ORTHODONTICS

1. Dr. Muzammil C

2. CONTENTS
 INTRODUCTION
 CLASSIFICATION OF ETIOLOGY OF MALOCCLUSON
 GENERAL FACTORS
 HEREDITY
 CONGENITAL DEFECTS
 ENVIRONMENT
 PREDISPOSING METABOLIC CLIMATE AND DISEASE
 DIETARY PROBLEMS
 POSTURE
 ACCIDENTS AND TRAUMA
 ABNORMAL PRESSURE HABITS

3. INTRODUCTION
Malocclusion is a developmental condition.
It is an interaction between genetic and environmental
factors
Malocclusions are caused by either genetic factors
or environmental factors.

4. In two-third of the cases the cause of
malocclusion is not known.
In the malocclusion group, a small minority have
problems attributable to a specific known cause ; the
remainder are the result of a complex and poorly
understood combination of hereditary and
environmental influences.
It is of great value in making preventive and
interceptive orthodontic procedures as possible
because malocclusion is prevented or intercepted by
timely removal of the cause.

5. SYSTEMS OF CLASSIFICATION
WHITE AND GARDENER’S CLASSIFICATION
A)DENTAL BASE ABNORMALITIES:
I. Anteroposterior malrelationship
II. Vertical malrelationship
III.Lateral malrelationship
IV.Disproportion of size between teeth and
basal bone
V. Congenital abnormalities

6. I. Abnormalities in position of developing tooth
germ
II. Missing teeth
III. Supernumerary teeth
IV. Prolonged retention of deciduous teeth
V. Large labial frenum
B.PRE-ERUPTION
ABNORMALITIES

7. 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
C . POST-ERUPTION ABNORMALITIES

8. Moyers identified primary etiologic sites , from where
the variations were expected to arise. These sites
included :
a. the craniofacial skeleton
b. the dentition
c. neuromuscular system
d. other soft tissues excepting muscle
1. Heredity
a. Neuromuscular system
b. Bone
c. Teeth
d. Soft parts
MOYERS CLASSIFICATION

9. 2. Development defects of unknown origin
3. Trauma
a. Prenatal trauma and birth injuries
b. Post natal trauma
4. Physical agents
a. Premature extraction of primary teeth
b. Nature of food
5. Habits
a. Thumb sucking and finger sucking
b. Tongue thrusting
c. Lip sucking and lip biting
d. Posture
e. Nail biting
f. Other habits

10. 6. Disease
a. Systemic disease
b. Endocrine disorders
c. Local diseases
- nasopharyngeal diseases and disturbed
respiratory function
- gingival and periodontal disease
- tumors
d. Caries
-early loss of permanent teeth
- premature loss of deciduous teeth
-disturbance in sequence of eruption of
permanent teeth

11. Graber’s classification
GENERAL FACTORS
1. Hereditary
2. Congenital defects ( cleft palate, torticollis ,
cleidocranial dystosis , cerebral palsy , syphilis etc )
3. Environment
a. prenatal(trauma , maternal diet , German measles)
b. postnatal ( birth injury , cerebral palsy , TMJ injury)
4. Predisposing metabolic climate and disease
a. endocrine imbalance
b. metabolic disturbances
c. infectious disease

12. 5. Dietary problems
6. Posture
7. Trauma and accidents
8. 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
f. speech defects
g. respiratory abnormalities
h. tonsil and adenoids
i. psychogenetics and bruxism

13. LOCAL FACTORS
1. Abnormalities of number
2. Anomalies of tooth shape
3. Abnormal labial frenum: mucosal barriers
4. Premature loss
5. Prolonged retention
6. Delayed eruption of permanent teeth
7. Abnormal eruptive path
8. Ankylosis
9. Dental caries
10. Improper dental restorations

14. GENERAL FACTORS
 Heridity
According to Lundstorm there exist a number of
human traits that are influenced by the genes that
include
A. Tooth size
B. Arch dimensions
C. Height of the palate
D. Crowding and spacing of teeth
E. Degree of sagittal overbite ( overjet)
F. Tooth shape
G. Tooth number
H. Interarch variations
I. Frenum

