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BDS3 Orthodontics > Facial Growth > Flashcards

Facial Growth Flashcards

1
Q

why is facial growth important

A

The size, shape and position of the underlying jaws determines the position of the teeth and therefore the malocclusion

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2
Q

describe

A

Class 3, reverse overjet, low angle

  • Jaw different sizes
  • Slight asymmetry
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3
Q

describe

A

Class 2 div 1, increased overjet, high angle, mandibular retrognathia, upper jaw in right place (lower jaw too small is the issue – functional app in young, orthognathic surgery in adult)

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4
Q

why is the study of facial growth important to orthodontics

A
  • Insight into growth of the face
    • predict changes – interceptive treatment
    • utilize growth to correct malocclusion – grow mandible (vertical more than AP)
    • time our orthodontics and surgery – only do surgery when completed growth
  • Understand development of facial anomalies
  • To measure changes in growth and treatment using cephalometry

treatment and favourable growth = success

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5
Q

2 phase of IUL

A

embryo 1-8 weeks (A - everything develops)

foetus 8 week to term (B - growing)

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6
Q

when are all limbs, organs and face formed

A

within the first 2 months and the embryo has a characteristic human form

  • External environmental influences can cause cranio-facial abnormalities very early on in the pregnancy
  • 10% of embryos miscarry – things don’t run like clockwork (deformities)*
  • After the initial 8 weeks significant drop*
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7
Q

day 1

A

fertilised egg (0.1mm)

2 nuclei

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8
Q

day 2-3

A

0.1mm still

Dividing – many cells (8-16)

Floating done fallopian tube

Still in egg like zona pellucida

Called morula

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9
Q

day 4-5

A

still 0.1-0.2mm

Blastocyst

Now 16-32 dells

  • Cells divided to make a cyst

1 – inner cell mass (ICM) -> baby

Everything else placenta etc

Just before implantation egg hatches – lose zona pellucida

Begin to form ectoderm and endoderm

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10
Q

day 9

A

still 0.1-0.2mm

implantation

begin to develop germ layers

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11
Q

day 17

A

still 0.2mm

Germ layers formed – germ disk (made of ectoderm and inside is endoderm (8))

Primitive node/streak – fold – ectoderm folds in to create 3rd layer mesoderm (7)

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12
Q

day 25-28 (week 4)

A

By 4 weeks beginning to grow in size

Somites along back

Neural grove forms  neural tube

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13
Q

neural crest cell migration

A

very important in the development of the face (cranial)

  • Ectomesenchyme
    • Originally ectoderm but migrate in, flood forward and help form pharyngeal arches = imp for facial development
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14
Q

cells develop into face

A

cranial neural crest cells (after migration)

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15
Q

migrated neural crest cells form

A

ECTOMESENCHYME

  • Originally ectoderm but migrate in, flood forward and help form pharyngeal arches = imp for facial development
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16
Q

neural tube

A
  • neural folds fuse to form the neural tube, towards the end of week three

failure to fuse will lead to spina bifida

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17
Q

failure of neural folds fusion

A

spina bifida

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18
Q

neural tube develops into

A
  • brain and spinal cord.
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19
Q

failure to develop neural tube

A

Failure to develop will lead to anencephaly

(in which the cerebral hemispheres and the cranial vault are absent)

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20
Q

neural crest cells form

A
  • During the folding of the neural plate, cells develop from the ectoderm along the edge of the groove, termed neural crest cells.
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21
Q

neural crest cell role

A

These undergo extensive migration within the developing embryo and ultimately differentiate into many cell types

e.g. spinal and autonomic ganglia; Schwann cells, adrenal medulla, meninges of the brain.

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22
Q

neural crest cells derived from ectomesenchy,e contribute to

A

branchial arch cartilage, bone and connective tissue proper, as well as dental tissues - pulp, dentine, cementum and periodontal ligament.

