Development of the face

29/07/2017 BY - Dr. Sanjana G. Patil 1

Development of the
face

29/07/201729/07/2017 BY - Dr. Sanjana G. PatilBY - Dr. Sanjana G. Patil 33
Development
Definition: “Development is a progress
towards maturity” – Todd (1931)
According to Moyers Development refers to
all the naturally occurring unidirectional
changes in the life of an individual from its
existence as a single cell to its elaboration as
a multifunctional unit terminating in death..

Branchial Apparatus
 Arches
– mesenchymal tissue surrounded by ectoderm
and endoderm
 „ Clefts (or grooves)
– Separate adjacent arches along ectodermal
surface
 „ Pouches
– Outpouching of endoderm from foregut
– Penetrate adjacent mesenchyme

Branchial Apparatus

Branchial Apparatus
 Each pharyngeal arch contains :
- A cartilaginous component.
- A nerve.
- A muscular component &
- An arch specific cranial nerve.

Musculature of Pharyngeal
arch

Cartilages of pharyngeal
arch

Cranial nerves of pharyngeal
arch

Arterial supply of pharyngeal
arch

Pharyngeal
Pouch
Derivative
1 Epithelium of tympanic cavity
and auditory tube
2 Epithelium of tonsil
3 Inferior parathyroid glands and
epithelium of thymus
4 Superior parathyroid glands.
5 Ultimobranchial body.

Pharyngeal clefts
 4 clefts
„
 The 2nd to 4th clefts become buried by the
overgrowth of the 2nd arch to form the cervical
sinus
„
 Cervical sinus has dissapeared by week 7
„
 The first cleft persists and invades the
mesenchyme
opposite the first pouch
„
 This becomes the EAM and ectoderm of the TM

Formation of the face
Both the frontonasal process and the branchial
arches play a large
part in the formation
of the face and the
oral cavity.

Maxillary process
1. Pharyngeal arch
(mandibular)
2. Pharyngeal arch
(hyoid arch)
3. Pharyngeal arch
4. And 6. Pharyngeal arch
Developing heart
Nasal placode
Frontonasal prominence

The face derives from five prominences that surround the
stomodeum.
The prominences are:
• the single median frontonasal
prominence and
• the paired maxillary prominences
• and mandibular prominences;
(derivatives of the ﬁrst
pharyngeal arch)

Tissues from the mandibular arches form all the lower
face and most of the midface while the other
pairs of arches, including branchial grooves and
pharyngeal pouches, are involved mainly in the
formation of the neck region.

The frontonasal prominence is the
largest and is composed of an
upper frontal and a lower nasal
portion.
In the fourth week, within 3 to 4 days,
two oval ectodermal thickenings,
the nasal placodes, appear
bilaterally, located on the nasal
process.

The mesenchyme beneath the
ectodermal thickenings rapidly
proliferate, causing a tissue
elevation around the placodes.
Each nasal placode possesses an
outer lateral nasal and an inner
medial nasal swelling.

In the fifth week, the lateral and
medial nasal swellings
enlarge rapidly, with the
medials advancing toward
one another and eventually
fusing.

The maxillary prominence is dimensionally not
impressive early in development.
With medial growth of its terminals and broadening of
its other borders, the maxillary
prominence presses onto the
nasal swellings forcing their
medial and lateral arms closer
together.

During the following week, the medial and lateral
nasal swellings unite and merge with the maxillary
process.
The line of fusion of the maxillary
process with the lateral nasal
swelling is marked by a trough,
the nasolacrimal groove.

The union of the medial nasal swellings
forms the intermaxillary process of
the maxillary arch.
The intermaxillary process produces:
• the philtrum of the lip,
• the segment of the maxilla bearing the
incisor teeth, and
• the primary
palate.
Fused
palatal
process

The lateral nasal prominences give rise to the wings
or alae of the nose.
The medial nasal processes produce the inferior
segment of the nasal septum.

