DEVELPOMENT OF JAW AND ANAMOLIES

CONTENTS

 INTRODUCTION
 GENERAL PRINCIPLES AND CONCEPTS
 DEFINITION – GROWTH, DEVELOPMENT AND
DIFFERENTIATION
 THEORIES OF GROWTH
 PRENATAL GROWTH
a) JAW
b) PALATE
c) MAXILLARY SINUS
 POST NATAL GROWTH
d) MAXILLA
e) MANDIBLE
 ANAMOLIES
 CLINICAL CONSIDERATIONS
 CONCLUSION
 REFERENCES
INTRODUCTION:
Growth is a universal phenomenon. All organisms grow from a single
cell to complex living structure performing varied function. During growth
person passes through different phases and these phases are unique in
themselves with multitude of factors affecting them and thus making them
significant.
So thorough knowledge of growth and development is necessary for
accurate diagnosis and treatment planning.
Growth and development are two terminologies that are often
confused, though closely related they are not synonymous.

Growth:
Definition: the self multiplication of living organism – J.S. Huxley
 Increase in size, change in proportion and progressive complexity –
Krogman.
 Entire series of sequential anatomic and physiologic changes taking
place from the beginning of prenatal life to senility – Meridith.
 Quantitative aspect of biologic development per unit of time – Moyer‘s.

Development: Todd – development is progress towards maturity.

Moyer’s: All 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.

Differentiation: defined as change from a generalized cell or tissue to one

that is more specialized.
THEORIES OF GROWTH:
Differentiation between growth site and control is important.
 Growth site is merely a location at which growth occurs.
 Growth center is a location at which independent genetically controlled
growth occurs. All centers of growth are sites but reverse is not true.

Genetic theory:
 Earliest theory simply states that all growth is controlled by genetic
influence.
 Doesn‘t recognize environmental factors.

Sutural theory: Sicher – suture between the membranous bone of the

cranium and jaws were considered growth centers, along with sites of
endochondral ossification in the cranial base.
 Growth, in this view, was the result of the expression of all these sites of
a genetic program.
Points raised against the theory
1) When an area of the suture is transplanted to another location, tissue
does not continue to grow.
2) Growth takes place in untreated cases of cleft palate.
3) Microcephaly and hydrocephaly.

Cartilagenous theory: James Scott

Intrinsic growth factors are present in cartilage and periosteum with
suture being only secondary cartilaginous sites throughout the skull as
primary centers of growth.
Maxilla – nasal septal cartilage
Mandible – cartilage present at head of condyle.
Tumour – if an epiphyseal plate is transplanted to a different location, it will
continue to grow in the new location.
 Experiments on rabbits – removal of nasal septal cartilage demonstrated
retarded mid face development.
But – neither transplantation experiments nor experiments in which the
condyle is removed lend any support to the idea that the cartilage of the
mandibular condyle is an important center.
 It appears that the growth at the mandibular condyles is much more
analogous to growth at the sutures of the maxilla – entirely reactive than
to growth at an epiphyseal plate.

Functional matrix theory: Melvin Moss

 A number of relatively independent functions are carried out in the
craniofacial region of the human body. Ex. respiration, olfaction, vision,
hearing, chewing, swallowing etc.
 Each of these functions is carried out by a functional cranial component
consisting of the tissues, organs, skeletal part to carry out the function.
Functional cranial component is divided into
1) Functional matrix
2) Skeletal unit
1) All the tissues, organs and functioning spaces taken as a whole comprise
the functional matrix, while the skeletal tissues related to this specific
functional matrix comprise the skeletal unit.
 Functional matrix consists of muscles, glands, nerve, vessel, fat, teeth
and functioning spaces.
Functional matrix is divided into two
1) Periosteal matrix
2) Capsular matrix
 Periosteal matrices act directly and actively upon their related skeletal
units. Alteration in their functional demands produce a secondary
compensatory transformation of size or shape of their skeletal units. Such
transformation are brought about by interrelated processes of bone
deposition and resorption.
 Capsular matrices acts indirectly and passively on their related skeletal
units producing a secondary compensatory translation in spaces.
 These alteration in spatial position of skeletal units are brought about by
the expansion of the orofacial capsule within which the facial bones
arise, grow and are maintained.
 The facial skeletal units are passively and secondarily moved in space as
their enveloping capsule is expanded.
 Neurocranial capsule and the orofacial capsule are examples of capsular
matrices. Each of these capsule is an envelop which contains a series of
functional cranial components. Which as whole are sandwiched in
between two covering layers. In neurocranial capsule, the cover consists
of the skin and duramater where as in orofacial capsule the skin and
mucosa form the covering.

Van limborgh’s theory: 1970 – multifactorial

He explains the process of growth and development in a view that
combines all the 3 existing theories.

Five factors that control growth

 Intrinsic genetic factors – genetic control of the skeletal units themselves.
 Local epigenetic factors – bone growth is determined by genetic control
originating from adjacent structure like brain, eyes etc.
 General epigenetic factors – genetic factors determining growth from
distant structure ex. sex hormones, growth hormones.
 Local environmental factors – they are nongenetic factors from local
external environment ex. habits, muscle force.
>General environmental factors – these are general non-genetic influences
such as nutrition, oxygen.

