Development of face and oral cavity 4/ oral surgery courses

DEVELOPMENT OF FACEDEVELOPMENT OF FACE
AND ORAL CAVITYAND ORAL CAVITY
INDIAN DENTAL ACADEMY
Leader in continuing Dental Education
www.indiandentalacademy.com

 Embryology : it is the study of the formation &
development of the embryo from the moment of
its inception up to the time when it is born as an
infant.
 The development of new individual begins at the
moment when one spermatozoon (male gamete)
meets & fuses with one ovum(female gamete).This
process is known as fertilization.
 Fertilization normally occurs in the ampullary
uterine tube, probably with in 24 hours of
ovulation. The fertilized ovum is called zygote.

 After completion of the second maturation
division, the zygote divides into 2
blastomeres of approximately equal size.
By repeated division & sub division of the
blastomere a mulberry shaped mass of cells
called morula forms. The human morula is
believed to enter the uterus at about 8-12
cell stage & about 72 hours after
fertilization.

 Formation of blastocyst: before zonapellucida
disappears, the fluid either secreted by the
trophoblastic cells or derived from the uterine
lumen ,begins to accumulate with in the morula.
This cavity is largely bound by mural trophoblast
cells except at one place where a clump of cell
mass projects into the cavity.
 The segmenting zygote has now been converted
into a unilaminar blastocyst. This is formed by the
end of 4th
or beginning of 5th
day after ovulation &
lies free in the uterine cavity.
 Within blastocyst 2 cell population can now be
distinguished i) trophoblast-lining the cavity
ii)embryoblast-small cluster of cells with
in the cavity forming inner cell mass.

The embryoblast cells forms embryo proper
& trophoblast cells are associated with
implantation of the embryo & formation of
placenta.
The cells of embryoblast rapidly
differentiate into 2 layers so that at about 8
days an outer ectodermal & inner
endodermal layer can be distinguished in
the bilaminar germ disk, resulting in the
formation of 2 cavities on either side of the
disk.

 During 3rd
week of development the bilaminar
embryonic disk is converted to a trilaminar disk
as follows, the floor of the amniotic cavity is
formed by ectoderm & with in it a structure called
the primitive streak develops forming the floor of
the amniotic cavity.
 primitive streak is a narrow groove with slight
bulging areas on either side. The head end of the
streak finishes in a small depression called the
primitive node or pit.
 At the node cells of ectoderm layer divide &
migrate between the ectoderm & endoderm to
form a solid column of cells that pushes forward
in as far as the prochordial plate. Through
canalization of this cord of cells the notochord is
formed to support the primitive embryo.www.indiandentalacademy.com

Else where alongside the primitive streak,
cells of ectodermal layer also divide &
migrate toward the streak, where they
invaginate & then spread laterally between
the ectodermal & endodermal layer to form
mesodermal layer.

 The nervous system develops as a thickening with
in the ectodermal layer at the head end of embryo
called neural plate. This rapidly forms raised
margins called as neural folds.
 The neural folds eventually fuse so that neural
tube separates from ectoderm forming the floor of
amniotic cavity.
 From neural tube the brain & spinal cord
develops.
 A group of cells differentiating at the lateral aspect
of the neural plate is called neural crest cells.
They have the capacity to differentiate
extensively giving rise to number of structures like
sensory ganglia, sympathetic neurons, schwann
cells, meninges & the cartilage of brachial arch.

In dental context the proper migration of
neural crest cells is essential for the
development of teeth & face. In Treacher
Collins syndrome full facial development is
prevented by interference in the migration
of neural crest cells to the facial region.

 Folding of the embryo
in 2 planes along
caudocephalic axis &
the lateral axis is
crucial.
 The head fold is
crucial in the
formation of the
primitive
stomatodeum(oral
cavity)

EMBRYOLOGY OF THE HEAD,EMBRYOLOGY OF THE HEAD,
FACE & ORAL CAVITYFACE & ORAL CAVITY
BRANCHIAL ARCHES & PRIMITIVE
MOUTH- When the stomatodeum first
forms, it is delimited above by the neural
plate & caudally by the developing cardiac
plate. It is separated from the fore gut by the
buccopharyngeal membrane, which soon
breaks down so that the stomatodeum
communicates with fore gut. Laterally the
stomatodeum becomes limited by first pair
of pharyngeal arches.

 The branchial arches form in the pharyngeal wall as a
result of proliferation of the lateral plate mesoderm
in the region reinforced by migrating neural crest
cells that eventually predominate.
 6 cylindrical thickenings thus form( 5th
arch is
transient structure in humans) that expand from the
lateral wall of the pharynx, pass beneath the floor of
the pharynx & approach their counterpart on the
opposite side. By this arches progressively separate
the primitive stomodeum from the developing heart.
 The arches are clearly seen as bulges on the lateral
aspect of embryo & are externally separated by small
clefts called branchial grooves. On the inner aspect
of pharyngeal wall are small depressions called
pharyngeal pouches.

Each branchial arch consists of an
ectodermal exterior,mesenchymal core & an
endodermal interior.
The mesenchyme produces a presumptive
skeletal elements which subsequently
chondrifies either wholly or partly. Much of
the remainder of the core of mesenchyme
becomes striated muscle which usually
migrate & may loose connection with
skeletal elements in arches. The identities of
the muscle mass where they assume new
function can nevertheless be inferred by
reference to their nerve supply.