By the end of the fourth week, the two mandibular
prominences have grown towards one another and
merged.
The mandible, the lower lip, the lower portion of the
cheek, the chin, and the gingiva take their origins
from the mandibular prominences.
The maxillary process gives rise to the lateral portions
of the upper lip and cheeks, the maxilla, and the
secondary palate with its associated gingiva.

A = Maxillary process
B = Mandibular process
C = Medial nasal process
D = Lateral nasal process

Development of the
palate

Formation of the palate
The formation of primary palate is a contribution of
the fusion of medial nasal processes.
The secondary palate
originates from lateral
palatine processes, a ledge
like outgrowths of the
maxillary process

These lateral palatine processes make their appearance
in the sixth week of development.
Early in their formation, they are located along the sides of
the developing tongue.
Indication of initiation of tooth development is also visible
(dental lamina).

 Another view of the same situation.
 The lateral palatine processes are situated besides
developing tongue.

Later as the tongue takes a deeper position in the primitive
oral cavity, the palatine processes rise and grow toward
each other.

By the eighth week, the lateral palatine processes fuse with
each other as well as with the primary palate and nasal
septum.
 These fusions complete
the formation of the ceiling
of the oral cavity and the
floor of the nasal cavity.
 The nasal septum
separates the right and left
passages of the nose.

 Fused palatine processes.

Development of face and oral
Cavity
Development of the tongue

Formation of the tongue
 The tongue is a muscular
organ composed of :
 An anterior movable part,
termed the body, and
 The posterior firmly attached
base/root or branchial part.

 The tongue originates from the first, second, and third
pharyngeal arches and from a migration of muscles
from the occipital somites.
 The anterior part arising from
the first arch is formed from
three masses, the two lateral
lingual swellings and the
tuberculum impar.

 These lateral lingual swellings rapidly enlarge, merge
with each other, and overgrow the tuberculum impar to
form the oral part of the tongue.
 An U-shaped sulcus develops in front of and on both
sides of this oral part, which allows it to be free and
highly mobile, except at the region of the lingual
frenulum where it remains attached to the floor of the
mouth.

 The root of the tongue develops mainly from the third
pharyngeal arch.
 Initially it is indicated by a midline elevation that appears
behind the tuberculum imper, which is a large branchial
eminence of the third and fourth arches (hypobranchial
eminence).
 Later this eminence
overgrows the second
pharyngeal arch, to
become continuous with
the body of the tongue.

The site of union between the base and the body of the
tongue is delineated by a V-shaped groove called the
sulcus terminalis.

Development of face and oral
Cavity
Development of the mandible

Development of the
mandible
The basic growth pattern of the mandibular body and
condyle appeared in week 7 of fertilization.
Histologically, the embryonic mandible originated in
the lower part of the first branchial arch from primary
intramembranous ossification in the fibrous
mesenchymal tissue around the Meckel's cartilage.

Development of the
mandible

Development of the
mandible
Before the begin of ossification the mandibular nerve
and its branches are developed and they ensure the
formation of canals around them.
From this initial ossification, the ramifying trabecular
bones developed forward, backward and upward, to
form the symphysis, mandibular body, and coronoid
process, respectively. (following the path way of the
incisive and the inferior alveolar nerve)

Development of the
mandible

Development of the
mandible
The accessory cartilages are:
• the condylar cartilage
• the coronoid cartilage
• the symphysial cartilage

Development of the
mandible
The condylar cartilage is the largest and most
important one. It appears in the 12th
week i. u. and is
quickly replaced by enchondral ossification.
A thin layer of cartilage remains in the condylar head
and persists until the 20
years of life providing
a mechanism of mandibular
growth.

Growth of the mandible
The shape and size of the mandible undergo
considerable transformation from embryonic to adult
mandible.

Growth of the mandible
The mandible grows in all directions:
• Anterio-posterior by bone deposition along the
posterior border of the ramus.
• Vertical by growth of the condyle, along the upper
border of the ramus and the formation of the alveolar
process.
• Transverse by bone deposition on the external
surface and bone resorption at the inner surface.

