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DEN203 > G&D- Bones, Growth > Flashcards

G&D- Bones, Growth Flashcards

1
Q

What is bone?

A

specialised connective tissue.

= living cells embedded in a mineralised extracellular matrix (ECM).

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2
Q

Name 3 bone types

A

1- trabecular
2- cortical
3- woven

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3
Q

Composition in % of bone

A

30% organic material (majority is collagen),

45% inorganic hydroxyapatite (HA)

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4
Q

What is HA

A

hydrated crystalline material of calcium and phosphate.

Hydroxyapatite provides strength.

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5
Q

HA content: in % in different connective tissues

A

Bone approx 45%
cementum 55%
dentine (70%),
enamel (90%)

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6
Q

What is in the bone matrix?

A 
Collagen fibres (95% type 1, 5% type 5)
Carbonated hydroxyapatite crystals.

Proteins (unique to calcified tissue) e.g. osteocalcin

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7
Q

Bone function- support

A

Mineralised when fully developed.

Supports/protects internal organs.

Allows movement

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8
Q

Bone function- metabolic

A

Haematopoiesis: bone marrow produces blood cells

Calcium homeostasis

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9
Q

Serum Ca2+ levels maintained by interplay between :

3

A

> intestinal absorption,
renal excretion
skeletal mobilisation or uptake.

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10
Q

What is cortical bone?

A

Cortical/Compact/laminar:-

approx 80% of skeleton,

dense, very strong, forms the outer layer of all bones.

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11
Q

What is trabecular bone?

A

porous meshwork of bone.

Makes up approx. 20% of the skeleton, mainly in axial skeleton.

Bone strength also determined by the trabecular microstructure-can change in disease e.g. osteoporosis.

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12
Q

What is woven bone?

A

forms quickly during periods of repair or rapid growth.

..remodelled into lamellar bone.

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13
Q

What is the periosteum?

A

lines the outer surface of cortical bone

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14
Q

How is bone a dynamic tissue?

Constant remodelling!

A

Changes all the time to

  • > meet stress loads
  • > release Ca++ and phosphate if required
  • Max strength, min weight
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15
Q

Cell-types in bone (5)

A 
Osteoclast
Osteoblast
Osteocyte
Bone lining cells
Osteoprogenitor cells (stromal)
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16
Q

What are Osteoclasts?

A

Large multinuceated cells. Bone resorbing cells

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17
Q

What are osteoblasts?

A

Bone forming cells

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18
Q

What are osteocytes?

A

Originate from osteoblasts.
- have become embeded in bone matrix.

  • Involved in sensing mechnaical loads and Ca homeostsis
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19
Q

What are bone lining cells?

A

Originate from osteoblasts

  • line quiescent periosteoal and endosteal surfaces of bone
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20
Q

What are osteoprogenitor cells (stromal cells)

A

Precursors of osteoblastic lineage

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21
Q

How many microscopic sites is remodelling estimated to be occuring at, at any one time

A

1-2 million

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22
Q

Why does bone remodelling occur? (i.e. bone is constantly being destroyed and reformed).

A
  • Release calcium

- Alter architecture of cancellous bone to meet new stresses

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23
Q

What is the resorption phase/ how long

A

bone ECM destroyed and removed.

This phase takes approx 3 weeks/remodelling site.

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24
Q

What is the bone formation phase and how long

A

New ECM is formed and mineralised

-this phase takes 3-4 months/remodelling site.

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25
Q

Mechanism of bone remodelling

A
  • Osteoclast precursors recruited to remodelling site
  • Mature to osteoclasts
  • Bone lining cells erode a little ECM, then leave the remodelling site
  • Osteoclasts bind to the ECM exposed by BLCs, they digest the bone matrix with enzyme
  • Resorption pit formed
  • Osteoclasts apoptose
  • Osteoblast precursors recruited
  • Mature into Osteoblasts
  • New ECM made by Ob
  • New bone surface becomes covered in bone lining cells
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26
Q

When might bone formation be needed?

A
  • during formation of the skeleton
  • during fracture repair
  • during tooth socket healing after extraction
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27
Q

NAme 2 types of bone formation

A

1- intramembranous ossification (IMO)

2- endochondral ossification (ECO)

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28
Q

What is Intramembranous ossification?

A

Bone is formed directly from condensed mesenchyme/ ectomesenchyme

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29
Q

What is endochondral ossification?

A

A cartilaginous precursor of the bone is formed and replaced by bone as it grows

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30
Q

Where does IMO occur?

