Growth and development /certified fixed orthodontic courses by Indian dental academy

Growth and
development
of cranium and maxilla

www.indiandentalacademy.com

INDIAN DENTAL ACADEMY
Leader in continuing dental education


 Growth- Robert Moyers defines growth as
the normal changes in amount of living
substance.
 Development-refers to all naturally occurring
unidirectional changes in life of an individual
from its existence as a single cell to its
elaboration as a multifunctional unit
terminating in death.
 Development=growth+differentiation+translo
cation

Controlling factors in craniofacial
growth
 Natural
genetic
function
general body growth
neurotrophism

 Disruptive forces
orthodontic forces
surgery
malnutrition
malfunctions
gross craniofacial anomalies

pre-natal Growth proper


 Pre-natal life of an individual can be
broadly divided into following three
phases
Period of ovum
Period of embryo
Period of fetus


Pharyngeal arches

pre-natal Growth and
development of cranium


 Mesodermally derived ectomeninx gives rise to
–
–
–
–
–

Frontal
Parietal
Sphenoid
Petrous temporal
Occipital

 Neural crest provides mesenchyme for
–
–
–
–
–
–

Lacrimal
Nasal
Squamous temporal
Zygomatic
Maxilla
Mandible


Calvaria


Frontal Bone
 Single primary ossification centre in the
region of superciliary arch at 8th week i.u.
 3 pairs of secondary centres in
 Zygomatic processes
 Nasal spine
 Trochlear fossae
 Fusion completes at 6-7 months i.u.
 Metopic suture-synostic fusion starts at 2 nd
year and completes by 7years

Parietal Bone
 Arises from two primary ossification centres
at parietal eminence in 8th week i.u.
 Fuses in 4th month i.u.
 Delayed ossification in region of parietal
foramina results in sagittal fontanelle at
birth.

Temporal bone
 Squamous portion ossifies intra
membranously from 1 centre appearing at
root of zygoma at 8th week i.u.
 Tymphanic ring ossifies I.M. from 4 centres
at 3rd month i.u. in the lateral wall of
tympanum.
 Pre-mastoid & styloid ossify endochondrally

Occipital bone
 Supranuchal squamous part ossifies I.M. at 8 th
week
 Below superior nuchal line, basilar part, condylar
part ossifies endochondrally at 10th ,11th, 12th
week respectively.
 Earliest centres of ossification first appear at 7 th
& 8th week i.u. but ossification is not completed
until well after birth
 Unusual ossification centres develop between
individual calvarial bones- sutural or wormian
bones`

 Ultimate shape & size of cranial vault depends on
internal pressure exerted on inner table of
neurocranial bones.
 Circumference of head is good indicator of brain
growth.
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18cm at mid gestational period
33cm at birth
46cm at 1yr of age
49cm at 2yrs
50cm at 3yrs


 Growth of calvarial bone is combination of
–
–
–

Sutural growth
Surface apposition & resorption
Centrifugal displacement by expanding brain

 Bones of new born calvaria are unilaminar & lack
diploe
 Inner table is related to brain & intracranial
pressures
 Outer table more responsive to extracranial
muscular & buttressing forces.

 Thickening of frontal bone at region of glabella
results from separation of inner & outer tables with
invasion of frontal sinus between cortical plates.
 Inner plate becomes stable at 6-7 yrs because of
cessation of cerebral growth. Used as stable
reference point for growth studies.
 Growth of external plate produces
–
–
–
–

Superciliary arches
Mastoid processes
External occipital protuberance
Temporal & nuchal lines


The cranial base
 Chondrocranium is important as a shared
junction between neurocranial & facial skeletons.
 Formation of the cartilages of chondrocranium is
dependent on presence of brain & other neural
structures & an appropriately staged inducing
epithelium.
 Chondrogenesis occurs only after an epithelialmesenchymal interaction has taken place.

