Etiology of malocclusion general factors

Etiology of malocclusion
Presented by
Dr Dimple Bedre M
Department of Orthodontics

Contents
Introduction
System Of Classification
Orthodontic Equation
Primary Etiologic Sites
General Factors
Local Factors
Conclusion

The beginning of wisdom is to call things by
their right names.
An old Chinese proverb
The origin of all sciences is in the desire to
know causes and the origin of all false
science and imposture is in the desire to
accept false causes rather than none or
which is the same thing in the unwillingness
to acknowledge our own ignorance.
Burke and Edinburgh Phrenologist

Introduction
Etiology of malocclusion is the study of its
causes.
Recognition and elimination of the
etiological factors is important so that one
can prevent and correct the malocclusion
and obtain a permanent result.
Etiologic factor contribute to the variance
more often than they simply “cause” it.

Current level of etiologic researchinherited pattern is polygenic.

Based on a multifactorial system with
additive polygenesis and threshold
effect – in order to become a
distinctive factor in the phenotype, the
inherited bundle of genes can be
„„tipped over the edge‟‟ for instance by
environmental factors.
Jorgensen 1966

Interaction b/w Hereditary factor
and Exogenous influences

Systems Of Classification
Inherited and Congenital Causes
Acquired causes
Indirect or predisposing Causes
Direct or determining causes
Various classification proposedWhite and Gardiner‟s Classification
Salzmann‟s Classification
Moyer‟s Classification
Graber‟s Classification
Proffit‟s Classification

White and Gardiner‟s Classification
A. Dental Base Abnormalities
1.Antero-posteror Malrelationship
2.vertical Malrelationships
3.Lateral Malrelationships
4.Disproportion of size b/w teeth and
basal bone
5.Congenital abnormalities

B. Pre-Eruption Abnormalities
1.Abnormalities in the 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

C. Post-Eruption Abnormalities
1.Muscular Forces:
a.Active Muscle Forces-Swallowing
b.Rest Position of the Musculature
c.Sucking habits
d.Abnormalities of path of closure
2.Premature Loss of Deciduous teeth
3.Extraction of Permanent Teeth

Salzmann‟s classification
Prenatal
1.Genetic:transmitted by genes.
may or may not be at birth.
2.Differentiative:
a.General or Constitutional: whole body
b.Local or dentofacial: face, jaws & teeth
3.Congenital:hereditary or acquired
exist at birth

Postnatal
A.Developmental
General
a.Abnormalities in relative
rate of growth.
b.Hypo/hypertonicity of
muscles.
c.Childhood diseases,
nutritional,Endocrine,&
metabolic disturbance
d.Radiation/Radiotherapy.

Local
a.Birth injuries.
b.Micro / macrognathia

c.Micro/macroglossia.
d.Abnormal labial frenum.
e.Facial hemiatrophy.
f.Anomalies of tooth
development & eruption.

B.Functional
General
a.Muscular hyper or
hypotonicity.
b.Neurotropic
disturbances.
c.Postural defects of the
tongue and jaws.
d.Masticatory and
respiratory
disturbances.

Local
a.Premature loss or
prolonged retention of
deciduous teeth.
b.Loss of proximal contact.
c.Temporomandibular
articulation disturbance.
d.Muscular hypo or
hyperactivity

C.Environmental or Acquired
General

Local

a.Diseases can affect the a.Eruption anomalies
b.Premature loss or
dentofacial tissue
prolonged retention of
directly or indirectly.
deciduous teeth.
b. Radiation.
c.Loss of permanent
teeth.
d.Periodontal disease
e.Harmful dentofacial
pressure habits.
f.Trauma
g.Infection
i.Temporomandibular
disturbance.

Moyer‟s Classification
Heredity
Developmental defects of unknown origin.
Trauma
a.Prenatal trauma &Birth injuries
b.Postnatal trauma.
Physical agents
a.Premature extraction of primary teeth
b.Nature of food

Habits
a.Thumb sucking and finger sucking
b.Tongue thursting
c.lip sucking & Lip biting
d.Posture
e.Nail biting
f.Other habits
Disease
a.systemic
b.Endocrine disorder.

c.Local disease
-nasopharyngeal diseases &
disturbed respiratory function.
-gingival & Periodontal disease
-tumors
-Caries
Malnutrition

Proffit‟s Classification
Specific causes1.Disturbances in embryologic development.
2.Skeletal growth disturbances
a.Fetal molding & birth injuries.
b.Birth trauma to the mandible.
c.Childhood fracture of the jaw.
3.Muscle dysfunction.
4.Acromegaly & hemimandibular
hypertrophy.

5.Disturbances in dental development.
a.Congenitally missing teeth.
b.Malformed teeth.
c.Supernumerary teeth.
d.Interference with eruption.
e.Ectopic eruption.
f.Early loss of primary teeth.
g.Traumatic displacement of teeth

Genetic Influences

Environmental Influences
1.Equilibrium Theory & Development of the
Dental Occlusion.
a.Equilibrium effect on the Dentition
-tooth contacts during mastication &
swallowing.
-soft tissue pressure of lip,cheek &
swallowing.
-external pressure like Habits &
orthodontics.
-Intrinsic pressures like PDL fibers &
Gingival fibers.
b.Equilibrium effects of Jaw size & shape

2.Functinal influences on Dentofacial
developmenta.Masticatory function
-Function & Dental arch size
-Biting force & Eruption
b.Sucking & Other Habits
c.Tongue thrusting
d.Respiratory pattern

Graber‟s Classification
General Factors
1.Heredity
2.Congenital Defectss
-Cleft palate
-Torticolis
-Cleidocranial dysostosis
-Cerebal palsy
-Syphilis

3.Environment
a.Prenatal
b.Postnatal
-Trauma
-Birth injuries
-Maternal Diet
-cerebral Palsy
-Maternal metabolism
-TMJ injury.
-German measles.
4.Predisposing Metabolic Climate & Disease
a.Endocrine Imbalance
b.Metabolic Disturbances
c.Infectious Diseases
5.Dietary Problems
-Nutritional Deficiency

6.Abnormal Pressure habits & Functional
aberration
a.Abnormal suckling
b.Thumb & Finger sucking
c.Tongue Thrust & Tongue sucking
d.Abnormal swallowing habits
f.Speech defects
g.Respiratory abnormalities
h.Tonsils & Adenoids
i.Psychogenic Tics & bruxism.
7.Posture
8.Trauma & Accidents

Local Factors
1.Anamolies of number
a.Supernumerary Teeth
b.Missing Teeth
2.Anamolies of Tooth Size
3.Anamolies of Tooth Shape
4.Abnormal Labial frenum; Mucosal
barriers
5.Premature Loss.