A

ONLY in:

  • Neurocranium- bone enclosing the skull
  • Viscerocranium- facial bones of skull
  • Clavicle
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31
Q

Where does ECO occur?

A

More common..
ALL bones except outside the skull…
- including the basicranium (chondrocranium)
- Except the clavicle

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32
Q

How does IMO occur?

A
  • Mesenchymal stem cells condense and Differentiate into osteoblasts
  • Secrete ECM (osteoid) in long strands
  • Obs lay down bone mineral on the strands of Osteoid
  • Consecutive growth rings of Osteoid (lamella) added on to increase thickness
  • Further bone growth by cycles of osteoid secretion and mineralisation (appositional growth)
  • Multiple trabecular within the developing bone contact one another to form a lattice structure
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33
Q

Name for bone containing lattice structures

A

Primary cancellous (trabecular) bones

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34
Q

Name for bones that completely fill in wtih mineralised osteoid

A

Compact (cortical)bone!

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35
Q

What is Cleidocranial dysostosis

A

a rare genetic disorder that interferes with intramembranous ossification (skeletal dysplasia)

Autosomal dominant-defect in the RUNX2 gene

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36
Q

Clinical symtpoms of cleidocranial dystosis

A

Neurocranium underdeveloped

Viscerocranium underdeveloped with severe dental malocclusion, delayed formation

Large head and frontal bossing

Clavicles reduced or absent-characteristic feature

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37
Q

How many affected by cleidocranial dystosis?

A

approx. 1 in 1million

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38
Q

hree phase processes in ECO

A

1) Miniature cartilage replica formed by diff of mesenchyman/ectomesen. cells -> into chondroblasts -> which mature into chondrocytes
2) Cartilage grows in a specific direction (interstitial and appositional growth)
3) cartilage is converted into bone!

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39
Q

What is the Epiphyseal growth plate?

A

Hyaline cartilage plate in the metaphysis at each end of a long bone

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40
Q

What are the 2 zones of epiphyseal growth plate?

A
  • Proliferation zone
  • Hypertrophic zone
  • Cartilage / bone interface
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41
Q

What is Achondroplasia?

A

recessive genetic condition that affects bone formation via ECO.

Autosomal dominant.
Incidence is 1 in 20,000.

Most common form of dwarfism.

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42
Q

What genetic defect results in achondroplasia?

A

Genetic defect is in the gene for FGFR-3

a membrane receptor that is important in the response of chondrocytes to..

growth factor (FGF-18) during development of the cartilage ‘template’.

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43
Q

Name 5 methods of assessing growth timing/rate

A
  1. measurement of change in height
  2. secondary sexual characteristics
  3. hand-wrist radiographs
  4. Radiographic assessment of cervical spine maturation
  5. Average growth increments
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44
Q

What is PHV?

A

Peak height velocity

  • Maximum rate of growth
  • During puberty, growth velocity curve rises to a max. and begins to fall again
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45
Q

What are the 4 major tissue systems plotted on Scammons growth curve-

A

General
Genital
Lymphoid
Neural

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46
Q

How are hand-wrist radiographs used?

A

Large number of centres of ossification present in the relatively small area

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47
Q

What is the atlas technique?

A

Ulnar sesamoid bone ossifies at the start of the pubertal growth spurt.
- Median bone maturity stage for each chronological age and sex was identified/ can compare/ use as a reference

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48
Q

What is a cephalogram?

A

A cephalogram is an X-ray of the craniofacial area. A cephalometric analysis could be used as means for measuring growth in children.

  • 3 cervical vertebrae
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49
Q

What craniofacial changes occur during puberty/growth

A

Facial dimensions increase…

  • Vertical changes are most prominent
  • Antero-posterior changes are less prominent
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50
Q

What soft tissue changes happen during growth

A

Greatest changes here rather than in hard tissues…

  • Lip incompetency… decreases with age
  • Lower lip grows more
  • LFH= lower facial height increase
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51
Q

Name 3 endocrine hormones involved in the control of growth

A 
Growth hormone
Oestrogen
Androgen
Glucocorticoids
Insulin
Insulin-growth factor 1
Thyroid
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52
Q

What is the human growth hormone?

A

Peptide hormone that stimulates growth, cell reproduction and cell regeneration in humans…

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53
Q

What gland secretes GH

A 
Pituitary gland (In brain)
- Regulated by neurosecretory nuclei of the hypothalamus
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54
Q

What is Gigantism

A

Occurs during childhood

- Excessive GH before growth plate closure…

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55
Q

What is acromegaly

A

middle-aged people
3 per million
Excessive GH due to benign tumours on pituitary?

