ETIO

Jai2008
LOG
pu
Y OF
MAL
r
OCC
LUSI
D
ON

en
tal
Co
lle
ge
 A SEMINAR REPORT
Submitted By-
Jaipur
Arpita Pareek
Final Year B D S Dental
College
Dhand, Tehsil -Amber, Jaipur-Delhi (N.H.-8), JAIPUR-303 101

CERTIFICATE
This is to Certify that Miss Arpita
Pareek Of BDS Final Year has
satisfactorily completed the Seminar
on Eiology of Malocclusion &
clinical and practical programmers ’
conducted by the Department of
Orthodontics and Dentofacial
Orthopeadics, during the academic
Year 2007-08
 Prof. & Head

Dept. of
Orthodontics

& Dentofacial
Orthopeadics

JAIPUR 28-05-08

ETIOLOGY OF
MALOCCLUSION

INTRODUCTION
What cozes a Malocclusion?

This question has to be answered correctly before

any decision can be taken regarding its prevention or
correction; hence, several classifications have been
put forward to help us understanding the etiology of
malocclusion.

The various classifications proposed are-

1. White & Gardiner’s classification

2. Salzmann’s classification
3. Moyer’s classification
4. Graber’s classification
WHITE & GARDINER’S CLASSIFICATION

It was the Ist attempt made to classify malocclusion

& to distinguish between skeletal & dental etiological
factors.
DENTURE BASE ABNORMALITIES

1. Anterio-posterior mal relationship

2. Vertical mal relationship
3. Lateral mal relationship

4. Disproportion of size between teeth and basal bone

5. Congenital abnormalities.
PRE-ERUPT1ON ABNORMAL1TIES

I. Abnormalities in position of developing tooth germ

2. Missing teeth

3. Supernumerary teeth and teeth abnormal in form

4. Prolonged retention of deciduous teeth

5. Large labial frenum

6. Traumatic injury. -
POSTERUPTION ABNORMALITIES

1. Muscular

a. Active muscle force

b. Rest position of musculature

c. Sucking habits

d. Abnormalities in path of closure

2. Premature loss of deciduous teeth

3. Extraction of permanent teeth.

GRABER’S CLASSIFICATION
GENERAL FACTORS
1. Heredity

2. Congenital

3. Environment

a. Prenatal (trauma, maternal diet, German

measles, material maternal metabolism, etc).

b. Postnatal (birth injury, cerebral palsy, TMJ

injury)

4. Predisposing metabolic climate and disease:

a. Endocrine imbalance

b. Metabolic disturbances

c. infectious diseases

5. Dietary problems (nutritional deficiency)

6. Abnormal pressure habits and functional

Aberrations:

a. Abnormal sucking

b. Thumb and finger sucking

c. Tongue thrust and tongue sucking

d. Lip and nail biting

e. Abnormal swallowing habits (improper

deglutition)

f. Speech defects

g. Respiratory abnormalities

h. Tonsils and adenoids

i. Psychogenetics and bruxism

7. Posture

8. Trauma and accidents.

LOCAL FACTORS
1. Anomalies of number:

• Supernumerary teeth

• Missing teeth (congenital absence or loss due to

Accidents , caries, etc.)

2. Anomalies of tooth size

3. Anomalies of tooth shape

4. Abnormal labial frenum: mucosal barriers

5. Premature loss

6. Prolonged retention

7. Delayed eruption of permanent teeth

8. Abnormal eruptive path

9. Ankylosis

10. Dental caries

11. Improper dental restorations

ETILOGY – GENERAL FACTORS

HEREDITARY

Hereditary causes of malocclusion include al factors

that result in amaLocc1usion and are inherited from

the parents by offspring’s. These may or may not he
evident at birth, but are likely to express themse1ve
as the child grows. These can be those influencing
the-

Neuromuscular system

Dentition

Skeletal structures

Soft tissues (other than the Neuromusculature).

NEUROMUSCULAR SYSTEM

The anomalies that have been found to possess some

inherited component include deformities in size,
position, tonicity, contractility, and in the
neuromuscular coordination pattern of facial, oral,
and tongue musculature.

DENTTION

Certain characteristics, especially related to the

dentition are definitely inherited. These include:
Size and Shape of the Teeth

Studies on twins have proved that the size and

relative shape of the teeth is inherited e.g. Peg
shaped

Lateral are the most commonly seen and noticed

abnormally shaped teeth encountered clinically. To
produce a malocclusion the discrepancy should exist
between the basal bone and the teeth size, or the
associated skeletal structures.

Number of teeth
Presence of either more or less no. of teeth can also
be inherited. This includes condition such as
Anodontia, Oligodontia, and Hypodontia.

Primary Position of Tooth, Germ and the

Path of Eruption
Considered to be inherited. eg., Crossbites, Ectopic
tooth eruption.