6.Prolonged Retention
7.Delayed Eruption of Permanent
teeth
8.Abnormal Eruption Path
9.Ankylosis
10.Dental Caries
11.Improper Dental Restorations.

Orthodontic Equation
[ Dockrell’s Classification ]
Causes
Act at

Times
On

Tissues
Producing

Results

Primary Etiologic Sites
Neuromuscular System
Bone of the facial skeleton

The Teeth
The Soft parts excepting muscles

Hereditary / Genetic factors in
malocclusion
Strong influence of inheritance on facial
features- obvious at a glance.
The Hapsburg jaw- prognathic mandible.
Two pertinent questions asked on the
inherited influences are1. Is malocclusion often caused by inherited
characteristics?
2.How much of these inherited characteristics
is modified by the pre & postnatal
environment?

Sir Francis Galton – first scientific
analysis of twins & concluded that it
is possible to separate „Nurture‟ from
„Nature‟.
The best way to find out about genetic
basis in malocclusion is by using1.Twin studies (difficult to obtain
samples).
2.Familial studies.
a.Parent child study (less comprehensive).
b.Sibling studies (more comprehensive).

Twin studies:
Lundstrom(1963) conducted a study on 100 pair
of twins,half of which were monozygotic and half
were dizygotic.
Both skeletal and dental overjets were measured

Conclusions
More variations in the dizygotic than
monozygotic.
Larger genetic variations for skeletal pattern than
dental overjet.
Indicates dentoalveolar compensation.

Lauweryns et al(1993) summarized a
number of twin studies and concluded that
40% of the dental and skeletal variations
that lead to malocclusion can be attributed
to hereditary factors.
The use of twins in dentofacial genetic research
Lauweryn I,Carels C,Vlietinck R
AJODO 1993;103:33-38

Familial Studies:
Parent-Child corelation co-efficient
 Facial skeletal dimension-0.5
 Dental characteristic
-maximum for overjet-0.5

-minimum for overbite-0.15

Suzuki(1961)studied 243 Japanese
families.
1 parent had anomaly-20% of children
affected.
Both parents had anomaly-40% of
children were affected.

Bolton & Brush Growth study(conducted on
siblings between 1930s & 1970s).
 Harris & Johnson concluded that-heritability of
craniofacial characters was high but dental was
low.
 Heritability estimates for skeletal characters
increases with age but for dental characters
decreased-indicates environmental contribution.
Heritability of craniometric & occlusal variables:
A longitudinal sib analysis.
Edward F Harris & Michelle G.Johnson
AJO-DO 1991;99:258-68

Harrs has shown that the craniofacial
skeletal pattern with class II
malocclusion is heritable & there is
high resemblance of skeletal pattern
in their siblings.
He concluded that the genetic basis
for their resemblance is polygenic.

Genuine Class II malocclusion in
three brother

Litton etal (1970) in their sibling study
have reported Class III malocclusion to
be heritable trait that is polygenic in
nature.
A genetic study of ClassIII malocclusion
Litton SF,Ackerman LV, Isarcson RJ
AJO-DO 1970;58(6) 565-577

Hereditary mandibular prognathism

Malocclusion could be produced by
inherited characteristics in two major ways:
 Disproportion between the size of the jaw
and size of the teeth.
 Disproportion between size and shape of
the upper and lower jaw.
More independently these characteristics
are inherited more likely is the
disproportion .

Studies done to find out if tooth & jaw size
discrepancy is due to independent inheritance.
Stockard’s study on cross-bred dogs (1930s)
• Observations
 Dramatic malocclusions did occur more from jaw
discrepancies than from tooth-size- jaw-size
discrepancy.
 This seemed to confirm that independent
inheritance of facial characteristics could be a

major cause of malocclusion

Study was misleading as many breeds of small
dogs carry genes for Achondroplasia.

Studies using out breeding in human
populations.

 In primitive human populations- malocclusions
less frequent since characterised by genetic
isolation & uniformity.
 Tooth-size jaw-size discrepancies were infrequent.
 Where out breeding occurs incidence of
malocclusion greatly increased.
 This seemed to show that the independent
inheritance could be a major cause of
malocclusion.

Hawaiian melting-pot study, Chung et al.

 One of the best investigations to examine the
hypothesis of independent inheritance of tooth &
jaw characteristics.
 Hawaii-homogenous Polynesian population.
 Large scale migration by Europeans, Chinese,
Japanese-Heterogeneous modern population.
 High prevalence of malocclusion would be
expected in this population but not so.

The prevalence of malocclusion though higher than
in the original population was only additive rather
than multiplicative.
Ex.10% of Chinese who had Cl III if mated with 10%
of Polynesians with crowded teeth, the offspring
seemed to have 10% prevalence of each
characteristic.
Conclusion that can be drawn from this study is if
malocclusion is inherited, the mechanism is not the
independent inheritance of discrete morphological
characteristics like tooth & jaw sizes.

Lundstrom made an intensive analysis of several
characteristics & found the followingHeredity significant1.Tooth size.
2.Width & length of arch.
3.Height of the palate.
4.Crowding & spacing.
5.Degree of sagittal overbite/overjet.
Heredity probable1.Position and conformation of perioral
musculature to tongue size and shape.
2.Soft tissue peculiarities(character and texture
of mucosa, frenum size, shape and position.)

