Prenatal growth & development /diploma orthodontic course by indian dental academy /certified fixed orthodontic courses by Indian dental academy

PRE-NATAL
GROWTH
&
DEVELOPMENT
INDIAN DENTAL ACADEMY
Leader in continuing dental education
www.indiandentalacademy.com

 What is EMBRYOLOGY?
Embryology is the study of prenatal development
of embryo and fetuses.
 SIGNIFICANCE OF EMBRYOLOGY
-Gives knowledge concerning beginning of human
life and changes occurring during prenatal
development.
-Understanding normal post-natal growth
-and development of various craniofacial
abnormalities
INTRODUCTION

 Period of ovum- fertilization to 2 weeks
 Period of embryo – 2nd to 8th week
 Period of fetus - 9th week to term
Imp-week 4-8,teratogens

He who sees things grow from the
beginning will have the finest view of
them……..
-ARISTOTLE

Day 0
FERTILIZATION
Human development begins at fertilization, the process
during which a male sperm unites with a female oocyte
to form a single zygote.
Human development begins at fertilization, which occurs
in the ampulla of the uterine tube

Zygote-contains
chromosomes and genes
that are derived from both
mother and father.

THE FIRST WEEK
 CLEAVAGE OF ZYGOTE:
-Cleavage usually occurs as the
zygote passes along the uterine
tube.
-Cleavage consist of repeated
mitotic divisions of zygote.
-The zygote divides into 2
cells, which then divides into 4,8
and so on.
-The cells are called
“BLASTOMERES‟‟.
- 12 to 16 blastomeres,
it is called as MORULA (fruit of
mulberry tree). www.indiandentalacademy.com

Day 1-3
 Cleavage
 blastomeres
 morula

2 cell 4 cell 8 cell
REF-THE DEVELOPING HUMAN, MOORE AND PERSAUDwww.indiandentalacademy.com

FORMATION OF BLASTOCYST
 As morula enters uterus, a fluid-filled space called
blastocyst cavity appears in morula.
 As fluid increases, it separates blastomeres into two
parts:- Outer cell layer, Trophoblast.
-Inner cell mass, which act as primordium of
embryo called Embryoblast
Day 4-7

Implantation
 6 days after
fertilization, blastocyst
adheres to endometrial
surface.
 As soon as it attaches, the
trophoblast starts
proliferating rapidly and
differentiates into 2 layers.
-Cytotrophoblast (inner layer).
-Syncytiotrophoblast (outer
mass with finger-like
processes).

Implantation

 Implantation of blastocyst
commences at the end
of 1st week and completed
by end of 2nd week.
 The syncytiotrophoblast
release proteolytic
enzymes which promotes
proteolysis and invasion
of maternal endometrium..
The Second week
Completion of implantation:
Day 8-14

DAY 9
 Isolated cavities
called lacunae
appear in
syncytiotrophoblast
 Adjacent lacunae
fuse to form lacunar
networks
Capillaries around
embryo become
dilated to form -
sinusoids

 Syncytiotrophoblast
erodes sinusoids
and maternal blood
flows freely In
lacunar networks
 Communication with
eroded endometrial
capillaries
 Primitive circulation
between
endometrium and
placenta-
uteroplacental
circulation
DAY 12

 Site at which blastocyst EMBRYONIC POLE.
gets implanted
CLINICAL RELEVANCE
Syncytiotrophoblast releases HUMAN CHORIONIC
GONADOTROPHIN ( HCG ) HORMONE… which gives
a positive pregnancy test at the end of the second week.

FORMATION OF AMNIOTIC CAVITY, EMBRYONIC
DISC AND YOLK SAC:
 As implantation of blastocyst progresses, a small cavity
appears in the inner cell mass called “AMNIOTIC CAVITY”.
 The blastocyst cavity / Exocoelomic cavity soon modifies to
form “PRIMARY YOLK-SAC”.

 So now there are 2 cavities:
1. “AMNIOTIC CAVITY” (above)
2. “PRIMARY YOLK-SAC” (below - later forms secondary yolk
sac)
Soon the inner cell mass form 2 types of cells which lie Between
these 2 cavities
Epiblast: High columnar cells related to amniotic cavity.
Hypoblast – squamous or cuboidal cell mass adjacent to
primary yolk sac
The epiblast and hypoblast
together forms the
“BILAMINAR EMBRYONIC
DISC”.
Second weekBILAMINAR DISC STAGE

 Defect in endometrium persists for 2 days- filled by a closing
plug- fibrinous coagulum of blood.
 In extra-embryonic mesoderm fluid filled spaces appear which
fuse to form Extraembryonic Coelom

DAY 14
2 processes occur
simultaneously:
Formation of
extraembryonic somatic
and splanchnic mesoderm
due to split of
extraembryonic mesoderm
by extraembryonic coelom.
Extraembryonic coelom is
now called chorionic cavity.