Intrinsic genetic factors Local

Genome
Local
Epigenetic factors
General
Local
Environment Factors
General

Periosteal matrix e.g. – coronoid process – temporalis

Capsular matrix – e.g.
1) Growth of cranial vault is a direct response to the growth of the brain.
Pressure exerted by growing brain separates the cranial bones at the
sutures and new bone passively till in at these sites.
2) Hydrocephaly – reabsorption of CSF is impeded

Current concepts of growth

1) Neurotrophic theory of growth
 The trophic substance is something that provides nutrition.
 The physiology of neutrotrophism is based on the fact that in nervous
system apart from conducting afferent and efferent is also concerned
with the integrity of the body structure. Nerves control of skeletal growth
assumable by transmission of a substance through axons.
 Genetic expression of the muscle is not within themselves but under the
influence of nerves sectioning of nerve lead to muscle degeneration.
 Bosma has showed that the epithelium and extra oral epithelium grows in
heaps and spurts as it comes in contact with sensory nerve endings. So
when deficiency exists in nerve one has to anticipate orofacial
hypoplasia, malgrowth and malformation.
 There are certain evidence that indicate that maxillary and mandibular
hypoplasia is often seen associated with a variety of intraoral and
intranasal sensory defects.

Enlow’s V-principle:
Many facial and cranial bones have a ‗v‘ shaped configuration. Note
that bone deposition occurs on the inner side of the V and resorption takes
place on the outside surface. Thus there is increase in wide end of the V.

Enlows counterpart principle: it simply states that growth of any given

facial or cranial part relates specifically to other structural and geometric
counter part in the face and the cranium,
Examples
1) Maxillary arch is counterpart of the mandibular arch
2) Anterior cranial fossa and palate are counterpart
3) Palate and maxillary apical base.
 If each regional part and its particular counterpart enlarge to same extent
balance growth between them results.

Pattern, variability and timing:

 Pattern reflects proportionality, usually of a complex set of proportions
rather than just a single proportional relationship. Ex. in fetal life – III
month of IUL. Head take up almost 50% of total body length by birth
head – 30% and in adult 12% of the adult.
 Another aspect is that not all the tissue systems of the body grow at the
same rate.
Body tissue can be classified into 4 types. They are lymphoids,
neural, general and genital tissue. Each of these tissue grow at different time
and rate as shown in diagnosis.

Concept of normality:
 Normal refers to that which is usually expected, is ordinarily seen or is
typical. The concept of normality must not be equated with that of the
ideal, while ideal denotes the central tendency for the group, normal
refers to range.
 Another aspect is normality changes with age. Thus what is normally
seen or is expected for one age group may not be necessary normal for a
different age group.

Growth spurts:
Growth does not take place uniformly at all times. These seems to be
periods when a sudden acceleration of growth occurs. This sudden increase
in growth is termed ―growth spurt‖. The physiological alteration in
hormonal secretion is believed to be the cause for such accentuated growth.
 Timing of growth spurt differs in boys and girls.
Timing
a) Just before birth
b) One yr after birth
c) Mixed dentition growth spurt
Boys – 8-11 yrs
Girls – 7-9 yrs
d) Pre-pubertal growth spurt
Boys – 14-16 yrs
Girls – 11-13 yrs

 Growth modification by means of functional and orthodontic appliance

better response during growth spurts.
 Surgical correction after cessation of growth, otherwise relapse.

Methods of studying physical growth:

Two main approaches

I) Measurement approaches
1) Craniometry – measurements of skulls found among human skeletal
remains.
Advantage: precise measurements can be made
Disadvantage: individual can be measured at only one point in time.
2) Anthropometry: distance between landmarks are measured by using
soft tissue points overlying these landmarks.
Advantage: soft tissue introduces variation
Disadvantage: growth of individual can be made repeatedly at different
times.
3) Cephalometric radiology – technique depends on precisely omenting the
head before a radiograph with precisely controlled magnification is
made.
 It allows direct measurement of bony skeletal dimensions, since the bone
can be seen through the soft tissue covering in a radiograph.
 Disadvantage –2D image so, all measurements not possible. (Broadbent
in 1931)

II. Experimental approaches

a) Vital staining – Belcher – 1936 – involves administration of certain dyes
to the experimental animal which get incorporated into the bones.
It is possible to study the manner in which bone is laid down, the site of
growth, the direction, duration and amount of growth dyes used are a)
alizarin b) leadacetate
b) Radioisotopes – gamma-emitting isotopes 99m Technetium can be used
to detect areas of bone growth. They get incorporated into the tissue and
emit weak radioactivity.
c) Implant – Bjork 1969 involves the implanting of small bits of
biologically inert alloys into growing bone. This serve as radiographic
reference for serial radiographic analysis.
 These implants are around 1.5mm in length and 0.5mm in diameter made
of tantalum metal.
 They are embedded in certain areas of the maxilla and mandible in order
to study growth of the skull.
Mechanism of bone growth:
 Bone is specialized tissue of mesodermal origin. It forms the structural
framework of the body.

Bone deposition and resorption – the process of bone deposition and

resorption together is called bone remodeling. The changes it can produce
a) Change in size
b) Change in shape
c) Change in proportion
d) Change in relationship of the bone with adjacent structures

Cortical drift: a combination of bone deposition and resorption resulting in

a growth movement towards the depositing surface is called cortical drift.
 E. g. if in case more bone is deposited on one side and less bone
resorbed on the opposite.

Displacement: Movement of whole bone as a unit.

Primary displacement:
 If a bone gets displaced because of its own growth it is called primary
displacement. For ex. growth of the maxilla at the tuberosity region
results in pushing of the maxilla against the cranial bone which results in
displacement of the maxilla in a forward and downward direction.
Secondary displacement:
 If bone gets displaced as a result of growth and enlargement of an
adjacent bone, it is called secondary displacement for e.g. the growth of
the cranial base causes forward and downward displacement of maxilla.

