Etiological basis of malocclusion theories /certified fixed orthodontic courses by Indian dental academy

MALOCCLUSION THEORIES

INDIAN DENTAL ACADEMY
Leader in continuing dental education
www.indiandentalacademy.com


Introduction


1.
2.

There is general agreement that an individual’s
occlusal status is described by two major
characteristics:
The relationship of the teeth within each arch to a
smoothly curving line of occlusion ( alignment ), and
The pattern of occlusal contacts between maxillary
and mandibular teeth in the transverse, anteroposterior, or vertical planes of space (occlusion).
It is difficult to implicate a single major cause for
malalignment or malocclusion.



Rather than having specific "causes," as do some
diseases, malocclusions are usually clinically
significant variations from the normal range of growth
and morphology. Etiologic factors contribute to the
variance more often than they simply "cause" it.

The primary etiologic sites of malocclusion are
(a) the craniofacial skeleton,
(b) the dentitions,
(c) the orofacial neuromusculature, and
(d) other "soft tissues" of the masticatory system,
(excluding muscle).

Incidence of Malocclusion
The most prevalent type of malocclusion in deciduous
dentitions is anterior open bite tied with tongue thrust
& finger habits.
Class II division 1 was next common.
 In mixed dentitions, crowding was most common, &
mandibular retrusion is the next common.
 In permanent dentitions, Class II, Division 1 &
crowding were equally distributed.



Prevalence
Brunelle JA et al J Dent Res 1996.





Angle I Normal: 30%
Angle Class I Malocclusion: 50%
Angle Class II Malocclusion: 20%
Angle Class III Malocclusion: <1%

Horizontal Plane:
Vertical Plane:
• Posterior Cross
• Open Bite (≥ 0 mm):< 3%
Bite
:9.1% • Vertical Deep
Bite
(≥5 mm): 16 %

Racial Differences:







Asian: increased Angle III prevalence
Afro-American: 10% anterior open bite,increased
Angle III
Northern European: increased prevalence of vertical
deep bite,increased prevalence Angle II
Hispanic: increased severe Angle II




In homogeneous racial groupings the incidence
of malocclusion seems relatively low. In certain
areas of the world for example, some of the
Philippine Islands malocclusion is almost
nonexistent Population groups there are
relatively pure genetically, and the occlusion of
the natives "normal."




A study was done by Stockard, C. R. (1932) on the
genetics of modified endocrine secretion and associated
form pattern among dog breeds. Proc. Sixth Internat.
Cong. Genetics,.



Results : gross deformities were seen after crossbreeding
of dogs. Racial crossbreeding may emulate these
experiments to a degree.



Conclusion :Where there has been a mixture of racial
strains the incidence of jaw size discrepancies and occlusal
disharmonies is significantly greater.

Chung, Niswander and Runck (1971) studied the effect of
intermixing of European, Japanese and Chinese races with
native Polynesians of Hawaii, on the malocclusion in their
descendents.
Their study showed that the effect of inter racial crosses on
malocclusion is additive rather than multiplicative.
No independent inheritance of discrete morphologic
characteristics like tooth and jaw sizes.

Systems of classification


The first useful orthodontic classification of
malocclusion was given by Angle (1890s).
Angle’s postulate was that the upper 1st molar
were the key to occlusion and that the upper &
the lower molars should be related so that the
mesiobuccal cusp of the upper molar occludes in
the buccal groove of lower molar.


Angle’s classification








Normal occlusion - Normal (Class I) molar relationship,
teeth on line of occlusion
Class I malocclusion - Normal (Class I) molar relationship
teeth crowded, rotated, etc.
Class II malocclusion -Lower molar distal to upper molar,
relationship of other teeth to line
of occlusion not specified
Class III malocclusion-Lower molar mesial to upper molar,
relationship of other teeth to line
of occlusion not specified

CLASS I Molar
and Jaw
Relationship

CLASS II Molar
and Jaw
Relationship

CLASS III Molar
and Jaw
Relationship


Simon’s method


One of the best classification efforts has been
made by Simon, using the gnathostatic approach
and orienting the dentition to anthropometric
landmarks in an attempt to better show the
actual relationship of the dentition in the face.
Simon took the suggestion made by Bennett in
1912 that malocclusions be categorized in three
planes.

Ackerman Profitt’s Classification


Classifications of etiology of
malocclusion
According to Dockrell
(1) Heredity;
(2) Developmental causes of unknown origin;
(3) Trauma;
(4) Physical agents;
(5) Habits;
(6) Disease; and
(7) Malnutrition

The primary etiologic sites of malocclusion are
(a) the craniofacial skeleton,
(b) the dentitions,
(c) the orofacial neuromusculature, and
(d) other "soft tissues" of the masticatory
system,(excluding muscle).


Dockrell’s Equation


Causes

ACT

Times

Tissues PRODUCING Results

ON

SOME PREDISPOSING

PRENATAL

SOME EXCITING

OR POSTNATAL

1.Heridity
2.Developmental
causes of
unknown origin
3.Trauma
4.Physical agents
5.Habits
6.Disease
7.Malnutrition

1.Continuous
OR
Intermittent
2.May act at
different age
levels.

May be following

SOME PRIMARILY
SOME SECONDARILY

1.Neuromuscular
tissue
2.Teeth
3.Soft tissue other
than muscles


or a combination
of these

1.Malfunction .
2.Malocclusion.
3.Osseous dysplasias.



McCoy and Shepard(1956)
a) Direct(determining)
b) Indirected(predisposing)


GRABER'S CLASSIFICATION


GENERAL FACTORS

1. Heredity
2. Congenital
3. Environment
 a: Pre-natal [trauma, maternal
diet, German measles,
maternal metabolism etc.,.]
 b. Post natal [birth injury,
cerebral palsy, T.M.J.injury.]

4. Pre-disposing 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 [mouth breathing etc.,.]
h. Tonsils and adenoids
i. Psychogenic tics and bruxism
7. Posture
8. Trauma and accidents

GRABER'S CLASSIFICATION


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 of deciduous teeth

6. Prolonged retention of deciduous teeth
7. Delayed eruption of permanent teeth
8. Abnormal eruptive path
9. Ankylosis
10Dental caries
11Improper dental restoration


MOYER'S CLASSIFICATION
1 Heredity
a.Neuromuscular System
b.Bone
c.Teeth
d.Soft Parts

3.Trauma
a.Prenatal trauma and
birth injuries
b.Postnatal trauma

4. Physical agents
a.Premature extraction
2.Developmental defects of
of primary teeth
unknown origin
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

6.Diseases
a.Systemic diseases
b.Endocrine disorders
c.Local diseases
i.Nasopharyngeal
diseases and disturbed
respiratory function
ii.Gingival and
periodontal disease
iii.Tumors
iv Caries
7.Malnutrition


WHITE AND GARDINER'S
CLASSIFICATION
B.Preeruption abnormalities
A. Dental base
abnormalities
1. Abnormalities in position of
developing tooth germ
1. Antero-posterior
2. Missing teeth
malrelationship
2. Vertical malrelationship 3. Supernumerary teeth and teeth
abnormal in form
3. Lateral mairelationship
4. Prolonged retention of
4. Disproportion of size
deciduous teeth
between teeth
5. Large labial frenum
and basal bone
6. Traumatic injury
5. Congenital abnormalities

C. Post-eruption 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

Salzman’s Classification
Prenatal
Postnatal

Developmental
A. General
B. Local
Functional
A. General
B. Local
Environmental Or Acquired
A. General
B. Local

Salzman’s classification
Prenatal
1.Genetic: Dentofacial anomalies may or may not
be in evidence at birth.
2. Differentiative –
a. General: affect the body as a whole
b. Local: affect the face, jaws, and teeth
3 Congenital a. General or constitutional
b. Local or dentofacial



Postnatal

1.