Basicranial ossification centres


Cranial base angulation


 Anterior & posterior parts of cranial base
grow at different rates
 10th-40th week i.u. anterior cranial base
increases its length & width sevenfold.
 Posterior cranial base grows only 5 fold.
 Growth of central ventral axis of brain is
slow providing a comparatively stable base.

Cartilages of fetal chondrocranium &
their derivatives


post- natal
development
of
cranium

Expansion of cranial base takes place as a
result of :-Growth at synchondroses
-Cortical drift & remodelling
-Sutural growth


synchondroses
 These are important growth sites of cranial
base. They are primary cartilages.
 Spheno- occipital -ossifies by 20yrs
 Spheno-ethmoidal -ossifies by 5-25yrs
 Intersphenoidal

-ossifies at birth

 Intraoccipital

-ossifies 3-5yrs of age

Spheno-occipital synchondroses
 Believed to be principal growth cartilage of cranial
base during childhood.
 Active upto 12-15yrs.
 Sphenoid & occipital segments become fused in
mid-line by 20yrs.
 Provides a pressure adapted bone growth.
 Fusion begins on its cerebral surface at
12-13yrs in girls
14-15yrs in boys

Cortical drift & remodelling
 Remodelling is a process where bone
resorption & deposition occur to bring about
change in size, shape & relationship of
bone.
 Clivus undergoes resorption on cerebral
surface, apposition on nasopharyngeal
surface of basioccipital bone & anterior
margin of foramen magnum.
 At birth, temporo-mandibular fossa is flat &
lacks articular tubercle.

Sutural growth


Cranial vault
 Fontanelles- areas of fibrous tissue
membrane which forms primitive cranial
vault before ossification begins.
 Posterior fontanelle- closes at birth
 Anterior - 1st yr
 Anterolateral- 15 months
 Posterolateral -18 months

Cranium at birth


 At birth cranial vault is about 8 times larger
than face.
 In embryonic period ,cranium to face ratio is
40:1. At 4 months 5:1. At birth 8:1.
 Post-natal facial growth causes it to reduce
to 2:1.
 Skull contains 45 separate bones at birth.
 During birth skull is altered in shape & part
of skull which lies more centrally in birth
canal is temporarily swollen & oedematous
due to interference with venous return–
CAPUT SUCCEDANEUM.
 By the end of 5th yr of life 90% of growth of
brain vault haswww.indiandentalacademy.com
been achieved.

Anomalies of development of
cranium
 Trisomy 13 syndrome
 Chromosomal disorder in which extra
chromosome 13 is present.
 Cleft lip & palate
 Micropthalmia
 Microcephaly
 Congenital heart defects
 polydactyly

Apert syndrome
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Single gene disorder characterized by
Pre-mature fusion of cranial sutures
Bizzare craniofacial appearance
Highly arched palate
Syndactyly
Congenital heart defects


craniosynostosis
 Condition resulting from premature fusion of cranial
sutures.
 Head shape depends on which sutures are pre- maturely
synostosed.
 Abnormal intra- uterine compression of cranium alters
immature sutural tissue & initiates mineralisation of sutural
ligament.
Dolicocephaly- sagittal suture is pre maturely synostosed
Brachycephaly- bilateral synostosis of coronal sutures
Plagiocephaly- premature synostosis of one side of coronal
or lambdoidal suture causing obliquity of skull
 Trigonocephaly- metopic suture closes pre-maturely
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achondroplasia
 Characterized by unusual craniofacial
configuration & dispropotional small stature.
 Enlarged calvaria
 Frontal bossing
 Large frontal sinus
 Occipital prominence
 Normal anterior cranial base
 Shortened posterior cranial base
 Acute cranial base angle
 Short nasal bone that is deformed & depressed
 Short upper facial height
 Recessed maxilla
 Prognathic mandible
 Bone that is preformed in cartilage is affected.