PRENATAL GROWTH OF JAW:

 Around 4th week of intra-uterine life a prominent bulge appears on the
ventral aspect of the embryo corresponding to the developing brain.
 Below the bulge a shallow depression which corresponds to the primitive
mouth appears called stomatodeum. The floor of the stomatodeum is
formed by the buccopharyngeal membrane which separates the
stomatodeum from the foregut.
 Mesoderm covering the developing forebrain proliferates and forms a
downward projection that overlaps the upper part of stomatodeum. This
downward projection is called frontonasal process.
 At around same time, five brachial arches form in the region of the future
head and neck. Each of these arches give rise to muscles, connective
tissue, vasculature skeletal and neural components.
 First brachial arch called mandibular arch forms important role in
development of major maxillary complex.
 The stomatodeum is thus overlapped superiorly by the fronto-nasal
process. The mandibular arches on both sides form the lateral walls of
the stomatodeum.
 Mandibular arch gives off a bud from its dorsal end called the maxillary
process.
 The maxillary process grows ventro-mediocranial to the main part of the
mandibular arch which is now called the mandibular process.
 Thus at this stage the primitive mouth or stomatodeum is overlapped
from above by the frontal process, below by the mandibular process and
on either side by the maxillary process.
Formation of mandibular and maxillary process:
 The ectoderm overlying the frontonasal process soon shows bilateral
localized thickening that are situated a little above the stomatodeum.
They are called nasal placodes. The formation of these placodes is
induced by the underlying forebrain. The placodes soon sink below the
surface to form nasal pits.
DEVELOPMENT OF JAW:
 The mandibular processes of the two sides grow towards each other fuse
in the midline. They form the lower margin of the stomatodeum which
give rise to lower lip and to lower jaw.
 Each maxillary process now grows medially and fuses, first with the
lateral nasal process and then with the medial nasal process. The medial
and lateral nasal processes also fuse with each other. Thus nasal pits are
cut off from stomatodeum.
 Maxillary process undergoes considerable growth. At the same time the
frontonasal process become much narrower from side to side, with the
result that the external nares come closer.
 The line of fusion of the maxillary process and the lateral nasal process
corresponds to the nasolacrimal duct.
DEVELOPMENT OF PALATE:
 Palate is formed by contributions of
a) Maxillary process
b) Palatal shelves given off by the maxillary process
c) Frontonasal process
 From each maxillary process palatal shelves grows medially called as
palatal process.

Constituents of developing palate:

 Each palatal process fuses with the posterior margin of the primitive
palate.
 The two palatal processes fuse with each other in the midline. Their
fusion begins anteriorly and proceeds backwards.
 Medial edges of the palatal processes fuse with the free lower edge of the
nasal septum, thus separating the two nasal cavities from each other and
from the mouth.
 At later stage, the mesoderm in the palate undergoes intramembranous
ossification to form hard palate. However ossification does not extend
into the most posterior portion, which remains as the soft palate.
 As the palatal shelves grow medially, their union is prevented by the
presence of the tongue. Thus initially the developing palatal shelves
grow vertically downwards towards the floor of the moth. Some time
during the seventh week of intra uterine life, a transformation in the
position of the palatal shelves occurs. They change from a vertical to
horizontal position.
 Withdrawal of the embryonic face from against the heart prominence
results in slight jaw opening. This results in withdrawal of the tongue
from between the palatal shelves and aids in the elevation of the palatal
shelves from a vertical to a horizontal position.
 Two palatal shelves, by 1 ½ weeks of I.U.L. are in close approximation
with each other initially the two palatal shelves are covered by an
epithelial lining as they join, the epithelial cells degenerate. The
connective tissue from the palatal shelves in interminglewith each other
resulting in their fusion.

DEVELOPMENT OF MAXILLARY SINUS:

 Initial development of the maxillary sinus follows a pumber of
morphogenic events in the differentiation of the nasal cavity in early
gestation. After fusion of nasal septum and palatal shelves the lateral
nasal wall begins to fold, thus 3 nasal conchae and 3 subjacent meatuses
arise.
 The inferior and superior meatuses remain as shallow depressions along
the lateral nasal wall for approximately first ½ of JUL. The middle
meatus expands immediately into the lateral nasal wall. Max sinus thus
established expands vertically into the primordium of the maxillary body
and reaches a diameter of 1mm in the 50mm CRL fetus.
3.5mm in 160mm
2.5mm in 250mm CRL fetus
 In prenatal period the human maxillary sinus measures about 7-16mm in
anterior posterior direction and 2-13mm in superio-inferior direction.
 In the course of development the maxillary sinus often pneumatizes the
maxilla beyond the boundaries of the maxillary body. Some of processes
of maxilla consequently become invaded by the air space.
 These expansions, referred to as the recesses, are found in the alveolar
process, zygomatic process, frontal, palatine process.
 The occurrence of the zygomatic recess brings the supalveolar
neurovascular bundles into proximity with the space of sinus. Frontal
recess invades and sometimes surrounds the content of the infraorbital
 canal, where as the alveolopalatine recesses reduce the account of the
bone between dental apices and the sinus space. The latter development
most often pneumatizes the floor of the sinus adjacent to the roots of the
first molar and less often to the roots of II premolar, I premolar and II
molar in that order of frequency.

PRENATAL GROWTH OF MANDIBLE:

 Pharangeal arches are laid down on the lateral and ventral aspects of the
cranial most part of the foregut which lies in close approximation with
the stomadeum. Initially there are six pharyngeal arches, but the fifth one
usually disappears as soon as it is formed leaving only five. They are
separated by four brachial grooves.
 The mandibular arch which is first arch forms lateral wall of
stomatodeum. The mandibular process of both sides grow toward each
other and fuse in the midline. They now form the lower border of the
stomatodeum i.e. lower lip and lower jaw.