 Defect in endometrium
disappears
 Cells from hypoblast
migrate along inside of
Primary yolk sac –
pinched off and smaller
secondary yolk sac forms
 Proliferation of
cytotrophoblastic cells
into syncytiotrophoblast
leads to Formation of
primary chorionic villi
(later forms placenta).
DAY 13

DAY 14
The amniotic cavity (epiblast
at floor)
and secondary yolk sac
(hypoblast at roof)
resembles 2 balloons
pressed together inside
larger balloon (chorionic sac)
suspended by connecting
stalk - umbilical cord

DAY 14
Epiblastic cells- formation of primitive streak
Hypoblastic cells in a localized area are now columnar and
form a thickened circular area called pre-chordal plate which
indicates the future site of the mouth and is an important
organizer of the head region

THE THIRD WEEK
 GASTRULATION : is a formative process by
which the 3 germ layers & axial orientation are
established in the embryo
-Primitive streak.
-Germ layers.
-Formation of notochord
 NEURULATION.
 NEURAL CREST FORMATION.

 GASTRULATION:
 the Bilaminar embryonic disc is converted to a
Trilaminar embryonic disc.
 It is the beginning of morphogenesis (development of
body form).
 It begins with formation of primitive streak at the
surface of the embryonic disk.
Third week

PRIMITIVE STREAK:
 It results from
proliferation and
migration of the cells of
epiblast to the median
plane of the embryonic
disc.
 The primitive streak
elongates by addition
of cells to its caudal
end
 its cranial end
proliferates to form
primitive node.
DAY 15,16

As soon as the primitive streak appear, it is possible to identify
the embryo‟s
Cranio -caudal axis
Primitive groove develops in the primitive streak that is
continuous with a small depression in the primitive node, the
primitive pit.

FATE OF PRIMITIVE STREAK
 Normally the primitive streak undergoes
disappears by the end of fourth week.
 Remnants of primitive streak may persist
and give rise to a large tumor –
SACROCOCCYGEAL TERATOMA.
 Need to be surgically excised .

Fetal Alcohol Syndrome
 clinically described 30 years ago (1973),
caused by maternal alcohol consumption during pregnancy.
 Alcohol crosses the placenta from maternal circulation into
fetal circulation
 consists of a variable degree of birth defects and mental
retardation, initially identified by a reduced head size and
distinctive facial features
 This Syndrome is 100% preventable.
FAS

Fetal Alcohol SyndromeFAS
•Maternal alcoholism causes effects of 2 types
•In moderation i.e. 1-2 ounces/day (30ml) can cause fetal
alcohol effects (FAE) -behavioral & learning defects
•Chronic consumption leads to FAS.
•Moderate &chronic consumption in the 1st trimester causes
these effects. However development of brain spans the entire
period of gestation, hence total abstinence from alcohol is
advised

FAS
CHARACTERISTICS:
Microcephaly - leads to small head
circumference
Palpebral fissure - short opening
of eye
Epicanthal folds - fold of skin at
inside of corner of eye
Midface - flat
Nasal Bridge - low
Philtrum - Indistinct,
Upper Lip - thin
Micrognathia - small jaw
Ears –the curve at top part of outer
ear is underdeveloped and folded
over parallel to curve beneath.
Gives the appearance of a "railroad
track"

 MANAGEMENT:
 early intervention is critical to determine prognosis for a
child with FAS
 earlier provision of medical, clinical and educational
intervention- better outcome
 special needs pre-school programme
 constant follow up

 FORMATION OF GERM
LAYERS:
 Soon after primitive streak
appears, cells leave its
deep surface and migrate
to form a loose network of
embryonic connective
tissue called Mesenchyme
 The mesenchyme forms
the supporting tissue of
the embryo.
Third week

 the mesenchyme forms a
layer called Intraembryonic
mesoderm.
 Some cells of the Epiblast
displace the Hypoblast
forming intraembryonic or
embryonic endoderm in the
roof of Yolk sac.
 Cells remaining in the
epiblast forms the
Intraembryonic or
Embryonic ectoderm in the
floor of the amnion.
Third week

 All the above cells have
the potential to
proliferate and
differentiate into diverse
types of cells, such as
fibroblast, chondroblast
and osteoblast.
 In short the cells of the
epiblast, through the
process of
gastrulation, give rise to
all 3 germ layers in the
embryo.
Third week

DERIVATIVES OF GERM LAYERS
 ECTODERM: Epidermis, hair, nail.
Central and peripheral nervous system.
Mammary, pituitary and subcutaneous gland.
Enamel of teeth.
 MESODERM :Connective tissue, cartilage, bone.
Striated and smooth muscle.
Heart, blood and lymphatic vessels.
kidneys, ovaries, testes, spleen, cortex of adrenal
gland.
 ENDODERM: Epithelial lining of gastrointestinal and respiratory
tracts, urinary bladder and urethra.
Epithelial lining of tympanic cavity, tympanic
antrum, auditory tube.

FORMATION OF NOTOCHORD
 Some mesenchymal cells
migrate cranially from the
primitive node and
pit, forming a median
cellular chord, the
notochordal process.
 The process soon acquires
a lumen, the notochordal
canal and grows cranially
until it reaches the
prechordal plate.
DAY 18

 The notochordal process cannot extent
beyond the prechordal plate.
 Place of fusion of upper ectoderm and
lower endoderm, which will form the
OROPHARYNGEAL MEMBRANE.
 Various cellular events take place in the
notochordal process which give rise to the
NOTOCHORD.

prochordal plate
Notochordal canal
cloacal membrane

IMPORTANCE OF NOTOCHORD:
 Defines primordial axis of embryo and gives
rigidity.
 Serves as basis for development of axial
skeleton (bones of head and vertebral column).
 Indicates future site of vertebral bodies.