Heredity also plays an important role in the foll.
conditions1.Congenital deformities.
2.Facial asymmetries.
3.Macro/micrognathia.
4.Macro/microdontia.
5.Oligodontia & anodontia.
6.Tooth shape variations.
7.Cleft-lip/palate.
8.Frenum diastemas.
9.Deep overbites.
10.Crowding & rotation of teeth.
11.Mandibular retrusion.
12.Mandibular prognathism.

Clinical implications
Heredity can affect the orthodontic treatment as
seen by the following examples1.Class II malocclusion caused due to habit much
easily corrected than one due to genetic causes.
2.Class III malocclusion mostly due to mandibular
prognathism(genetic) as against maxillary
retrusion.
The greater the genetic component, the worse the
prognosis for a successful outcome by means of
orthodontic intervention.

Congenital malformations
1.Single gene abnormality
Genetic
disorder
2.Chromosomal disorders
3.Multifactorial disorder- Genetic +environment
4.Disorder cause by Teratogens
NG & E
5.Disorders of unknown etiology

Autosomal Dominant Disorder
Treacher collins syndrome
Achondroplasia
Crouzon Disease [cranio facial dysostosis]
Cleido cranial dysostosis
Marfan syndrome
Dentinogenesis imperfecta
Hemifacial microsomia [goldenhar
syndrome]
Basal cell nevus syndrome
Neuro fibromatosis

Autosomal Recessive Disorders
Cerebro-Costo-mandibular syndrome
[micrognathia with Pierre Robin Syndrome]

Bloom syndrome [with Skin lesion]Maxillary hyperplasia
Stickler symdrome
Nagar Aerofacial dysostosis.

Multi Factorial Inheritance
Cleft Lip and Palate
Disease with which we deal
malocclusion, Dental Caries,
Periodontal disease which are
multifactorial triats.

Disorder Caused By Teratogens
A group of congenital malformation caused
by maternal exposure to teratogens
[malformation inducing] agents during
pregnancy.
The best known teratogenic agents are
Viruses [Rubella], heavy dose natural
irradiation and maternal exposure to
various chemical substances.
Heavy alcohol consumption during
pregnancy.

Teratogens affecting dentofacial development

Contemporary Orthodontics: William R Proffit

Cleft Lip And Palate
Cleft Palate can defined as a furrow in the
palatal vault or Breach in continuity of
palate.
Most commonly seen congenital deformity
at the time of birth.
Incidence of cleft of the lip & palate varies
from 1 in 500 to 1 in 2500 of live
births,depending on geographic origin,
racial & ethnic background &
socioeconomic status.

Both dental & skeletal components
affected.
More common in maxilla-damage to
profile due to maxillary deficiency.
Influenced byType of surgery.
Type of deformity.
Timing of intervention.

Etiology of cleft
Fogh & Anderson – Genetic in origin
Bhatia – Either by single mutant gene or by
number of genes .
Bixler – 1.Probably polygenic.
2.Monogenic or syndromic.
Various environmental factor.
-Alcohol [Munger et. al 1996]
-Maternal illness & smoking [Werler et. Al
1990]

Classification of cleft lip & palate
Veau‟s
classification[1931]
Group I: Soft palate
Group II: Hard & soft
palate
Group III: Comp.
Unilateral cleft
Group IV: Comp.
bilateral cleft

Kernahan & Stark‟s classification
Cleft of pri. Palate only
a. Unilateral - Complete
- Incomplete
b. Median - Comp.[ premaxilla absent]
- Incomplete[PM rudiment]
c. Bilateral - Complete
- Incomplete
Cleft of sec. palate only
- Complete
- Incomplete
- Submucous

Cleft of pri. & sec. palate
a. Unilateral - Complete
- Incomplete
b. Median - Complete
- Incomplete
c. Bilateral - Complete
- Incomplete

Schuchardt & Pfeifer symbolic
classification

Kernahan’s Striped Y Classification

Millard’s modification of the striped Y

Problems associated with CL & CP
Dental
Esthetics.
Speech & hearing.
Psychology.

Dental problem
Congenitally missing teeth [U LI ]
Mobile premaxilla
Anterior & post. Cross bite
Ectopically erupting teeth
Impacted teeth
Supernumerary teeth

Poor alignment – poor oral hygiene
Multiple decayed teeth
Periodontal complications
Enamel hypoplasia & microdontia
Protruding premaxilla
Deep bite
Spacing / crowding

Speech & hearing
Speech depends on timing of palatal
surgery.
Velopharngeal sphincter dysfunction.

The term Cleft Palate Speech include:

Abnormal nasal resonance
Abnormal nasal airflow
Altered laryngeal voice quality
Nasal or facial grimace
Atypical consonant production
McWilliam etal 1990, Trost-Cardemone 1990, Sell etal 1994
Wyatt etal 1996

Clinical significance
Surgically repaired with excellent cosmetic
& functional result
Best operated bfore the pt. is 1 mth old.
3 mths - CL , 18 mths – CP
Physical & psychological effect of CP on pt.
are considered
Eating & drinking are difficult because of
regurgitation of food & liquid through the
nose
Speech problem is serious & tends to
increase mental trauma suffered by the pt.

Cliedocranial dysplasia
Hereditary – important cause of
malocclusion
Unilateral/bilateral absence of clavicles.
Delayed closure of cranial sutures.
High, narrow,arched palate and actual cleft
palate appears to be common.
Maxillary retrusion.
Mandibular protrusion.
Retarded eruption of permanent teeth
Retained deciduous teeth.
Multiple impacted supernumerary teeth

Ectodermal Dysplasia
Specific syndrome characterised by a
congenital dysplasia of one or more
ectodermal structures manifested
primarily by hypohydrosis,
hypotricosis & hypodontia.
X-linked recessive mendelian
character.
EDSs may manifest in association
with midfacial defect- CL &CP.

