolated cleft)
results from growth distortions in palatine shelves causing defective midline fusion & w/ nasal septum
soft palate may or may not be involved
Lateral facial cleft: macrostomia
poor merging of max and man prominences; condition manifests as a large mouth on one or both sides
congenital craniofacial defects
most craniofacial malformations occur during the embryonic period (weeks 2 to 8)
deformations and growth disturbances (diruptions) occur in the fetal period (weeks 9 to 40)
Fetal alcohol syndrome
caused by maternal intake of alcohol
different effects due to timing of exposure(s)
affects development of all structures; apoptosis of early cell populations; damaged DNA; cognitive defects
may stimulate premature differentiation of mesenchyme of facial primordia
characteristic facial features
Holoprosencephaly
defective formation of forebrain resulting in malformation of structures depending on molecular signaling from this region; reduction in frontonasal process structures
Frontonasal dysplasia
excessive tissue in frontonasal process structures