NEURULATION
 Formation of neural plate and neural folds and closure
of these folds to form the neural tube constitute
Neurulation.
Neural plate and Neural tube:
 As the notochord develops, the embryonic ectoderm
over it thickens to form an elongated, slipper-like plate
of thickened epithelial cells, the “neural plate” .
DAY 19,20

 Neural plate formation is induced by developing
notochord.
 The ectoderm of neural plate called Neuroectoderm
gives rise to the “CENTRAL NERVOUS SYSTEM” i.e.
the Brain and spinal chord

NEURULATION
 At about 18th day, the neural plate invaginates along
its central axis to form median “Neural
groove”, which has neural folds on each side.

 The neural fold are the first signs of brain
development.
 By the end of 3rd week the neural folds begin to move
together and fuse, converting neural plate into a
“neural tube”
NEURULATION

NEURAL CREST FORMATION
 As the neural folds
fuse to form the neural
tube, some
neuroectodermal cells
lying along the crest of
each neural fold lose
their epithelial affinities
and attachments to
neighboring cells.

 Soon it forms a flattened irregular mass, the neural
crest, between the neural tube and the overlying surface
ectoderm.
 Neural crest soon separates into right and left parts that
migrates to the dorsolateral aspects of the neural tube
and give rise to the sensory ganglia of the spinal and
cranial nerves.

 CREST CELLS DERIVATIVES.
 Neurolemmal sheath of peripherl nerves.
 Meningeal coverings of the brain and the
spinal cord.
 Formation of pigment cells.
 Several skeletal and muscular components in
the head

 NEURAL TUBE DEFECTS- primarily
results from failure of neural folds to fuse
and form the neural tube in the brain
region.
 e.g.- ANENCEPHALY- anterior brain
structures are lost and replaced by soft
spongy mass.

Development of somites
 As the notochord and neural tube
form,intraembryonic mesoderm on each
side proliferates to form a column of
PARAXIAL MESODERM.
 INTERMEDIATE MESODERM
 LATERAL MESODERM

Development of somites DAYS 20-30
•Paraxial mesoderm
differentiates into paired
cuboidal bodies- somites
•First appear in occipital
region
•42-44 pairs of Surface
elevations by 5th week
•Develop craniocaudally
•Form axial skeleton www.indiandentalacademy.com

4th week
onwards...

 Paraxial mesoderm.
 Lateral plate mesoderm.
 Neural crest cells .
 Ectodermal placodes
Mesenchyme for formation of head region is
derived from:

PHARYNGEAL APARATUS
 “Branchial”- branchia, gill
resemblance to fish embryo
 - Pharyngeal arches (mesoderm)
 - Pharyngeal clefts (ectoderm)
 - Pharyngeal pouches (endoderm)
 - Pharyngeal membranes
clefts separate arches
externally.
Pouches separate arches
internally.

PHARYNGEAL ARCHES
 Pharyngeal arches consist of core of mesenchymal tissue
covered on the outside by surface ectoderm and on inside by
endoderm.
 Apart from this, the arches also have migrated neural crest
cells, which contribute to skeletal components of the face.

 By the end of the 4th week , 4 pairs of pharyngeal
arches are visible externally as rounded ridges on
each side of the future head and neck regions.
 5tharch-often absent. If present the 5th and 6th arches
are rudimentary & not visible on the surface.
 Neural crest cells, in addition to forming nerve
tissue, produce the bones of the cranium.
 Within the pharyngeal arches, neural crest cells and
lateral plate mesoderm give rise to bones of the jaw
and lower face, the viscerocranium

Each arch is characterized by its own
 Cartilaginous rod that forms the skeleton of the arch
 muscular component
 nerve component and
 arterial component.

DERIVATIVES OF PHARYNGEAL
Apparatus

SKELETAL DERIVATIVES

MUSCLE DERIVATIVES

NERVE SUPPLY

ARTERIAL SUPPLY

 The first pharyngeal arch is often called the mandibular arch.
 First arch splits giving rise to 2 regions:
- cranial part called Maxillary Process
- Caudal part called Mandibular Process
 MAXILLARY PROCESS gives rise to Maxilla
 MANDIBULAR PROCESS gives rise to Mandible
FIRST PHARYNGEAL ARCH

MAXILLARY PROCESS:
mesenchyme of the maxillary
process gives rise to
 premaxilla,
 maxilla,
 zygomatic bone and
 part of temporal bone
through membranous
ossification.

MANDIBULAR
PROCESS:
Cartilage of the 1st arch
is meckel‟s cartilage.
Dorsal end-ossifies to
form malleus and incus
Middle part regresses,
but perichondrium forms
sphenomandibular ligament

Meckle‟s cartilage
 Ventral part-forms horse shoe shaped structure in the
shape of future mandible and has close positional
relationship to developing mandible but makes no
contribution to it.
 Mesenchymal tissue lateral to cartilage undergoes
intramembranous ossification to form mandible and
meckel‟s cartilage disappears

 MUSCULATURE:
 Temporalis
 Masseter
 Pterygoids
 Anterior belly of digastric
 Mylohyoid
 Tensor tympani
 Tensor palatini.

NERVE SUPPLY:
 Nerve supply to muscles
of the 1st arch is by
mandibular branch of
trigeminal nerve.
 Sensory supply to the
skin of face by
ophthalmic, maxillary, an
d mandibular branches
of trigeminal nerve.