  • Vital for tooth development
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23
Q

tooth development from

A

neural crest cells derived from ectomesenchyme

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24
Q

day 30

A
  • Embryo getting larger*
  • Beginning to get pharyngeal arches*
  • Frontal nasal processes at top (P) neural crest cells flooding in from here*
  • Learn arches and what they formed*
  • 1st, 2nd and 3rd formed and bulked by neural crest cells flooding in*
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25
Q

day 32

A
  • 4th pharyngeal arch appearing*
  • Embryo is folding over*
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26
Q

day 33-36

A
  • Embryo is folding over*
  • Ear beginning to form*
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27
Q

day 39 - 44

A
  • Embryo is folding over*
  • Ear beginning to form*

Facial development beginning

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28
Q

day 46

A
  • begins to fold back the way at day 46*
  • pretty much formed*
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29
Q

day 54

A

fully formed - now growth

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30
Q

formation of face when

A

during the first eight weeks after fertilisation

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31
Q

malformations of face due to

A
  • Environmental factors may lead to significant malformations during this early period (initial 8 weeks)

Defects of the face, particularly in the midline, may be closely related to defects of the anterior parts of the brain.

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32
Q

most of face forms from

A

migrating neural crest cells, either in the frontonasal process or the branchial arches.

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33
Q

issue if migrating neural crest cells interfered with

A

can lead to severe facial deformities.

Cells flood forward to fill out pharyngeal arches

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34
Q

failure of fusion of facial processes or between palatine processes

A

may lead to cleft formation.

  • Need fuse at certain times – separate events for lip and palate
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35
Q

cleft lip region

A

nose to incisive forman

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36
Q

cleft palate region

A

incisive foramen backwards

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37
Q

cleft palate effect on teeth

A

doesn’t cross alveolus = normal teeth

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38
Q

cleft lip effect on teeth

A

does cross over alveolar = issue in teeth – supernumerary, missing etc

upper lip and anterior part of the palate have different embryological origins from the posterior palate and they fuse at different times.

  • Therefore, cleft lip and alveolus can occur independently of cleft palate and vice versa.
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39
Q

week 4

neural cell migration forms

A

Migrating neural crest cells form the frontonasal process and laterally the branchial arches

Frontal prominence coming down

Maxillary and mandibular processes come over

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40
Q

week 5-7 facial processes

A

early phase

See the extension and fusion of the facial processes

Lateral and medial nasal processes

Maxillary process coming round to fuse in middle

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41
Q

development of pharyngeal arches

A
  • Fish stage of development - gills*
  • Cartilage, vein, blood vessel and nerve associated with it
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42
Q

nerve supply to maxilla and mandible

A

trigeminal – nerve of 1st arch

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43
Q

nerve supply to all muscles of facial expression

A

Nerve 2nd arch – facial

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44
Q

pharyngeal arches fuse to form

A

various structures

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45
Q

blastocyst layers

A

2nd week development

2 layers inside blastocyst – hypoblast and epiblast

Together form an oval shape disc like structure

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46
Q

3 weeks development

A

Streak developed on surface of epiblast

Cells of epiblast detatch and migrate

  • Create 3 layers – ectoderm, endoderm and mesoderm
47
Q

3-4 weeks

A

Neural cord forms – induces thickening in ectoderm (blue) cells forming neural plate and edges elevate to form neural folds -> neural tube

Neural crest cells are formed along entire length at tip of folds

48
Q

CNNCs

A

cranial neural crest cell

move in distinct pattern from neural tube to make face

Growth and migration and subsequent differentiation of CNCCs are critical important for normal development of facial region

49
Q

CNNCs movement

A

migrate from back to front of embryo in distinct paths

Once arrive at final destination in facial region, CNCCs further develop and ultimately contribute to substantial amount of tissue in head and neck – bones, cartilage and nerves

Growth and migration and subsequent differentiation of CNCCs are critical important for normal development of facial region

50
Q

4th week face development

A

CNCCs at destination – facial area is externally characterised by 5 swellings

  • Frontonasal prominence
  • Paired – maxillary and mandibular prominences
51
Q

5th week face development

A

Nasal placodes -> olfactory

Optic placodes -> eye lenses

Maxillary and mandibular prominences enlarge and grow forward towards midline

  • Eventual giving rise to jaws
52
Q

6th week face development

A

Mandibular prominences fuse

  • Outline of jaw evident
53
Q

7th week face development

A

Maxillary prominences grow and fuse to form the border of the nostril and upper lip