Light very thin hair
Underdeveloped eye brows
Broad nose
Ridge like lip configuration
Pronounced mentolabial
sulcus.

Underdevelopment of
middle face & lower facial
height

Frontal bossing ,Collapsed middle
third face & Spare hair on the Scalp
Anodontia or oligodontia.
Growth of jaw is normal.
Alveolar process does not developreduced vertical dimensionprotuberant lips.
High Palatal arch & CP.

Mandibulofacial Dysostosis
[Treacher Collins-Franceschetti Syndrome]
Encompasses a group of closely
related defects of the head & face.
Hereditary or familial in pattern.

Clinical manifestations
Antimongoloid palpebral fissures with a
coloboma of the outer portion of the lower
lids & deficency of the eyelashes.
Hypoplasia of facial bone.
Malformation of external ear.
Macrostomia, high palate & abnormal
position & malocclusion of teeth.
Blind fistulas b/w the angle of the ears &
angle of mouth.
Facial cleft and deformity.
Micrognathia & Openbite.
Characteristic facies of patient-Birdlike or
Fishlike

Craniofacial Dysostosis
[Crouzon Disease]
Autosomal dominant pattern.
Mutation of FGFR-2 gene.
Early synostosis of the sutures.
Facial deformities is observed at birth.
AP diameter is smaller than transverse
Wide face & hypoplastic maxilla producing
pseudoprognathism.
Deviation of nasal septum, narrowed ant nare &
wide beaked nose
Mimicks frog face.
Upper lip is shortened & cleaved.
Impair vision & earing.
Malocclusion, malposed teeth & dysplasia noted.

Craniofacial Dysostosis
Cranial & facial deformities.
Hypoplasia of maxilla.
Mandibular prognathism.
High-arched palates & clefts.

Pierre Robin Syndrome
May/may not be genetic.
Characterised by- Cleft Palate,
Micrognathia,Glossoptosis.
Primary defect in the mandible.
U or V shaped hard & soft palate.
Respiratory difficulty due to epiglottic
obstruction.

Achondroplasia
Caused by mutations in the gene for
FGFR-3[fibroblast growth factor receptor]
Characteristic form of dwarfism.
Disease begins in utero.
80% of affected infants are still born.
Maxilla retruded & mand prognathism.
Midfacial hypoplasia & prominent
fore head.

Down‟s Syndrome
First described by John Langdon Down in 1866.
Form of mental retardation.
Somatic abnormalies due to number of
chromosomal aberrations.
Three Cytogenetic variants:
Trisomy-21
Trisomy-18
Trisomy-13
Small head,flat face,depressed nasal bridge, flat
occiput & broad short neck.
Small slanting eyes with epicanthal folds, open
mouth, frequent prognathism & sexual
underdevelopment.

Protrusion of tongue [macroglossia]
with difficulty in eating & speaking.
Scrotal teeth
Hypoplasia of maxilla.
Delayed tooth eruption, partial
anodontia, enamel hypoplasia, jevinile
periodontitis & Clept lip or palate.
Fissuring & thickening of lips &
angular Cheilitis are frequent.

Stickler Syndrome
Autosomal dominant
connective tissue
disorder.
Greater b/w families
rather than with in
families.
Manifest as three main
groups- the Eyes , Joints
& facial appearance.
At birth only features of
pierre Robin sequence.
The facial appearance at
birth –mid face
hypoplasia, flat nasal
bridge,anteverted nares
& prominent eyes.

Syphilis
Caused by treponema palladium.
Classified as Congenital & Acquired.
Congenital syphilis is transmitted to
offspring only by an infected mother.
Manifest variety of lesions including frontal
bossae, short maxilla, high palatal arch,
saddle nose, mulberry molars,
Higoumenakis‟s sign [ irregular thickening
of the sternoclavicular portion of clavicle],
protruberance of mandible.

Hutchinson‟s triad:
- hypoplasia of incisor & molar teeth
-eight nerve deafness
-Interstitial Keratitis.
Malocclusion frequently observed is
open bite & lack of development of
maxilla.

Environmental factors
Skeletal growth disturbancesFetal moulding and birth injuries
Injuries apparent at birth :
1.Intra uterine moulding [prenatal]
2.Trauma to mandible during the birth
process [postnatal]

Prenatal
Intrauterine moulding:
Pressure against rapidly
growing areas leads to
distortion
Arm pressed against the facemaxillary deficiency
Head flexed against the chestmandibular deficiency.

Decreased amniotic fluid-small mandible-cleft
palate results due to upward displacement of
tongue.
Catch-up growth occurs when pressure is
released except when cartilage is affected-Stickler
syndrome

Rubella [German Measles]
Caused by togavirus which spread by
droplet infection.
When the disease occurs in women during
the first trimester of pregnancy, the
offspring has a high incidence of congenital
defects such as blindness, deafness, &
cardiovascular abnormalities.
Occasionally can cause enamel hypoplasia
high carious incidence & delayed eruption
of deciduous teeth.

Post-Natal
Birth injuries
1.Trauma to mandible
Most mandibular deformities-due to
congenital anomalies-but thought to be
due to birth trauma.

Forceps delivery –TMJ damage.
2.Vogelgeschist: development
ankylosis of TMJ,may be due to birth
injury.

Childhood Fractures of the jaw
 Mandible more common than the maxilla.
 Condylar neck is vulnerable.
 75% of these fractures –normal growth
occurs.
 Asymmetric growth due to injury to the soft
tissue matrix –scarring restricts the
growth.
 Management of fractures very critical-early
immobilisation.

Muscular trauma
 Part of soft tissue matrix
responsible for bone growth.

 Malocclusion can be
caused by,
a.Decreased tone of the
muscles-due to muscular
dystrophy,or loss of motor
nerve supply-muscle atrophy
b.Excessive muscle
contraction-torticollis or
scaring after a injury.