Developmental
A. General
a. Birth injuries
b. Abnormalities of relative rate of growth in
different body organs
c. Hypo or hypertonicity of muscles
d. Endocrine disturbances
e. Nutritional disturbances
f. Childhood diseases that affect the growth
pattern
g. Radiation

B. Local
a. Abnormalities of the
dentofacial Complex
(1) Birth injuries of the
head, face and jaws
(2) Micrognathia or
macrognathia
(3) Microglossia or
macroglossia
(4) Abnormal frenum labil
(5) Facial hemiatrophy

b. Anomalies of tooth
development
(1) Delayed or premature
eruption of the deciduous
or permanent teeth
(2) Delayed or premature
shedding of deciduous teeth.
(3) Ectopic eruption
(4) Impacted teeth
(5) Aplasia of teeth




Functional

2. Local
A. Malfunction of forces exerted
A. Muscular hyper- or
by the inclined planes of the
hypotonicity.
cusps of the teeth
B. Endocrine disturbances B. Loss of force caused by failure
of proximal contact of teeth
C. Neurotrophic
C. Temporomandibular
disturbances
articulation disturbances
1. General

D. Nutritional deficiencies
E. Postural defects
F. Respiratory
disturbances, mouth
breathing.

D. Masticatory and facial
muscular hypo- or hyperactivity
E. Faulty masticatory function,
(during tooth eruption).


Environmental Or Acquired.
1. General
A. Disease
B. Nutritional disturbances
(during tooth formation).
C. Endocrines.
D.Metabolic disturbances
E.Trauma. Accidental injuries
F.Radiation

2. Local
A. Disturbed forces of occlusion
B. Early loss of deciduous teeth
C. Prolonged retention of deciduous
teeth
D. Delayed eruption of permanent teeth
E. Loss of permanent teeth
F. Periodontal diseases
G. Temporomandibular articulation
disturbances
H, Infections in the oral cavity
I. Pressure habits
J. Traumatic injuries, fractures of jaws




Equilibrium Theory first given by Weinstein.S et al A O
1963 revisited by William R Proffit A O 1978 states that
Equilibrium theory, as applied in engineering, that an
object subjected to unequal forces will be accelerated and
thereby will move to a different position in space .It
follows that if any object is subjected to a set of forces
but remains in the same position, those forces must be in
balance or equilibrium. From this perspective, the
dentition is obviously in equilibrium, since the teeth are
subjected to a variety of forces but do not move to a new
location under usual circumstances. Even when teeth are
moving, the movements are so slow that a static
equilibrium can be presumed to exist at any instant in
time.

Equilibrium components
Four major primary factors
1. Intrinsic forces by tongue &
lips
2. Extrinsic forces:
Habits (thumb-sucking, etc)
Orthodontic appliances.
3. Forces from dental occlusion
4. Forces from the periodontal
membrane.


.


25 After a paralytic stroke in this patient, the side of the tongue rested
A large portion of die cheek has been lost because of a
against the mandibular left posterior teeth. A, Intraoral view; B, casts
tropical infection. The outward splaying of die teeth when
mounted on an articulator. The extreme displacement of teeth in this adult
the restraining force of the check :s lost illustrates the effect
resulted from the increased tongue pressure, altering the equilibrium.
of a change in equilibrium. (From Moss JP, Picton DCA:
(Courtesy Dr. T. Wallen.)
Arch OralBiol 12:13131320, 1967.)

GENETICS AND
MALOCCLUSION


Heredity





Two Facts
1.For each individual there is a basic pattern or
blueprint for dentofacial development , not
really which may be masked but not really
changed. (unless by surgery).
2.Racial and familial characteristics repeat


Inheritance and Malocclusion
Familial

occurrence of Class II division 2 has been
documented in several published reports
including twin and triplet studies e.g. Korkhaus
(1930), Markovic (1992), Peck et al. (1998).

Markovic

(1992) carried out a clinical and
cephalometric study of 114 Class II division 2
malocclusions (48 twin pairs and six sets of
triplets)





Of the monozygotic twin pairs, 100 per cent
demonstrated concordance for the Class II division
2 malocclusion, while almost 90 per cent of the
dizygotic twin pairs were discordant.
This is strong evidence for genetics as the main
etiological factor. Genetic influence is probably
Autosomal dominant with incomplete penetrance
and variable expressivity.






It could also be explained by a Polygenic model with a
simultaneous expression of a number of genetically
determined morphological traits acting additively rather
than being the effect of a single controlling gene for the
entire occlusal malformation.
Controversy regarding the etiology arises from a failure
to appreciate the synergistic effects of genetics and
environment.




The most famous example of a genetic trait passing
through several generations is the pedigree of the so
called Hapsburg jaw.( Hungarian /Austrian dual
monarchy)



Strohmayer (1937) concluded from pedigree analysis of
the Hapsburg family line that the mandibular
prognathism was transmitted as an Autosomal
dominant trait.

King Charles II of Spain who had a Hapsburg jaw.

Heritability of craniofacial skeletal dimensions
and tooth-based occlusal variables








Craniometric measures have higher heritabilities than occlusal
variables of tooth position.
Mild occlusal relationship problems may be largely
environmental, while the more severe ones probably have a
stronger genetic component.
A number of cranio-facial features are under polygenic control.
Mesiodistal dimensions of teeth are strongly influenced by
genetic determinants. All teeth have about the same amount of
heritability.
MZ twins show greater concordance in tooth morphology than
DZ twins.

Affected by Heredity
According to Lundstrom. A – (1949).
 Tooth size
 Arch length and width
 Height of the palatal vault
 Crowding or spacing of teeth.
 Overbite and overjet
 Position and configuration of muscles
 Tongue size and shape
 Character of the oral mucosa, frenum size,shape &
position.

Heredity also plays a role in:












Facial asymmetries
Macrognathia and micrognathia
Macrodontia and microdontia
Oligodontia and anodontia
Tooth shape variations (peg-shaped lateral incisors.
Carabeli's cusps,mamelons, etc.)
Cleft palate and harelip
Frenum diastemas
Deep overbite
Crowding and rotation of teeth
Mandibular retrusion
Mandibular prognathism



Robert S. Corruccini,, and Rosario H. Yap Potter: AJO-DO,
1980. Genetic variance and heritability were estimated for a
series of arch and occlusal traits in sixty twins using recently
developed methods that are unbiased by variance
heterogeneity between zygosities. Heterogeneity was
demonstrated for 20 of the 40 traits, suggesting considerable
amounts of hidden environmental determinance. Toothdisplacement means differed between monozygotes and
dizygotes, indicating bias in that trait's genetic variance
analysis.


Significant heritability could not be
demonstrated for overbite, overjet, buccal
segment relation, total tooth displacement, and
occlusal discrepancies in arch shape.
 Arch size, individual tooth displacement scores,
and cross-bite show significant genetic variance,
averaging only about 36 percent of the total
variance of these traits.



Jedidiah R. Gass, Manish Valiathan, Hemant K. Tiwari, Mark
G. Hans, and Robert C. Elston, (AJODO 2003) to estimate
familial correlations and heritability to evaluate familial
aggregation patterns of maxillary midline diastemas. The
sample consisted of 30 extended families: 15 black, 14 white
and 1 mixed race. Family data were collected with a 7-question
survey.