Development of the
mandible
The alveolar bone formation begins as the teeth
reach the early bell stage.
The bone begins to grow around the tooth germs and
upward in occlusal direction.
Later this area is called alveolar bone and is divided
into alveoli by septa.

Formation of Nose
 Receives contributions from 
• Frontonasal process
• Medial & lateral nasal process
of right & left side
56

 Nasal placode: by the 5th
week, thickening
of ectoderm of lower part of frontonasal
prominence
 Nasal pit: depressions in nasal placode
 Median nasal prominence and lateral
nasal prominence: proliferation of
mesenchyme at the margins of the nasal
placodes

The formation of these Nasal
Pits divides the Fronto -nasal
process into two parts :
a. The Medial nasal process
b.The lateral nasal process
Formation of Nose

Under influence of developing forebrain
ectoderm overlying frontonasal process
shows
bilateral localized thickening ( known as Nasal placodes)
sink below surface
Nasal pits
continuous with stomatodeum
medial raised edge lateral raised edge
medial nasal process lateral nasal process

 Nasal pits later on cut off from stomatodeum and fusion of
maxillary process with medial nasal process
formation
external nares
approach each other
narrowing of frontonasal process
 mesoderm heaped up in median plane
prominence of nose
 external nares open downward instead of
forward

Formation of Eyes
 Formation starts – 8th
week in utero
 Firstly, ectodermal thickening known as
lens placode appears on ventrolateral
side of developing forebrain, lateral &
cranial – nasal placode

Formation of Eyes
 At first, it is directed laterally & in the angle
between maxillary & lateral nasal process.
 With narrowing of frontonasal process, they
lie forward.

Formation of
External Ear
 External acoustic meatus –
 dorsal part of 1st
ectodermal cleft
 deeper part  proliferation of its lining epithelium
which grows towards middle ear.
 Firstly this proliferation – solid , later on canalized.

 Auricle ( pinna )
• Series of 6 mesodermal thickenings appear –
mandibular & hyoid arch around opening of
external acoustic meatus
• Fusion of these thickenings leads to pinna
• Firstly it lies caudal – developing jaw , later on
pushed upward & backward to its definitive
position because of great enlargement of
mandibular process

 Mandibular arch forms only tragus & small
area around it.
 Rest of auricle formed from hyoid arch.

References
 J.W Larsen, 1998. Essentials of Human
Embryology. 2nd
Ed Churchill Livingstone
publisher, New York. Pg-345-370.
 K L Moore, and T. V. N. Persaud. 1998. The
Developing Human, 6th Ed. Saunders,
Philadelphia. Pg- 236-254
 T W Sadler,1985. Langman’s Medical
Embryology, 5th Ed. Williams and Wilkins,
Baltimore. Pg-345-390

Developmental Anomalies
of Face
 Formation of various part of Face 
fusion of diverse components
 This fusion occasionally incomplete 
various anomalies
 Formation of various part of Face 
fusion of diverse components
 This fusion occasionally incomplete 
various anomalies

Developmental anomalies
of face
 Oblique facial cleft
 Manidibulofacial dysostosis

Oblique facial
cleft
• Non fusion of the maxillary and lateral
nasal process  cleft running from the
medial angle of the eye to the mouth.
• Nasolacrimal duct not formed.

Mandibulo-facial
dysostosis
 also known as 1st
arch syndrome
 Condition results  entire 1st
arch remain
underdeveloped on one/ both side ,
affecting lower eyelid , maxilla , mandible &
external ear displaced ventrally & caudally.
 Absence of prominence of cheek.

of lip and palate
 Cleft lip
 Cleft palate
 Vander woude syndrome
 Double pit
 Ascher’s syndrome

Cleft lip
a) Unilateral cleft lip:
Results from failure
of the maxillary
prominence to
merge with medial
nasal prominence on
the affected side

b. Bilateral cleft lip : Results from failure
of the maxillary prominences to merge
with the medial nasal prominence on
both sides
c. Median cleft lip: Results from failure of
the medial nasal prominences to merge
and form the intermaxillary segments

Cleft palate
 Congenital defect → non fusion of right
and left palatal processes
 May be of different degrees
Least severe types → soft palate.
Most severe → cleft in palate is
continuous involving cleft lip.