 Called the hyoid
arch as part of the
hyoid bone develops
here
 The cartilage of 2nd
arch is called as
Reichert‟s cartilage.
SECOND PHARYNGEAL ARCH

 It gives rise to,
 Stapes
 Styloid process of
temporal bone
 Stylohyoid ligament
 Lesser horn and
upper part of body of
hyoid bone.

MUSCLES:
 Stepedius.
 Posterior belly of
digastric.
 Auricular.
 Muscles of facial
expression

NERVE:
 Facial nerve supplies
all these muscles.

CARTILAGE of 3rd
pharyngeal arch
produces,
 Lower part of body of
hyoid bone.
 Greater horn of hyoid
bone.
THIRD PHARYNGEAL ARCH

MUSCLE:
 Stylopharyngeus
muscle.
NERVE:
 Glossopharyngeal
nerve.
THIRD PHARYNGEAL ARCH

CARTILAGINOUS
component of 4th and 6th
pharyngeal arches fuse
to form,
 Thyroid cartilage.
 Cricoid cartilage.
 Arytenoid cartilage.
 Corniculate cartilage.
 Cuneiform cartilage.
FOURTH AND SIXTH PHARYNGEAL ARCHES

MUSCLES:
4th arch:
 cricothyroid,
 levator palatini,
 constrictors of pharynx ,
6th arch:
 intrinsic muscles of
larynx.

NERVE:
 4TH arch: Superior laryngeal branch of vagus nerve.
 6th arch: Recurrent laryngeal branch of vagus nerve.

ARTERIAL SUPPLY
 Pharyngeal arch arteries are called aortic arches
 from arch 1 & 2-arteries significantly smaller
 Arch 1- part of maxillary artery
 Arch 2- hyoid & stapedial arteries
 Arch 3- part of carotid system
 Arch 4- left side-arch of aorta
Right side-subclavian artery
 Arch 6- pulmonary arteries

 Human embryo has 5 pairs of pharyngeal pouches, the last one
is atypical and often considered as part of the 4th pouch.
 Composed of Endoderm
PHARYNGEAL POUCHES

 It comes in contact with the
epithelial lining of the 1st
pharyngeal cleft, which is a
future external auditory meatus.
 The distal portion widens into
sac-like structure forming
primitive tympanic cavity, the
proximal part remains
narrow, forming Auditory
(Eustachian) tube.
 lining of the tympanic cavity-
forms tympanic membrane or
eardrum.
FIRST PHARYNGEAL POUCH
1st pouch forms stalk-like diverticulum- Tubotympanic recess.

 Buds are secondarily invaded
by mesodermal tissue thus
forming primordium of palatine
tonsil
 3rd and 5th month- tonsil is
infiltrated by lymphatic tissue.
 Part of pouch remains and
forms tonsillar fossa in adult.
second PHARYNGEAL POUCH
The epithelial lining of 2nd pouch proliferates and form Buds that
penetrate into surrounding mesenchyme.

3rd and 4th pouches are characterized by ,
 DORSAL WING and VENTRAL WING
In 5th week, from 3rd pouch
 Dorsal wing- Inferior parathyroid gland.
 Ventral wing- Thymus gland.
THIRD PHARYNGEAL POUCH

Both gland primordia lose their connection with pharyngeal
wall, the thymus then migrates in a caudal and medial
direction, pulling the Inferior parathyroid gland with it.

 The primordia finally rest on the dorsal surface of the thyroid
gland and forms inferior parathyroid gland.
 The thymus gland moves rapidly to its final position in the
thorax, fuses with counterpart from opposite side.
THIRD PHARYNGEAL POUCH

 Of the 4th pouch
Dorsal wing- superior
parathyroid gland.
 It also loses contact with
wall of pharynx and
migrate caudally and
medially and finally is
located on the dorsal
surface of thyroid.
FOURTH PHARYNGEAL POUCH

 Last pharyngeal pouch to develop
 Usually considered to be a part of 4th pouch.
 Gives rise to – Ultimobranchial body, which gets incorporated
into thyroid gland giving rise to parafollicular or „c‟ cells of
thyroid gland which secrete calcitonin, hormone involved in
regulation of calcium level in blood.
FIFTH PHARYNGEAL POUCH

Derivatives PHARYNGEAL POUCHES

 located between arches
externally
 these are spaces, thus
contain no germ layer
components
 Four pharyngeal clefts, of
which only 1st contributes
to the definitive structure -
external auditory meatus.
DERIVATIVES OF PHARYNGEAL CLEFTS/grooves

 Active proliferation of mesenchymal tissue of 2nd arch, results in
overlapping of it over 3rd and 4th arch causing the 2nd , 3rd and
4th clefts lose contact with the outside and forms a cervical
sinus which eventually obliterates as neck develops.
DERIVATIVES OF PHARYNGEAL CLEFTS

Pharyngeal Membranes:
 Appear in the floors of the pharyngeal grooves and form where
the epithelia of the groove & pouches approach each other
 as most clefts are filled in, only first membrane develops.
 this lies close to external auditory meatus and develops into the
Tympanic membrane

 Primordial mouth or stomodeum appears as slight depression
of surface ectoderm
 It is separated from cavity of primordial pharynx by
oropharyngeal membrane
 Bilaminar-ectoderm and endoderm
STOMODEUM

•Ruptures at 26 days
•Communication of primordial cavity and foregut with amniotic
cavity

CLINICAL COMMENT
Most congenital anomalies in head-
neck region originate during
transformation of the pharyngeal
apparatus into its adult derivatives.
Thus the term “branchial anomalies”
results from persistence of parts that
normally disappear as adult
structures develop.