 Branchial arch cartilage: the initial skeleton of
the branchial arches develop from the
mesenchymal tissues as cartilage bars. In the first
arch bilateral meckel`s cartilage arise. Malleus &
incus develop & ossify at the dorsal end of
meckel` cartilage. The rest of meckel`s cartilage
disappears which leaves part of the
perichondrium as the sphenomalleolar ligament &
spheno mandibular ligament.
 In the second arch reichert`s cartilage develop. It
gives rise to stapes ,styloid process, lesser horn &
upper part of body of hyoid bone. Stylohyoid
ligament is formed by the perichondrium at the
site of disappearance of this second arch cartilage.


Third arch cartilage- forms greater horn &
lower part of the body of hyoid.
Fourth arch cartilage – forms greater horn
& lower part of the body of the hyoid bone.
Sixth arch cartilage- forms laryngeal
cartilage.

 Branchial arch vasculature- Each of 5 branchial
arches contains a pair of blood vessels that
conduct blood from the heart dorsal through the
arch tissues to the brain & to the posterior regions.
These are called aortic arches.
 The anterior right & left aortic arches develops
first & after a week begin to disappear as more
posterior arches develop.
 The posterior arch vessels then enlarge & mature.
 Fifth arch vessels disappear next.
 3rd
,4th
& 6th
arch vessels are important in function.

 3rd
arch arteries become common carotid arteries;
4th
arch vessels become dorsal aorta which supply
blood to entire body. 6th
arch vessels supply blood
to lungs.
 By 5th
week , the 1st
& 2nd
branchial arch vessels
have disappeared & then the blood supply to the
face is carried by the 3rd
branchial artery( which
becomes common carotid artery) which gives rise
to external & internal carotid artery.
 The External carotid artery supplies blood to the
ventral part of the 1st
& 2nd
branchial arches
 The Internal carotid artery gives blood supply to
brain.

 In the region of the ear the internal carotid artery
gives rise to small vessel called the Stapedial
artery, which supplies most of the blood to the
upper face & palate.
 Shift in blood supply to the face-in the 7th
week the
stapedial artery suddenly occludes & separates
from the internal carotid artery, which thus
discontinues its blood supply to the face & palatal
tissues. Many of the terminal branches fuse with
ECA`s peripheral vessels. This results in the most
unusual shift in the blood of face from ICA to
ECA . This occurs in 7th
week which is an
important period of rapid growth expansion &
fusion of facial process.

 Timing of this process is important as the
vessels begins to degenerate at one site &
rapidly expands at other , if timing is not
precise there will be a period when the face
is deprived of oxygen & nutrition.
 Since development of lip & palate will be
maximum at this time any discrepancy in
supply of oxygen & nutrition will result in
cleft lip ,cleft palate or both.

 Fate of grooves & pouches:
The 1st
groove & pouch are involved in the
formation of external auditory meatus , tympanic
membrane,tympanic antrum, the mastoid antrum & the
pharyngotympanic and eustachian tube.
 2nd
, 3rd
4th
grooves are normally obliterated by overgrowth
of 2nd
arch, but sometimes they persist as cervical sinus.
 The 2nd
pouch is also obliterated by the development of
palatine tonsil.
 The 3rd
pouch expands dorsally & ventrally into 2
compartments . The dorsal component gives origin to
inferior parathyroid gland. While the ventral component
forms thymus gland.
 4th
pouch- dorsal component forms superior parathyroid
glands-ventral component forms Para follicular cells of
thyroid . www.indiandentalacademy.com

FORMATION OF THE FACEFORMATION OF THE FACE
Early development of face is dominated by the
proliferation & migration of ectomesenchyme
involved in the formation of primitive nasal
cavity.
At about 28 days , localized thickening
develops with in the ectoderm of the frontal
prominence, just above the opening of
stomatodeum.these thickenings are NASAL
PLACODES.

Rapid proliferation of underlying
mesenchyme around the placode produce a
horse shoe shaped ridge that converts the
placode into NASAL PIT.
The lateral arm of the horseshoe is called
LATERAL NASAL PROCESS & the medial
arm the MEDIAL NASAL PROCESS.
Between the 2 nasal process is the depressed
area of frontonasal process
The medial nasal process with frontonasal
process forms middle portion of nose, mid
portion of upper lip, anterior portion of
maxilla & primary palate.

The maxillary process grows medially &
approaches both the lateral & medial nasal
process, but remain separated from them by
distinct grooves.
The medial growth of maxillary process
pushes the medial nasal process toward the
midline, where it fuses with its anatomic
counterpart from the opposite side. In this way
the upper lip is formed from the maxillary
process & the medial nasal process.

Development of teethDevelopment of teeth
The face develops between 24-38 days. By this
time it is already possible to distinguish some of
the epithelium covering the facial processes as
odontogenic or tooth forming.
On inferior border of maxillary process & the
superior border of the mandibular arch where
the lateral margin of the stomatodeum is
formed,the epithelial begins to proliferate &
form thickening as ODONTOGENIC
EPITHELIUM.

These bands of epithelial are roughly horse
shoe shaped & correspond in position to the
future dental arches. This band very quickly
gives rise to vestibular lamina & dental
lamina.

 Vestibular lamina: vestibule forms as a result of the
proliferation of vestibular lamina into the
ectomesenchyme. Its cells rapidly enlarge & then
degenerate to form a cleft which becomes the
vestibule between the cheek & the tooth bearing area.
 Dental lamina: with in dental lamina , continued &
localized proliferative activity leads to the formation
of a series of epithelial ingrowths into the
ectomesenchyme, at sites corresponding to the
positions of the future deciduous teeth.
 from this point the tooth development
proceeds in 3 stages- bud,cap & bell stages.