Merging of the maxillary and mandibular prominences forms the cheeks and corners of mouth

Philtrum of upper lip created

54
Q

facial development from 8 week on

A

Next months development – initial cartilaginous skeleton replaced by bone

  • Face continues to develop from further and growth and remodelling from childhood to adulthood

If doesn’t happen at prescribed time = cleft (2-3 months)

55
Q

foetal stage

A

8 weeks to term

56
Q

skull divided into

A
  • the neurocranium, which forms a protective case around the brain
  • the viscerocranium, which forms the skeleton of the face.
57
Q

neurocranium divided into

A

the flat bones of the vault which develop intramembranously

the endochondral elements of the base of the skull

58
Q

intramembranous bone formation

A
  • Bone is deposited directly into primitive mesenchymal tissue.
  • Intramembranous bones include the vault of the skull, the maxilla and most of the mandible.
  • Needle-like bone spicules form, which progressively radiate from the primary ossification centres to the periphery.
  • Progressive bone formation results in the fusion of adjacent bony centres.

Most bone in skull, maxilla and mandible

59
Q

endochondral bone formation

A
  • bones are preceded by a hyaline cartilage ‘model’
    • blood vessels come in and change cartilage to bone
    • islands of cartilage often left for growth (epiphyseal plates in long bones)
  • Forms base of skull
    • Several centres of ossification which eventually fuse
60
Q

base of skull formation (neurocranium)

A
  • series of cartilages forms the base of skull.
  • undergo endochondral ossification from multiple centres, starting with the basi-occiput at 10-12 weeks.
  • At birth cartilagenous growth centres remain between the sphenoid and occipital bones and in the nasal septum
61
Q

vault of skull formation (neurocranium)

A

Intramembranous ossification of the vault commences in the third month in several centres

  • Fusion is incomplete at birth, leaving widenings known as fontanelles to allow flexibility in the skull during birth.
  • Growth occurs at fibrous sutures in response to intracranial pressure.
    • As brain grows the skull grows too
      • Bone laid down at sutures – come apart as required for bone deposition
        *
62
Q

anterior fontanelle closes

A

arount 2 years

63
Q

posterior fontanelle closes

A

at around 1 year

64
Q

growth of skull continues until

A

continues until the 7th year but some of the sutures remain open until adulthood

65
Q

embryonic facial cartilages

A

Although the maxilla and mandible form intramembranously, they develop adjacent to a pre-existing cartilaginous skeleton

  • the nasal capsule
  • Meckel’s cartilage

(6 weeks)

Closely associated with the bones that are forming but it is the intramembranous ossification

66
Q

growth of mandible

A
  • The mandible develops as several units all responding to different growth stimulae.
67
Q

how many units are there in mandible growth

A

5

  • condylar
  • angular
  • coronoid
  • alveolar
  • body
68
Q

condylar unit of mandible

A

forms the articulation and contains the largest secondary cartilage formation

  • Continual growth of mandible is due to the cartilage here
    • Secondary cartilage – as not nasal capsule or Meckel’s cartilage it is later cartilage
      • Can be switched on and off
      • Can create asymmetry in adulthood is one side begins to grow
69
Q

angular unit of mandible

A
  • forms in response to the medial pterygoid and masseter muscles;
    • Born without either muscles– will not have angle
70
Q

coronoid unit of mandible

A
  • which responds to temporalis muscle development (muscular processes).
    • Only there due to temporalis
71
Q

alveolar unit of manidble

A
  • which forms only if teeth are developing.
    • No teeth – no alveolar bone on top of skeletal bone
72
Q

body of mandible

A
  • body of the mandible forms in response to the inferior dental nerve
    • Starts where inferior dental nerve splits from mental nerve – fork is site of beginning of intramembranous ossification of mandible
73
Q

3 main sites of secondary cartilage in mandible

A
  • the condylar cartilage
    • most important – growth in childhood
  • the coronoid cartilage – tends to disappear
  • at the symphyseal end of each half of the bony mandible – tends to disappear, thought to allow a little bit of compression during birth
    • The cartilages appear between 12 and 14 weeks I.U.
74
Q

growth of mandible after birth due to

A

secondary cartilages

The coronoid cartilage disappears long before birth and the symphyseal just after birth.