In all, the sample of 430 subjects consisted of 220 females,
210 males, 99 nuclear families, 534 sibling pairs, 422
avuncular pairs, 318 grandparent pairs, and 27 cousin
pairs. Data were analyzed. Heritability was found to be
0.32 ± 0.14 in the white sample and 0.04 ± 0.16 in the
black sample. The preliminary results suggest a possible
genetic basis for maxillary midline diastema and a greater
role of environmental factors in the black sample than in
the white sample.






A study was done by Lisa King et al ( AJODO 1993 )
to estimate heritabilities of skeletodental variables. Of
only that portion of the adolescent population receiving
comprehensive orthodontics. Initial treatment records
of 104 pairs of siblings were studied, all of whom
subsequently received full-banded treatment.
In this selected series of overt malocclusions,
heritability estimates for craniometric variables were
significantly lower than in a comparable series of
adolescents with naturally occurring good occlusions,
whereas heritability estimates for occlusal variations
(e.g., rotations, crossbites, displacements) were
significantly higher.







This indicates the clinical perception that siblings often
present with similar malocclusions.
They propose that the substantive measures of intersib
similarity for occlusal traits reflect similar responses to
environmental factors common to both siblings. That is,
given genetically influenced facial types and growth
patterns, siblings are likely to respond to environmental
factors (e.g., reduced masticatory stress, chronic mouth
breathing) in similar fashions.
Malocclusions appear to be acquired, but the fundamental
genetic control of craniofacial form often diverts siblings
into comparable physiologic responses leading to
development of similar malocclusions.



Hasund and Sivertsen ( A O – 1971) point out the sexlinked nature of facial width and dental arch shape.
Females demonstrate a positive correlation the wider
the face, the wider the arch. Unless we can change
cranial and facial superstructures and reorient bony
trabeculae, stress trajectories and supporting pillars and
buttresses, along with their muscle attachments, we
cannot significantly alter the hereditary pattern
determinant that furnishes the blueprint for arch form,
arch size, arch shape, etc.




According to Pruzhansky (1959), the individual never
fully realizes the genetic pattern in postnatal life.
Human potentialities are determined by the genotype,
but their manifestation depends on environment. With
the exception of identical twins, no two persons have
the same genotype.


Examples of Congenital Defects






Clefts of the lip and palate
Cerebral Palsy
Crouzons syndrome
Cleido-Cranial Dysostosis
Cranial Synostosis


Craniosynostoses


The sutures ( or lines of fusion ) between the bones of
the cranium are the areas across which the skull
expands as growth occurs. Craniosynostosis describes
the premature fusion of skull sutures. Those which
particularly affect skull shape are the coronal, sagittal
and lamboid sutures.




It is the constraint on neurocranial growth by
prematurely closed sutures that results in the
characteristic shape. Head shape depends on which
sutures are prematurely synostosed, the order in which
they synostose, and the timing at which they synostose.
As a general rule, growth restriction occurs at right
angles to the fused suture with compensatory expansion
in the same direction as the fused suture.


Crouzon Syndrome


Autosomal dominant with almost complete penetrance



Considerable variability of cranial form depending upon
the sequence and degree of sutural synostosis. The
most characteristic type is represented by the premature
closing of the lamboid and coronal sutures resulting in
an abnormally high, peaked or conically shaped skull.




Malformations of the
face lend the disease its
characteristics. The face
is flattened, sometimes
concave.




Protrusion of the
eyeballs is a constant,
cardinal sign and is often
quite marked.






Wide-set eyes may be
present
Nasal root is flat, the
dorsum and the nostrils
are wide




Because of recession of
the maxillary bone, there
is the impression of
protruded mandible
despite the fact that the
latter is normal or even
reduced in size.




Orally, the dental arch
may be V-shaped. The
palate is usually higharched and narrow


Apert’s Syndrome




Autosomal dominant. High
infant mortality.Advanced
male parental age consistently
noted.
The occiput is flat and not
clearly demarcated from the
plane of the back of the neck.
The forehead is steep, high
and flat. Temporal bulging is
evident




Osseous and / or
cutaneous syndactyly of
hands and feet




Downward slanting of
the eyes with a drooping
of the upper eyelids




The mouth remains open
in the shape of an
isosceles triangle. The
upper lip is retracted.
The cheeks are rounded
while the dangling lower
lip juts out.




Class III malocclusion


Treacher-Collins Syndrome
(Mandibulofacial Dysostosis)


The term “ dysostosis refers to a malformation of
individual bones either singly or in combination, but it
is not a generalized skeletal disorder. Thus,
mandibulofacial dysostosis is limited to facial structures.



Autosomal dominant trait.






Varying degrees of
hypoplasia of the
mandible, maxilla, and
zygoma.
Sagging lower eyelid


Cleiocranial Dysplasia






Autosomal dominant inheritance. Penetrance is high,
although expressivity may be low requiring careful
examination to establish proper diagnosis.
Sagitally diminished cranial base and transverse
enlargement of the cranium, resulting in a large head.
Facial bones and paranasal sinuses are hypoplastic
giving the face a small and short appearance




Orally, delayed eruption
of secondary dentition,
supernumerary teeth,
more frequent caries, and
malformed teeth or
roots. The cause of
delayed or failed eruption
of the teeth has been
associated with lack of
cellular cementum.
Dentigerous cysts



Partial to complete
aplasia of clavicles, which
allows the patient to
oppose the shoulders.
Severely sloped and
hypermobile shoulders


Cleft lip & palate


The literature on tooth formation in children with cleft lip
and/or palate is reviewed by Reijo Ranta, (AJODO 1986.)
1.

The upper lateral incisor is the most susceptible to injury
in the area of cleft in both deciduous and permanent
dentitions. This tooth is affected in most instances, even
in the cases of microforms of the cleft lip.

2.

The prevalence of hypodontia increases strongly with
the severity of cleft. More teeth are congenially missing
from the upper jaw than from the lower jaw; however,
in the permanent dentition both jaws are affected.

3. Very high prevalence of hypodontia are observed in
connection with the Van der Woude syndrome
associated with cleft and with the Pierre Robin anomaly.
4. Hypodontia is similarly prevalent in subjects with isolated cleft
palate with and without a positive family history of clefts.
5.Asymmetric formation of the contralateral teeth is a milder form of
hypodontia.
6. The prevalence of asymmetrically developing pairs of teeth is far
more common in children with clefts than in children with
normal palates or lips.

7. In the permanent dentition the timing of tooth formation
is delayed in children from all cleft groups compared to
noncfeft children. The delay lengthens (with increasing
severity of cleft) from 0.3 to 0.7 years and is similar in
all permanent teeth in both jaws.
8. In children with hypodontia, the delay is still more
severe. As the child becomes older, the delay may
increase.
9. The size of the permanent teeth is smaller than in non cleft children and the metric asymmetry of the crown or
root size is apparent in both jaws.

10. Enamel defects and abnormalities in shape and size of
both deciduous and permanent teeth are far more
common in children and fetuses affected with cleft than
in normal subjects. These abnormalities occur in both
jaws.
11. Dental abnormalities in number, size, shape, timing of
formation, eruption, and the cleft itself seem to have a
common cause in most instances. The postnatal
environmental factors nutrition, infections, and surgical
treatment may have an effect only on enamel defects
and, perhaps, in some instances, on agenesis of the
permanent teeth

Cerebral Palsy.







Cerebral palsy is a paralysis or lack of muscular coordination attributed
to an intracranial lesion.
It is most commonly considered to be the result of a birth injury.
Effects of this neuromuscular disorder may be seen in the integrity of
the occlusion .
Unlike cleft palate, where there are abnormal structures, the tissues are
quite normal but the patient, because of his comparative lack of motor
control, docs not know how to use them properly.
Varying degrees of abnormal muscular function may occur in
mastication, deglutition, respiration and speech. The uncontrolled or
aberrant activities upset the muscle balance that is necessary for the
establishment and maintenance of a normal occlusion.