15. CONGENITAL DEFECTS
Malformations seen at the birth
GENERAL CONGENITAL DEFECTS
A. Abnormal state of mother during pregnancy
B. Malnutrition
C. Endocrinopathies
D. Infectious diseases
E. Metabolic and nutritional disturbances
F. Accidents during pregnancy and child birth
G. Intra uterine pressure
H. Accidental traumatisation of the foetus by external
forces

16. LOCAL CONGENITAL FACTORS
a. Abnormalities of jaw development due to
intra uterine position
b. Clefts of the face and palate
c. Macro and microglossia
d. Cleidocranial dystosis

17. Other congenital conditions
a. Cerebral palsy
b. Torticollis
c. Maternal rubella infections
d. Congenital syphilis

18. ENVIRONMENT
PRENATAL FACTORS
a. Abnormal fetal posture
b. Fibroids of the mother
c. Amniotic lesions
d. Maternal diet and
metabolism
e. Drug induced deformities-
thalidomide
f. German measles

19. 1. Disturbances in embryologic development
Any problem in germ cell layer formation and initiation
of organization(17th day) causes the fetal alcohol
syndrome.
Anencephaly results when there is a disturbance during
neural tube formation(18-23 days of IU life) .

20. Subsequent to neural tube formation there is origin,
migration and interaction of neural crest cells
between 19 and 28 days, and defects during this
stage causes hemifacial microsomia and
mandibulofacial dystosis.
Cleft lip and or palate and other facial clefts result due
to defective organ system function( 28-55 days).

21. From the 50 th day of IU life to birth , final
differentiation into skeletal , muscular and nervous
tissue takes place and disturbance during this phase
can result in achondroplasia, crouzan syndrome or
Apert syndrome.

22. 2. Teratogens
TERATOGENS EFFECTS
AMINOPTERIN ANENCEPHALY
ASPIRIN CLEFT LIP AND PALATE
CIGRATTE SMOKE CLEFT LIP AND PALATE
CYTOMEGALOVIRUS MICROCEPHALY, HYDROCEPHALY
DILATIN CLEFT LIP AND PALATE
ETHYL ALCOHOL CENTRAL MID FACE DEFICIENCY
6- MERCAPTOPURINE CLEFT PALATE
13-CIS- RETINOIC ACID RETINOIC ACID SYNDROME
RUBELLA VIRUS MICROPHTHALMIA , DEAFNESS
THALIDOMIDE HEMIFACIAL MICROSOMIA
TOXOPLASMA MICROCEPHALY, HYDROCEPHALY
X-RADIATION MICROCEPHALY
VALIUM CLEFT LIP AND PALATE
VITAMIN D EXCESS PREMATURE SUTURE CLOSURE

23. 3. FETAL MOLDING
During IU life , any pressure effect on rapidly
growing areas lead to distortion of growth.
On rare occasions, arm is pressed against the face ,
resulting in maxillary deficiency.
Sometimes, fetal head is flexed tightly against the
chest in utero. This retards the mandibular
growth due to decreased volume of amniotic
fluid.

24. The restriction of the mandible , forces the tongue
upwards and , therefore , closure of the palate is
stopped leading to cleft palate.
This happens in Pierre Robin Syndrome in which
combination of micrognathia with cleft palate occurs.

25. POSTNATAL FACTORS
a. Forceps delivery causes TMJ injury , undergo ankylosis
and results in hypoplastic mandible.
b. Cerebral palsy conditions can exhibit malocclusion due
to loss of muscle balance.
c. Traumatic injuries that causes condylar fracture and
results in facial asymmetry.
d. Scar tissue caused by burns or cleft surgery.
e. Milwaukee braces- in scoliosis – causes mandibular
growth retardation

26. Predisposing metabolic climate and disease
ENDOCRINE IMBALANCE
HYPOTHYROIDISM
 Retardation in rate of calcium deposition in bones and teeth.
 Marked delay in tooth bud formation and eruption of teeth.
 Delayed carpel and epiphyseal calcification
 The deciduous teeth are often over retained and the
permanent teeth are slow to erupt.
 Abnormal root resorption
 Irregularities in tooth arrangement and crowding of teeth can
occur.

27. HYPERTHYROIDISM
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 indicates
orthodontic treatment.
HYPOPARATHYROIDISM
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 hypoplastic teeth.