  • Growth continues at the condylar cartilage until about 20 years of age, sometimes longer
75
Q

manible form at birth

A
  • two halves, the midline symphysis fuses a few months afterward
76
Q

mandible growth until

A
  • Growth continues at the condylar cartilage until about 20 years of age, sometimes longer
77
Q

ossification of face and skull commences at abot

A

7-8 weeks

(bone laid down)

78
Q

what encases the brain

A

neurocranium

79
Q

what forms the face

A

viscerocranium

80
Q

vault of skull formation

A

intramembranous

81
Q

base of skull formation

A

endochondral ossification

cartilage precursors

82
Q

maxilla and mandible formation

A

develop intramembranously but are preceded by a cartilagenous facial skeleton

83
Q

Meckel’s cartilage preceeds

A

the mandible

84
Q

the nasal capsule is the primary skeleton of

A

upper face

85
Q

primary abnormality

A
  • Defect in the structure of an organ or part of an organ that can be traced back to an anomaly in it’s development (spina bifida, cleft lip, CHD)
86
Q

secondary abnormality

A

Interruption of the normal development of an organ that can be traced back to other influences

  • Teratogenic agents; infection (rubella virus), chemical (thalidomide), chemical (lithium)
  • Trauma; amniotic bands
87
Q

deformation

A
  • Anomalies that occur due to outer mechanical effects on existing structures
88
Q

agenesia

A
  • Absence of an organ due to failed development during embryonic period
89
Q

sequence

A
  • Single factor results in numerous secondary effects (Pierre Robin)
90
Q

syndrome

A
  • Group of anomalies that can be traced to a common origin (Trisomy 21 in Down’s Syndrome)
91
Q

example facial syndromes

A
  • Maxillary Hypoplasia
    • Apert’s Syndrome*
      • (acrosyndactyly)
    • Crouzon’s Syndrome*
      • (craniofacial dysostosis)
    • Oral-Facial Digital Syndrome*
    • Binder’s Syndrome
    • Achondroplasia
    • Down’s Syndrome
    • Cleidocranial dysostosis*
    • Foetal Alcohol Syndrome
    • Cleft lip/palate*​
  • Mandibular problems
    • Treacher Collin’s Syndrome* (mandibulofacial dysostosis)
    • Pierre-Robin*
    • Stickler’s Syndrome*
    • Van der Woude Syndrome*
    • Turner’s Syndrome Hemifacial Microsomia*

* can be associated with cleft

92
Q

why is it good to know if pt has syndroe

A
  • Good to know if pt has syndrome as other things can occur*
  • e.g. cleft lip and palate – higher risk of kidney defects, heart defects, ear defects, eye defects – can check*
93
Q

when do many syndromes occur

A

Many syndromes arise from defects early in pregnancy (inital 8)

94
Q

environmental caused facial syndrome arising in early pregnancy

A

foetal alcohol syndrome

95
Q

genetic/multifactorial caused facial syndrome arising in early pregnancy

A
  • Hemifacial microsomia
  • Treacher Collins syndrome (mandibulofacial dysostosis)
  • Clefts of lip and palate
96
Q

foetal alcohol syndrom cause and prevalence

A
  • A high maternal intake of alcohol
    • 1:750-1:100 live births
      • A microform is present in 1:300 live births

DAY 17 - mum not aware she is pregnant

97
Q

foetal alcohol syndrom characteristics

A
  • microcephaly (small head)
  • typical faces having
    • short palpebral fissures (eyeslits small)
    • short nose,
    • long upper lip with deficient philtrum,
    • small midface (maxilla small)
    • small mandible.
  • Mild mental retardation
98
Q

hemifacial microsomia

A

1:3500 Live births

Multifactorial

  • Neural crest cell migration? (day 19-28)
    • Less cells come down – unsure why

3D Progressive facial asymmetry

  • Unilateral mandibular hypolasia, zygomatic arch hypoplasia, high arched palate, malformed pinna
    • More and apparent with growth