TORTICOLLIS. The farreaching effects of abnormal
muscle forces are visible also in
torticollis, or "wry neck." The
foreshortening of the
sternocleidomastoid muscle can
cause profound changes in the
bony morphology of the cranium
and face. Torticollis provides an
example of the thesis that in a
struggle between muscle and
bone, bone yields. Bizarre facial
asymmetries with uncorrectable
dental maloccluslons may be
created if this problem is not
treated fairly early.



a.
b.
c.
d.
e.
f.

Congenital Syphilis - Abnormally shaped teeth and
malposed teeth are considered characteristic disease
phenomena
Hutchinson’s incisors.
Mulberry molars
Enamel deficiencies.
Extensive dental decay.
The maxilla may be smaller in size relative to maxilla.
Anterior crossbite.



a.
b.
c.

Maternal Rubella infection :
Dental Hypoplasia.
Retarded eruption of teeth.
Extensive caries.


ENVIRONMENT
Prenatal Influence –
 Uterine posture,
 fibroids of the mother,
 amniotic lesions,
 maternal diet and metabolism,
 drug-induced deformities (thalidomide),
 possible injury or trauma and
 German measles

Intrautcrinc moulding, showing probable intrauterine posture
distortion & assymetry in view. But may be temporary.

Phocomelia


Paulo Frazãoa and Paulo Capel Narvai (AJODO 2006) The
aim of their study was to assess the severity of occlusal
disorders in Brazilian adolescents, 12 and 18 years old, and
to investigate associations between occlusal disorders and
demographic, socio-environmental, and clinical variables.
Secondary data from a cross-sectional study, including
13,801 dental occlusion status records from a sample
randomly selected from public and private schools in 131
cities in the state of São Paulo, Brazil, were analyzed.


Results: The mean DAI score for the sample was 24.33
(SD 7.54), and 16.5% of the subjects had DAI scores of
30 or more (severe or very severe malocclusion). The
rate of DAI 31 was significantly higher among 12-yearolds, nonwhites, public-school students, those from
smaller municipalities, those without fluoridated tap
water, and those with a CI 51%, a DMFT score 4 at age
12 years, or a DMFT score 6 at age 18 years. At age 18,
fewer subjects had DAI scores 30; the components
responsible for this reduction were spacing in at least 1
incisal segment, midline diastema 1, and anterior
maxillary overjet 4.
Conclusion: Some socio-environmental factors are
associated with severity of malocclusion in adolescents.

Postnatal Influence.



Birth
Forceps delivery



Another possibility, is the delivery-induced deformation of the
upper jaw. Obstetricians frequently insert the forefinger and middle
finger into the baby's mouth to ease passage through the birth
canal. Because of the plasticity of the maxillary and premaxillary
region, temporary deformation is quite likely and permanent
damage may result



Accidents
Extensive scar tissue




Birth Injury 8 year old girl

Extensive scar tissue


Milwaukee brace


PREDISPOSING METABOLIC
CLIMATE AND DISEASE
Exanthematous fevers
 Diseases like Poliomyelitis which have
paralytic effect
 Endocrinopathies (pituitary and
parathyroid disturbances)



Acromegaly


In acromegaly, which is caused by an anterior pituitary
tumor that secretes excessive amounts of growth
hormone, excessive growth of the mandible may occur,
creating a skeletal Class III malocclusion in adult life .
Often (but not always sometimes the mandible is
unaffected) mandibular growth accelerates again to the
levels seen in the adolescent growth spurt, years after
adolescent growth was completed. The condylar
cartilage proliferates, but it is difficult to be sure
whether this is the cause the mandibular growth or
merely accompanies it. Although the excessive growth
stops when the tumor is removed irradiated, the skeletal
deformity persists.

Hemimandibular Hypertrophy







Occasionally, unilateral excessive growth of
mandible occurs in individuals who seem
metabolic normal.
Aetiology - entirely unknown.
It is more likely in girls between the ages of 15
and 20yrs, but may occur as early as age 10 or as
late as the early 30s .
Formerly was called condylar byperplasia.

Achondroplasia






Achondroplasia is rare in humans, but it does occur,
and it produces the expected changes.
Clinical Features
short limbs, the cranial base does not lengthen normally
because of the deficient growth at the synchondroses,
the maxilla is not translated forward to the normal
extent, and a relative midface deficiency occurs.
In a number of relatively rare genetic syndromes like
achondroplasia, influences on the form of the face,
jaws, and teeth can be discerned, but those cause only a
small percentage of orthodontic problems.

DIETARY PROBLEMS
(NUTRITIONAL DEFICIENCY)


Disturbances such as rickets, scurvy and
beri beri can produce severe malocclusions.
(Main problem is the upseting of the dental
developmental timetables. The resultant premature loss
prolonged retention, poor tissue health and abnormal
eruptive paths mean malocclusion).





Muscle Dysfunction
The facial muscles can affect jaw growth in two ways.
First, the formation of bone at the point of muscle
attachments depends on the activity of the muscle;
second, the musculature is an important part of the
total soft tissue matrix whose growth normally carries
the jaws downward and forward. Loss of part of the
musculature can occur from unknown causes in utero
or as a result of a birth injury, but is most likely to result
from damage to the motor nerve (the muscle atrophies
when its motor nerve supply is lost). The result would
be underdevelopment of that part of the face

Abnormal muscle activity


In Class III
malocclusions, the lower
lip is impotent, while the
upper lip is quite active
as it lengthens and is
drawn against the
maxillary incisors and
alveolar process by the
contracting buccinator
mechanism.



In the Class II, Division I
malocclusion, the lower lip
is constantly forcing the
premaxillary segment
upward and outward
against a hypotonic,
flaccid, relatively
functionless upper lip. If
there is a negative overbite
(open bite), the tongue
may actually assist in this
deformation.

Habits
Duration
Frequency
Intensity




ORAL HABITS
S U C K I N G ME C H A N I S M







Coordinated Reflex
Nourishment
Security/Warmth
Prevalence – 60%
Persistency


Note collapse of cheeks and bottle due to
vacuum created during excessive sucking.

EXCESSIVE digit sucking can set up abnormal
forces on the oral cavity and surrounding structures.

Labbok / Hendershot 1987
• Principle finding - the longer the duration of
breastfeeding, the lower the incidence of
malocclusion.
• Bottle feeding leads to a habit of forward tongue
thrusting and a weakened development of the
orbicularis muscles.
• There is a significant decrease in tongue thrusting
with an increased duration of breastfeeding .

Thumb sucking



Incidence & Damage –
Kjellgren, in a study of 167 thumb suckers,
found 87 per cent with a malocclusion;
Popovitch, in the Burlington study, reported 52
per cent of the 689 children from 3 to 12 years
of age with malocclusion that could be
attributed to oral habits.




Gesell and Ilg of Yale's Child Development Laboratory
contend that finger sucking is perfectly normal at one
stage of a child's development. They concur with this
opinion and feel that most finger sucking and tongue
sucking habits, which may be considered normal for the
first year and a half of life, will disappear spontaneously
by the end of the second year with proper attention to
nursing. For the first three years of life, damage to the
occlusion is confined largely to the anterior segment.
This damage is usually temporary, provided the child
starts with a normal occlusion.




The original morphology is quite important because
there is much controversy over the damage that may
result from finger and thumb sucking habits, because
some of damaging consequences of the habit are similar
to the characteristics of a typical hereditary pattern type of
Class II , Division I malocclusion, it is easy to assume that
the retrognathic mandible, prognathic premaxillary
segment, deep overbite, flaccid upper lip, high palatal
vault and narrow dental arches are the result of finger
sucking.