28. HYPERPARATHYROIDISM
 Hyperparathyroidism produces increase in blood calcium.
 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 slow down pace of growth
and development.
 These conditions may cause disturbance in tooth
eruption and shedding hence increases risk of
malocclusion.

29. DIETARY PROBLEMS ( NUTRITIONAL DEFICIENCY)
 Nutritional deficiencies during growth may result in
abnormal development , causing malocclusion.
 The diseases are more common in the developing
countries than in the developing countries than in
the developed world.
 Nutrition related disturbances such as rickets ,
scurvy and beriberi can produce severe malocclusion
and may upset the dental developmental timetable.

30. POSTURE
Poor postural habits are said to be cause for malocclusion.
Although not substantiated, they may be imbalance thereby
increasing the risk of 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 are observed to have mandibular deficiency
Poor posture as a cause of malocclusion although not proved
may nevertheless be an accentuating factor for other
malocclusions.

31. ACCIDENTS AND TRAUMA
Children are more prone to injuries of dento-facial region
during the early years of life when they learn to crawl,
walk or during play.
Resulting in non vital teeth that do not resorb and
deflection of erupting permanent teeth into abnormal
position.

32. ABNORMAL PRESSURE HABITS
THUMB AND DIGITAL SUCKING
 Digital sucking is defined as placement of the
thumb or one or more fingers in varying depths into
the mouth.
EFFECTS
 Labial tipping of the maxillary anterior teeth
resulting in proclination of maxillary anteriors.
 The overjet increases due to proclination of the
maxillary anteriors

33. Anterior open bite can occur as a
result of restriction of incisor
eruption and supraeruption of the
buccal teeth.
The cheek muscles contract during
thumb sucking resulting in
narrow maxillary arch , which
predisposes to posterior cross bite.
The child may develop tongue
thrust habit as a result of the open
bite.
The upper lip is generally
hypotonic while the lower part of
the face exhibits hyperactive
mentalis activity.

34. TONGUE THRUST HABIT
 Tongue thrust is defined as a condition in
which the tongue makes contact with any
teeth anterior to the molars during
swallowing.
CLINICAL FEATURES
 Proclination of anterior teeth.
 Anterior open bite.
 Bimaxillary protrusion .
 Posterior open bite in case of lateral
tongue thrust.
 Posterior cross bite.

35. BRUXISM
 Bruxism can be defined as the
grinding of teeth for non-functional
purposes.
CLINICAL FEATURES
 Occlusal wear facets can be
observed on the teeth.
 Fractures of teeth and restoration.
 Mobility of teeth.
 Tenderness and hypertrophy of
masticatory muscles.
 Muscle pain when the patient
wakes up in the morning.
 Temporomandibular joint pain and
discomfort can occur.

36. LIP BITING
CLINICAL FEATURES
 Proclined upper anteriors and
retroclined lower anteriors.
 Hypertrophic and redundant lower
lip.
 Cracking of lips.
NAIL BITING
 CLINICAL FEATURES
 Rotation
 Wear of incisal edge
 Minor crowding

37. RESPIRATORY ABNORMALITIES
 This may lead to anterior proclination , short upper lip,
everted lower lip and v shaped arch, can be corrected by
using oral vestibular screen. The typical profile is
called as “ adenoid facies “.
 Prolonged inflammation of tonsils causes tongue and
jaw posture alteration leading to development of
adenoid facies

38. CONCLUSION
Malocclusion has an important impact on the function and
esthetics on the self esteem of many children,adolescent and
adult.If a malocclusion is not recognized by either the dentist
or the patient,it cannot be assessed and treated.
Knowledge about the various etiological factors of
malocclusion will help us to plan the various interceptive and
preventive orthodontic procedures.
It also eliminating the etiological factor if it is of a
environmental type.
A sound knowledge about the various factors that lead to
malocclusion,will definitely help is to render excellent
treatment for patients with good retention and stability.

39. REFERENCES
ORTHODONTICS - THE ART AND SCIENCE - SIXTH
EDITION – S I BHALAJI
TEXTBOOK OF ORTHODONTICS – FIRST EDITION – S
GOWRI SHANKAR
CONTEMPORARY ORTHODONTICS – SIXTH EDITION
– WILLIAM R. PROFITT