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56
Q

What affect does Oestrogen have on GH?

A

Increases GH secretion

  • Induces epiphyseal plate closure
  • Direct and indirect effects
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57
Q

What role do Androgens have on Growth?

A

Play a role in male traits and reproductive activity

e.g. Testosterone

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58
Q

Androgen affect on bones…

A

Radial bone growth-> bones get fatter
… Make growth plate increase in size

  • Androgen receptors in bone
  • Can be converted to oestrogen
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59
Q

Why are males bigger?

A

Less oestrogen!

Oestrogen also inhibits condylar growth-> masculine contour of the mandibular angle

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60
Q

GH affect on muscle growth?

A

GH acts on IGF1 for myofibril proliferation.

Paracrine IGF1 has a role in load-induced hypertrophy.

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61
Q

GH as a performance-enhancing drug(3)

A

1- positive effect on CT strength
2- Reduce recovery time (anticatabolic)
3- Increased VO2 max

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62
Q

What do glucocorticoids do?

A

Increase GH secretion.
Affects SST and GHRH release.

Chronic Glucocorticoid exposure reduces GH release (leasds to glucose intolerance)

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63
Q

Insulin involvement in growth due to GH= diabetogenic…

A

GH promotes gluconeogenesis (making of glucose), glucogenolysis (break down) and lipolysis… GH is therefore diabetogenic (causes diabetes)

Insulin is released to compensate for this.

Long term.. can lead to insulin resistance

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64
Q

Insulin as a IGF1 homologue

A

Can cause insulinopenia (reduction in insulin levels)… reduces children’s growth

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65
Q

What effect does thyroid hormone have on growth

A
  • Increases linear growth

T3 affects chondrocytes and osteoblasts in growth plate
- Drives IGF1 synthesis pre-pubertal

  • Stimulates GH synthesis

Hypothyroidism= reduces adult height

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66
Q

What is IGF1???

A

Insulin growth factor 1

  • Similar molecular struc to insulin
  • childhood growth
  • Anabolic effects in adults
  • Tx for child growth failrure
  • Produce in liver
  • Production is stimulated by GH, can be retarded by undernutrition, GH intensity, lack of GH receptors
  • Produced throughout life
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67
Q

What is calcium?

A

1kg in the body.
99% in bone
Blood and ECF total = 2mM = 60% Ca2+

  • Involved in intracellular signalling
68
Q

What is trousseau’s sign

A

Reduced blood flow.

  • Neuromuscular irritability
  • Hypocalcaemia causes Na+ influx (sustained muscle contraction, high AP rate)
69
Q

How much calcium needed in mg

A

Adults= 1300mg (or 700?)

70
Q

Food sources of calcium

A

milk, oily fish, bread, broccolli

71
Q

Processes by which small intestine absorbs calcium from diet

A

Transcellular: low intake, active
Paracellular: high intake, passive

72
Q

What hormone does thyroid gland release (involved in calcium homeostasis)

A

Calcitonin

parafollicular cells in thyroid

73
Q

What does Calcitonin do?

A

Increases bone mineralisation.
Decreases Ca2+ reabsorption in kidneys.

Overall: causes a decrease in Plasma Ca2+ levels

74
Q

What hormone does parathyroid gland release (involved in calcium homeostasis)

A

Parathyroid hormone

75
Q

Parathyroid hormone functions

A
  • Causes osteolysis (bone breakdown and release of Ca)
  • Increases Ca2+ reabsorption in kidneys
  • Increase in Ca2+ absorption from gut?? (diet)

Overall: causes a INcrease in Plasma Ca2+ levels

76
Q

What does the 1,2,4-dihydroxy-cholecalciferol hormone do?

A
  • Increases Ca2+ reabsorption in kidneys
  • Increase in Ca2+ absorption from gut?? (diet)

Overall: causes a INcrease in Plasma Ca2+ levels

77
Q

What is the name for Vit. D?

A

Calcitrol

78
Q

Vit. D in calcium homeostasis

Crucial for uptake!

A

Vit. D allows SI absorption of calcium by:

  • Upregulates carriers/ Ca pumps (transcellular)
  • Makes gap junctions more porous to Ca
79
Q

What is rickets?

A

Skeletal disorder caused by lack of vit.D, calcium or phosphate.