Cerebral Palsy
Cerebral palsy is a paralysis or lack of
muscular co-ordination attributed to an
intracranial lesion.
Result of birth injuries.
Effect of this neuromuscular disorder may
be seen in the integrity of occlusion.
Varying degree of abnormal muscular
function may occur in mastication,
deglutition, respiration and speech.

Predisposing metabolic Climate
And Disease
Endocrine imbalance.
Hypopituitarism:
 Dwarf
 Delayed eruption of permanent teeth and
delayed shedding of primary teeth.
 Crowding due to smaller arch size.
 Mandibular growth more affected than
maxilla.

Hyperpituitarism:

Gigantism-large teeth and jaws.
Acromegaly-occurs after growth and ossification is
complete.
Lips thick,tongue enlarged,shows scalloping.
Accelerated condylar growth-large mandible.
Teeth tipped buccally due to large tongue.

Hypothyroidism:
Delayed eruption.
Abnormal resorption pattern.
Retained deciduous teeth.
Malposed teeth-deflected from eruption path.
Gingival disturbances.

Hyperthyroidism:
Early shedding and eruption
Atrophy of alveolar bone.

Nutritional Deficiency
Disturbances in the developmental
timetable.
Rickets, scurvy and beri-beri can produce
severe malocclusions.
Premature loss of teeth /Prolonged
retention.
Abnormal eruptive path.
Poor tissue health
Poor absorption-hormonal /enzymatic
deficiency.
Decreased fluoride intake-loss of teeth due
to caries-malocclusion.

Abnormal Pressure Habits And
Functional Aberration
EQUILIBRIUM THEORY
If an object is acted upon by a set of forces
but remains in the same position, then the
forces must be in balance.
Dentition is in equilibrium.
Movement occurs when equilibrium is
disturbed.

4 PRIMARY FACTORS IN
EQUILIBRIUM:
1.Intrinsic forces of tongue and lips.
2.Extrinsic forces-habits &orthodontic
appliances.
3.Forces from dental occlusion.
4.Forces from periodontal membrane.

Equilibrium effects on the dentition.
1.Intrinsic forces -Tongue Vs. Lip.

Duration of force more important than the
magnitude.
Chewing force - heavy.
Periodontal ligament -shock absorber.
Force maintained longer -pain is felt.
Heavy but intermittent force no change in
tooth position.

Forces from lips, cheek and
tongue- lighter but act for a
longer duration.
Capable of causing tooth
movement.
Since no tooth movement
occurs-forces are in
equilibrium.
Electronic measurement
showed- pressures are
unequal.

Study by Walter Straub(1950)- clinical
observation.
Tongue and lip pressures during swallowing varied
among individuals.
Did not correlate with the position of the teeth.
The tongue and lip pressures were never
balanced.
Tongue pressure several times higher during
swallowing.
Thought lip pressure acts for longer time but was
disproved.
Concluded that incorrect swallowing – major
cause of anterior open bite & incisor protrusion.

Lear & Moorrees studied tongue and lip
pressures.
Tongue and lips pressures measured over
a 4 hour period and projected over 24
hours.
In the 24 hour period, summary of tongue
and lip pressures are close to the
equilibrium.
Total tongue and lip pressures still
imbalanced.
Other forces must be considered, if
equilibrium is to be explained.

2.Extrinsic forces: Pressure habits &
orthodontic appliances.
a.Orthodontic treatment causing tooth
movement interferes with the equilibrium.

b.Same can be concluded about habits.
c.Extrinsic forces effective only when
duration exceeds 6 hours.

Factors affecting equilibrium in the
vertical direction:
1.Tongue & lips.
2.Forces of occlusion.
3.Forces of eruption.

Studies by Wallen- to find if tongue
pressure leads to anterior open bite:
1.Tongue pressure in patients with anterior
open bite less than persons with normal
vertical relationships.
2.Due to relatively high position of the
incisors the tongue doesn‟t contact them
during swallowing.

3. Forces from dental occlusion:
Attachment apparatus effective hydrodynamic
damping system.
The occlusal forces influence vertical position of
teeth.
Maximum force of 100kg or more sustained for
fraction of a second.
Vertical position of teeth when changed can alter
the rest position of the mandible.
Extrusion of molar teeth rotates the mandible
downward & backward & intrusion causes the
mandible to move to a closed position.
These changes mediated by proprioceptors in the
periodontal ligament.

Forces of eruption:
Eruptive force moves the tooth through the bone.
Remains active till tooth has come into occlusion.
Extraction of antagonist restarts the eruption
process again.
Studies show eruptive force generated in the
periodontal membrane rather than the root apex.
Strain gauge pressure transducer shows the
eruptive force can be between 2 to 10gms

Biting forces & Eruption:
Patients with deep / openbite show
infra/supra eruptive posterior teeth – how
much a tooth erupts depends on how much
force is placed on it.
Studies to find if long faced persons have
lower maximum biting force & short faced
persons have high biting forces were done.
Swallowing, chewing & maximum biting
forces were evaluated.

3 groups measured were- children with long faces, children
with normal faces & long faced adults.
All 3 groups had less biting forces than normal adults.
Difference in occlusal forces arises at puberty -when the
normal faced individual gains muscle strength.
Tendency towards long face before the difference in force
appears- difference is an effect rather than the cause.

4. Forces from the periodontal
membrane:
Form an important part in stabilizing teeth.
Though the tongue & lip pressure are unequal
postulated that periodontal ligament maintains
teeth in stable position.
Pathological migration – break down of periodontal
ligament.
Final position of teeth influenced by two factors1.Resting positions of lip, cheek & tongue.
2.Metabolic activity within the periodontal membrane

Abnormal Habits
All habits are learned patterns of muscle
contraction of a very complex nature.
Habits such as normal lip action and
mastication-stimulants for normal growth,
Undesirable habits –malocclusion.

Duration not the only determinant but
frequency & intensity affect the end
result.
The trident of habit factors.