Cleidocranial dysplasia
 Dominant mendelian characteristic of inheritance
 Men & women equally affected
 Abnormalities of skull,teeth,jaws,shoulder gridle,stunting of
long bones.
 Fontanelles exhibit delayed closure.
 Paranasal sinuses are underdeveloped & narrow.
 Head is brachycephalic with transverse diameter of skull
being incerased.
 Patient exhibits unusual mobility of shoulders . Maybe able
to bring shoulders forwards till they meet in mid- line.

Marfan syndrome
 Hereditary disease transmitted by
autosomal dominant trait.
 Disease of connective tissue related to
defective organization of collagen.
 Shape of skull & face is characteristically
narrow & long.
 Excessive length of tubular bones.
 Arachnodactyly & high arched palatal vault.

Down’s syndrome / trisomy 21
syndrome
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Most common chromosomal abnormality
Flat face, large anterior fontanelle
open sutures
small slanting eyes with epicanthal folds
open mouth
Frequent prognathism
Sexual underdevelopment
Hypermobility of jaws
Cardiac abnormalities

hypothyroidism
 Base of skull is shortened leading to
retraction of bridge of nose.
 Face is widened & fails to develop in
longitudinal direction.
 Mandible is underdeveloped.
 Maxilla is overdeveloped.
 Mental retardation.

Development
maxilla

of


 Pharyngeal arches begin to develop early in 4 th
week as neural crest cells migrate into future
head & neck region.
 1st pharyngeal arch develops two prominences
 Maxillary prominence gives rise to maxilla,
zygomatic bone & squamous part of temporal
bone.
 Mandibular prominence forms lower jaw.


Development of face
 Facial primordia appear early in 4 th week
around large primordial stomodeum.
 The 5 facial primordia that appears as
prominences around stomodeum are: Single frontonasal prominence
 Paired maxillary prominence
 Paired mandibular prominence

 Facial development occurs mainly between 4 th
& 8th weeks
 By the end of 4th week bilateral oval thickenings
of surface ectoderm –nasal placodes-have
developed on inferolateral parts of fronto nasal
process.
 Each lateral nasal prominence is separated
from maxillary prominence by cleft called
nasolacrimal groove.
 Nasolacrimal duct develops from rod like
thickening of ectoderm in floor of nasolacrimal
groove.

 Part of nasolacrimal duct fails to canalize resulting in –
atresia of nasolacrimal duct.
 By end of 5th week , primordia of auricles of ear begin
to develop.
 During 7th week there is shift in blood supply of face
from internal to external carotid artery.
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Intermaxillary segment gives rise to:Philtrum of upper lip
Pre maxillary part of maxilla & its associated gingiva
Primary palate

 Recent clinical & embryological studies
suggest upper lip is formed entirely from
maxillary prominences. Lower parts of
medial nasal prominences appear to have
become deeply positioned & covered by
medial extensions of the maxillary
prominences to form philtrum.breitsprecher et al,2002.


Pre natal develoPment of
maxillary comPlex


 Until bone formation occurs, the nasal
capsule is the only skeletal support of
upper face
 Lateral & inferior to cranial base
cartilages, ossification centers appear &
face begins to develop in width.
 Nasal, premaxillary, maxillary, Lacrimal,
Zygomatic, palatine & temporal
ossification centers appear & expand until
they appear as bones separated only by
sutures.

Development of palate
 Palatogenesis begins at end of 5 th week & is
not completed until 12th week.
 Critical period of palate development is 6 th
week until beginning of 9th week.
 Bones of palate arise from several ossification
centers.
 In 8th week bilaterally located bony centers in
anterior palate give rise to pre-maxilla &
maxilla.

 Three elements that make up secondary
palate
-2 lateral maxillary palatal shelves
-primary palate of frontonasal
prominence
 At 8th week I.U. life lateral shelves alter from
vertical position to horizontal


Mechanisms proposed for rapid
elevation of palatal shelves
 Biochemical transformations in physical
consistency of connective tissue matrix of
shelves
 Variations in vasculature & blood flow to
these structures
 Sudden increase in tissue turgor
 Rapid differential mitotic growth
 An “intrinsic shelf force” generated by
accumulation & hydration hyaluronic acid.