Meckels cartilage: the meckels cartilage is derived from the I brachial arch
around 41-45th day of I.U.L. it extends from the cartilaginous otic capsule to
the midline or symphysis and provides a template for guiding the growth of
the mandible.
A major part of the meckels cartilage disappear during growth and the
remaining part develops into the following structures.
1) Mental ossicles
2) Incus and malleus
3) Spine of sphenoid bone
4) Anterior ligament of malleus
5) Sphenomandibular ligament
 The first structure to develop in the primiordium of the lower jaw is the
mandibular division of the trigeminal nerve. This is followed by the
mesenchymal condensation forming the I brachial arch.
 Neurotrophic factors produced by the nerve induce osteogenesis in the
ossification centers. A single ossification centre for each half of the
mandible arises in the 6th week of intrauterine life in the region of the
bifurcation of the inferior alveolar nerve into mental and incisive branch.
 The ossifying membrane is located lateral to the meckels cartilage and its
accompanying neurovascular bundle. From this primary center
ossification spreads below and around the inferior alveolar nerve and its
incisive branch and upwards to form a trough for accommodation of the
developing tooth buds. Spread of the intramembranous ossification
dorsally and ventrally forms the body and the ramus of the mandible.
 As the ossification continues, the meckels cartilage becomes. Surrounded
and invaded by the bone ossification stops at the site that will later
become the mandibular lingula.
Endochondral bone formation is seen only in 3 areas of the mandible
1) Condylar process Coronoid
2) Mental region

Condylar process:
At about the V week of intrauterine life, on area of mesenchymal
condensation can be seen above the ventral part of developing mandible.
This develops into a cone shaped cartilage by about 10 th week and starts
ossification by 14th. It then migrates inferiorly and fuses with the
mandibular ramusby about 4 months. Much of the cone cartilage is replaced
by bone by the middle of fetus life but its upper end persists into adulthood
acting both as growth cartilage and an articular cartilage.
Coronoid process:
Secondary accessory cartilage appear in the region of the coronoid
process by about the 10-14 week of intra-uterine life the secondary cartilage
of coronoid process is believed to grow as a response to the developing
temporalis muscle. The coronoid accessory cartilage becomes incorporated
into expanding intramembranous bone of the ramus and disappear from
birth.
Mental region: in the mental region on either side of the symphysis, one or
two small cartilage appear and ossify in the 7th month of intrauterine life to
form variable numbers of mental ossicle in the fibrous tissues to the
symphyses. These ossicles become incorporated into the intramembranous
bone when the symphysis ossifices completely during the first year of post-
natal life.

POST NATAL GROWTH OF MAXILLA:

The growth of the nasomaxillary complex is produced by the
following mechanisms.
a) Displacement
b) Growth of sutures
c) Surface remodeling

Displacement:
Maxilla is attached to the cranial base by means of a number of
sutures. Thus growth of the cranial base has a direct bearing on the
nasomaxillary growth.
 Passive or secondary displacement of the nasomaxillary complex occurs
in a downward and forward direction as the cranial base grows. This is a
secondary type of displacement as the actual enlargement of these parts
is not directly involved.
 The passive displacement of the maxilla is an important growth
mechanism during the primary dentition years but becomes less
important as growth of cranial base slows.
 In addition, a primary type of displacement is also seen in a forward
direction. This occurs by growth of the maxillary tuberosity in a
posterior direction. This results in the whole maxilla being carried
anteriorly. The amount of this forward displacement equals the amount
 of posterior lengthening. This a primary type of displacement as the bone
is displaced by its own enlargement.

Growth at sutures: the maxilla is connected to the cranium and cranial

base by a number of sutures
These sutures include
a) Fronto-nasal suture
b) Fronto-maxillary suture
c) Zygomatico-temporal suture
d) Zygomatic-maxillary suture
e) Pterygo-palatine suture
 These sutures are all oblique and more or less parallel to each other. This
allows the downward and forward repositioning of the maxilla as growth
occurs at these sutures. As growth of the surrounding soft tissue occurs,
the maxilla is carried downward and forward. This new bone is formed
on either side of the suture. Thus the overall size of the bones on either
side increases. Hence a tension related bone formation occurs at the
sutures.

Surface remodeling:
Massive remodeling by bone deposition and resorption occurs to
bring about
a) Increase in size
b) Change in shape of bone
c) Change in functional relationship
Following are remodeling changes that are seen in the naso-maxillary
complex.
1) Resorption occurs on the lateral surface of the orbital rim leading to
lateral movements of the eye ball. To compensate, there is bone
 deposition on the medial rim of the orbit and on the external surface of
the lateral rim.
2) The floor of the orbit faces superiorly, laterally and anteriorly. Surface
deposition occurs here and results in growth in a superior, lateral and
anterior direction.
3) Bone deposition occurs along the posterior margin of the maxillary
tuberosity. This cause lengthening of the dental arch and enlargement of
the antero-posterior dimension of the entire maxillary body. This helps to
accommodate the erupting molars.
4) Bone resorption occurs on the lateral wall of the nose leading to an
increase in size of the nasal cavity.
5) Bone resorption is seen on the floor of nasal cavity. To compensate there
is bone deposition on the palatal side. Thus a net downward shift occurs
leading to increase in maxillary height.
6) Zygomatic bone moves in a posterior direction. This is achieved by
resorption on the anterior surface and deposition on the posterior surface.
7) The face enlarges in width by bone formation on the lateral surface of the
zygomatic arch and resorption on its medial surface.
8) The anterior nasal spine prominence increase due to bone deposition. In
addition there is resorption from the periosteal surface of a labial cortex.
As a compensatory mechanism, bone deposition occurs on the endosteal
surface of the labial cortex and periosteal surface of the lingual cortex.
9) As the teeth start erupting, bone deposition occurs at the alveolar
margins. This increases the maxillary height and depth of the palate.
10) The entire wall of the sinus except the mesial wall undergoes
resorption. This results in increase in size of the maxillary antrum.
SURFACE REMODELLING
POST NATAL GROWTH OF MANDIBLE:
 Of the facial bones, the mandible undergoes the largest amount of
growth postnatally and also exhibits the largest variability in
morphology.
 While the mandible appears in the adult as a single bone, it is
developmentally and functionally divisible into several skeletal sub units.
The basal bone or the body of the mandible forms one unit, to which is
attached the alveolar process, the coronoid process, the condylar process,
the angular process, the ramus, the lingual tuberosity and the chin. Thus
the study of post-natal growth of the mandible is made easier and more
meaningful when each of the developmental and functional parts are
considered separately.