There is clinical evidence
that deglutitional
maturation is retarded in
confirmed finger suckers.
The finger habit in duration
and intensity may be
relatively innocuous
(perhaps at bed time only)
but the tongue thrust
continues to adapt to the
morphology and the,
tongue does not drop back,
hump up or spread out.

More damage may be expected with the
dorsal surface of the finger resting fulcrum

Ogaard B, Larsson E, Lindsten R Pacifiers A J O D O
1994.
• Positive association between pacifiers use
and posterior cross bite and reduced upper
arch width.
• Probable mechanism
– Sucking activity in the cheeks
– Reduced palatal support as the tongue takes a
lower position

Peter H. Lam et al (AJODO 1999)
to determine if condylar position in children with
functional unilateral crossbites was different from that
found in children with Class I noncrossbite
malocclusions. Mandibular asymmetry in children with
functional unilateral posterior crossbite was also
compared to that of a Class I noncrossbite group. It
was revealed that the mandibles of children in the
functional unilateral posterior crossbite group exhibited
asymmetry in both anteroposterior and transverse
dimensions when compared with the Class I
noncrossbite group (P < .05).

These asymmetries were the result of a functional
deviation of the mandible that was present in all
subjects in the crossbite group. This deviation was
manifested occlusally by a Class II subdivision on the
crossbite side as indicated from the study model
analysis (P < .05). Examination of condylar position as
evidenced by horizontally corrected tomograms
demonstrated a large standard deviation, resulting in an
inability to detect any significant differences within or
between groups at both T1 and T2 (P > .05).


Chang Liua et al Angle Orthodontist,, 2007
To evaluate the morphological and histological responses of
the glenoid fossa to mandibular lateral shift in growing rats.
It is suggested that the mandibular lateral shift causes
asymmetry in the position and size of the glenoid fossa and
that this phenomenon can be related to different bilateral
directional new bone formation in the posterior region.


Etiological Basis of
Malocclusion:theories &
contemporary view
Presented by- Dr.Neelesh Shah
Done Under The Guidance OfProfessor.Ashima.Valiathan
B.D.S {Pb}, D.D.S, M.S{U.S.A}
Director of P.G studies
Department of Orthodontics,
Manipal College Of Dental Sciences,
Manipal.

Part-2

Habits



Tongue thrust habit




A case report by Valiathan A. & Shaikh.S. (J I OS 1998;31:53-57)
showed the effect of an abnormally large tongue in producing the spaces
similar in appearance to primate spaces. A 28 year male patient of south
Indian origin was presented with a chief complain of proclination of
upper anterior teeth along with spacing between the same. His face was
fairly symmetrical with convex facial profile, prominent nose, acute
nasolabial angle and incompetence of lip. An additional lateral ceph was
taken following the administration of radio- opaque contrast medium to
highlight the dorsum of tongue and related soft tissue. Based on detailed
examination of the tongue dimension, tongue volume,
electromyographic activity and force exerted by the tongue, it was
concluded that excessively large volume tongue and dimension produce
excessive force which possibly causes the malocclusion.


Wallen, T. R.: Vertically directed forces and
malocclusion: A new approach. J. Dent. Res., 1974.


Studies by Wallen (1974)
indicate that vertically
directed pressures during
swallowing actually are less in
patients with anterior open
bite than in patients with
normal vertical
relationships .If the tongue
pressures were greater in the
open bite patients than in the
normal occlusion patients, it
would be easy to understand
how the tongue was
preventing eruption.





Birte Melsen et al A O April, 1987 to evaluate the
relationships between swallowing pattern and mode of
respiration and different malocclusion traits.
Considering malocclusion, it was observed that the frequency
was higher among children swallowing without tooth contact,
and that this was especially pronounced when a tongue thrust
was involved. The malocclusion traits most affected by the
swallowing pattern were the sagittal discrepancies.




The frequencies of both distal and mesial molar
occlusion were higher, as were the frequencies of
extreme maxillary overjet and mandibular overjet.
Children with a tongue thrust also had a slightly higher
frequency of openbite, although only 9.8% of the
subjects exhibited lack of incisal overlap. In the
transverse plane, both groups with a swallowing
anomaly exhibited an higher frequency of crossbite.
Comparing children with nasal respiration with mouth
breathers, the latter category exhibited a higher
frequency of distal occlusion, openbite, crossbite, and
crowding.

Conclusions - Tongue-thrust swallowing is more detrimental
to occlusal development than teeth-apart swallowing.
Respiration pattern may influence the development of the
transverse relationship, resulting in development of
crossbite. The influence of deviation in swallowing and
respiratory pattern depends on the interaction between
genetic and environmental factors. The isolated effect of
change in respiratory and swallowing pattern is still to be
elucidated.




A study by Dr.Ashima Valiathan & Padmapriya C V was done
on tongue volume & tongue force exerted during swallowing to
evaluate their effect on the dentition. cephalometric findings of
the study group were compared with normal cases as well as
togue volume & pressure were measured. The results showed an
increase in tongue pressure of 33 cN compared to 20.5 cN in
control group & also an increase in the occurance of mouth
breathing & tongue & lip habits in the study group.Thus in the
complex etiology of bimaxillary protrusion,environmental factors
in the form of various habits & excessive tongue force play an
important role.


Lischer’s
drawing




John J. Warren Samir E. Bishara, (A J O D O 2002) to
determine the association between the duration of nutritive
and nonnutritive sucking behaviors and various occlusal
characteristics in the primary dentition. The results indicated
no relationship between duration of breast-feeding during the
first year of life and any dental arch or occlusal parameters.
The study found that prolonged pacifier habits resulted in
changes to the dental arches and the occlusal parameters that
were different from the effects of digit sucking.




In addition, some changes in the dental arch
parameters and occlusal characteristics (eg, prevalence
of posterior crossbite and increased amount of overjet)
persisted well beyond the cessation of the pacifier or
digit habit , the results suggest that current
recommendations for discontinuing these habits may
not be optimal in preventing habit-related
malocclusions.


Lip sucking


Arm sucking




Posture


Yocheved Ben-Bassat et al (AJODO 2006)
Patients with idiopathic scoliosis have asymmetric features
of malocclusion compared with a random population.
Carsten Lippold et al (AO 2006)
Significant correlations could be obtained with respect to
the facial axis and the lordotic angle, the facial axis and the
pelvic inclination, the inner gonial angle and the lordotic
angle, the inner gonial angle and the pelvic inclination, the
mandibular plane angle and the lordotic angle, the
mandibular plane angle and the pelvic inclination, as well
as the facial depth and the pelvic inclination



Beni Solow et al (AO, 1977) demonstrated a
relationship between the craniocervical angulation (the
way the head is carried on the neck) and both facial
proportions and dentoalveolar proportions. The farther
the head is carried forward on the neck, the more likely
the face is to be long vertically, and vice versa. There
are corresponding differences in dentoalveolar
morphology relating to head posture. For instance, the
more the head is held forward, the more likely it is that
upper dentoalveolar height will be increased, especially
in its basal portion. Forward head posture also
correlates strongly with a steep occlusal plane.

John R. C The postural basis of malocclusion: A
philosophical overview (AJODO 2004).
Our current environment and diet are dramatically
different from those of our ancestors of 30,000 years ago
when malocclusion was rare; no evidence suggests that
there has been a significant change in our genes since then.
This questions all hypotheses that are based on the longheld belief that most malocclusions are inherited. There is
strong scientific, logical, and clinical evidence to suggest
that the weak muscles and open mouth postures that are
now endemic in our society can cause increased vertical
growth, whereas parafunction of the tongue, lips, and
cheeks is known to displace both the teeth and their
supporting bone. Such a malocclusion would be a postural
deformity.