 BUD STAGE:
represented by the first
epithelial incursion
into the
ectomesenchyme of
the jaw. The
epithelium shows little
change. The
supporting cells are
closely packed
beneath lining
epithelium around the
epithelial bud.

 CAP STAGE: as epithelial bud continues to
proliferate into the ectomesenchyme , cellular density
increases immediately adjacent to the epithelial
ingrowth & results from a local group of cells failing
to produce extra cellular substance & not separating
from each other. The epithelial ingrowth which
superficially resembles a cap sitting on a ball of
condensed ectomesenchyme, is called as DENTAL
ORGAN
 The ball of condensed ectomesenchymal cells called
DENATL PAPILLA forms dentin & pulp. The
condensed ectomesenchymal cells limiting the dental
papilla & enclosing the dental organ is known as
DENTAL FOLLICLE- gives rise to the supporting
structures of tooth.

 BELL STAGE: continued growth of tooth germ leads
to bell stage – called so because the dental organ
comes to resemble a bell as the under surface of
epithelial cap deepens.
 As growth takes place histo differentiation takes place.
 The cells in the center of the dental organ continue to
synthesize & secrete glycosaminoglycans into the
extra cellular compartment- these are hydrophilic –so
absorb water into the dental organ- increase in the
volume of extra cellular compartment-cells are forced
apart. Since cells retain their connection with each
other through their desmosomal contacts they become
star shaped- called as stellate reticulum.

 At the periphery of dental organ cells assume a cuboid
shape & form external dental epithelium.
 The cells adjacent to dental papilla assume a short
columnar shape & are characterized by high glycogen
content, they are known as inner dental epithelium.
 Between inner dental epithelium & stellate reticulum
the epithelial cells differentiate into a layer of flattened
cells – stratum intermedium which is characterized by
high activity of the enzyme alkaline phosphatase.
 Stratum intermedium along with inner dental
epithelium is responsible for enamel formation.
 Inner dental epithelium along with external dental
epithelium forms cervical loop at the rim of dental
organ.

2 important events takes place during bell
stage-i) the dental lamina joining the tooth
germ to the oral epithelium breaks up into
discrete island of cells,thus separating the
developing tooth from the oral epithelium
 ii) the internal dental epithelium folds
making it now possible to recognize the shape
of the future crown pattern of tooth.

 ROOT FORMATION: epithelial cells of dental
organ proliferate to from the cervical loop of
dental organ to form a double layer of cells known
as hertwigs epithelial root sheath.
 This sheath of epithelial cells grows around the
dental papilla between papilla & follicle, until it
closes all but the basal portion of the papilla. The
rim of this root sheath, the epithelial diaphragm
encloses the apical foramen.
 As the root sheath progressively moves
downward they initiate the differentiation of
odontoblasts from the cells at the periphery of
dental papilla.

Development of facialDevelopment of facial
musclesmuscles
 During 5th
& 6th
weeks myoblasts with in the
mandible arch begin proliferation. The muscle
cells become oriented to the sites of origin &
insertion of the masticatory muscle which they
will form
 By 7th
week the mandible muscle mass has begun
to differentiate into the 4 muscles of mastication
 Muscle cell migration occurs prior to the time that
the skeletal ossification centers of mandible begin
to appear.

 At 7th
week muscle cells with in the hyoid arch
undergo proliferation & muscle cells in occipital
myotomes have begun proliferation & anterior
migration toward the floor of the mouth to become
the muscles of the tongue.
 Muscle cells of hyoid arch continue migration over
the mandible muscle mass & by 10th
week have
migrated up over the face. These muscle cells forms
a thin sheet as they extend up over the face, with one
group of cells extending anterior to the ear & a 2nd
group extending posterior to it. They initially follow a
path like the location of platysma muscle up the side
of the neck over the mandible.

 Innervation : Trigeminal nerve supplies sensory
fibers to the mandible & maxilla, motor fibers to
the 4 muscles of mastication & to the mylohyoid,
tensor palatini, tensor tympani& anterior belly of
digastric.
 The facial nerve follows the migration of facial
muscle mass from neck onto the face, where loop
of motor nerve will be distributed to these
muscles. This nerve also supplies stylohyoid,
stapedius & posterior belly of digastric.
 Glossopharyngeal nerve supplies the
stylopharyngeal & upper pharyngeal muscles.
 Vagus supplies the pharyngeal constrictor &
laryngeal muscles.

Formation of the palateFormation of the palate
 Initially there is a common oronasal cavity occupied
by tongue & only after the development of the palate
there is distinction between oral & nasal cavity.
 Palate develops from 3 parts-one medial & 2 lateral
palatine process. The medial palatine process is also
called primary palate. Lateral palatine process forms
secondary palate.
 At the end of 6th
week the lateral palatine process
which forms the secondary palate develops from the
mesial edges of the maxillary process that bound the
stomodeum.

The lateral palatine process grow medially first &
then grow downward or vertically on either side
of the tongue. At this stage of development the
tongue is narrow & tall almost completely filling
the oronasal cavity.

 Shelf elevation: at about eight & half week of
IUL the lateral palatine shelves slide or roll over
the body of the tongue. The process of elevation of
secondary palate involves an intrinsic force in the
palatal shelves whose nature has not yet been
determined.
 The high glycosaminoglycan content of the
shelves which attract water & makes the shelf
turgid & presence of contractile fibroblasts in the
palatal shelves has been suggested as intrinsic
force in palatal closure. Another factor in the
closure of secondary palate is the displacement of
the tongue from between the palatal shelves by the
growth pattern of head.

