Facial Growth Flashcards
why is facial growth important
The size, shape and position of the underlying jaws determines the position of the teeth and therefore the malocclusion
describe
Class 3, reverse overjet, low angle
- Jaw different sizes
- Slight asymmetry
describe
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)
why is the study of facial growth important to orthodontics
- 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
2 phase of IUL
embryo 1-8 weeks (A - everything develops)
foetus 8 week to term (B - growing)
when are all limbs, organs and face formed
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*
day 1
fertilised egg (0.1mm)
2 nuclei
day 2-3
0.1mm still
Dividing – many cells (8-16)
Floating done fallopian tube
Still in egg like zona pellucida
Called morula
day 4-5
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
day 9
still 0.1-0.2mm
implantation
begin to develop germ layers
day 17
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)
day 25-28 (week 4)
By 4 weeks beginning to grow in size
Somites along back
Neural grove forms neural tube
neural crest cell migration
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
cells develop into face
cranial neural crest cells (after migration)
migrated neural crest cells form
ECTOMESENCHYME
- Originally ectoderm but migrate in, flood forward and help form pharyngeal arches = imp for facial development
neural tube
- neural folds fuse to form the neural tube, towards the end of week three
failure to fuse will lead to spina bifida
failure of neural folds fusion
spina bifida
neural tube develops into
- brain and spinal cord.
failure to develop neural tube
Failure to develop will lead to anencephaly
(in which the cerebral hemispheres and the cranial vault are absent)
neural crest cells form
- During the folding of the neural plate, cells develop from the ectoderm along the edge of the groove, termed neural crest cells.
neural crest cell role
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.
neural crest cells derived from ectomesenchy,e contribute to
branchial arch cartilage, bone and connective tissue proper, as well as dental tissues - pulp, dentine, cementum and periodontal ligament.
- Vital for tooth development
tooth development from
neural crest cells derived from ectomesenchyme
day 30
- 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*
day 32
- 4th pharyngeal arch appearing*
- Embryo is folding over*
day 33-36
- Embryo is folding over*
- Ear beginning to form*
day 39 - 44
- Embryo is folding over*
- Ear beginning to form*
Facial development beginning
day 46
- begins to fold back the way at day 46*
- pretty much formed*
day 54
fully formed - now growth
formation of face when
during the first eight weeks after fertilisation
malformations of face due to
- 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.
most of face forms from
migrating neural crest cells, either in the frontonasal process or the branchial arches.
issue if migrating neural crest cells interfered with
can lead to severe facial deformities.
Cells flood forward to fill out pharyngeal arches
failure of fusion of facial processes or between palatine processes
may lead to cleft formation.
- Need fuse at certain times – separate events for lip and palate
cleft lip region
nose to incisive forman
cleft palate region
incisive foramen backwards
cleft palate effect on teeth
doesn’t cross alveolus = normal teeth
cleft lip effect on teeth
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.
week 4
neural cell migration forms
Migrating neural crest cells form the frontonasal process and laterally the branchial arches
Frontal prominence coming down
Maxillary and mandibular processes come over
week 5-7 facial processes
early phase
See the extension and fusion of the facial processes
Lateral and medial nasal processes
Maxillary process coming round to fuse in middle
development of pharyngeal arches
- Fish stage of development - gills*
- Cartilage, vein, blood vessel and nerve associated with it
nerve supply to maxilla and mandible
trigeminal – nerve of 1st arch
nerve supply to all muscles of facial expression
Nerve 2nd arch – facial
pharyngeal arches fuse to form
various structures
blastocyst layers
2nd week development
2 layers inside blastocyst – hypoblast and epiblast
Together form an oval shape disc like structure
3 weeks development
Streak developed on surface of epiblast
Cells of epiblast detatch and migrate
- Create 3 layers – ectoderm, endoderm and mesoderm
3-4 weeks
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
CNNCs
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
CNNCs movement
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
4th week face development
CNCCs at destination – facial area is externally characterised by 5 swellings
- Frontonasal prominence
- Paired – maxillary and mandibular prominences
5th week face development
Nasal placodes -> olfactory
Optic placodes -> eye lenses
Maxillary and mandibular prominences enlarge and grow forward towards midline
- Eventual giving rise to jaws
6th week face development
Mandibular prominences fuse
- Outline of jaw evident
7th week face development
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
facial development from 8 week on
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)
foetal stage
8 weeks to term
skull divided into
- the neurocranium, which forms a protective case around the brain
- the viscerocranium, which forms the skeleton of the face.