Perverse oral postures have proved difficult to measure,
diagnose, and treat, and, in these circumstances, we should
perhaps be guided by basic research in preference to clinical
evidence. The tropic premise seems the best fit of the
hypotheses that have been considered, and no evidence
appears to disprove it. It suggests that environmental factors
disrupt resting oral posture, increasing vertical skeletal growth
and creating a dental malocclusion, the occlusal characteristics
of which are determined by inherited muscle patterns,
primarily of the tongue.








Bengt Ingerval Urs Thuer ( AO 1988). To measure
maxillary cheek pressures in the molar area, at the teeth
and high in the buccal sulcus, in both natural and
extended head positions, with teeth at rest and in
function.
In the rest position, the pressure on the alveolar
process was greater than that on the teeth, and at both
locations it was slightly greater with the head extended
than in the natural position.
The pressures on the teeth did not vary noticeably with
head position or among rest, chewing, or swallowing;
but the pressure on the alveolar process during chewing
was greater with the head extended then in the natural
position.




Local factors


Missing Teeth

(4)

Muller,T.P et al (J.A.D.A,1970)
The order of frequency of absence tooth is :
Maxillary & Mandibular third molars.
Maxillary lateral incisors.
Mandibular second premolar.
Mandibular incisor.

(5)

Maxillary second premolar.



(1)
(2)
(3)









Anodontia - the total absence of teeth
Oligodontia - atleast 6 teeth are missing
Hypodontia - the absence of only a few teeth.
Anodontia or oligodontia , is usually associated with an
usual but mild systemic abnormality, ectodermal
dysplasia .
Occasionally, oligodontia occurs in a patient with no
apparent systemic problem or congenital syndrome.


Supernumerary or extra teeth






Disturbances during - initiation and proliferation stages.
The most common supernumerary tooth appears in the
maxillary midline and is called a mesiodens.
Gupta L.D etal 1970 They may form prior to birth or as
late as 10 -12 years of age.
When it erupts at an advanced age “a third set of teeth”
In few cases Supernumerary lateral incisors;
Extra premolars appear;
Fourth & third molars may be present



A.Hall & A.Onn (JO 2006) showed 4 cases in which
delayed formation & late eruption of supernumerary
teeth in the mandible occurred in patients with history
of supernumerary formation in the premaxillary region.
In all cases the premaxillary supernumeraries prevented
eruption of the associated permanent incisors & they
concluded that an opportune time for further
radiographic review old young adult with history of
previous supernumerary teeth may be around 16 – 18
years when assessment of the third molars is often
desirable .

Malformed Teeth









Disturbances during - morphodifferentiation stage
(some carry over) histodifferentiation stage.
The most common abnormality is a variation in size,
maxillary lateral incisors and second premolars.
About 5 % of the total population have a significant
tooth size discrepancy because of disproportionate
sizes of the upper and lower teeth.
Fusion
Gemination.





As dietary habits in humans adapt from a
hunter/gatherer to a refined food culture evolutionary
selection pressures are tending to reduce tooth volume,
which is manifested in the 3rd molar , 2nd premolar and
lateral incisor “fields” ( Butler's Field Theory )
Clinical evidence suggest that congenital absence of
teeth and reduction in tooth size are related. example
hypodontia and hypoplasia of the maxillary lateral
incisors present simultaneously.





Douglas R. Crosby et al (A J O D O 1989 )
Occurrence of tooth size discrepancies among
different malocclusion groups The results showed
that there was no significant difference in the incidence
of tooth size discrepancies among malocclusion groups,
there was a large number of tooth size discrepancies in
each group. Therefore it is suggested that Bolton's
tooth size analysis be performed before initiation of
orthodontic treatment.


Abnormal Labial Frenum


At birth the frenum is attached to the alveolar ridge,
with fibers actually running into the lingual interdental
papilla. As the teeth erupt and as alveolar bone is
deposited, the frenum attachment migrates superiorly
with respect to the alveolar ridge. Fibers may persist
between the maxillary central incisors and in the Vshaped intermaxillary suture ,attaching to the outer
layer of the periosteum and connective tissue of the
suture.














As Faustin Weber has noted, the diastema may be due
to other factors, the following list should be eliminated
as possible causative factors:
microdontia,
macrognathia,
supernumerary teeth (especially a mesiodens),
peg laterals,
missing lateral incisors,
heavy occlusion against the lingual surfaces of the
maxillary incisors,
habits such as thumb sucking,
tongue thrust, lip biting or lip sucking, and
midline cysts.







Existence of a heavy fibrous frenum does not
always mean that spacing is present.
Frequently during the course of orthodontic
therapy the interposed fibers will atrophy,
making a frenectomy unnecessary
“Blanche test" At 10 to 12 years of age no
demonstrable change at the maxillary central
inderdental papilla.






Where there is a heavy fibrous frenum that may be
contributory, however, a "blanching" of the tissue just
lingual to the maxillary central incisors can be noted.
This usually means that the fibrous attachment still
remains in this area.
The difficulty lies in establishing whether this fibrous
attachment is "causative" or "resultant" or whether it is
primary or secondary to such problems as excessive
overbite, local habits, tooth size discrepancy. The
hereditary component is a major factor in persistent
diastemas.

Jedidiah R. Gass, Manish Valiathan, Hemant K. Tiwari, Mark
G. Hans, and Robert C. Elston, (AJODO 2003) to estimate
familial correlations and heritability to evaluate familial
aggregation patterns of maxillary midline diastemas. The
preliminary results suggest a possible genetic basis for
maxillary midline diastema and a greater role of environmental
factors in the black sample than in the white sample.


Interference with Eruption.







For a permanent tooth to erupt, the overlying bone as
well as the primary tooth roots must resorb .
Factors that obstruct eruption Supernumerary teeth,
Sclerotic bone, and
Heavy fibrous gingiva .
All of these interferences are present in cleidocranial
dysplasia. The multiple supernumerary teeth contribute
an element of mechanical interference.
Children with this condition have a defect in bone
resorption, and the gingiva is quite heavy and fibrous.



In patients with less severe interferences with eruption,
delayed eruption of some permanent teeth contributes
to malocclusion only when other teeth drift to
improper positions in the arch.


Ectopic Eruption.







Cause - Malposition of a permanent tooth bud .
Most likely seen with - Maxillary first molars
If the eruption path of the maxillary first molar carries
it too far mesially at an early stage, the permanent molar
is unable to erupt. The mesial position of the
permanent molar leads crowded arch.
Ectopic eruption of other teeth is rare but can result in
transposition of teeth or bizarre eruption positions.
Other teeth especially , maxillary canines , usually is due
the eruption path altered by a lack of space.

Sune Ericson etal (A O 2001) The Dental Follicle in
Normally and Ectopically Erupting Maxillary Canines:
A Computed Tomography Study
The dental follicles of the ectopically erupting canines
were, on average, wider than those of the normally
erupting canines.




Sheldon Peck, Leena Peck, Matti Kataja,
(AO 1994)
Palatal displacement of the maxillary canine tooth is a
positional variation thought generally to develop as a
result of local factors, such as retained deciduous
canines, anomalous permanent lateral incisors, or dental
crowding. From analysis of available evidence, the PDC
positional anomaly appears to be a product of
polygenic, multifactorial inheritance.