Deleterious habitual patterns of
muscles behavior produce:
1.Perverted osseous growth.
2.Tooth malpositions.
3.Disturbed breathing.
4.Difficulty in speech.
5.Upset balance of facial musculature.
6.Psychological problems.

Thumb/Finger sucking
One of the most
important factors in
producing and
maintaining
malocclusion.
Begins at birth and
outgrown by 3-4
years.

Finger sucking from birth to 4 years:
Suckling mechanism –most important
exchange with the outside world.
Through suckling child obtainsnutrients, feelings of euphoria, sense
of security and feeling of warmth.

Time of appearance of digital suckingFirst few weeks- feeding problems.
During the eruption of teeth- Teething device.
Older children- release of emotional tensions.
THEORIES FOR NON-NUTRITIVE SUCKING:
1. Classical Freudian theory(1905)
Orality of the infant related to pregenital
organisation.
Sexual activity not separated from taking of
nourishment.
Abrupt stopping of habit leads to substitution by
other antisocial tendencies.

2.The learning theory- Davidson(1967)
Association of non-nutritive sucking with
pleasurable feelings like hunger.
3. The oral drive theory- Sears and Wise
(1982)
Strength of the oral drive is proportional to
how long a child continues to feed by
suckling.
Thumb sucking is due to the oral drive and
not the result of frustration of weaning.
Agrees with the Freudien theory- suckling
increases the erotogenesis of the mouth.

Studies done to evaluate feeding
pattern:
Children fed had less thumb sucking habit than
children whose feedings were widely separated.
Non-thumb suckers took a longer time to feed.
Digital sucking related to inadequate sucking
activity.
Benjamin did a series of experiments with
monkeys and found – less thumb sucking in those
in whom the nutritive suckling experience is less
Thumb sucking is an expression of a need to suck
– associated thumb-sucking with primary
reinforcing aspects of feeding.
Thumb sucking – reflex common to all mammalian
infants.

Studies done to evaluate psychological
aspects:

Thumb sucking result of inadequate
attention.
Manifestation of feeling of insecurity.
Should be screened for underlying
psychological disturbances.
Psychological consultation needed
when trying to break the habit.
Studies in the university of Alberta
disproved the above facts.

This study was done with 66 children divided into
6 groups.
a. Control group.
b. Psychologic treatment.
c. Palatal arch only.
d. Palatal arch & psychological treatment.
e. Palatal crib only.
f. Palatal crib reinforced by psychological
treatment.
Children who suck their thumbs failed to
demonstrate any consistent psychological
difference from the control group.

Results support the theory that digital
sucking is a simple learned habit.
No support for interpretation of thumb
sucking as a symptom of psychological
disturbance.
Orthodontic intervention failed to produce
any increase in alternative or substitute
undesirable behaviour.
Palatal crib with spurs was most effective
and associated habits like hair-twisting,
fondling, disappeared with finger habits.

Palermo- thumb-sucking arises out of a
progressive stimulus & reward reaction;
spontaneously disappears unless becomes an
attention getting mechanism.
Eysenek- learning theory regards neurotic
symptoms as simple learned habits; no neurosis
underlying the symptom but the symptom itself.
Various theories of non-nutritive digit sucking are
not completely incompatible.
Findings support the learning theory – associated
with prolonged nutritive sucking.

Classification of Sucking Habits
1.O’Brien (1996)
Nutritive sucking habit – breast feeding/bottle
feeding.
Non-nutritive sucking habit – thumb / finger
sucking, pacifier sucking.
2.Subtelny (1973) – 4 grades of thumb sucking
Type A
50% of children – whole digit is placed inside the
mouth.
Pad of the thumb presses against the palate.
Maxillary & mandibular anterior contact is
maintained

Type B
13-24% of children.
Thumb is placed without touching the palate.
Maxillary & mandibular anterior contact is
maintained.
Type C
18% of the children.
Thumb is placed just beyond the first joint.
Contacts the hard palate.
Contacts only the maxillary incisors.

Type D
6% of the children.
Tip of the thumb inside the mouth.

Digit Sucking & Malocclusion.
Large percentage of children practicing digit sucking but little
correlation with malocclusion.
Sucking habits in primary dentition – little or no long term
effects.
Habits persist beyond the time that the permanent teeth
erupt - malocclusion occurs.
Characterized by flared & spaced maxillary incisors, lingually
positioned lower incisors, anterior open bite, narrow upper
arch.
Rarely due to finger pressure alone, assistance from perioral
musculature.

Burlington Orthodontic Research Center –
Popovitch & Thompson report.
 High association of abnormal sucking
habits with malocclusion.
Cook measured forces of thumb sucking:
 Three distinct patterns of force application
during sucking.
 All forces sufficient to displace teeth &
deform growing bone.

How does malocclusion actually occur?
 When thumb / finger placed
between the teeth –
positioned at an angle.
 Presses lingually against
the lower incisors & labially
against the upper incisors.
 There can be variation
depending on which teeth
are contacted.
 Duration of the sucking is
most important.
 Child who sucks vigorously
but intermittently does not
displace incisors but when
continuous light pressure is
applied – malocclusion
results.

 Anterior open bite –
Combination of thumb
sucking & interference
with normal eruption.
 Excessive eruption of
posterior teeth & impedes
eruption of incisors.
 Mandible positioned in a
downward
manner
to
accommodate
the
interposed
thumbcausing
increased
eruption of posterior teeth.
 Direct
impediment
of
incisor eruption.
 Maxillary constriction- not
due to negative pressure.

Imbalance between tongue & cheek
pressures.
Tongue is lowered which decreases the
pressure on the upper posterior teeth.
Cheek pressure increased as buccinator
muscle contracts during suckling.

Constricted maxillary arch least likely
to correct spontaneously.
When maxillary arch expanded,
incisor protrusion & anterior open bite
improves spontaneously.
No use beginning orthodontic therapy
till habit is stopped.

Tongue Thrusting

Often associated with thumb sucking.