Weak, stunted bones/growth/deformities

Growth plates have vit.D receptors

80
Q

Vit. D effects on developing teeth-

A 
6-24 months of age
Enamel hypoplasia
Enlarged pulp horns
Delayed eruption
Caries risk
Prevention: take vit.D and fluoride supplements
81
Q

How does bone turnover occur…

A

In low levels of vit.D…

  • Ob release RANK ligand
  • Osteoclasts differentiation
  • Oc activation
  • Resorption of bone
  • Calcium release
82
Q

Name some Non-skeletal roles of calcium…

A 
Cancer
Autoimmune disease
Schizophrenia
Depression
Diabetes
muscle strength
83
Q

What is osteomalacia?

A

Closed growth plates

  • Low density bones
  • Lack of remineralisation
  • Pathological amount of callus matrix
  • Pseudofractures, including in mandible
  • Bone pain
  • Muscle weakness
  • Periodontitis
84
Q

What is osteoporosis?

A

Fragile, weak bones… resulting in fracture?
More spongy, porous,..
Loss in density

85
Q

Pathogenesis of osteoporosis:

A
  • Reduced uptake of dietary calcium
  • Imbalance of bone turnover
  • Reduced bone mineral density
86
Q

Oestrogen affect on bone?

A

Reduced inhibition of osteoclasts…
- Inhibits bone breakdown, resorption /reabsorption of Ca

  • Levels of oestrogen fall after menopause leading to more bone resorption … get more fragile…
87
Q

Name 2 drugs used to Tx of osteoporosis

A

1- Adcal

2- Alendronic acid

88
Q

what is Adcal

A

Calcium carbonate with vitD

89
Q

What is Alendronic acid

A

Bisphosphonate drug which inhibits osteoclasts and stops over-activation of them…

(stops breakdown!)

90
Q

2 mechanisms of bone growth

A

1- Interstitial growth

2- Direct growth

91
Q

What is interstitial growth?

A

soft tissues- combination of hyperplasia (increase in number of cells) and hypertrophy (increase in size of cells).

In the craniofacial skeleton, it occurs in cartilages, synchondroses and sutures.

92
Q

Examples of interstitial growth

A

Endochondral ossification is the conversion of cartilage.

Intramembranous ossification occurs only in the embryo and is the direct transformation of mesenchymal cells into osteoblasts.

93
Q

What is direct bone growth

A

surface apposition (bone being added on the surface by osteoblasts) and resorption (bone being removed by osteoclasts).

94
Q

What is the primary mechanism that shapes the craniofacial skeleton?

A

Direct growth.

In fully formed bone, growth activity can only occur in the periosteum - periosteal surface remodelling (including sutural deposition)

The processes of apposition and resorption constitute remodelling.

95
Q

Name 3 theories of control mechanisms of craniofacial growth

A

1- Sutural directed growth in sutures
2- Cartilage directed growth theory (genetically determined)
3- Functional matrix theory

96
Q

What is the Sutural directed growth in sutures theory

A

sutures in bones are growth centres.

There is expression of growth at these sites which causes changes in shape.

97
Q

How is growth of cranial vault determined?

A

NOT determined by sutures but by pressure from growing neural tissues.

98
Q

What is the Cartilage directed growth theory?

A 
Growing cartilage is replaced by bone...
Cartilage growth sites:
- Spheno-occipital and spheno-ethmoidal synchondroses
- Nasal septum
- Mandibular condyle
99
Q

What are synchondroses?

A

@ cranial base…

  • Possible cartilage growth sites
  • Immovable joints between bones, bound by layer of cartilage

2 epiphyseal cartilages placed back to back (with a common central zone of resting cells)

100
Q

What is the functional matrix theory?

A
  • Bone growth in response to growth of surrounding tissues

- Craniofacial growth as a response to functional needs that is mediated by tissue growth

101
Q

What are the 2 matrices in the functional matrix theory:

A

1- Periosteal matrix: muscles, nerves, glands, teeth

2- Capsular matrix: neurocranial, orbital and pharyngeal fossae

102
Q

Examples of functional matrix

A

Coronoid process only grows if subject to functional forces from masseter and medial pterygoid muscles

Aleolar bone loss if teeth loss

103
Q

At birth, what % of body length is head

A

25%

104
Q

At adulthood, what % of body length is head

A

12%

105
Q

Age 1, what % of total wt is the brain

A

50%

106
Q

Age 3, what % of total wt is the brain

A

75%

107
Q

Age 7, what % of total wt is the brain

A

90%

108
Q

Age 11, what % of total wt is the brain

A

FULL

109
Q

What are sutures

A

Formed in membranous bone without cartilagenous precursors

  • Secondary growth centres
  • Periosteal growth activity
  • Fast rate of growth
  • Begin to fuse by age 7
  • Fused by 17
110
Q

Functional matrix theory- cranial vault perspective

A

Sutures allow expansion for brain.