Ramus: ramus moves progressively posterior by a combination of

deposition and resorption. Resorption occurs on the anterior part of the
ramus while bone deposition occurs on the posterior region. This results in a
drift of the ramus in a posterior direction. The functions of remodeling of
the ramus are
1) Accommodate the increasing mass of masticatory muscles inserted
into it.
2) To accommodate the enlarged breadth of the pharyngeal space.
3) To facilitate the lengthening of the mandibular body, which in turn
accommodate the erupting molars.

Body of mandible / corpus of mandible:

 As anterior border of the adult ramus exhibits bone resorption while the
posterior border shows bone deposition. That is, the displacement of the
ramus results in the conversion of former ramal bone into the posterior
part of the body of mandible. In this manner body of the mandible
 lengthens. Thus additional space made available by means of resorption
of the anterior border of ramus is made use to accommodate the erupting
permanent molars.

Angle of the mandible:

 On the lingual side of the angle of the mandible, resorption takes place
on the postero, inferior aspect while deposition occurs on the anterio-
superior aspect.
 On buccal side, resorption occurs on the anterior-superior part while
deposition takes place on the posterio-superior part. This result in flaring
of the angle of the mandible as age advances.

The lingual tuberosity:

Is direct equivalent of the maxillary tuberosity, which forms a major
site of growth for the lower bony arch. It forms the boundary between the
ramus and the body.
 Lingual tuberosity moves posteriorly by deposition on its posteriorly
facing surface. Lingual tuberosity protrudes noticeably in a lingual
direction and it lies well towards the midline of the ramus.
 The prominence of the tuberosity is increased by presence of a large
resorption field just below it. This resorption field produced a sizeable
depression, the lingual fossa. The combination of resorption in the fossa
and deposition on the medial surface of the tuberosity itself accentuates
the prominence of the lingual tuberosity.

Alveolar process:
Develops in response to the presence of tooth buds. As the teeth
erupts the alveolar process develop and increases in height by bone
deposition at the margins. The alveolar bone adds to the height and
thickness of the body of the mandible and is particularly manifested as a
ledge extending lingual to the ramus to accommodate III molars. In case of
absence of teeth, the alveolar bone fails to develop and it resorbs in the
event of tooth extraction.

The chin:
Specific human characteristic and in found its fully developed form in
recent man only.
 In infancy, the chin is usually underdeveloped as age advances growth of
chin becomes significant.
 Males are seen to have prominent chins compared to females. The
mental protroberance forms by bone deposition during childhood.
 Its prominence is accentuated by bone resorption that occurs in the
alveolar region above it, creating a concavity. Deepest portion is known
as point ‗B‘ in Cephalometric terminology.

Condyle:
Mandibular condyle has been recognized as an important growth site.
The head of the condyle is covered by a thin layer of cartilage caused the
condylar cartilage. The presence of the condylar cartilage is an adaptation to
withstand the compression that occurs at the joint.
The role of the condyle in the growth of mandible has remained a
controversy. There are 2 schools of thought.
a) It was earlier believed that growth occurs at the surface of the condylar
cartilage by means of bone deposition. Thus the condyle grows towards
the cranial base. As the condyle pushes against the cranial base, the
entire mandible gets displaced fowards and downwards.
b) It is now believed that growth of soft tissues include the muscle and
connective tissue carries the mandible forwards away from the cranial
 base. Bone growth follows secondarily at the condyle to maintain
constant contact with the cranial base.
 Condylar growth rate increases at puberty reaching a peak between 12 ½
- 14 yrs. the growth ceases around 20yrs of age.

Coronoid process: follows the enlarging ‗V‘ principle.

 Viewing the longitudinal section of the coronoid process from the
posterior aspect. It can be seen that deposition occurs on the lingual
surfaces of the left and right coronoid process. Although additions takes
place on the lingual side, the vertical dimension of the coronoid process
also increases. This follows the ‗V‘ principle.
 Viewing it from occlusal aspect, the deposition on the lingual of the
coronoid process brings about a posterior growth movement in the V
bottom. Briefly the coronoid process has propeller like twist, so that its
lingual side faces 3 general directions all at once i.e posteriorly,
superiorly and medially.

SURFACE REMODELLING
DEVELOPMENTAL ANAMOLIES OF THE JAW:

Agnathia: extremely rare, absence of maxilla or mandible. More

commonly, only a portion of one jaw is missing.
 Ex one maxillary process / premaxilla / entire mandible on one side /
only condyle condyle / ramus / bilateral agenesis of condyles and of
ramus has also been reported.