 For fusion of palatal shelves to occur it is
necessary to eliminate their covering epithelium.
As the 2 palatal shelves meet ,there is adhesion of
the epithelium so that the epithelium of one shelf
becomes indistinguishable from that of the other
& a midline epithelium seam forms.
 To achieve fusion there is cessation of DNA
synthesis with in the epithelium some 24-36
hours prior to epithelium contact.
 Surface epithelium cells are sloughed off & basal
cells are exposed. These basal epithelial cells have
carbohydrate rich surface coat that permits ready
adhesion & the formation of junction to achieve
fusion of the process.

The midline seam thus formed should be
removed to permit ectomesenchymal
continuity between fused process. Even
though epithelial cells of seam divide
growth of the seam fails to keep pace with
palatal growth so that the seam first thins to
a single layer of cells & then breaks up into
discrete islands of epithelial cells & the
surrounding basal lamina is lost & the
epithelial cells assume fibroblast like
features.

Formation of tongueFormation of tongue
Tongue begins to develop at about 4 weeks .
First tuberculum impar arises in the midline in
mandibular process & is flanked by 2 lingual
swellings.
Very quickly the lateral lingual swellings
enlarge & merge with each other &
tuberculum impar to form a large mass from
which the mucous membrane of the anterior of
tongue is formed.

 The root of the tongue is formed by hypobranchial
eminence, a large midline swelling developed
from the mesoderm of the third arch. The
hypobranchial eminence gives rise to the mucosa
covering the root, posterior 1/3rd
of the tongue.
 Hypobranchial eminence can be divided into
i) anterior copula which gives origin to the mucosa
covering the root of the tongue
 ii) hypobranchial eminence which give rise to
epiglottis.
 Tongue separates from the floor of the mouth by
downward growth of ectoderm around its
periphery which subsequently degenerates to form
the lingual sulcus & gives the tongue the mobility.

The muscles of tongue arise form occipital
somites which have migrated forward into
the tongue area carrying with them
hypoglossal nerve. This unusual
development of tongue explains the nerve
supply of the tongue. Since the anterior 2/3rd
is derived from the first arch it is supplied
by fifth cranial nerve.
Posterior 1/3rd
is supplied by
Glossopharyngeal nerve
Motor supply is through hypoglossal nerve.

Development of mandibleDevelopment of mandible
 Meckels cartilage forms the lower jaw in primitive
vertebrates. In humans it has close positional
relationship to the developing mandible but makes
no contribution to it.
 At 6 weeks of development this cartilage extends as a
solid hyaline cartilaginous rod, surrounded by a fibro
cellular capsule, from the otic capsule to the midline
of the fused mandibular process.
 The cartilage of each side do not meet each other at
midline but are separated by a thin band of
mesenchyme.

 The mandibular branch of fifth cranial nerve is
closely associated with Meckels cartilage, where
in the inferior alveolar nerve & lingual nerve run
along the lateral & medial aspect of the cartilage.
 On the lateral aspect of Meckels cartilage, during
6th
week of development –a condensation of
mesenchyme occurs in the angle formed by
division of inferior alveolar nerve & its incisive &
mental branches.
 At 7 week intramembranous ossification begins in
this condensation forming the first bone of
mandible.from this center of ossification bone
formation spreads rapidly both anteriorly &
posteriorly.

 In anterior aspect this new bone formation occurs
along the lateral aspect of Meckels cartilage, forming
a trough consisting of lateral & medial plates that
unite beneath incisive nerve.
 The trough of bone extends to the midline, where it
comes into close approximation with a similar trough
formed in the adjoining mandibular process. These 2
separate centers of ossification remain separate until
shortly after birth. The trough is converted into a
canal as bone forms over the nerve joining the lateral
& medial plate.
 Similarly extension of ossification continues
backward until it reaches the point of division of
mandibular nerve into inferior alveolar & lingual
nerve.

From inferior alveolar canal medial & lateral
alveolar plates develop in relation to the
forming tooth germs, so that the tooth germs
occupy a secondary trough of bone.
This trough is partitioned ,thus teeth occupies
individual compartment,which finally become
totally enclosed by growth of bone over the
tooth germ. In this way body of mandible is
formed.

 The ramus of mandible develops by a rapid spread of
ossification backward into the mesenchyme of the first
arch,diverging away from meckel`s cartilage. This
point of divergence is marked by lingula in the adult
mandible.

 Thus by 10 week the rudimentary mandible is
formed entirely by membranous ossification. The
fibrocellular capsule of meckel`s cartilage persists
as sphenomandibular ligament. In the ear region
the cartilage forms the malleus of inner ear &
spheno lamellar ligament.
 The further growth of mandible until birth is
strongly influenced by the appearance of 3
secondary growth cartilage & the development of
muscular attachments.
 The secondary growth cartilage are – condylar
cartilage, coronoid cartilage & the symphysial
cartilage.

 Condylar cartilage appears during the 12th
week of
development & rapidly forms a cone or carrot shaped
mass that occupies the most of developing ramus. This
mass of cartilage is quickly converted into bone by
endochondral ossification so that at 20 week only a thin
layer of cartilage remains in the condylar head.