Adrian Becker (AO 1995)
1.Their conclusion does not contradict the possibility that
environmental factors may give rise to palatal
displacement of canines generated by genetic anomaly
of the adjacent teeth.
2.The buccally displaced canine finds itself similarly
environmentally compromised by the different factor of
crowding which leads to its characteristic buccally
ectopic guidance pattern.



3.(a) Canines that are transposed with the premolar.
(b) Others that have erupted ectopically, high in the
buccal sulcus and in the absence of crowding ,
(c) Certain palatal canines whose root apex is located
markedly distant from their designated site, may all
be labeled as genetically controlled with a fair degree
of confidence.


4. In between these clearly defined entities there exists a
“gray area” in which it is probable that the etiology of
the individual displaced teeth may be linked to a
combination of circumstances that obey premise
number 1 and premise number 2, to varying degrees.
The guidance theory cannot provide the complete
answer to the etiology of the palatally displaced canine.
Were this so, we would find PDC every time there was
an anomalous or missing lateral incisor. Equally, it may
not yet be discounted out of hand and certainly not on
the basis of the evidence provided in the article in
question.


Early Loss of Primary Teeth


When a unit within the dental arch is lost, the arch
tends to contract and the space to close. At one time,
this space closure was attributed entirely to mesial drift
of posterior teeth, which in turn was confidently
ascribed to forces from occlusion. Although a mesially
directed force can accompany occlusion, it probably is
not a major factor in closure of spaces within the dental
arches.






Thomas E. Southard, Rolf G. Behrents, and Elizabeth
A. Tolley – A J O DO 1989
to design and develop instrumentation to measure the
anterior component of occlusal force generated by a
single tooth under a known axial load. An additional
objective was to quantify the distribution and
dissipation of this force as it progressed anteriorly. The
distribution and dissipation of the anterior component
of the occlusal force anteriorly approximated an
exponential decay function.



The contemporary view is that mesial drift is a
phenomenon of the permanent molars only. The major
reason these teeth move mesially when a space opens
up is their mesial inclination , so that they erupt
mesially as well as occlusally.


Leeway space


In the mandibular arch the combined width of the
deciduous canine, first deciduous molar and second
deciduous molar is on the average of 1.7 mm greater on
each side than the permanent successors. In the
maxillary arch this "leeway" space averages only 0.9 mm
because of the greater size of the permanent canine and
first and second premolar teeth. This space differential
is necessary to allow for the occlusal adjustment and
final alignment of the incisors and a settling in of the
occlusion as the terminal plane relationship is corrected.








Experimental data suggest that, occlusal forces rather
than causing mesial drift, actually retard it.( i.e. :
permanent molar is likely to drift mesially more, rapidly
in the absence of occlusal contacts than if they are
present)
Mesial drift of the permanent first molar after a primary
second molar is lost prematurely can significantly
contribute to the development of crowding in the
posterior part of the dental arch. This has been a
significant cause of crowding and malalignment of
premolars.
If a primary canine or first molar is lost prematurely on
only one side, the permanent teeth drift distally only on
that side, leading to an asymmetry in the occlusion as
well as a tendency toward crowding.

When a primary first molar or canine is lost
prematurely, there is also a tendency for the space to
close. This occurs primarily by distal drift of incisors,
not by mesial drift of posterior teeth
The impetus for distal drift appears to have two sources:
 Force from active contraction of transseptal fibers in
the gingiva, and pressures from the lips and cheeks.
 The pull from transseptal fibers probably is the more
consistent contributor to this space closure tendency,
whereas lip pressure adds a variable component.



Ibrahim Yavuz et al (A J O D O) 2006 Effects of early
loss of the permanent first molars on 3rd molars Early
loss of the permanent first molars might have an
accelerating effect on the development of the third
molar on the extraction side compared with the contra
lateral teeth. Therefore, emergence of the third molars
on the extraction side might be hastened, and these
teeth might erupt earlier than the contra lateral teeth.


ABNORMAL ERUPTIVE PATH





This is usually a secondary manifestation of primary
disturbance.
With a hereditary pattern of severe crowding and totally
inadequate space to accommodate all the teeth,
deflection of the erupting tooth may be merely an
adaptive response to the conditions present
Because of the presence of a supernumerary tooth,
retained deciduous tooth or root fragment, or possible
bony barrier, a physical barrier often influences the
direction of eruption, setting up an abnormal path as a
result.

ANKYLOSIS







Accidents or trauma, certain endocrine conditions and
congenital diseases like cleidocranial dysostosis
predispose an indivdual to ankylosis
Ankylosis or partial ankylosis is encountered relatively
frequently during the 6 to 12year age period.
Ankylosis is probably due to an injury
Submerging of the offending tooth is seen.
In actuality, the other teeth are erupting and the
ankylosed tooth is not The contiguous teeth often
migrate into the space, effectively locking the tooth in
the process.

Traumatic Displacement of Teeth
Dental trauma can lead to the development of
malocclusion in three ways:
(1) Damage to permanent tooth buds from an injury to
primary teeth
(2) Drift of permanent teeth after premature loss of
primary teeth, and
(3) Direct injury to permanent teeth.





1.

2.

Trauma to a primary tooth can displace the
permanent tooth bud underlying it. There are two
possible results.
If the trauma occurs while the crown of the
permanent tooth is forming, enamel formation will be
disturbed and there will be a defect in the crown of
the permanent tooth. (Turner’s Tooth ).
If the trauma occurs after the crown is complete, the
crown may be displaced relative to the root. Root
formation may stop, leaving a permanently shortened
root or root formation continues, but the remaining
portion of the root then forms at an angle to the
traumatically displaced crown .( Dilacerated root )

DENTAL CARIES





Caries, which leads to the premature loss of a
deciduous or permanent tooth, subsequent drifting of
contiguous teeth, abnormal axial inclination, over
eruption, bone loss, etc.
Loss of arch length due to a series of proximal carious
lesions that are unrepaired .
Immediate and correct anatomic restoration should be
made of all teeth as a preventive orthodontic
procedure.

Effect of proximal caries on. arch length. Great care must be
exercised in maintaining the mesio-distal dimension through
proper restoration of tooth Contours and the contact
relationship.

IMPROPER DENTAL
RESTORATIONS







Overextended proximal restorations
irregular mandibular
incisors .
Snap ligature concept (super-tight mesial and distal contacts)
Too tight a contact causes elongation of either the tooth being
restored or approximating teeth, creates functional prematurities
and severely strains the canine-lateral contact .With more than
one restoration in a segment placed with "snap-ligature"
precision, the arch length is increased that leads to break in the
continuity of the arch.
Gutta-percha filling left in occlusion or the slightest bit high has
plunger-like action of the rubberoid mass.
Mechanical separation also encourages increase of arch length as
the dentist strives for a tight contact

An increase in arch length through improper restoration of one or more carious
proximal surfaces may result in the creation of broken contacts, rotations,
cross-bite conditions and functional prematurities.

Conclusion


Malocclusion can occur due to number of possible
causes. It can be caused by either genetic factors or by
environmental factors. Comprehensive Orthodontic
management involves identification of the possible
etiologic factors & an attempt to eliminate the same.
Although it may not be possible to eliminate the cause
in most cases of malocclusion it nevertheless is of value
in preventive & interceptive orthodontic procedure
where a possible malocclusion is prevented or
intercepted by timely removal of the cause .