 Withdrawal of embryo’s face from against
heart prominence by uprighting of head
facilitates jaw opening.

 Pressure differences between nasal & oral
regions due to tongue muscle contraction
may account for palatal shelf elevation.


 Epithelium overlying edges of palatal
shelves are thickened , & their fusion on
mutual contact is crucial for intact palatal
development
 Fusion seam forms initially anteriorly in hard
palate region.
 Combination of degenerating epithelial cells
& a surface coat accumulation of
glycoprotiens & desmosomes facilitate
epithelial adherence b/w contacting palatal
shelves.

 Ossification of palate begins at 8th week I.U.
by spread of bone into mesenchyme of
fused lateral palatal shelves & from
trabeculae appearing in primary palate as
“pre-maxillary centres”.
 Posteriorly hard palate is ossified by
trabeculae spreading from single primary
ossification centres of each palatine bone.
 Ossification does not occur in most
posterior part of palate ,giving rise to region
of soft palate. www.indiandentalacademy.com

muscles of the Palate


 Muscles of soft palate are derived from
myogenic mesenchymal tissue of first, second
& fourth branchial arches.
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Tensor veli palatini – 1st arch
Palatopharyngeus Palatoglossus Levator palatini – 4th arch
Uvular - 4th arch

( 40 days) I.U.
(45 days)
(9 th week)
(8th week)
(11th week)


 Palatoglossus attaches to soft palate during 11 th week
I.U.
 Hard palate grows in length, breadth, height to
become arched shaped roof of mouth.
 b/w 7 & 18 wks i.u. fetal palate increase in length more
rapidly than in width.
 From 4th month i.u. palate widens as a result of mid
palatal sutural growth & appositional growth along
lateral alveolar margins.
 At birth length & breadth of hard palate are almost
equal.

Post – natal develoPment of
Palate


 Palate increases in length due to appositional
growth in maxillary tuberosity region & at
transverse maxillopalatine suture.
 Growth at mid-palatine suture ceases b/w 1
-2yrs of age.
 Growth in width of mid-palatine suture is more
posteriorly than anteriorly.
 Obliteration in mid-palatine suture may start in
adolescence, but complete fusion is rarely
found before 30 yrs of age.

 Lateral appositional growth continues till
7yrs of age, by which time palate achieves
ultimate anterior width.
 Posterior appositional growth continues
after lateral growth has ceased ,so that
palate becomes longer than wider during
late childhood.
 During infancy & childhood , bone
apposition occurs on entire inferior surface
of palate , accompanied by resorption from
nasal surface.

Factors in normal palatal
development
 Elevation of head to erect posture maybe related
to elevation of palatal shelves.
 Deficiencies of oxygen, various food stuffs or
vitamins.
 Excess of certain endocrine substances , drugs &
irradiation.
 Delay in the shift of blood supply of face & palate
from internal to external carotid artery during
critical period of palatofacial develoment.

Post-natal develoPment of
maxilla


Mechanisms & sites
 Sutures
 Nasal septum
 Periosteal & endosteal surfaces
 Alveolar bone

Amounts & direction
 Maxillary height – classic implant studies of bjork
& skeiller confirm that maxillary height increases
by sutural growth towards frontal & zygomatic
bones & appositional growth in the alveolar
process.
 Maxillary width – growth at median suture is more
important than appositional remodeling .