The coronoid cartilage appears at about 4
months of development, surmounting the
anterior border & top of the coronoid
process. It is relatively transient cartilage &
disappears before birth.
The symphysial cartilage are 2 in number,
appears in the connective tissue between 2
ends of Meckels cartilage & is obliterated
with in 1st
year of birth.
 Coronoid process develops in response to
the insertion & function of temporalis
muscle.

Development of maxillaDevelopment of maxilla
 Maxilla develops from center of ossification in the
mesenchyme of 1st
arch. No arch or primary cartilage
exists in the maxillary process, but the center of
ossification is closely associated with the cartilage of
the nasal capsule.
 The center of ossification appears in the angle
between division of anterior superior dental nerve &
infra orbital nerve.
 From this center the bone formation spreads
backward below the orbit toward the developing
zygoma & forward towards the future incisor region.

 Ossification also spreads upward from this
extension to form frontal process. As a result of
this a bony trough forms for inferior orbital nerve.
From this trough a downward extension of bone
forms the lateral alveolar plate for maxillary tooth
germs. Ossification also spreads into the palatine
process to form the hard palate.
 The medial alveolar plate develop from the
junction of palatal process & the main body of the
forming maxilla. This plate together with lateral
counter part forms a trough of bone around
maxillary tooth.

A second cartilage also contributes to the
development of maxilla. A zygomatic or
malar cartilage appears in the developing
zygomatic process & for a short time adds
considerably to the development of maxilla.
At birth the frontal process of maxilla is
well marked ,but the body of maxilla
consists of little more than the alveolar
process containing tooth germs & small
zygomatic & palatal process.

POST NATAL GROWTH OFPOST NATAL GROWTH OF
FACEFACE
THEORIES OF GROWTH-
a) sutural dominance theory by sicher
b)Scott hypothesis
c) moss hypothesis

SICHER says that major development occurs due
to intrinsic genetic factors, with only modeling
resorptive and depository changes under the
influence of muscles and other environmental
factors. He says that primary event in the sutural
growth is proliferation of connective tissue
between two bones.

 Scott hypothesis- emphasizes that intrinsic growth
controlling factors are present in the cartilage and in the
periosteum , with sutures being only secondary and
dependant on extra sutural influence. He says that
cartilagenous parts of the skull must be recognized as
primary centers of growth, with nasal septum being a
major contributor in maxillary growth.

 Moss hypothesis- he emphasizes that osseous growth of
the skull is entirely secondary. Based on the functional
cranial component theory, moss supports the concept of
functional matrix, where in growth of bone is largely
dependant on the growth of bone,

LIMBORGH states that
 growth of synchondroses & the ensuing
endochondral ossification is almost exclusively
controlled by intrinsic genetic factors.
 the intrinsic factors controlling intra membranous
bone growth are small in number & of general
nature.
Cartilagenous skull parts must be seen as growth
centers.
Extent of periosteal bone growth largely depends
on the growth of adjacent structures.

GROWTH OF CRANIUMGROWTH OF CRANIUM
Cranial base grows primarily by cartilage
growth in sphenoethmoidal, inter
sphenoidal, spheno occipital & intra
occipital synchondroses.
Activity at intersphenoidal synchondroses
disappears at birth, the intra occipital
synchondroses closes in 3rd
– 5th
year of life.
Spheno occipital synchondroses is a major
contributor of growth & it continues upto
20 year of life.

GROWTH OF MAXILLAGROWTH OF MAXILLA
Cranial base influences the development of
maxilla, the position of which is dependant on
growth at spheno occipital & spheno ethmoidal
synchondroses.
During maxillary growth 2 changes occurs
 I) translation- brought by endochondral
ossification at cranial base
II) transposition – brought by intra membranous
ossification of maxilla.

 A major factor in the increase of height of maxilla is
the continued apposition of alveolar bone on the free
borders of the alveolar process as teeth erupts.
 Palatal growth follows principle of expanding V. The
buccal segments move downwards & outwards.
 Bone deposition also occurs along the posterior margin
of the maxillary tuberosity. This increases the antero
posterior dimension of entire maxillary body. Along
with this increase the zygomatic process moves in
posterior direction. The face simultaneously in breadth
by proportionate bone apposition on the lateral surface
of the zygomatic arch with corresponding resorption
from medial surface

 The palatine process of maxilla grow in
downward direction by a combination of
surface deposition on the oral side of the
palate with resorptive removal from the
opposite nasal side .
 The post natal growth of maxilla is similar to
mandible in that forward & downward
movement of the growing bone is caused by
growth which takes place in a posterior
direction with corresponding repositioning of
the entire bone in a forward course.

GROWTH OF MANDIBLEGROWTH OF MANDIBLE
 At birth the 2 rami of mandible are short, condylar
development is minimal . A thin line of fibro cartilage
exist at the midline of the symphysis to separate the
left & right halves of mandible.
 Between 4 months & I year the symphyseal cartilage
is replaced by bone.
 During first year appositional growth is especially
active at alveolar border, at the distal & superior
surface of the ramus, along the lower border of the
mandible & on its lateral surface.

 CONDYLAR GROWTH –endochondral growth occur at
condyles with differentiation & proliferation of hyaline
cartilage & its replacement by bone . The hyaline cartilage
of bone is covered by a dense & thick fibrous connective
tissue layer . This is protect the prechondroblastic layer in
the neck of the condyle which is under constant pressure.

Mandibular growth after 1st
year of life becomes
selective . The condyle shows considerable
activity as the mandible moves & grows
downward & forward.
 Growth of condyle along with apposition of
bone on its posterior border of ramus contributes
to the length of the mandible & alveolar growth
contributes to the height.
Width of mandible is increased by expansion of
posterior part of mandible in an expanding V
pattern.