Shedding of Deciduous Teeth &

Sequence of Eruption
Mineralization of Teeth
Inherited defects of the tooth structure differ from
defects in mineralization as they are present in both
the deciduous dentition as well as permanent dentition
and are localized in the enamel or the dentine.
SKELETAL STRUCTURES

Skeletal structures r partially inherited

e.g, Class III skeletal pattern is associated with

familial tendency

SOFT TISSUES (OTHER THAN THE

NEUROMUSCULATU RE)
These generally includes the size & shape of the
frenum especially the maxillary labial frenum.

CONGENITAL FACTORS
Congenital defects include those malformations that
are seen at the time of birth. These are –

a. Micrognathism
b. Oligodontia
c. Anodontia , etc.

Endocrine imbalance
Certain endocrinal disorders may result in mal
occlusion. The following are some of the endocrinal
disturbances that can cause malocclusion.

Hypothyroidism: Hypothyroidism is characterized by

the presence of one or more of the following
features:

a) Retardation in rate of calcium deposition in

bones and teeth
b) Marked delay in tooth bud formation and
eruption of teeth
c)Delayed carpel and epiphyseal calcification
d) The deciduous teeth are often over-retained and
the permanent teeth are slow to erupt Abnormal
root resorption
e)Irregularities in tooth arrangement and crowding
of teeth can occur

Hyperthyroidism: This condition is characterized by

increase in the rate of maturation, and an increase in
metabolic rate. The patient exhibits premature
eruption of deciduous teeth, disturbed root
resorption of deciduous teeth and early eruption of
permanent teeth. The patient may have osteoporosis
which contra-indicates orthodontic treatment.

Hyperparathyroidism : This endocrinal disorder is

associated with changes in calcium metabolism. It
can cause delay in tooth eruption, altered tooth
morphology, delayed eruption of deciduous and
permanent teeth and hypo plastic teeth.

Hyperparathyroidism : Hyperparathyroidism
produces increase in blood calcium. There is
demineralization of bone and disruption of
trabecular pattern. In growing children, interruption
of tooth development occurs. The teeth may become
mobile due to loss of cortical bone and resorption of
the alveolar process.
METABOLIC DISTURBANCES
Acute febrile diseases are believed to slow down +he
pace of growth and development. These conditions
may cause a disturbance in tooth eruption and
shedding thereby increasing the risk of
malocclusion.

DIETARY PROBLEMS (NUTRITIONAL

DEFICIENCY)
Nutritional deficiencies during growth may result in
abnormal development, causing malocclusion.
Nutrition related disturbances such as rickets,
scurvy and beriberi can produce severe malocclusion.

POSTURE
Poor postural habits are said to be a cause for
malocclusion.
Children who support their head by resting the chin
on their hand and those who hang their head so that
the chin rests against the chest ore observed to
have Mandibular deficiency.

ACCIDEINTS AND TRAUMA

Children are highly prone to injuries of the dento-
facial region during the early years of life when they
learn to crawl, walk or during play. Most of These
injuries go unnoticed and may be responsible for non-
vital teeth that do not resorb and deflection of
erupting permanent teeth into abnormal positions.

Etiology – Local
Factors
ANOMALIES OF NUMBER
Each jaw is designed to hold only a specific number
of teeth at a particular age. However, if the number
of teeth present increases, or size of teeth is
abnormally ige, it can cause crowding or hamper the
eruption i succedaneous teeth in their ideal
positions. Similarly, if the number of teeth present
is less than normal then gaps will be seen in the
dental arch. The anomalies in the number of teeth
can be of two types (I) supernumerary teeth, (II)
less number of teeth or missing teeth.

SUPERNUMERARY TEETH
Supernumerary teeth can vary remarkably size,
shape and location. They may closely resemble a
teeth of the group to which they belong, i.e. mimics,
premolars or molars, etc

Supernumerary teeth, which bear a close

resemblance to a particular group of teeth and erupt
close to the original sight of these teeth, are called
supplemental teeth. Commonly seen in the premolar
region or the lateral incisor region

The most commonly seen supernumerary tooth is the

“mesiodens”

Supernumerary teeth can cause

a. Non-eruption of adjacent teeth

b. Delay the eruption of adjacent teeth

c. Deflect the erupting adjacent teeth into

abnormal locations

d. Increase the arch perimeter.

e. Crowding in the dental arch

MISSING TEETH
Congenitally missing teeth are far more commonly
seen as compared to supernumerary teeth (true
partial anodontia or hypodontia or Oligodontia)
Certain teeth show a greater predilection to be
congenita1ly missing .The most commonly

are the third molars, followed by the maxillary

lateral incisors.