 BRANCHIAL FISTULAS:
 -an abnormal canal that opens internally into tonsillar sinus and
externally in the side of the neck.
 persistence of parts of the 2nd pharyngeal groove and pouch.
 Fistula ascends from its opening in the neck through the
subcutaneous tissue and platysma muscle to reach the carotid
sheath – passes between the internal & external carotid arteries
and opens into the tonsillar sinus
CLINICAL CORRELATION

BRANCHIAL CYST:
 Remnants of parts of cervical sinus and/or the
2nd pharyngeal groove may persist and form a
spherical or elongated cyst.
 They may be associated with
branchial sinuses and drain
through them,
 these cysts often
lie free in the neck just inferior
to the angle of the mandible

 May develop anywhere
along the anterior border
of SCM muscle
 Slowly enlarging painless
swelling in the neck.

 NEURAL CREST CELLS:
Essential for formation of craniofacial region but
disruption results in severe craniofacial malformation :
 1ST ARCH SYNDROME-
Treacher collins syndrome (mandibulofacial dysostosis)
Pierre-Robin sequence
 Digeorge sequence (3rd and 4th pharyngeal pouch
syndrome).
 Goldenhar syndrome (Hemifacial microsomia ).
CLINICAL CORRELATION

TCS
 First described by Thomson and Toynbee in 1846-47
Later, essential components described by Treacher Collins
in 1960
 Autosomal dominant inheritance
 Associated with increased paternal age
 Prevalence of 1 in 50,000
Treacher collins syndrome
(mandibulofacial dysostosis)

Characteristics:
 Fishlike” facial appearance
 Usually bilateral and symmetric expression
 Degree of malformation at birth is stable and non-progressive
 Dolichofacial pattern
 Hypoplastic supraorbital rims and underdeveloped zygomatic
bones resulting in malar
hypoplasia.
TCS

TCS
 “Cleft palate in 35%
 Downward slanting palpebral
fissures
 Retrusive mandible and maxilla
 High mandibular plane
angle– Anterior open bite
 Antegonial notching
 Malformed external ear
 Normal intelligence

Treacher Collins syndrome
1. Preoperative frontal view of 16-year-old patient with Treacher
Collins Syndrome. No previous correction had been performed.
2. Postoperative frontal view 1 year after orthognathic surgery.
3. Pre and postoperative lateral views of same patient.
1. 2. 3.

PRS
 Triad of micrognathia, glossoptosis and cleft palate
 First described by St. Hilaire in 1822
 Pierre Robin first recognized the association of
micrognathia and glossoptosis in 1923
 Prevalence: 1 of every 8,500 newborns
PIERRE ROBIN SEQUENCE
Alters 1st arch structures, with mandible most severely
affected. www.indiandentalacademy.com

 The initiating defect is micrognathia which results in
posterior displacement of the tongue i.e. glossoptosis
and obstruction to full closure of palatine processes
resulting in bilateral cleft palate
PRS

 Occurs because the 3rd and 4th pharyngeal pouches fail to
differentiate into thymus and parathyroid glands.
 Congenital thymic aplasia and absence of parathyroid glands
with or without cardiovascular defects.
DIGEORGE SEQUENCE:

characteristics
 Congenital hypo-parathyroidism
 Increased susceptibility to infections
 Shortened philtrum of lip
 Low set notched ears
 Nasal clefts
 micrognathia,
 And cardiac abnormalities – defects of aortic
arch & heart

Characteristics
 Maxilla, temporal,& zygomatic bones are reduced in size and
flattened.
 Facial asymmetry
 Ear, eye, and vertebral defects
are common.
i.e. Occuloauriculovertebral
disease
 Epibulbar Dermoids which are
benign tumors located just inside
the opening of the eye or the
eyeballs, cause problems with
vision.
HEMIFACIAL MICROSOMIA/GOLDENHAR
SYNDROME:

Preoperative frontal view of 17-year-old patient after
inadequate orthognathic surgical correction.
Postoperative frontal view after distraction osteogenesis and
dermal fat graft to left cheek.
Preoperative left oblique view shows deformity and after
reconstruction
GS

Development of
face

2 organizing centers-
 Forebrain (prosencephalic) centre
 Hindbrain (rhombencephalic) centre

 5 facial primordia
 Neural crest: source for almost all connective tissues in the face
DEVELOPMENT OF FACE

Boundaries of stomodeum.
 Paired maxillary prominences- lateral
boundary
 Paired mandibular prominences- caudal
boundary
 Nasal part of FNP- rostral boundary

 Facial prominences-active centers of growth – 4th to 8th week
 Connective tissue continuous from one prominence to another.
DEVELOPMENT OF FACE

 Lower jaw and lower lip are the first parts
of the face to form.

 Nasal placodes & nasal pits- by the end of fourth week
 Primodia of the nose and and nasal cavities.
DEVELOPMENT OF FACE

Nasal prominences , nasal pits

Maxillary prominences grow- pushing nasal prominences
medially
Nasolacrimal groove

MNP
MP
LNP

•Auricular hillocks- seen by the
end of fifth week.
•Neck region
•Primordia for external acoustic
meatus and auricle.