Applied aspects of growth andApplied aspects of growth and
developmentdevelopment
Disturbances during gastrulation-
 The beginning of 3rd
week of development ,
when gastrulation is initiated is a highly sensitive
stage, during which foetus is susceptible for
various teratogens. For example high doses of
alcohol kills cells in the anterior midline of the
germ disc, producing a deficiency in the midline
in the craniofacial structure and resulting in
holoprosencephaly, where in the fore brain is
small and eyes are closer together.

 Some times remnants of the primitive streak persist in
the sacro coccygeal region. These cluster of pluripotent
cells proliferate and form sacro coccygeal teratomas that
commonly contain tissues derived from all the 3 germ
layers.

 Teratogens- These are factors that cause birth defects.
Various types of teratogens like infectious agents,
physical agents, chemical agents are there.

Fetal alcohol syndrome- caused by maternal
alcohol ingestion. Neural tissue more sensitive.

 Neural crest cells & cranio facial defects-
neural crest cells are essential for the formation of
much of the craniofacial region. Since neural crest cells
also contribute to the conotruncal endocardial cushions
which separate the out flow tract of the heart into
pulmonary and aortic channels, hence infants having
craniofacial defects also have cardiac abnormalities like
persistent ductus arterioses, tetralogy of fallot and
transposition of great vessels.
Neural crest cells are vulnerable to teratogens because
they lack super oxide dismutase and catalse enzyme
which are responsible for scavenging free radicals.
In some cases cranial vault fails to form (cranioschisis)
and brain tissue exposed to amniotic fluid degenerates
leading to anencephaly.

 Treacher Collins syndrome- craniofacial defect
involving crest cells. The main cause for this is thought
to be defect in stapedial artery, which results in defective
stapes and incus, also the failure of inferior alveolar
artery to develop an ancillary vascular supply gives rise
to mandibular abnormalities. Improper orientation and
hypoplasia of the mandibular elevator muscles resulting
from an aplastic or hypo plastic zygomatic arch, may also
be contributory.
 Clinical features include various degrees of hypoplasia
of the mandible, maxilla, zygomatic process of the
temporal bone, external & middle ear. Abnormalities of
medial pterygoid plates & hypoplasia of the lateral
pterygoid muscles are common. Patients have bird like or
fish like face.

 Notched linear colobomas of outer one third of
eyelids, anti mongoloid obliquity, congenital
atresia of the external auditory canal, deformed or
absent pinnae, conductive hearing loss, atypical
hair growth, cleft palate, macrostomia, high arch
palate and malocclusion with apertognathia is seen

 Robin sequence – cranio facial defect involving
crest cells where in first arch structures are
severely affected. Affected infants have a triad of
micrognathia, cleft palate and glossoptosis.
 this sequence may be genetic or environmental.
This may also result from deformation like when
chin is compressed against the chest in cases of
oligohydramnious.
 The primary defect includes poor growth of
mandible as a result posteriorly placed tongue that
fails to drop from between the palatal shelves,
preventing their fusion.

Di George sequence-( 3rd
& 4th
pharyngeal pouch
syndrome)- includes hypoplasia or absence of
thymus ( because crest cells contribute to the
connective tissue stroma of the gland) and para
thyroid gland with or with out cardiovascular
defects, abnormal external ear, micrognathia and
hyper telorism( wide spaced eyes). Patient with
complete Di George sequence have
immunological problems, hypocalcaemia, and
poor prognosis.

Hemifacial microsomia-( goldenhar syndrome)-
craniofacial abnormalities that involve the maxilla,
temporal and zygomatic bone, which are small and
flat. Ear , eye , vertebral defects are commonly
observed.

 Cleido cranial dysplasia- it is notable for aplasia or
hypoplasia of the clavicles,cranio facial malformation
and the presence of supernumerary and unerupted teeth.
It is inherited as autosomal dominant trait,
intramembranous and endochondral bones in the skull
are affected, resulting in sagitally diminished cranial
base, transverse enlargement of the calvarium, delayed
closure of the fontanelles and sutures, complete or
partial absence of clavicles.
 The head is large and brachycephalic, prominent
frontal ,parietal and occipital bossing, facial bones and
Para nasal sinuses are hypoplastic, giving the face short
and small appearance. Maxillary hypoplasia gives
mandible relative prognathic appearance, the palate is
narrow and high arched.

Delayed or failed eruption of the teeth has been
associated with lack of cellular cementum. The
formation of supernumerary teeth is due to
incomplete or severely delayed resorption of the
dental lamina. Extreme delay in physiologic root
resorption of the primary teeth occurs, eruption of
permanent teeth is severely delayed.