Congenitally missing teeth can lead to:

a. Gaps between teeth

b. Aberrant swallowing patterns

c. Abnormal tilting

d. Multiple missing teeth can cause a multitude of

problems

ANOMALIES OF TOOTH SIZE

Only two anomalies of tooth size are of interest to
an orthodontist-microdontia and macrodontia. The
true generalized form of microdontia is rarely seen.
It is usually associated with cases of pituitary
dwarfism and, true generalized macrodontia, is seen
in cases of pituitary gigantism .Most common
localized microdontia involves maxillary lateral
incisors. The tooth is called a ‘peg lateral”

ANOMALIES OF TOOTH SHAPE

Anomalies of tooth shape include true fusion,
gemination, concrescence, talon cusp, and ‘dens in
dente’. Dilaceration is also an anomaly of the tooth

a) True fusion is seen when the tooth arises

through the union of two normally separated
tooth germs - It might lead to spacing
b) Geminated teeth are anomalies, which arise
from division of a single germ by an
invagination, leading to the formation of two
incomplete teeth
c)The term ‘twinning’ has been used to designate
the production of equivalent structures
 d)The term concrescence refers to fusion of
teeth which occurs after root formation has
been completed

LABIAL FRENUM
At the birth the Labia1 frenum is attached to the
alveolar same fibers crossing over and attaching with
the dental papilla. As the teeth erupt, bone is
deposited and the frenal attachment migrates

Superiorly with respect to the alveolar ridge. Some

may persist between the maxillary central incisor

These fibers which persist between these teeth of

preventing the two contra-lateral central incisor
from coming into close approximation. It. Midline
diastema may persist even after the “ugly duckling
stage” or close simultaneously upon the amount of
fibers crossing over interdentally. A midline
diastema can exist due to various cozes and the
‘blanch test’ is used to determine the role of frenum
as a causative factor.

PREMATURE LOSS OF DECIDUOUS TEETH

The permanent successor does not erupt for
sometime following the loss of the deciduous tooth,
during which the adjacent teeth get time to migrate
in its space. This can lead to a decrease in the over
all arch length as the posterior teeth have a
tendency to migrate mesially. This might cause the
permanent successor to erupt malpositioned or get
impacted or cause a shift in the midline (in case of
anterior teeth).

In case an anterior deciduous is lost prematurely,

there is a tendency for spacing to occur between the
erupted anterior teeth. It might also lead to a shift
in the midline, towards the side where the deciduous
Compensatory extraction for anterior deciduous
tooth loss and space maintainer or the use of space
regainers is highly recommended in case of the early
loss of deciduous tooth

Which ever deciduous tooth may be retained beyond

the usual eruption age of their permanent successor,
is capable of causing:

i. Buccal/labial or palatal/lingual

deflection in its path of eruption; or

ii. Impaction of the permanent tooth

DELAYED ERUPTION OF PERMANENT TEETH

Nature has provided for a particular sequence for
the eruption of individual teeth in each arch, but if
one of the teeth does not occupy its designated
place in this sequence there is a likelihood of
migration of other teeth into the available space.
Whatever the reasons for the delay in eruption ,it is
important from a clinicians point of view to maintain
and if required to create space for its eruption.

ABNORMAL ERUPTIVE PATH

Generally each tooth travels on a distinct path since
its inception to the location at which it erupts. It
can deviate from this eruption path because of many
reasons . The tooth that most frequently erupts in
an abnormal location is the maximally canine

Various reasons have been attributed for this

behavior. These include:

1. Early loss adjacent primary teeth with a

consequential flaring or spacing between
erupted permanent teeth.
2. Early loss of primary tooth leading to
mucosal thickening over the succedaneous
tooth

3. Early loss of the primary tooth might cause

excessive bone deposition over the
succedaneous tooth

4. Hereditary, in certain children teeth erupt

much later than established norms

5. Presence of supernumerary tooth can block

the erupting permanent tooth

6. Presence of odontomas or other cysts and

tumors in the path of eruption

7. Presence of deciduous root fragment

8. Presence of ankylosed deciduous teeth

9. The succedaneous tooth might be

congenitally missing, delaying the loss of the
primary tooth
10. In certain endocrine disorders the eruption
of permanent teeth might be delayed, e.g.
hypothyroidism

ANKYLOSIS
Ankylosis is a condition which involves the
union of the root or part of a root directly to
the bone, without the intervening periodontal
membrane ,its encountered relatively
frequently during the mixed dentition stage.
Its seen more commonly associated with
certain infections ,endocrine disorders and
congenital disorders, e.g. Cleidocranial
dysostosis, but these are rare occurrences.

Ankylosis should generally be suspected ,

where there is a past history of trauma, or a

tooth has regained stability or apicoectomy

has been performed.

DENTAL CARIES
Caries can lead to premature loss of
deciduous or permanent teeth thereby
causing migration of contiguous teeth,
abnormal axial inclination and supra-eruption
of opposing teeth.

Proximal caries that has not been restored

can cause migration of the adjacent teeth
into the space leading to a reduction in arch
length.

A substantial reduction in arch length can be

expected if several adjacent teeth involved by
proximal caries are left unrestored.
IMPROPER DENTAL RESTORATIONS
a. Under contoured proximal restoration lead
to a significant decrease in the arch
length. Over contoured proximal
restorations might bulge into the space to
be occupied by a succedaneous tooth and
result in a reduction of this space.
b. Overhang or poor proximal contacts may
predispose to periodontal breakdown.
c. Premature contacts on over contoured
occlusal restoration can cause a functional
shift of the mandible during jaw closure,
d. Under-contoured occlusal restorations can
lead to the supra-eruption of the opposing
dentition.