Veau’s classification
 Group I - cleft of soft palate only
 Group II - cleft of hard & soft palate
 Group III – complete unilateral cleft …uvula to
incisive foramen.. deviates to one side extending
through the alveolus
 Group IV – complete bilateral alveolar cleft

29/07/2017 BY - Dr. Sanjana G. Patil 77 77

Treatment
 Cleft lip repair — within the first 12 months
of age
 Cleft palate repair — by the age of 18
months, or earlier if possible
 Follow-up surgeries — between age 2 and
late teen years

 Cleft lip repair. To close the separation in the
lip, the surgeon makes incisions on both sides
of the cleft and creates flaps of tissue. The
flaps are then stitched together. The repair
should create a more normal lip appearance,
structure and function. Initial nasal repair, if
needed, is usually done at the same time.
 Cleft palate repair. Various procedures may
be used to close the separation and rebuild the
roof of the mouth (hard and soft palate),
depending on your child's situation. The
surgeon makes incisions on both sides of the
cleft and repositions the tissue and muscles.
The repair is then stitched closed.

 Ear tube surgery. For children with cleft
palate, ear tubes may be placed, typically at 6
months of age, to reduce the risk of chronic ear
fluid, which can lead to hearing loss. Ear tube
surgery involves placing tiny bobbin-shaped
tubes in the eardrum to create an opening to
prevent fluid buildup.
 Surgery to reconstruct
appearance. Additional surgeries may be
needed to improve the appearance of the
mouth, lip and nose.

Vander woude syndrome
• Known as dimpled papillae of lip, lip pit
syndrome
• Autosomal dominant syndrome – association of
cleft lip & palate with lower lip pits
Bilateral lip pits

• Diagnosis – hyper nasal voice & bifid
uvula.
• May have maxillary
hypodontia( missing incisors /
premolars) ,ankyloglossia , high arched
palate.

Double Lip
 A redundant fold of tissue on the mucosa
side of the lip.
 Usually congenital but can be acquired.
 Acquired may be associated with Ascher’s
Syndrome (double lip, blepharochalasis,
non toxic thyroid enlargement)
 Treatment – Removal of accessory lip.

Ascher’s Syndrome
Blepharochalasis
Double Lip
Thyroid Enlargement

of nose
 Encephalocele
 Glioma
 Dermal fistula ( Nasal dermoid)

Encephalocele
Extra cranial herniation of meninges and brain tissue
through a defect in the skull.
Meningocele presents similarly without herniation of
brain tissue
a) Sincipital Encephalocele b) Basal Encephalocele.

 A) Sincipital encephaloceles are also
known as Frontoethmoidal
encephaloceles. They occur between the
frontal and ethmoid bones at the foramen
cecum immediately anterior to the cribiform
plate. They may be further subdivided as
nasofrontal, nasoethmoidal and naso-orbital
and manifest as external nasal masses.
 B) Generally Basal Encephaloceles arise
through the cribiform plate or through the
superior orbital fissure and manifest as an
intranasal mass.

Nasal Glioma
 Heterotopic glial tissue that lacks a patent
CSF communication to subarachnoid
space
 Abnormal closure of the fonticulus frontalis
 During retraction of the
embryonic Dural
diverticulum, rests of glial
tissue become sequeatered

Extra nasal (60%)
 Smooth, firm, non-compressible masses,
skin telangiectasia
 Glabella (most common), nasomaxillary
suture line
Intranasal (30%)
 Polypoid, pale masses
 Arise in the lateral nasal wall near the
middle turbinate
 Nasal septum (rare)

 During development, dura projects
through the foramen cecum and attaches
to skin
 Separates from the nasal skin and retracts
through foramen cecum
 If there is a persistent attachment to
underling fibrous tissue, nasal capsule or
dura, epithelial elements are trapped in
the prenasal space
Nasal dermoids


. Dermoids contain ectodermal and mesodermal
embryonic elements. The latter include hair follicles,
sebaceous glands, and sweat glands and keratin debris.
from deremoid cysts, Dermoids lack glial features of
encephaloceles and gliomas.

