Development of Pharyngeal Arches Flashcards

1
Q

Describe how the pharyngeal arches begin to develop

A

After closure of the neuropores, the arches appear as tissue bulges in the cranial region separated by clefts.

Made up of 3 embryological layers;

  • mesenchyme core (mesoderm and neural crest cells)
  • internal endodermal pouch
  • external ectodermal cleft
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2
Q

What are the components of the pharyngeal arches?

A
  • muscle
  • cartilage
  • artery
  • cranial nerve
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3
Q

Describe the origins of the cells that give rise to the pharyngeal arch components

A
  • paraxial mesoderm: voluntary muscles, arteries, neurocranium, meninges, dorsal skin (arches 1-3)
  • lateral plate mesoderm: laryngeal structures (arches 4 and 6)
  • neural crest cells: mesenchyme, ganglia, nerves, viscerocranium
  • ectodermal placodes: sensory neurons/glia
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4
Q

What are the components of the first pharyngeal arch?

A
  • maxillary part of external carotid artery
  • trigeminal nerve (CNV)
  • maxilla, mandible, malleus, incus, zygomatic, (Meckel’s cartilage)
  • muscles of mastication, tensor tympani, tensor veli tympani, mylohyoid, anterior belly of digastric
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5
Q

What are the components of the second pharyngeal arch?

A
  • hyoid and stapedial arteries
  • facial nerve (CNVII)
  • stapes, styloid process, lesser horn and upper body of hyoid
  • muscles of facial expression, stylohyoid, stapedius, posterior belly of digastric
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6
Q

What are the components of the third pharyngeal arch?

A
  • common carotid and proximal internal carotid arteries
  • glossopharyngeal nerve (CNIX)
  • greater horn of hyoid and lower body of hyoid
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7
Q

What are the components of the 4th pharyngeal arch?

A
  • left: aortic arch
  • right: subclavian artery
  • superior laryngeal nerve (of vagus n. (CNX))
  • epiglottis, laryngeal cartilages, thyroid, cunieform, corniculate, arytendoids
  • all muscles of pharynx except stylopharyngeus
  • all muscles of palate except tensor veli palatini and cricothyroid
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8
Q

What are the components of the 6th pharyngeal arch?

A
  • pulmonary arteries and ductus arteriosus
  • recurrent laryngeal nerve (of vagus n. (CNX))
  • all muscles of larynx
  • cricoid cartilage
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9
Q

What are the derivatives of the pharyngeal arches?

A

1: primitive tympanic cavity
2: palatine tonsil/tonsillar fissure
3: inferior parathyroid glad (dorsal pouch), thymus (ventral pouch)
4: superior parathyroid gland (dorsal pouch), ultimobranchial body (ventral pouch) - produces parafollicular Ca2+ producing cells in thyroid

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10
Q

What are the derivatives of the pharyngeal clefts and its clinical relevance?

A

1: external auditory meatus and external part of tympanic membrane (dorsal), tympanic membrane (deep)

2nd cleft will proliferate and overgrow clefts 3 and 4 obliterating them.
2, 3, and 4 lose contact with the exterior forming the cervical sinus which usually disappears.

CLINICAL RELEVACE: no obliteration of clefts 3 and 4 by 2nd:

  • causes cysts in adults
  • causes fistulas/sinuses in children
  • located anywhere along anterior border of SCM, cancer risk
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11
Q

Describe the process of molecular determination

A
  • 3 streams of neural crest cells migrate from rhombomeres carrying the homeodomain to the pharyngeal arches
  • homeodomain = OTX transcription factor and HOX gene
  • these respond to local endodermal signals at the arches (FGF, BMP, PAX, SHH etc) which determines mesenchymal expression pattern and arch characteristics
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12
Q

Describe some craniofacial defects

A

Treacher Collins Syndrome (arches 1 and 2)

  • abnormal eye shape
  • micrognathia
  • malformed ears
  • conductive hearing loss
  • underdeveloped zygoma

Di George Syndrome (arches 3 and 4)

  • defective thymus and parathyroids
  • CATCH 22: cardiac abnormality (esp. Teratology of Fallot), abnormal facies (cleft lip and palate, small jaw and upper lip, slanted eyes, low set abnormal folding ears)
  • cleft palate
  • hypocalcaemia

SHH:

  • inadequate function = less pairing of structures, narrowing and fusion (eg. cylopia)
  • excessive function = excessive duplication and widening of structures (eg. diprosopus)

Craniosynostosis Syndromes:
(FGFR2 and FGFR3 mutations)
* results in gain of function leading to activation of receptors
* activates bone calcification to cause premature fusion and decreases cell proliferation in mesenchyme at the suture
* also causes syndactyly

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