References
1. Weinstein.S et al :On an equilibrium theory of tooth
position. A O 1963;33: 1 -26.
2. Proffit . W .R Equilibrium Theory Revisited : Factors
Influencing Tooth Position A O 1978;48:175 – 86.
3. Wallen, T. R.: Vertically directed forces and
malocclusion: A new approach. J. Dent. Res.,
1974.53:1015-1022.
4. Robert S. Corruccini,, and Rosario H. Yap Potter
Genetic analysis of occlusal variation in twins : AJODO, 1980;44(140 - 154):

5. Ashima Valiathan. Malocclusion and Genetics. JIOS
1976, vol 8, no 1; 29-33.
6. Gass J, Valiathan M, Tiwari H, Hans M, Elston
R.Familial correlations and heritability of maxillary
midline diastema AJODO 2003 123 (1):35-39.
7. Chung C, Niswander J. Genetic and epidemiologic
studies of oral characteristics in Hawaiian
schoolchildren V. J Dent Res 1975;54:324-29
8. Peck S, Peck L, Kataja M. The palatally displaced canine
as a dental anomaly of genetic origin. Angle Orthod
1994;64:249-56.

9. Valiathan A. and Sameer H Shaikh. (J Ind Ortho Soc
1998;31:53-57)
10. Moyers, R. E.: Handbook of Orthodontics. 3rd ed.
Chicago, Year Book Medical Publishers,Inc., 1972.
11. Reijo Ranta A review of tooth formation in children
with cleft lip/palate, (AJODO, 1986;90: 11-18,.)
12. Ben-Bassat Y,Yitschky M ,Kaplan L,Brin I Occlusal
patterns in patients with idiopathic scoliosis..
AJODO. 2006 ;130(5):629-33.

13. Wen-hua Ruana; Min-dong Chenb; Zhi-yuan Guc; Yuan Lud;
Ji-mei Sue; Qi Guof Muscular Forces Exerted on the Normal
Deciduous Dentition (Angle Orthod 2005;75:785–790.)
14. Hasund, A., and Sivertsen, R.: Dental arch space and facial type.
Angle Orthodont, 1971;41:140-145,.
15. Stockard, C. R.: The genetics of modified endocrine secretion
and associated form pattern among dog breeds. Proc. Sixth
Internat. Cong. Genetics, 1932.
16. John J. Warren Samir E. Bishara Duration of nutritive and
nonnutritive sucking behaviors and their effects on dental
arches in primary dentition (AJODO 2002;121:347-56)


17. Paulo Frazãoa and Paulo Capel Narvai Socioenvironmental
factors associated with dental occlusion in adolescents
(AJODO 2006;129:809-16)
18. Beni Solow et al Dentoalveolar morphology in relation to
craniocervical posture. Angle Ortho., 1977;47:157-165,.
19. Melsen, B., Stensgaard, K., and Pedersen, J. 1979. Sucking
habits and their influence on swallowing pattern and
prevalence of malocclusion. E.J.O. 1979;1:271-180.
20. Carsten Lippold et al Relationship between Thoracic, Lordotic,
and Pelvic AO, 2006;76, 779-85.

21. Ashima Valiathan ,Padmapriya C V- Comparison of tongue
pressure, tongue volume and cephalometric values in kerela
population with and without bimaxillary protrusion-a
clinical study- J Ind Orthod Soc ,2003, 36;Page-158-163
22. John R. C The postural basis of malocclusion: A philosophical
overview(Am J Orthod Dentofacial Orthop 2004;126:729-38)
23. Birte Melsen, Laura Attina, Maria santuari Relationships
between Swallowing Pattern,Mode of respiration, and
Development of Malocclusion A O April, 1987 113 – 20
24. Brunelle JA et al.: Prevalence and distribution of selected
occlusal characteristics In the US Population, 1988-1991, J
Dent Res
1996;75:706-713.

25. Ogaard B et al. The effect of sucking habits,cohort, sex,
intercanine arch widths, and breast or bottle feeding on
posterior cross bite in Norwegian and Swedish 3-year-old
Children (AJODO 1994;106:161-6).
26. Peter H. Lam, Cyril Sadowsky, and Frank Omerza, Mandibular
asymmetry and condylar position in children with uniateral
posterior crossbite (AJODO 1999;115:569-75)
27. Sune Ericson, Krister Bjerklin The Dental Follicle in Normally
and Ectopically Erupting maxillary Canines: A Computed
Tomography Study (A O 2001;71:333–342 )
28. Heritability of cephalometric and occlusal variables as assessed
from siblings with overt malocclusions
Lisa King et al ( AJODO 1993;104:121-31 )

29. Valiathan Ashima & John KK. Racial comparison of
Dentoskeleto-facial patterns of adults from Kerala with
Caucasian, Chinese, Japanese and Negroes. Journal of Pierre
Fauchard Academy 1992; 6(3): 80-89.
30. Bengt Ingerval Urs Thuer Cheek Pressure and Head Posture
Angle Orthodontist 1988 January, (47 – 57).
31. Labbok M et al. Does breast-feeding protect against
malocclusion? Am J Prev Med, 1987;3(4):227-32
32. Thomas E. Southard, Rolf G. Behrents, and Elizabeth A. Tolley
- A Anterior component of occlusal force Part 1. Measurement
and distrubution – (A J O DO 1989;96:493-500.)

33. Chang Liua; Sawa Kanekob; Kunimichi Somac Glenoid Fossa
Responses to Mandibular Lateral Shift in Growing Rats Angle
Orthodontist, Vol 77, No 4, 2007 660 – 667
34. Sune Ericson Krister Bjerklin : The Dental Follicle in Normally
and Ectopically Erupting Maxillary Canines: A Computed
Tomography Study A O Vol 71, 333 No 5, 2001.
35. Effects of early loss of the permanent first molars on 3rd molars
Ibrahim Yavuz et al (A J O D O) 2006; 130:634-8
36. Douglas R. Crosby, and Charles G. Alexander Richardson and
Dallas : Occurrence of tooth size discrepancies among
different malocclusion groups (A J O D O 1989;95:457-61.)

37. Thomas P George, Valiathan Ashima, Arji I George &
Denny J Payyappilly: Oral habits (Part II) Tongue
thrusting. Kerala Dental Association. 1992; 15(3 & 4):
721-724
38. William.R. Proffit- Contemporary Orthodontics,3rd
Edition.—Henry W.Fields.JR 3rd Edition Mosby 2000.
39. T.M.Graber - Orthodontics Principles and Practice 4th Edition Elsevier - 2005.
40. Adrian Becker Palatal canine displacement:

Guidance theory or an anomaly of genetic
origin?. (AO 1995 ; 65 : 95 – 98)

41. Muller,T.P.,Hill,.I. N, Petersen,A.C : A Survey Of
Congenitally Missing Teeth.J.A.D.A,1970;81:101-7
42.J H Gardiner., B C Leighton., J K Luffingham., Ashima
Valiathan. Orthodontics For Dental Students Oxford
University Press.1998.
43. A.Hall., A.Onn The development of supernumerary
teeth in the mandible in cases with a history of
supernumeraries in the premaxillary region.(J.O
2006;33:250-56).



Either we must presume premise number 1–the
existence of these genetically-determined
anomalies has brought about an
environmentally-generated alteration in the
eruption pattern of the canine, as the guidance
theory would hold, or we must presume premise
number 2–the PDC is also genetically
determined, which is the stand these authors
take.

Thank you
Leader in continuing dental education


Etiological basis of malocclusion theories /certified fixed orthodontic courses by Indian dental academy

Recommended

Recommended

More Related Content

What's hot

What's hot (20)

Similar to Etiological basis of malocclusion theories /certified fixed orthodontic courses by Indian dental academy

Similar to Etiological basis of malocclusion theories /certified fixed orthodontic courses by Indian dental academy (20)

More from Indian dental academy

More from Indian dental academy (20)

Recently uploaded

Recently uploaded (20)

Etiological basis of malocclusion theories /certified fixed orthodontic courses by Indian dental academy

Editor's Notes