 Present at birth - first two decades of life
Midline mass or cyst with sinus opening
 Firm lobulated non compressible mass
 Sinus opening sebaceous or purulent
material
 Widened nasal bridge
 Protruding hair (path gnomonic)

 Up to 50% have a fistula or
sinus tract
 Tract transverses via the
cribiform plate or foramen
cecum
 Tract may attach to dura,
falx cerebri or other
intracranial structures

of jaws
 Agnathia
 Micrognathia
 Macrognathia
 Piere robin syndrome

Agnathia

Micrognathia

 Congenital –
1) It is associated with congenital heart disease &
Pierre Robin syndrome
2) Maxillary Micrognathia due to deficiency in
premaxillary area.
3) Retracted middle third of face.
4) Etiology – mouth breathing.
 Mandibular micrognathia may be due to
posterior positioning of mandible, steep
mandibular angle, agenesis of condyle.

 Acquired type is post natal –
 Due to disturbance in TMJ region.
 Ankylosis due to trauma or infection of mastoid.
Clinical features
 Severe retrusion of chin
 Steep mandibular angle
 Deficient chin button.

Pierre robin syndrome
 Cleft palate
 Micrognathia
 Glossoptosis
 Congenital heart defect
 Ocular anomalies
 Skeletal defects

Macrognathia
 Abnormally large jaws
 Pituitary gigantism – both jaws
 Maxillary enlargement – Paget’s disease, Leontiasis
ossea, Cherubism.
 Mandibular enlargement – Acromegaly.
Treatment
 Surgical correction of defect.

Facial hemihypertrophy /
hyperplasia
 Characterized by asymmetric overgrowth of one or
more body parts.
 Etiology
 Hormonal imbalance
 Incomplete twinning
 Chromosal abnormalities
 Lymphatic abnormalities
 Vascular abnormalities
 Neurogenic abnormalities.

Syndromes associated

Clinical features

 Treatment
• Cosmetic repair
 Differential diagnosis
• Neurofibromatosis
• Fibrous dysplasia

Facial hemiatrophy / Parry
Romberg Syndrome
 Slowly progressive atrophy of the soft tissue of
essentially half the face – progressive wasting of
subcutaneous fat, accompanied by atrophy of skin,
cartilage, bone, muscle.
 May spread to one side of neck & body.

 Etiology
 Cerebral disturbances leading to increased &
unregulated activity of sympathetic nervous system.
 Trauma
 Infection
 Hereditary
 Peripheral trigeminal neuritis
 Localized scleroderma

Clinical features
 Atrophy of skin, subcutaneous tissue, muscle,
bone & cartilage on affected side.
 Begins in 1st
decade & lasts for 3years before
becomes quiscent.
 Basilar kyphosis.
 Misshapen ear or small ear.
 Dark pigmentation of affected side.
 Trigeminal neuralgia, facial parathesia.

oral manifestations
 Atrophy of half lip & tongue
 Shorter ramus & body of mandible resulting in
malocclusion.
 Delayed eruption of teeth on affected side.
Treatment
 A new technic for the treatment of facial hemiatrophy
(Romberg's disease) in children with multiple
subcutaneous injections of dimethylpolysiloxane has
been highly satisfactory. The technic is investigative in
nature and will remain so for several years.
 Surgical corrections.

of tongue
• Microglossia
• Macroglossia
• Tongue tie

Microglossia
 May be mild and difficult to detect to
aglossia
(very rare).
 May be a presence of rudimentary or small
tongue

Macroglossia
 Caused by a wide variety of conditions.
 Congenital and hereditary: vascular
malformations (lymphangioma and
hemangioma), hemihyperplasia, cretinism,
Beckwith-hypogycemic syndrome, down
syndrome,
 Acquired; amyloidosis, myxedema, acromegaly,
angioedema, tumors.