Micrognathia: means small jaw

 More no of case are not true micrognathia but rather due to abnormal
positioning / relation of one jaw to the other or to the skull which
produces illusion of micrognathia.
True: classified
 Congenital – cause unknown but – generally associated with syndrome
Ex Pierre robin syndrome
Maxilla – generally in premaxillary area
 Acquired – disturbance in area of

TM joint: ex ankylosis of joint, may be caused by trauma / infection of the

mastoid / infection of joint itself.
 Since manual growth of the mandible depends on to a considerable
extent on normally developing condyles as well as on muscle function
and hence can result in deficient mandible.

Pierre Robin syndrome: cleft palate, micrognathia and glossoptosis heart

and skeletal anamolies.
Mandibulofacial dysostosis:
1) Hypoplasia of facial bone, malar bones and mandible
2) Malformation of external ear
3) Macrostomia, high palate
4) Skeletal deformities also called tracher Collins syndrome

Craniofacial dysostosis: protuberant frontal region, hypoplasia of maxillae

and mandibular prognathism, patient nose resembles parrot beak,
hypertelorism, exopthalmus, blindness – frequently, may be mentally
retarded – normal life span.

Cleidocranial dysplasia: dominant

Abnormalities of skull – frontanels remain open / exhibit delayed closing
o Paranasal sinus are narrow
o Clavicular absent
o Smaller maxilla than mandible
 Micrognathia of maxilla is frequently due to a deficiency in the
premaxillary area, and patients with this deformity appear to have the
middle third of the face retracted.
 Micrognathia may be one of predisposing factors in the mouthbreathing,
owing to associated maldevelopment of the nasal and nasopharyngeal
structures.
 Clinical appearance of mandibular micrognathia is characterized by
severe retrusion of the chin, a steep mandibular angle and a deficient
chin.
Macrognathia: abnormally large jaws
Both jaws with increase size of skeleton – pituitary gignatism.
Macrognathia – where only jaws are affected.
a) Paget‘s disease of bone
b) Acromegaly – increase size of mandible owing to increase in growth
hormone in adults.
 number of cases with mandibular prognathism – etiology is
unknown but some cases follow hereditary pattern.
Factors that would influence and tend to favour mandibular
prognathism are as follows
1) Increased height of ramus
2) Increased mandibular body length
3) Increased gonial angle
4) Anterior positioning of glenoid fossa
5) Decreased maxillary length
6) Prominent chin button.
7) Varying soft tissue contours

Treatment: surgical correction is feasible – resection of a portion of the

mandible to decrease the size is an established procedure.

Cleft lip and palate:

 Most commonly seen congenital deformities that occur at the time of
birth.
Incidence of cleft lip and palate is found to be different among different
races.
India – 600 - 1000 births
Negroid – Least one in every 2000 births
Mongoloid – highest
 Unilateral clefts accounts for 80% of incidence while bilateral remaining
20%.
 Among unilateral cleft, cleft involving left side are seen in 70% of the
cases.

Etiology: is yet to be understood

Factors responsible are
a) Genetic factors – in 1/5th to 2/5th of patient the family history can be
elicited.
 Vander woudes syndrome where lip pit are associated with cleft lip and
palate or autosomal recessive inherence.
Cleft palate alone – more in females
Cleft lip associated with cleft palate more in males

Environmental factors: rubella, exposure to radiation, drugs, trauma and

complication of pregnancy during I trimester of pregnancy can lead to
development of ramus types of defects.
 Ex  incidence of cleft was noted in off springs of pregnant women in
Nagasaki and Hiroshima after atomic explosions.
 Drugs like thalidomide, antiepileptic drugs, quinine, deficiency of vit A,
steroid.
 Consumption of alcohol, smoking and hypoxia conditions in the mother
are also considered to play an important role in development of clefts.

Polygenic interactions:
Interaction between multiple genes with small defects and
environmental factors result in defect. Increased evidence states that most
clefts on human beings appear due to multifactorial causes i.e. due to
combined effect of genetic influence and various environmental influences.
Associated syndromes:
 Vander woudes syndrome – with lip pits
 Orofacial digital syndrome – median cleft lip, bilateral accessory toes.
 Teacher Collins syndrome
 Pierre robin syndrome

Classification:
Morphological
Veau classification:
Group I: cleft on soft palate only
Group II: cleft of the hard and soft palate till the incessive foramen.
Group III: complete unilateral cleft of the soft palate, hard palate, the
alveolar ridge and the lip on one side.
Group IV: complete cleft of the soft palate, hard palate, alveolar ridge and
the lip on both side.

Embryological classification:
Kernahan and Stark classification

Group I: Cleft of the primary palate only

 Unilateral
 Bilateral
 Total
 Subtotal

Group II: cleft of the secondary palate only

 Total
 Subtotal
 Submucous
Group III: cleft of both primary and secondary palate
 Unilateral – total, subtotal
 Median – total, subtotal
 Bilateral - total, subtotal

Kernahans stripped ‘Y’ classification:

1 4
Right 2 5 Left

3 6
1 – lip
7 2 and 5 - alveolus
8

3 and 6 – hard palate anterior to the incisive foramen.

7 and 8 – hard palate posterior to incisive foramen
9 – soft palate
Blocks are shaded in areas where clefts have occurred.