neurocranium divided into
the flat bones of the vault which develop intramembranously
the endochondral elements of the base of the skull
intramembranous bone formation
- 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
endochondral bone formation
- 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
base of skull formation (neurocranium)
- 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
vault of skull formation (neurocranium)
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
*
- Bone laid down at sutures – come apart as required for bone deposition
- As brain grows the skull grows too
anterior fontanelle closes
arount 2 years
posterior fontanelle closes
at around 1 year
growth of skull continues until
continues until the 7th year but some of the sutures remain open until adulthood
embryonic facial cartilages
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
growth of mandible
- The mandible develops as several units all responding to different growth stimulae.
how many units are there in mandible growth
5
- condylar
- angular
- coronoid
- alveolar
- body
condylar unit of mandible
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
- Secondary cartilage – as not nasal capsule or Meckel’s cartilage it is later cartilage
angular unit of mandible
- forms in response to the medial pterygoid and masseter muscles;
- Born without either muscles– will not have angle
coronoid unit of mandible
- which responds to temporalis muscle development (muscular processes).
- Only there due to temporalis
alveolar unit of manidble
- which forms only if teeth are developing.
- No teeth – no alveolar bone on top of skeletal bone
body of mandible
- 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
3 main sites of secondary cartilage in mandible
- 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.
growth of mandible after birth due to
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
manible form at birth
- two halves, the midline symphysis fuses a few months afterward
mandible growth until
- Growth continues at the condylar cartilage until about 20 years of age, sometimes longer
ossification of face and skull commences at abot
7-8 weeks
(bone laid down)
what encases the brain
neurocranium
what forms the face
viscerocranium
vault of skull formation
intramembranous
base of skull formation
endochondral ossification
cartilage precursors
maxilla and mandible formation
develop intramembranously but are preceded by a cartilagenous facial skeleton
Meckel’s cartilage preceeds
the mandible
the nasal capsule is the primary skeleton of
upper face
primary abnormality
- 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)
secondary abnormality
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
deformation
- Anomalies that occur due to outer mechanical effects on existing structures
agenesia
- Absence of an organ due to failed development during embryonic period
sequence
- Single factor results in numerous secondary effects (Pierre Robin)
syndrome
- Group of anomalies that can be traced to a common origin (Trisomy 21 in Down’s Syndrome)
example facial syndromes
- 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*
- Apert’s Syndrome*
- 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
why is it good to know if pt has syndroe
- 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*
when do many syndromes occur
Many syndromes arise from defects early in pregnancy (inital 8)
environmental caused facial syndrome arising in early pregnancy
foetal alcohol syndrome
genetic/multifactorial caused facial syndrome arising in early pregnancy
- Hemifacial microsomia
- Treacher Collins syndrome (mandibulofacial dysostosis)
- Clefts of lip and palate
foetal alcohol syndrom cause and prevalence
- A high maternal intake of alcohol
- 1:750-1:100 live births
- A microform is present in 1:300 live births
- 1:750-1:100 live births
DAY 17 - mum not aware she is pregnant
foetal alcohol syndrom characteristics
- 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
hemifacial microsomia
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
treacher collins - mandibulofacial dyostosis
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
cleft lip and palate prevalence
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
cleft lip occurs
day 28-38
cleft palate occurs
day 42-55
describe
Unilateral cleft lip and palate of right hand side
descrive
bilateral clefr lip and palate
genetic aetiology of cleft lip/ palate
- Monozygotic twins
- Syndromes
- Familial pattern
- Epidemiology:
- Sex ratio
- Laterality 66% Left
- Ethnic distribution
environmental aetiology of cleft lip/palate
- Social deprivation
- Smoking (2.5x)
- Alcohol
- Anti-epileptics
- Multivitamins (dec 25%)
dental features of cleft lip
- Impacted Teeth
- Crowding
- Hypodontia
- Supernumeraries
- Hypoplastic teeth
- Caries
cleft palate NONE – doesn’t cross alveolus
cleft treatment team
- Specialist cleft nurse
- Speech Therapist
- Orthodontist
- Paediatric dentist
- Cleft surgeon (OMFS/Plastics)
- ENT
- Geneticist
- Psychologist
Long treatment – birth to 20s
achondroplasia
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
crouzon’s (craniofacial dyostosis)
- 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
crouzon’s effect
- 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
possible crouzon’s treatment
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
Apert’s (acrosyndactyly)
AD, 1:160,000
Premature closure of almost all cranial sutures (not just 2)
*
Apert’s (acrosyndactyly)
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