•By the end of sixth week
•Maxillary prominence merges
with lateral nasal prominence
•Continuity between side of
nose and cheek region
•Nasolacrimal duct NLG

NASOLACRIMAL DUCT
Rod like ectodermal thickening in the floor of
Nasolacrimal groove.
Later as a result of cell degeneration cord
canalizes into Nasolacrimal duct.
Part of duct which fails to canalize –
ATRESIA OF NASOLACRIMAL DUCT.

 Medial nasal prominences merge with each other and with
fused lateral nasal & maxillary prominences
 Intermaxillary segment

Intermaxillary segment gives
rise to
 Philtrum of the upper lip.
 Premaxillary part of the maxilla and its
associated gingiva.
 The primary palate.

MNPLNP
MP

1. Frontonasal prominence: forehead, dorsum & apex of nose
2. Lateral nasal prominence: alae of nose
3. Medial nasal prominence: nasal septum, philtrum, premaxilla,
primary palate
4. Maxillary prominence: upper cheek, most of maxilla and lip
5. Mandibular prominence: mandible, chin, lower lip, lower cheek
Disruptions in the
formation of these
prominences leads
to facial clefting and
other defects.
Summary of Facial
Development

DEVELOPMENT OF PRIMARY
PALATE
 Palatal development spans week 5-12 , but weeks 6-9 are most
critical
 Formation of intermaxillary segment from merged medial nasal
prominences

 Primary palate begins to develop from
deep part of the intermaxillary segment of
maxilla.
 Initially this segment is a wedge shaped
mass of mesenchyme between internal
surface of maxillary prominence.
 Primary palate forms the premaxillary part
of the maxilla.

DEVELOPMENT OF SECONDARY
PALATE

Sixth week
Secondary palate develops from two
mesenchymal projections that extend from
internal aspects of the maxillary
prominences. ( lateral palatine processes )
project inferomedially.

 As jaw develops tongue moves
inferiorly palatal shelves ascend to
a horizontal position and fuse in the
median plane.
 Palatal shelves also fuse with the nasal
septum and posterior part of primary
palate.

 NASAL SEPTUM develops as a
downgrowth from internal aspects of
merged medial nasal prominences.
 Fusion between nasal septum and
palatine processes ninth to twelfth
week.

 Bone develops in the primary palate,
forming Premaxillary part of the maxilla.
 Gradually bone extends into the lateral
palatine processes to form HARD
PALATE.
 Posterior part do not ossify SOFT
PALATE.

Nasal septum
Bone development

Theories for palatal shelf elevation
 Causes extrinsic to palatal shelves
1. Descent of the tongue due to pronounced sagittal growth
spurt of the Meckle's cartilage and the mandible (Coleman
1965; Burdi & Silvey 1969)
2. Myoneural activity within the tongue causing descent
(Wragg et al 1969)
3. shelves being pushed up by the tongue (Walker 1971)
4.mouth opening reflexes (Humphrey 1969)

Intrinsic causes –
1. Hydration and polymerization of intercellular substances
producing an elastic elevating force (Walker 1961)
2. differential growth of one side of the palatal shelf (Wood &
Kraus, 1962)
3. turgor produced by a build up of mucopolysaccharides
, predominantly hyaluronic acid (Andersen et al 1967)
4. serotonin release from neural tissue (Zimmerman et al 1981)
5. degree of mesenchymal cell activity at different sites and
stages of palatal development (Singh and Moxham 1993)
Ref- fundamentals of craniofacial growth - Sperberwww.indiandentalacademy.com

 Most accepted theory-
elevation of the palatal shelves to horizontal
position is believed to be caused by an intrinsic shelf
elevating force that is generated by the hydration of
hyaluronic acid in the mesenchymal cells within the
palatal process

CLEFT LIP & PALATE
 Cleft lip and cleft palate are related embryologically but
are distinct entities
 Cleft lip: 1 in 750; Cleft palate: 1 in 2500
 Effects on appearance, speech, feeding
Associated Dental Abnormalities
 Supernumerary Teeth- 20%
 Dystrophic Teeth- 30%
 Missing Teeth- 50%
 Malocclusion- 100%

Genetics
 Non-syndromic inheritance is multifactorial
 Cleft Lip, With or Without Cleft Palate:
• One Parent-2%
• One Sibling- 4% Two Siblings- 9%
• One Parent + One Sibling- 15%
 Cleft Palate:
• One Parent- 7%
• One Sibling- 2% Two Siblings- 1%
• One Parent + One Sibling- 17%

Genetics
 Increased clefts with chromosome aberrations
 Clefts a part of a Syndrome 15-60% of time
 More than 200 syndromes include clefts
 Cleft Palate- Apert‟s, Stickler‟s, Treacher
 Cleft Lip +/- Palate- Van der Woude‟s, Waardenberg‟s

Epidemiology
 Cleft Lip +/- Palate- 2 Male: 1 Female
 Cleft Palate - 2 Female: 1 Male
(palatine processes fuse one week later in females)
 Cleft Lip +/- Palate- Native Americans > Oriental and
Caucasians > Blacks
 Cleft Palate- Same among ethnic groups
 Environmental: Ethanol, Rubella
virus, thalidomide, aminopterin, smoking
 Increased Clefts with maternal diabetes mellitus and
amniotic band syndrome
 Increased Clefts with increased paternal age