But clinical spectrum

  • ear tags only, to complete lack of condyle, coronoid and ramus

Normal intellect, deafness (ear formation issue), cardiac and renal problems – check them out

Treatment – none most, costochondral graft (cartilage from ribs in place of glenoid fossa) to try growth – varying success, sort out occlusal issues if teeth absent

99
Q

treacher collins - mandibulofacial dyostosis

A

Deformity of 1st and 2nd branchial arches,

  • (day 19-28)

characteristics

  • Anti-mongoloid slant palpebral fissures
  • Colomboma of lower lid outer 1/3rd (notch in eye)
  • Hypoplastic or missing zygomatic arches
  • Hypoplastic mandible with antigonial notch
  • Deformed pinna, conductive deafness

1;10,000 Live births

100
Q

cleft lip and palate prevalence

A

1: 700 live births
* 70% sporadic

Cleft Lip+/-Palate: males> females

Cleft Lip : males:females

  • 3:1 (Scotland)

Cleft palate: females >males

  • 3:2 (EU)

CLP>CP England and Wales

CP = CLP Scotland

Left side predisposition – more likely on left to occur

101
Q

cleft lip occurs

A

day 28-38

102
Q

cleft palate occurs

A

day 42-55

103
Q

describe

A

Unilateral cleft lip and palate of right hand side

104
Q

descrive

A

bilateral clefr lip and palate

105
Q

genetic aetiology of cleft lip/ palate

A
  • Monozygotic twins
  • Syndromes
  • Familial pattern
  • Epidemiology:
    • Sex ratio
    • Laterality 66% Left
    • Ethnic distribution
106
Q

environmental aetiology of cleft lip/palate

A
  • Social deprivation
  • Smoking (2.5x)
  • Alcohol
  • Anti-epileptics
  • Multivitamins (dec 25%)
107
Q

dental features of cleft lip

A
  • Impacted Teeth
  • Crowding
  • Hypodontia
  • Supernumeraries
  • Hypoplastic teeth
  • Caries

cleft palate NONE – doesn’t cross alveolus

108
Q

cleft treatment team

A
  • Specialist cleft nurse
  • Speech Therapist
  • Orthodontist
  • Paediatric dentist
  • Cleft surgeon (OMFS/Plastics)
  • ENT
  • Geneticist
  • Psychologist

Long treatment – birth to 20s

109
Q

achondroplasia

A

cartilaginous defect

  • AD, 1:14,000
  • Problem with endochondrial ossification
  • Defects in long bones, short limbs = dwarfism (70%)
  • Defects in base of the skull,
    • retrusive middle third of the face (no nasal capsule to drive forward) frontal bossing, depressed nasal bridge
110
Q

crouzon’s (craniofacial dyostosis)

A
  • AD, 1:25,000
  • Premature closure of cranial sutures
    • esp coronal and lamdoid

causes effects

  • Proptosis (shallow orbits – eyes pop out), orbital dystopia (eyes in different direction), mild hypertelorism (larger interorbit difference)
  • Retusion and vertical shortening of midface
  • Prominent nose
  • Class III malocclusion
  • Narrow spaced teeth
111
Q

crouzon’s effect

A
  • Proptosis (shallow orbits – eyes pop out), orbital dystopia (eyes in different direction), mild hypertelorism (larger interorbit difference)
  • Retusion and vertical shortening of midface
  • Prominent nose
  • Class III malocclusion
  • Narrow spaced teeth
112
Q

possible crouzon’s treatment

A

Early closure of the sutures is termed cranial synostosis and requires surgical intervention. e.g. Crouzon’s syndrome.

  • Distraction osteogenesis treatment – get bone growing where you want it
113
Q

Apert’s (acrosyndactyly)

A

AD, 1:160,000

Premature closure of almost all cranial sutures (not just 2)

*

114
Q

Apert’s (acrosyndactyly)

A

Increased ICP, delayed development of brain

Exopthalmos, hypertelorism,

Maxillary hypoplasia

Class III occlusion

  • AOB
  • narrow spaced teeth

Narrow high arched palate

  • 30% have cleft palate

Parrot’s beak nose

Syndactyly of fingers and toes

Conductive deafness

BDS3 Orthodontics (13 decks)

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