111
Q

What separates the anterior/posterior regions of the cranial base

A

Spheno-occipital synchondrosis

112
Q

Anterior region - cranial base

A

spheno- ETHMOIDAL synchrondrosis

  • Neural pattern of growth
    Stable by age 8
    Active until age 18
113
Q

Posterior region

A

Spheno OCCIPITAL synchondrosis

Somatic pattern of growth
Active until age 16

114
Q

What happens to the facial bones from 0-12 years

A

Enlargement, make space to accommodate airway and masticatory growth/function

115
Q

What happens 12-18yrs, puberty to face:

A
  • Forward growth of jaws
  • Forward elongation of nose
  • Backward shift of orbits
  • Posterior movement of zygoma
  • Posterior extension of dental arches in tuberosity of maxilla
116
Q

How does growth of Maxilla occur?

-Downwards and forwards

A

Surface and sutural deposition

Sutures respond to separating forces caused by soft tissue growth.

  • Bone added at sutures and tuberosity areas.
  • Floor of nose is resorbing
  • Bone being added to FOM
117
Q

Growth of mandible?

  • Grows in length and upwards

Condylar head is remodelled
Ramus is remodelled

More height growth than length.

A

Resorption and apposition at condylar head.
- Cartilage replacement in 2ndary growth cartilage

Resorption from ANTERIOR surface.
Deposition on POST. surface.

118
Q

What is the condyle made of?

A

Condylar cartilage (not true cartilage)

  • Resembles epiphyseal cartilage of long bone
119
Q

What happens to cells of proliferative zone in condyle

A

They differentiate into chondroblasts, once this happens,

Chondrogenesis is appositional (NOT organised into parallel columns)

120
Q

What are jaw rotations?

A

50% true rotation

- Rotation masked by surface apposition and resorption

121
Q

What 2 types of rotation occur and waht %

A

25% Matrix rotation (around condyle)

75% Intra-matrix rotation; within body of mandible

122
Q

Mandible rotation?

A

M. plane decreases by 2-4 degrees

- Forward 4 out 5 cases

123
Q

Maxilla rotation?

A

Forward rotation by 3 degrees

124
Q

What might cause a long face?

A 
Backwards rotation.
- Matrix rotation
- Open bite
- Incisors thrust forward...
Class 2?
125
Q

What might cause a short face?

A 
Forwards roation
- Short ant. face height
- Forward rotation of mandible...
Deep bite
- Crowded incisors
126
Q

What is adenoidal facies?

Posterior nasal obstruction
Increased face height

A
  • increased lower and total face height
  • narrow upper arches
  • retroclined incisors

Difficulty with nasal breathing…

127
Q

2 phases of facial soft tissue growth during puberty:

A

1- mainly growth of midface downwards

2- significant growth of face downwards

128
Q

Craniofacial anomaly classification (2)

3% of births

A
  • Embryological

- Developmental (worsen with growth?)

129
Q

Name 2 embryological craniofacial anomalies

A

1- Facial clefts

2- First arch anomalies

130
Q

What is cleft-palate

A

1 in 680 births

  • Hearing and speech difficulties
  • Dental anomalies
131
Q

What are mid-face clefts

A

HPE- cephalic disorder, the prosencephalon fails to develop into 2 hemespheres…
- Midline features are affected

132
Q

What is hemi-facial microsomia?

first arch anomaly

A

Early mixed dentition.
1 in 4000
Interrupted blood supply to branchial arch.

Restricted facial development…

133
Q

What is treacher collins

first arch anomaly

A

1 in 50,000

Autosomal dominant.

Affects mesenchymal flow in 1st/2nd p arches.

  • Hypoplastic maxilla/mand.
  • Ear anomalies
  • Cleft palate
134
Q

What is craniosynostoses?

A

Premature fusion of 1+ fibrous sutures resulting in distortion of cranial development and facial features

135
Q

Examples of craniosynostoses

A
  • Crouzon’s syndrome
  • Apert’s syndrome
  • Achondroplasia
136
Q

Prevalence of craniosynostoses

A

1 in 2000

137
Q

What is Crouzon’s syndrome

A 
1 in 25,000
Autosomal dominant
Premature fusion of sutures
- Raised ICP
- Facial appearance...
- Restricted mid-face
- High arched palate
- Speech diff
Class 3?
138
Q

What is Apert’s syndrome?