Tongue thrust is forward placement of the tongue
between the anterior teeth & against the lower lip
during swallowing- Schneider (1982).
Normal swallow – the teeth are in occlusion, lips
lightly closed, the tongue held against the palate
behind the anterior teeth.

CLASSIFICATION OF TONGUE THRUST
SWALLOW:

1.Simple tongue-thrust swallow –
Normal teeth together swallow.
Associated with digit sucking habit.
Needed to maintain anterior seal.

2. Complex tongue thrust swallow.
Associated with chronic nasorespiratory
distress, mouth-breathing, tonsillitis or
pharyngitis.
Inflamed tonsils produce pain due to
encroachment of the root of the tongue.
Reflex drop of mandible – separating the
teeth & provides more room for the tongue
to thrust - assuming a more comfortable
position.

In chronic mouth breathers - large
freeway space due to dropping of the
mandible & protrusion of the tongue –
adequate airway.
Jaws held apart during swallow –
tongue remains in a protracted
position.

 Studies by Melsen et al showed tongue thrust
swallow & teeth apart swallow favor development
of disto-cclusion, maxillary overjet & openbite.

 Tongue thrust a misnomer – Proffit.
 Swallowing not a learnt behavior but is integrated
& controlled physiologically at subconscious
levels.

Mature adult swallow develops at 3 years of age, in
majority of people seen by the age of 6 yrs.
Only brain damaged children retain a true infantile
swallow.
Transition stage characterized by muscular activity
which brings the lips together, separates the
posterior teeth & there is forward protrusion of the
tongue.
Delayed normal swallow transition associated with
previous history of sucking habit

 Upper incisor protrusion or anterior open bite –
Difficult to seal the mouth by bringing lips together.
 Bringing the tongue forward – a successful
maneuver to form an anterior seal.
 Too short a duration to have impact on the tooth
position-1 second.
 Total swallows per day approx.-1000.

Tongue thrust swallow present in children with
good anterior occlusion.
Due to stoppage of sucking habit & where the
open bite is closing – tongue position persists for a
while.
Tongue thrusting seen in two circumstances1. Children with normal occlusion passing through
the transition stage.
2. Where there is an anterior openbite or protracted
anterior teeth.

Tongue thrusting result of malocclusion not
the cause.

Tongue Posture & Tongue Size
 TONGUE POSTURE:

 Tongue thrust swallowing
– short duration to have
impact on tooth position.
 If posture of tongue is
forward resting for long
duration effects tooth
position.

TONGUE SIZE:
Macroglossia can lead to proclination of
anteriors & anterior openbite.

Aglossia/Microglossia can lead to crowding
and lingual inclination of teeth.

Skeletal openbite
Steep mandibular plane.
Increased anterior facial height.
Tongue thrusting results due to lack
of anterior seal.

Respiratory Pattern
Respiratory needs – Primary
determinants of the jaw & tongue.
Breathing through the mouth alters
equilibrium of the jaws & teeth.
Lowering of the mandible & tongue &
extension of the head is seen.

Effects of mouth-breathing:
-Increase in facial height.
-Supraeruption of posterior teeth.
-Rotation of mandible downwards &
backwards.
-Open bite anteriorly.
-Increase in overjet.
-Pressures from stretched cheeks – narrow
maxillary arch.-Posterior crossbite .
&class II malocclusion.

Causes leading to mouth breathing:
Chronic respiratory obstruction.
Mechanical obstruction.
Size of the nostril.
Pharyngeal tonsils or adenoids (adenoid
facies).
Greater effort required to breath through
the nose – tortuous nasal passages.
Partial blockage of the nose leads to
resistance of airflow – person shifts to
mouth breathing

Studies to Find Association of Respiratory
Pattern & Craniofacial Growth.
D‟Arcy Thompson – „Form of an object is
its diagram of forces‟.
Methods to evaluate nasal obstruction:
1.Clinical tests- fogging of mirror, movement
of cotton wisps.
2.Cephalometric Radiographs.
3.Rhinomanometric tests

1. CLINICAL STUDIES OF
RESPIRATORY OBSTRUCTION:
Classic example – „adenoid facies‟
Characterized by separated lips, small
nose, nostrils poorly developed, pout in
the lower lip, vacant facial expression.
All patients with this facial
characteristics are not mouth breathers.
a. Case- children with nasal
obstruction- downward &
backward rotation of mandible.
Subsequent growth increases
lower facial height.

b. Howard reviewed 500 patients.
 159 patients classified as mouth breathers.
 59% - normal occlusion.
 14% with Class II malocclusion.
 27% with Class III / Class I malocclusion.
c. Linder – Aronson & Backstrom compared facial
types & type of occlusion in nose breathers and
mouth breathers.
 Greater nasal resistance – children with long
narrow faces & high narrow palate.
 No direct correlation between mouth breathing &
type of occlusion - particularly overbite / jet.

d. James A. McNamara Jr. – Preliminary
analysis of skeletal & dental characteristics
of 40 patients.
Tonsil & adenoid study (children‟s hospital
Pittsburgh).
Prospective study – Each subject met 1
criterion (at least) for adenoidectomy.
Recurrent otitis media.
Nasal obstruction due to large adenoids.
Both.

Classified as surgical/non-surgical groups.
Lateral radiographs analyzed77% - Class I molar relation.
13% - Class II molar relation.
10% - Class III molar relation.
On an average – excessive anterior facial height &
steep mandibular plane (31.5°) was characteristic.
4 patients – steep mandibular plane, 4 fell within
normal limits.
Results indicate craniofacial relationships with
mouth breathing are variable & associated with no.
of facial patterns.

. Fields et al-compared respiratory modes
of normal and long-faced subjects using
respirometric studies.
1/3rd of the long-faced individuals have
less than 50% nasal respiration and none
of the normal-faced individuals have such
low values.
Most of the long faced individuals are
predominantly nasal breathers.