 Crouzon’s syndrome- characterized by variable cranial
deformity, maxillary hypoplasia and shallow orbits with
exophthalmoses. Craniosynostosis results when premature
fusion of the cranial sutures occurs. The premature closure
of these sutures can initiate changes in the brain secondary
to increased intra cranial pressure. The character of cranial
deformity depends on the sutures affected, the degree of
involvement and the sequence of sutural fusion. Increased
interpupillary distance and exophthalmoses are constant
features. The face is described as froglike , mid face
hypoplasia is seen. Patient have relative mandibular
prognathism, with the nose resembling parrots beak. Upper
lip and philtrum are short, severe maxillary hypoplasia with
compressed and high arch palate is seen. Bilateral posterior
lingual cross bite and anterior open bite are common.www.indiandentalacademy.com

 Down syndrome- common and recognizable chromosome
aberration, caused by non disjunction resulting in an extra
chromosome. Skull is brachycephalic with flat occiput and
prominent fore head. Sagittal suture separation greater than
5 mm present in 98% of affected individuals.maxillary sinus
is hypoplastic, mid face skeletal deficiency is quite marked,
relative mandibular prognathism seen.tongue is fissured,
macroglossia( both true & relative) is seen. An open mouth
posture because of narrow nasopharynx and hypertrophied
tonsils causing airway blockage. Drying and cracked lips
seen. Palatal width and length are significantly decreased &
a bifid uvula & cleft lip & cleft palate seen. Increased
concentration of sodium, calcium, phosphate ion have been
seen in parotid gland. Periodontal disease is more common,
because of defective immune system & neutrophil motility
defect.

Eruption of teeth delayed, abnormalities in eruption
sequence, hypodontia, microdontia, enamel
hypocalcification seen. Occlusal disharmonies
consisting of mesiocclusion due to relative
prognathism, posterior cross bite, apertognathia,
severe crowding of the anterior teeth are common.
Posterior cross bites are of maxillary basal bone
origin, where as anterior open bite are due to dento-
alveolar origin.

Birth defects involving pharyngeal region
Ectopic thymic & parathyroid tissue- Since the
glandular tissue derived from the pouches undergo
migration, the presence of accessory glands or
remnants of glandular tissues along the path of
migration is common. This is common with
thymic tissue & parathyroid glands. Inferior
parathyroid are more variable in position than
superior ones and are some times found at the
bifurcation of common carotid artery.

Branchial fistula- occurs when 2nd
pharyngeal arch
fails to grow caudally over the 3rd
& 4th
arches,
leaving remnants of the 2nd
,3rd
,4th
clefts in contact
with the surface by a narrow canal. These fistulas
are found on the lateral aspect of the neck directly
anterior to sternocleidomastoid muscle . These
cysts, remnants of cervical sinus, are most often
just below the angle of the jaw, although they
may be found anywhere along the anterior border
of sternocleidomastoid muscle .

Thyroglossal duct & thyroid abnormalities-
thyroglossal cyst may lie at any point along the
migratory pathway of the thyroid gland but is
always near or in the midline of the neck.
 50% of these cysts are close to or just inferior to
the body of the hyoid bone, they may also be
found at the base of the tongue or close to the
thyroid cartilage. Thyroglossal fistula arises
secondary to rupture of the cyst.

Developmental Disturbances of JawDevelopmental Disturbances of Jaw
 Micrognathia- is of 2 types, namely congenital or
acquired.
 Etiology of the congenital form is unknown, but usually
associated with other congenital deformities like
congenital heart anomalies, Pierre-robin syndrome.
 Micrognathia of maxilla is due deficiency in the
premaxillary area. True mandibular micrognathia may be
caused by agenesis of condyles.
 Acquired type of micrognathia results due to disturbance
in the area of TMJ, ankylosis of joint may caused by
trauma or infection of mastoid or middle ear or of the joint
space itself

Macrognathia- cases of mandibular
prognathism uncomplicated by any systemic
condition are rather common. The etiology of
this problem is unknown, although hereditary is
said to be the main cause. In some cases
prognathism is due to disparity in the size of the
maxilla in relation to mandible. The angle
between the body & ramus also appears to
influence the relation the relation of the mandible
to the maxilla, and also the actual height of the
maxilla.

 Facial hemi hypertrophy- exact cause is not known, but
hormonal imbalance, chromosomal abnormality ,
localized alteration of intra uterine development,
lymphatic & vascular abnormalities has been suggested
as the possible causes.
 patient affected by this condition exhibit enlargement
of one half of the face, with the enlarged side growing at
same rate as uninvolved side so that disparity is
maintained.
 females are more prone to be affected than males.
 Dentition of hypertrophic side is affected. They have
abnormal crown size, root size & shape, rate of
development. Usually cuspids, pre molars & 1st
molars
are affected more. Permanent teeth are affected more, and
on the affected side erupt earlier than unaffected side.

The maxilla and mandible is also enlarged, some
times trabecular pattern is also altered.
 Tongue & buccal mucosa are also involved.
Buccal mucosa appears velvety & seems to hang
in soft, pendulous folds on the affected side.

Facial hemi atrophy- exact cause is unknown,
but trophic malfunction of cervical sympathetic
nervous system, trauma, infection, heredity,
peripheral trigeminal neuritis have been
suggested as possible causes. Left side is more
common than right side.
 Initial lesion extends progressively to include
atrophy of skin, subcutaneous tissue, muscle ,
bone resulting in facial deformity of varying
degree. The cartilage of nose, ear, larynx also
becomes involved. Lips, tongue, teeth are also
involved. Roots of teeth may exhibit deficiency
of root development and decrease growth of jaw
on the affected side.www.indiandentalacademy.com

 Developmental Disturbances of Lip and Palate
 Mandibular cleft lip- it is an extremely rare condition
caused due to failure of copula to give rise to mandibular
arch or due to persistence of central groove of the
mandibular process.
 Maxillary cleft lip – it is more common.earlier it was
thought to be due to failure of the globular portion of the
median nasal process to unite with lateral nasal process and
maxillary process. But recently it is said to be caused by
failure of mesodermal penetration & the obliteration of the
ectodermal grooves separating these mesodermal masses
that actually constitute the facial process.
 2 types – a) cleft lip with or with out associated cleft palate
 b) isolated cleft lip

 Hereditary is said to be the main cause, but
environmental factors also affect the formation cleft. In
hereditary transmission , polygenic nature of
transmission is said to be more common( determined by
several different genes acting together)
 other factors suggested are- defective vascular supply to
the area involved, mechanical disturbance in which the
size of the tongue prevents the union of parts, circulating
substances like alcohol, drugs and toxins, infections and
lack of inherent developmental forces.
 Cleft lip & cleft palate more common in boys than girls,
left side more common than right side.