Lashal classification:
prephase of the anatomic areas affected by the cleft
L – lip
A – alveolus Areas involved on the cleft are denoted by

H – hard palate specifically indicating the alphabet standing for

S – soft palate it. Example – L … S….. stands for cleft of right

H – hard palate lip and soft palate

A – alveolus
L – lip
Problems associated with clefts:
Cleft lip and palate patient are affected by number of problems.
Broadly classified as
a) Dental problems
b) Esthetic
c) Speech and hearing
d) Psychologic

Dental: one / more of following features

 Congenital missing teeth commonly upper laterals
 Presence of natal / neonatal teeth
 Presence of supernumerary teeth
 Ectopically erupting teeth
 Microdontia
 Fused teeth
 Macrodontia
 Posterior and anterior cross bite
 Enamel hypoplasia
 Aberration in crown shape
 Deep bite
 Spacing / crowding

Esthetic: can lead to facial disfigurement varying from mild to severe.

deformities of nose are common and esthetic is greatly affected

Hearing and speech:

Sometimes associated with disorders of the middle ear which may
affect hearing. The presence of hearing problems can cause difficulty in
language uptake and speech.
 Nasal regurgitation, middle ear infection, inability to suck mothers
milk.

Psychological problems: under lot of psychological stress. Due to

abnormal facial appearance they have to put up with staring, curiosity, pity.

Management of cleft lip and palate:

Multidisciplinary approach comprising of the pediatrician
pedodontist, orthodontist, oral and maxillofacial surgeon, prosthodontist,
ENT, plastic surgeon, psychiatrist and speech pathologist.

Management can be divided into 4 stages:

Stage one: Birth-18 month
 Fabrication of a passive obturator
 Presurgical orthopaedics
 Surgical lip closure – millard role of 10 – 10 wks, 10 pounds, 10 gram %
Hb.
 Surgical palatal closure

Stage two: 18 months – 5 yr of life – treatment in primary dentition.

 To maintain check on eruption pattern and timing
 Oral hygiene instructions
 Restoration of decayed teeth
 No orthodontic treatment initiated

Stage three: 6-11yr mixed dentition

1) Orthodontic procedures – correction of cross bite by using fixed or
removable appliance.
2) Buccal segment cross bite by quadhelix or expansion screw.
Stage four: permanent dentition
 Fixed orthodontics – all irregularities like crowding, over jet, over bite,
spacing.
 Prosthesis can be given for missing teeth after completion of orthodontic
therapy.
Key to successful rehabilitation of a cleft lip and palate patient is
inderdisciplinary approach and moreover the patient should be treated with
sympathy and concern.

Dental considerations:
 More no of dental problems.
 Motivation for proper oral hygiene as  chance of caries due to
crowding.
 Regular oral prophylaxis
 Fluoride therapy – varnish application / mouth rinse
 Rarely an adult patient with cleft palate may be encountered in dental
operatory – treatment carried out under rubber dam.

Mental retardation: general term is applied to person whose intellectual

development is significantly lower than that of the normal persons and
whose ability to adapt to environment is consequently limited McDonald.
 Mental retardation translates an intelligence quotient which is calculated
as
Mental age
X 100
Chronological age
IQ, classification
Above 140 – very superior
120-139 – superior
110-119 – high average
90-109 – average
80-89 – low average
70-79 – borderline impaired
< 69% - mental retarded

Treatment considerations: short attention span, restlessness, hyperactivity

and erratic emotional behaviour.
 Familiarize patient to the office
 Speech should be slow and simple
 One instructions at a time
 Appointments short and scheduled during early part of the day.
 Careful listening to patient as they have trouble with communication.
 Should be managed with a blend of kindness and furriness
 Permanent restoration with preventive procedure with regular recalls.

Down’s syndrome: occur due to trisomy of chrosome 21, translocation or

due to monosaicism incidence – 1 in 600.

Clinical feature: round skull, with flattening of face and occiput.

 Small maxilla
 Oblique palpebral tissue
 IQ – retarded
 Congenital heart lesion
  chance of cleft lip and palate
Consideration:
1) Mental retardation precaution
2) Prophylaxis for heart disease
3) Preventive procedures

Hemifacial hypertrophy: congenital hemihypertrophy may occur including

1) Entire half of the body
2) One or both limbs
3) Face, head and associated structures

Etiology: cause is unknown but condition is variously ascribed to

1) Hormonal imbalance
2) Incomplete twinning
3) Chromosomal abnormality
4) Localized alteration in intrauterine development
5) Lymphatic / vascular /neurogenic abnormalities

Clinical features: enlargement of ½ of the head, enlarged site grows at a

rate proportional to uninvolved side so that disproportion is maintained
through out the life, although growth of the entire face ceases by the age of
20 yrs.
F>M with equal involvement of right and left sides.

O/M: dentition of hypertrophic side, according to rowe is abnormal in 3

aspects.
1) Crown size
2) Root size and shape
3) Rate of development
 But not all teeth in the enlarged area are necessarily affected in a similar
fashion.
 Enlargement is frequently in the cuspid, premolars, and first molar.
 Permanent teeth on the affected side develop more rapidly and erupt
before their counterpart on the uninvolved side.
 Tongue is commonly involved and exhibit enlargement of lingual
papillae in addition to the general unilateral enlargement and
contralateral displacement.

Treatment and prognosis: no specific treatment for this condition other

than attempts at cosmetic repair.
 Normal life span

D/D: certain disease of the jaws – neurofibromatosis and fibrous dysplasia

of the jaws – but can be readily by the lack of effect on tooth size and rate of
eruption.

Facial hemiatrophy / Parry Romberg syndrome:

 Progressive atrophy of some or all the tissues on one side of the face,
occasionally extending to other parts of the body.