Tongue tie
 Tongue -Tie (Ankyloglossia) is a problem caused
by abnormal development of the tongue.It is a
congenital condition, in which the tongue is tied
down to the floor of the mouth. The tongue is
normally connected to the floor of the mouth by a
thin cord, called a frenum.
 With tongue-tie the frenum is too short and thick. It
prevents the tongue from moving freely.
 Effect of Tongue-Tie (Ankyloglossia)
 Ankyloglossia in breastfeeding infants can cause
ineffective latch, inadequate milk transfer, and
maternal nipple pain, resulting in ultimately weaning.
It also causes the speech problem and there is
difficulty in swallowing.

Treatment
 Frenotomy – The lingual frenum is given a cut to
release the tongue
 Frenectomy – Removal of frenum
 Revision of the frenum by laser without a
general anaesthetic.
 Revision by electrocautery using a local
anaesthetic.

Developmental anomalies of
ear
 Microtia
 Auditory canal atresia.

Microtia
 Microtia is a developmental abnormality in which the
external part of the ear (the pinna or auricle) has not
fully developed. There are varying degrees of microtia
depending on how well developed the auricle is. The
degree of auricle development can range from simply
a small ear that has all the proper cartilage (grade I) to
a small "nubbin" or peanut ear that has no cartilage
and only a mound of skin and soft tissue (grade III).
Rarely, people are born without an auricle, a condition
called anotia.

Treatment
A plastic surgeon skilled in microtia repair can often
rebuild the auricle to a very favorable appearance using
a prosthesis, the person's own rib cartilage, or an
implant.

Auditory canal atresia
 Auditory canal atresia is the partial or total failure of
the ear canal to develop. Absence of the ear canal is
usually associated with absence of the eardrum
(tympanic membrane) and underdevelopment of the
middle ear and middle ear bones (hammer, anvil, and
stirrup). Children with auditory canal atresia have
hearing loss because sound is not efficiently carried,
or conducted, into the middle and inner ear. Usually
the inner ear (cochlea) is healthy and normally
developed in these children.

Treatment
 In some children, doctors can
surgically open the ear canal, build an
eardrum, and restore the natural
sound-conducting pathway of the ear
canal and middle ear to the healthy
inner ear. Although surgical correction
of auditory canal atresia, called
canalplasty, can improve hearing, it
seldom results in normal hearing at all
pitches (frequencies) of sound.

of eye
 Anopthalmia & Micropthalmia.
 Colombomas.

Anopthalmia &
Micropthalmos Complete failure of eye development is
extremely rare. Only histologic examination can
differentiate between true anophthalmia and
severe microphthalmia. In cases of
microphthalmia, ocular structures are identified,
whereas they are absent in primary
anophthalmia. Microphthalmos is considered
simple or pure when the eye is small but
anatomically correct, and complex when the eye
is malformed

Treatment (anopthalmia)
 Inflatable expander
 Self expanding hydrophilic, osmotic expanders.
 Injectable calcium hydroxylapatite
 Eyelid surgery

Treatment (micropthalmia)
Conformer expansion therapy

Colombomas
 Colobomas The term coloboma is of Greek origin
meaning curtailment and is used in ophthalmology to
refer to defects in ocular structures. Those colobomas
that result from failure of the embryonic.
 choroidal fissure to close properly are classified as
typical colobomas. Colobomas are common
malformations, constituting about 2% of all congenital
abnormalities. They are usually bilateral. A variant of
typical coloboma of the disc is designated the morning
glory syndrome, because in this malformation the optic
disc is posteriorly displaced at the apex of a funnel-
shaped staphylomatous excavation. This configuration
is thought to resemble the flower.

Treatment
 There is no proper treatment .
 Use of contact lens can be done.

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