Unilateral Cleft Lip
• Forms as a persistent labial groove
• Labial groove should disappear as the maxillary prom. fuse with
merged medial nasal prominences
• Stretching of epithelium causes tissue breakdown and cleft
formation www.indiandentalacademy.com

 Nasal floor communicates with oral cavity
 Maxilla on cleft side is hypoplastic
 Columella is displaced to normal side
 Nasal ala on cleft side is laterally, posteriorly, and inferiorly
displaced www.indiandentalacademy.com

Bilateral Cleft Lip
• Similar to unilateral cleft lip
• Central soft-tissue mass that moves freely

 Clefting of alveolar process of maxilla as well as lip
 Complete cleft extends to incisive foramen
 Complete bilateral anterior cleft isolates the anterior and
posterior parts of the palate
 Result from failure of lateral palatine processes to fuse to
primary palate
Anterior Cleft Anomalies

Posterior Cleft Anomalies
 Clefts extending through both soft and hard palate to the
incisive fossa
 Isolates anterior and posterior parts of palate
 Result from failure of lateral palatine processes to grow
medially and fuse to each other

Complete Cleft Palate
 Complete bilateral cleft
of the lip and alveolar
process of the maxillae
with complete bilateral
cleft of the anterior and
posterior palate
Complete bilateral cleft of
the lip and alveolar
process of the maxillae
with bilateral cleft of the
anterior palate and
unilateral cleft of the
posterior palate

Development of tongue
Development begins
around the end of
fourth week in relation
to pharyngeal arches
in the floor of mouth.

 Swellings from the first pharyngeal arch
Median tongue bud 2 distal buds
(tuberculum impar)
anterior two thirds of
epithelium proliferates tongue
Downwards (thyroglossal duct)
To form the thyroid gland.

 Two swellings caudal to foramen cecum
COPULA HYPOBRACHIAL
EMINENCE
Ventromedial parts ventromedial parts
of 2nd arch of 3rd and 4th arch
Overgrown by hypo forms the posterior
Brachialeminence two thirds of the
tongue.www.indiandentalacademy.com

1st Brachial Arch
2nd Brachial Arch
3rd Brachial Arch

Copula overgrown by
hypopharyngeal
eminence

1st Brachial Arch
2nd Brachial Arch
3rd Brachial Arch
4th Brachial Arch

Terminal sulcus-line
of fusion of the
anterior and
posterior parts of
the tongue.

Nerve supply of tongue
 Anterior two-thirds
 lingual branch of chorda tympani
mandibular div of tri- branch of facial.n ( taste
geminal.n (sensory) buds except for vallate
papillae )

Posterior third
glossopharyngeal.n superior laryngeal
branch of vagus.n
MUSCLES – all muscles of tounge are
supplied by hypoglossal nerve except for
palatoglossus which is supplied by
pharyngeal plexus fibres from the vagus
nerve.

•Aglossia.
In this condition, a portion or all of the tongue
is absent. Rarely is all the tongue absent.
Microglossia
Migrognathia and limb defects (Hanhart‟s syndrome)
APPLIED ASPECTS

 Macroglossia
 A congenital macroglossia is generally
caused by an overdevelopment of the
muscular portion of the tongue.
 Lymphangiomas may occur alone or (more frequently) in
association with hemangiomas The tongue is the most
common oral location for this lesion. Together with
hemangioma, lymphangioma is an important cause of
congenital macroglossia.
 Macroglossia may develop after removal of teeth. This
develops as a hypertrophy (increase in cell size) when the
teeth no longer contain the tongue within the previously
established boundaries.

Ankyloglossia :
In this condition, the tongue is restricted in its movements by a
strand of mucosa - lingual frenum that attaches the anterior third
of the tongue to the floor of the mouth and the lingual gingival
mucosa.
Extends to the tip of tongue interfering with free protrusion
Persons with this condition are commonly called "tongue-tied."
Treatment is surgical. www.indiandentalacademy.com

Congenital Lingual Cysts and Fistulas
Remnants of thyroglossal duct
Dysphagia
Fistulas open through foramen caecum

SKULL
NEUROCRANIUM VISCEROCRANIUM
( clavaria & base of skull ) ( skeleton of face and associat
ed structures )
•Membranous
•cartilaginous

Cartilagenous neurocranium
Development of neurocranium
Neural crest
cells
Paraxial
mesoderm

 Ossification pattern-
• Occipital bone
• Body of sphenoid
• Ethmoid bone
 Other structures-
• Vomer bone of nasal septum
• Petrous and mastoid part of temporal bone

Membranous neurocranium
Origin of mesenchyme
Neural crest
cells Paraxial
mesoderm

Membranous neurocranium
Calvaria
•Frontal bone
•Parietal bone
•Squamous part of temporal bone
•Occipital bone

Role of fontanelle

VISCEROCRANIUM
CARTILAGINOUS VISCEROCRANIUM
•Middle ear ossicles
•Styloid process
•Hyoid bone
•Laryngeal cartilages

MEMBRANOUS VISCEROCRANIUM
•Maxilla
•Zygomatic bone
•Squamous
temporal
•mandible

Apert and Crouzon
Syndrome‟s
1906, Apert described a child with
acrocephalosyndactyly
1912, Crouzon described mother & daughter with
craniofacial dysostosis
Both are autosomal dominant
Incidence is ~ 15 to 16 per 1,000,000 births