Etiology: etiology unknown suggested factors

 Trophic malfunction of the cervical sympathetic nervous system.
 Trauma
 Infection
 Hereditary
 Peripheral trigeminal neuritis
 Localized scleroderma
 Clinical features: onset of condition noticed in the first or second
decade of life as a white line, furrow or mark on one side of the face or
brow near the midline.
 There is atrophy of the skin, subcutaneous tissue, muscle and bone,
resulting in facial deformity of varying degree depending upon severity
of the atrophy.
 Hollowing of the cheek, eye depressed in the orbit, atrophic facial
muscle, cartilage of nose, ear are involved. Affected skin becomes darkly
pigmented.
  for left side

O/M:
 Hemiatrophy of lips and the tongue is reported.
 Teeth may also be affected and may show deficiency of root
development and reduced growth of the jaws on the affected side.
 Eruption of teeth on affected side may also be retarded.

Treatment and prognosis: no specific treatment

 Disease will be progressive for period of several years and then remain
unchanged for remainder of patient life.

Dental considerations:
 Differentiation diagnosis is important – other tissues of face is also
affected.
 Roots of teeth – affected are frequently short
 And irregular size of teeth -  prove for malocclusion like individual
tooth cross bite / posterior cross bite.
 Then can be associated abnormalities like mental deficiency, skin
abnormalities like nevi, haemangioma, telangiectasia, varicose cons etc.
Coronoid hyperplasia:
M : F is 5:1
May be unilateral / bilateral – more common is bilateral

C/F: enlarged coronoid process may impinge on posterior surface of

zygoma, restricting mandibular opening.

Treatment and prognosis: surgical removal of elongated coronoid process

– coronoidectomy.

Condylar hyperplasia: cause unknown but local circulatory problems,

endocrine disturbances, and trauma have been suggested as possible
etiologic factor.

C/F: facial asymmetry, prognathism, cross bites, sometime there is

compensatory maxillary growth and tilting of the occlusal plane.
Radiographic feature: varies with some elongation of condylar neck /
enlargement of condylar heat.

Treatment and prognosis: self limiting condition, and treatment is

determined by the degree of functional difficulty and aesthetic change.
 Unilateral Condylectomy, or condylotomy with concomitant orthodontic
therapy frequently is necessary.

Condylar hypoplasia: congenital / acquired

Congenital is often associated with head and neck syndrome
 Mandibulofacial dysostosis
 Oculoauiculovertebral syndrome / goldenbar syndrome
 Hemifacial microsomia
Acquired: disturbances of growth center of the developing condyle – cause
trauma during infancy / childhood, infections, radiation therapy, rheumatoid
or degenerative arthritis.

C/F: unilateral – distortion and depression of face on the affected side,

mandibular midline shifts to the involved side when the mouth is opened,
accentuating the deformity.
Bilateral – small mandible with a class II malocclsuion.

Diagnosis: panorama films in severe cases condyle or ramusmay be totally

absent.
Milder process – short condylar process and shallow sigmoid notch.

Treatment and prognosis: surgery is often required

 If condyle is missing, a costochondral Hb graft can be placed to help
establish an active growth centre.

Exostosis: localized bony protruberances that arise from the cortical plate.
Common oral exostosis are torus palatinus and torus mandibularis.

Torus palatinus: common exostosis that occurs in the midline of the vault
of the hard palate.

Etiology: not exactly known

 Autosomal dominant trait
 Multifactorial both genetic and environmental influences.
C/F and radiological features: hard mass along the midline suture of hard
palate.
Classified as
a) Flat torus – broad base and slightly convex smooth surfaces. Extends
symmetrically on both sides of midline rephae.
b) Spindle torus – has midline ridge along with palatal raphae.
c) Nodular torus – arise as multiple protruberance each with an
individual base.
d) Lobular torus – lobulated mass but arise from single base.
 Generally no symptoms but if overlying mucosa becomes thin then can
result in ulceration secondary to trivial trauma.

Prevalence: Varying 9-60%

 in Asian and Eskima
F-M = 2:1

Radiograph: radiopacity on periapical films

H/P: mass of dense lamellar cortical bone and inner zone of trabecular bone
sometimes seen.

Treatment: generally no treatment

In denture / if repeatedly ulcerated than can be surgically removed.
Torus mandibularis:
 Common arising from lingual aspect of the mandible.

Clinical and radiological features: presents as bony protruberance along

the lingual aspect of the mandible above the mylohyoid line in the region of
the premolars.
 Bilateral involvement in 90% of cases.
 Most are generally single nodules
 Prevalence 5-40%  in Asians and Eskimos
 Thought to be multifactorial
 A large mandibular tori may appear on periapical radiograph as a
radioopacity superimposed on the roots of the teeth.

H/P: mass of dense lamellar cortical bone and inner zone of trabecular bone
sometimes seen.

Treatment and prognosis: similar to torus palatinus.

CONCLUSION:
Birth defects are leading cause of infant mortality. So, for effective
management of these disabilities a thorough understanding of fundamental
principles of embryology is a necessary requisite.
Development is a complex process, embryology gives insight to
formation of various organ with which be deal with step further, on which
researchers are banking on are gene mapping of 46 chromosomes that
human have. So in coming days it would be possible to replace damaged
genes inutero and prevent birth defects which are leading cause of infant
mortality.
REFERENCES

1) HUMAN EMBRYOLOGY –INDERBIR SINGH, VII EDITION

2) LANGMANS MEDICALO EMBRYOLOGY---TW SADLER, IX
EDITION
3) ORAL AND MAXILLOFACIAL PATHOLOGY – NEVILLE,
DAMM, ALLEN & BOUQUET, II EDITION.
4) ORAL PATHOLOGY—SHAFER, HINE AND LEVY, V EDITION
5) ORTHODONTICS. THE ART AND SIENCE ---BHALAJHI.
6) CONTEMPORARY ORTHODONTICS---WILLIAM PROFFIT
III EDITION.