A

1 in 50,000

  • similar to Crouzon
  • united fingers?
139
Q

What is Achondroplasia?

A

1 in 15,000 and 1 in 40,000
ADominant
Abnormality in cartilage formation, causing shortening of limbs (dwarf)

140
Q

What does this embryonic germ layer make: ectoderm

A

Epidermis, glands, enamel

141
Q

What does this embryonic germ layer make: Endoderm

A

Gut lining

Glands

142
Q

What does this embryonic germ layer make: Ventral mesoderm

A

Blood vessels and cells

143
Q

What does this embryonic germ layer make: dorsal mesoderm/ neural crest

A

Muscle, CT, bone, sensory nerves

144
Q

What does this embryonic germ layer make: Neural tube

A

CNS and motor nerves

145
Q

What does each pharyngeal arch contain

A
  • Artery, vein, cranial nerve
  • Skeletal element
  • Muscle (migrates into each arch)
146
Q

What nerves innverates arch 1

A

Trigeminal (V), third division

147
Q

What nerves innverates arch 2

A

Facial (VII)

148
Q

What nerves innverates arch 3

A

Glossopharyngeal (IX)

149
Q

What nerves innverates arch 4

A

Vagus (X)

150
Q

What muscles are in Arch 1

A

muscles of mastication
some suprahyoids
tensor veli palatini

Supplied by third division of CNV

151
Q

What muscles are in Arch 2

A

muscles of facial expression
some suprahyoids
stapedius

All supplied by CNVII

152
Q

What muscles are in Arch 3

A

one trivial muscle (stylopharyngeus)

Supplied by CNIX

153
Q

What muscles are in Arch 4

A

pharyngeal constrictors
muscles of soft palate and larynx

All supplied by CNX

154
Q

Innervation of the tongue by which arches…

A

Anterior 2/3= 1st and 2nd arches

Posterior 1/3= 2nd, 3rd and 4th
(2nd is overgrown)

Epiglottis= 4th

155
Q

Examples of what arch malformations can result in

A

(majortiy affect 1st arch)

  • clearest impact on skeletal structures
  • hypotrophic mandible
  • Conductive hearing loss (incus and malleus)
  • Part of syndrome??
156
Q

What happens from 4th week of development

A

Formation of nasal cavity and primary palate.
- Invagination of the nasal placodes forms the nasal pits (primitive nasal cavity)

Primary plate begins the separation of the nasal and oral cavities anteriorly…

157
Q

What happens from 6th week of developement

A

Maxillary processes extend from posterior aspect of mandibular arch.
- Forms the lateral borders of the mouth

2 processes grow mesially from the maxillary arches (tectospetal and palatine processes)

158
Q

What happens from the 8th week of development

A

Palatal elevation

Embryo develop a cervical flexure- lifting the head away from cardiac bulge.

Tongue drops into FOM as mandible widens.
Palatal processes have no restraint and elevate into a horizontal position.

159
Q

Intrinsic factors of palatal elevation

A
  • Water
  • Turgor
  • Agents that dirsupt GAG synthesis tend to inhibit palate elevation
160
Q

Week 10- Fusion of palatine processes

Completes at week 12

A

Processes contact and fuse.

Fusion requires breakdown of the ectodermal covering of the processes to allow underlying ectomesenchyme to fuse.

161
Q

Post-week 12…

A

Anterior 2/3 is invaded by bone.

Posterior 1/3rd invaded by muscle from 4th pharyngeal arch to form muscles of soft palate.

162
Q

How is nose formed?

A

Frontonasal processes are compressed between max. processes to form a protruding nose

163
Q

How is mouth formed?

A

Fusion of max. and mand. processes

164
Q

What is macrostomia?

A

Failure of fusion of mand. and max. processes

165
Q

What if cleft palateis?

A

800-1000 in uk/annum

Rare familial cleft carried on Chromosome

166
Q

Contributory environmental factors to c.palate

A

During pregnancy:

  • Heavy smoking
  • heavy alcohol consump
  • Folic acid deficiency
167
Q

What is cyclops feti?

A

Failure of nasal placodes to develop so no nasal cavities

  • eyes fused at midline
  • excess tissue is pushed out as proboscis

DEN203 (11 decks)

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