 Typical characteristics
 Craniosynostosis
• Coronal sutures fused at birth
• Larger than average head circumference at birth
 Midfacial malformation and hypoplasia
 Shallow orbits with exophthalmos
 Apert Syndrome: symmetric syndactyly (=fusion of digits)
of hands and feet
Apert and
Crouzon

Apert and
Crouzon
syndactyly

 Facial features
 Shallow orbits with exophthalmos
 Retruded midface with relative prognathism
 Beaked nose
 Hypertelorism
 Downward slanting palpebral fissures
Apert and
Crouzon

Development of mandible
 Intramembranous
 Meckle‟s cartilage – role
• Primitive structural support
• Morphogenic template

MECKLE’S
CARTILAGE

DEVELOPING MANDIBLE MECKEL‟S CARTILAGE

 Mandibular nerve – lingual branch
• inferior alveolar branch – mental
- incisive

 Primary ossification center
 Anterior and posterior extension of growth

 Height of bone is increasing at the same time as antero
– posterior growth.
 Mental nerve comes to lie in a shallow groove & then a
definite notch
 Formation of trough composed of lateral and medial
plates. Notch containing nerve converted into foramen.
 Closure & formation of incisive canal – part of
mandibular canal
 Neural element

 Developing tooth germs
 Formation of alveolar process – upward extension of
neural element
 Medial and lateral alveolar plates - formation of
secondary trough

Development of ramus
 Backward extension of neural
element behind and above mandibular
foramen
 Pre-osteoblast condensation
 Coronoid and angular processes added
for muscular attachment
 Point of divergence is marked by
– Lingula www.indiandentalacademy.com

By 10TH week the rudimentary mandible is formed almost
entirely by membranous ossification, with little direct involvement
of MECKEL‟S CARTILAGE

 Secondary cartilages
Condylar cartilage
Coronoid cartilage
Symphyseal cartilage
 Distinguish from the primary Meckel's cartilage:-
 histologic structure
(large haphazardly arranged chondrocytes
& sparse intercellular matrix)

CONDYLAR CARTILAGE
 10 week of IUL –first appears as a fringe
 Cone shaped structure
 14TH week of IUL – By endochondral ossification this mass of
cartilage converted quickly to bone.
 This cartilage persists until the end of the second decade of
life, providing a mechanism for growth of the mandible.

CORONOID CARTILAGE
 About 16th week of IUL
 Strip along anterior border and tip of coronoid process
 Grows as response to the developing temporalis muscle
 Fuses with ramus & disappears before birth

SYMPHYSEAL CARTILAGE
 Two in number
 7 month of IUL in the mental region
 Fuses with mandible during the first year of post-natal life

Development of nasomaxillary complex
 Maxilla – intramembranous
 Maxilla develops from the centre of ossification in the
mesenchyme of the maxillary process of the first arch

 No arch cartilage or PRIMARY CARTILAGE , but centre of
ossification is associated closely with the cartilage of the nasal
capsule.
 Centre of ossification-at division of infraorbital into
anterosuperior dental nerve.
 spread of ossification –
 Upwards – frontal
 Downwards – lateral alveolar plate
 Inward – palatal process
 Backward – zygomatic process
 Forwards – pre-maxillary region
 Medial alveolar plate along with Lateral alveolar plate trough
around maxillary tooth germ
MAXILLA

SECONDARY CARTILAGE
 Zygomatic or malar cartilage appears in the developing
zygomatic process and for a short time adds
considerably to development of maxilla.
 Body of maxilla is relatively small because the maxillary
sinus is not developed.
 Formation of sinus takes place in 16th week as a shallow
groove on the nasal aspect of the developing maxilla.
 At birth sinus is still the rudimentary structure about the

COMMON FEATURE OF
DEVELOPMENT OF JAWS
 Both maxilla and mandible start developing from centres
of ossification in close relation to bifurcation of
corresponding nerves
 They form from 2 facial swellings which have the same
origin
 Each has a relation to a primary cartilaginous skeleton
 Both form a neural element & alveolar element.
 Finally, both develop SECONDARY CARTILAGE to
assist in their growth.

CLINICAL
CONSIDERATIONS

Down Syndrome (Trisomy 21)
 1866, described by John
Landon Down
 Most common
 Prevalence 1 in 700 births
 Maternal age >35 carries
increased risk

 Etiology: non-disjunction mutation
resulting in Trisomy 21
 Non-disjunction-error in cell division;
 Failure of chromatids of a chromosome to disjoin during
meiosis
Down
Syndrome

 Trisomy=3 chromosomes present instead of the
usual pair; associated with 3 main syndromes
 Trisomy 21 – Down syndrome
 Trisomy 18 – Edwards syndrome
 Trisomy 13 – Patau syndrome
 Infants with trisomy 18 &13 are severely malformed and mentally
retarded and usually die early in infancy
Down
Syndrome

•Growth retardation
•Mental retardation
•Clinodactyly of 5th digit
(=incurving)
•Simian crease
(=single transverse palmar crease)
•Congenital heart defects
Characteristic features:
Down
Syndrome

Facial Characteristics
 Broad face
 Midface hypoplasia
 Flat occiput
 Flat nasal bridge
 Epicanthal folds
 Up-slanting palpebral fissures
 Progressive enlargement of lips
 Small ears
Down
Syndrome

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