Veau classification of cleft lip –
Class I –unilateral notching of the vermilion
border that doesn’t extend into lip.
Class II – unilateral notching of the vermilion
that extends into the lip but does not involve the
floor of the nose.
Class III – unilateral clefts of the lip extending
through the lip into the floor of the nose.
Class IV – bilateral cleft of the lip.

 Veau classification of cleft palate-
 Class I – cleft limited to the soft palate
 Class II- cleft of the hard(secondary) & soft palate.
 Class III- complete unilateral clefts extending from the
uvula to the incisive foramen & alveolar process.
 Class IV- complete bilateral clefts involving the soft & hard
palate & the alveolar process on both sides of pre-maxilla.
 The prevalence of dental abnormalities associated with cleft
lip & palate is remarkable. Abnormalities of tooth number,
size, morphology, calcification and eruption are seen. Both
deciduous & permanent dentition are affected. The lateral
incisor in the vicinity of the cleft is often involved. The
prevalence of hypodontia increases proportionally with the
severity of cleft. www.indiandentalacademy.com

 Treatment- this often requires multi disciplinary approach.
 cleft lip repair is done when child is stable & weighs 10
pounds, has hemoglobin level of 10 mg%.
 For cleft palate surgery is done only after the child is 18
months old.
 Orthodontic devices are used to guide the dento-alveolar
segments into normal anatomic relationship
 once into mixed dentition phase of development ,
conventional orthodontic therapy to be initiated to establish
normal maxillary arch form.
 palatal obturators to be given to patients having difficulty
in swallowing.

Developmental Disturbances of Tongue
Macroglossia- congenital macroglossia due to over
growth of musculature. This produces displacement
of teeth, malocclusion because of strength of muscle
involved. Crenation & scalloping of lateral borders
of tongue are common
Beckwith’s hypoglycemic syndrome – has
macroglossia,neo natal hypoglycemia, mild micro
cephaly, umbilical hernia, fetal visceromegaly.

Ankyloglossia- complete fusion of the tongue & the
floor of the mouth.
Partial Ankyloglossia( tongue tie)- has a short
lingual frenum, or frenum attached too near the tip
of the tongue. Because of restricted movement –
speech difficulty is seen.
Can be surgically treated by clipping the frenum.

Cleft tongue- occurs due lack of merging of the
lateral lingual swellings of the tongue. A partial cleft
is more common & is seen as deep groove in the
dorsal surface of tongue & is caused by incomplete
merging & failure of groove obliteration by
underlying mesenchymal tissue proliferation.
 Cleft tongue is usually seen in orofacial digital
syndrome, where in thick fibrous bands in lower
anterior mucobuccal fold eliminating the sulcus &
with clefting of the hypoplastic mandibular alveolar
process. Food debris & microorganisms may collect
in these cleft & cause irritation

Median rhomboid glossitis- congenital
abnormality of the tongue, presumably due to failure
of tuberculum impar to retract before fusion of the
lateral halves of the tongue, so that structure devoid
of papilla is interspersed between them.
Clinically it appears as an ovoid or diamond shaped
reddish plaque on dorsal surface of tongue
immediately anterior to circumvallate papilla. It has
no filiform papilla.
Histologically loss of papilla with varying degree of
hyper parakeratosis, proliferation of rete ridges,
lymphocytic infiltrate with in connective tissue ,
hyaline formation is seen.www.indiandentalacademy.com

Anomalies of TeethAnomalies of Teeth
Microdontia- a)generalized-actual- ex-pituitary
dwarfism
 relative- ex- macrognathia
 b) localized- ex- peg laterals

Macrodontia-a)generalized actual- ex pituitary
gigantism
 relative- ex- micrognathia
 b) localized – ex hemifacial hypertrophy
Alterations in shape
I)Gemination- fusion of 2 teeth from a single enamel
organ. Typically partial cleavage with appearance of
2 crowns that share the same root canal
II) fusion- joining of 2 developing tooth germs,
resulting in single large tooth structure. It may
involve entire length of tooth or only a part of it.www.indiandentalacademy.com

 Concrescence- a form of fusion where in already formed
teeth are joined by cementum.commonly seen in
maxillary 2nd
& 3rd
molars. Surgical sectioning might be
required during extraction.

Dilaceration- An extraordinary curving or
angulations of teeth, caused by trauma during
development. Difficulty will be faced during
extraction & during root canal treatment.

 Dens invaginatus- also known as dens in dente, it
represents an accentuation of the lingual pit. Severity
ranges from just coronal involvement to both coronal
& radicular involvement. Anterior teeth are more
commonly involved. This condition predisposes to
early caries & pulpitis.

 Dens evaginatus- premolars predominantly affected
(LEUNG’S PREMOLARS). The defect is anomalous
cusp located in center of occlusion, subsequent wear
causes exposure of accessory pulp horn, leading to
periapical pathology in disease free pulp.

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