 Maxillary length – length increases in
maxilla after second year by apposition on
the maxillary tuberosity & by sutural
growth toward palatine bone.
 Maxilla rotates forward in relation to
anterior cranial base
 Timing – increase in alveolar process size
is closely related with eruption of teeth.
 Increase in overall maxillay height
coincides with vertical growth in mandible

AnomAlies of pAlAtAl
development


 Epstein’s pearls – entrapment of epithelial
rests or pearls in line of fusion of palatal
shelves.
 Mucosal gland retention cysts or bohn’s
nodules may occur on buccal & lingual
aspects of alveolar ridges ,& dental lamina
cysts composed of epithelial remnants of
this lamina may develop on crests of
alveolar ridges.
 Torus palatinus

Cleft lip & palate
 Delay in elevation of palatal shelves from
vertical to horizontal while head is growing
continuously results in widening gap
between shelves so that they cannot meet &
fuse.
 Failure of medial edge epithelial cell death
 Post –fusion rupture & failure of
mesenchymal consolidation &
differentiation.

 Cleft palate is a feature of many
congenital syndromes
 Mandibulofacial dysostosis/treacher
collins’ syndrome
 Pierre robin syndrome
 Orodigitofacial dysostosis syndrome
 Palate is narrower,shorter & lower than
normal in down syndrome. High mid-line
elevation ,horizontally flattened laterally
along alveolar ridges , creating a “steeple
palate”.

 Conditions displaying high arched palate
-Marfan’s syndrome
-Cleidocranial dysostosis
-Craniofacial dysostosis/ crouzan
syndrome
-Acrocephalosyndactyly / apert
syndrome
-Progeria
-Turner syndrome
-Oculodentodigital dysplasia

The para-nasal sinuses


 4 sets of paranasal sinuses
-maxillary
-sphenoidal
-frontal
-ethmoidal
 Begins development at end of 3rd month i.u.
as outpouchings of mucous membranes of
middle & superior nasal meatus &
sphenoethmoidal recesses.

Primary Pneumatization
 Early paranasal sinuses expand into
cartilage walls & roof of nasal fossae by
growth of mucous membrane sacs into
maxillary, sphenoid, frontal, ethmoid bones.
Secondary Pneumatization
 Sinuses enlarge into bone from their initial
small outpocketings, retaining
communication with nasal fossae through
ostia.

MAXILLARY SINUS
 1ST to develop at 10 wks from middle meatus
by primary pnumatization into ectethmoid
cartilage.
 Secondary pneumatization into ossifying
maxilla starts in 5th month i.u.
 At birth it is large enough to be clinically
imp. & radiographically identifiable.
 Sinus enlarges by resorption of cancellous
bone except on medial wall.

 Rapid & continuous downward growth of
sinus after birth brings its wall in close
proximity to roots of maxillary cheek teeth.
 As each tooth erupts ,vacated bone
becomes pneumatized by expanding sinus.
 In adulthood, roots of molar teeth commonly
project into sinus lumen.


 Absence of the development of frontal &
shenoidal sinuses is characteristic of down
syndrome.
 Diminution or absence of sinuses is also
found in Apert’s syndrome.
 If a metopic suture persists ,the frontal
sinuses are small or even absent.


Coronal section of paranasal sinuses


NEW INSIGHTS IN FACIAL
DEVELOPMENT


The fate of the neural crest mesenchymal
precursors into differentiated facial tissue is
strongly restricted by homeobox (HOX)
gene expression.
The HOX genes are expressed in a stepwise
manner ,delineating the cascading streams
of ectomesenchyme that migrate from their
dorsal origin to their ventral destination to
create six pharyngeal arches and five facial
prominences.

 Five key secreted growth factors control
facial growth by regulation of cell
proliferation ,survival & apoptosis.
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Endothelins
Fibroblast growth factor
Sonic hedgehog
Wingless
Bone morphogenetic proteins


New genetic lineage markers are identifying
the expression changes occurring in the
early embryonic face at different stages.
173 genes expressed in frontonasal
prominence like TBX10, TBX21, BARX1,
BAPX1, MNT, located of different
chromosomes.
During 4th week ,64 genes are upregulated.
During 5th week further 26 genes upregulated
in frontonasal prominence

COGENE
CRANIOFACIAL AND ORAL GENE
EXPRESSION NETWORK


Thank you
Leader in continuing dental education


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