Nasal impairment may contribute to long –face but
not the sole and major cause.
Multifactoral nature of association between nasal
obstruction and facial growth.

Conclusion of clinical studies:
Relationship exists between upper respiratory
obstruction & configuration of craniofacial
structures for a given individual.

No specific pattern can be directly co-related with
mouth-breathing

2. EXPERIMENTAL STUDIES OF
RESPIRATORY OBSTRUCTION:
James Mcnamaracaused complete nasal obstruction in
primates using silicon plugs.
Found downward & backward rotation of
mandible & increased lower facial height.
b. Harvold Miller – Classical studies in
young rhesus monkey.
Latex plugs inserted into the nasal
passages – forcing to breathe through the
mouth.
Gradual adaptation from nasal to oral
respiration.

Some animals positioned
mandibles downward &
backward.
Some, rhythmically lowered
and raised the mandibles.
Some positioned the
mandible downward &
forward.
Morphological changes –
Soft tissue changes
occurred first – notching of
upper lip & grooving of the
tongue.
Moderate skeletal changes
in animals who lowered
mandible for each breath

Dramatic changes

In mandibular morphology –at the gonial
region and chin in animals which
maintained lowered mandibular posture.
Distance from nasion to chin increasedlowering of mandible.
Distance from nasion to hard palate
increased –downward displacement of
maxilla.

Lower border of the mandible became steeper,
increase in gonial angle.
The ramus height maintained its normal relation –
masticatory muscles attaching the ramus to the
skull are unaffected.
Conclusions:
Every animal adapted to the environmental insult
with unique neuromuscular adaptation.
Occlusal effects variedRotation of the mandible in a posteroinferior
direction – Class I skeletal open bite or Class II
malocclusion.
Maintained more anterior position of mandible –
Class III malocclusion.
Total nasal obstruction- rare in human beings.

3. STUDIES FOR ADAPTATIONS FOLLOWING REMOVAL OF
NASAL OBSTRUCTIONS:

Linder- Aronson studied 41 children who
underwent adenoidectomies- 5 years.
34 children who switched to oral respiration
compared with 54 normal children.
Significant group mean difference found initially.
Greatest change occurred in the dentition and the
sagittal depth of the nasopharynx in the first year.

Mandibular plane angle diminished by 4
degrees (gradual change).
Results were statistically significant but no
large measurement differences – facial
height only 3 mm larger in adenoidectomy
group.

Solow & associates studied relationship of
craniofacial angulations & nasal respiratory
resistance.

2 months after adenoidectomy – 2% reduction in
the craniocervical angulation & position of the
head in relation to true vertical.
Bushey-Compared lateral cephalograms –pre and
post surgically.
 Found no relationship between linear
measurements of the adenoids and nasal
respiration.

Research leads to 2 opposing principles:
Total nasal obstruction – highly likely to
alter the pattern of growth & lead to
malocclusion.
Majority of individuals with long face
pattern of deformity have no evidence of
nasal obstruction & must have some other
etiological factor as the principle cause.

Roles of the Muscles in Producing
Class I, II & III Malocclusion
Class I malocclusion –
Muscle function usually normal & in a state of
balance.
Class I open bite – exception – attributable to
thumb/finger sucking or abnormal swallow or both.
Displacement of maxillary incisors labially results
in tongue thrusting to „close off‟ the oral cavity –
accentuation of open bite occurs.

Tongue thrusting enhances as lips
become hypotonic & no longer contact.
Mouth breathing aggravated as tonsils
& adenoids are larger at this stage.

If maxillary incisors are very proclined –
cushions to the lingual aspect of maxillary
incisors making them more proclined.
Mentalis activity increases – puckering of
the skin with each swallow.
Tongue drops lower in the mouth – no
longer approximates the palate

 Disturbance of the equilibrium – narrowing
of the maxillary arch.
 Over eruption of the posterior teeth
because lateral portion of tongue do not
overlay occlusal surfaces of posterior teeth.
 Interocclusal space eliminated.
 Crossbite occurs – leading to mandibular
displacement.
Though malocclusion not entirely caused
by the finger habit, it was the first assault
on the integrity of the dentition.
Compensatory tongue & lip activity resulted
in significant deforming mechanism.

Class II Div. 1 malocclusion:
Change in the muscle function – requisite.
Proclination of anterior teeth leads to excessive
overjet.
Lip sucking habit develops – hypertrophic lower
lip.
Incisors move further labially – no resistance from
hypotonic functionless upper lip.
Lower incisors pushed lingually by abnormal
mentalis activity.
Lower tongue position – Narrowing of the maxillary
arch.

Class II Div. 2 malocclusion:
 Muscle function usually normal.
 Tongue occupies the interocclusal space – increases
interocclusal clearance.
 Interferes with eruption & accentuate curve of spee.
 Due to lingual inclination, excessive interocclusal clearance
& infraocclusion of posterior teeth – forced retrusion of
mandible occurs.
 TMJ problems can arise.

„Forced retrusion‟- controversial.

Swann (1954)-functional displacement of mandible
when teeth are occluded.
Ricketts (1955),Jarabac(1963),Graber(1969)-also
agreed that there was a displacement of mandible
posteriorly and superiorly.
Recent studies have challenged this concept.

Gianelly (1989)-studied 19 asymtomatic
subjects with no overjet,deep bite and
upright incisors against 21 Cl II subjects
with normal overbite,overjet and interincisal
angulations.
Concluded that condylar positions in both
groups were essentially centered.
Demisch(1992)-concluded that-if there is
distal positioning of the mandible,it would
spontaneously reposition anteriorly on
treatment. As this phenomenon not noticedmandible not displaced posteriorly.

Assessment of the condylar position in class II div
2,using the mandibular position indicator-30
subjects.
Conclusions:
1.Although no particular predisposition to condylar
retrusion,it is seen in (uni/bilatrelly)in more than
50% of cases.
2.No association between condylar retrusion and
overjet, overbite and incisal inclinations.
3.Significant association between mandibular size
and condylar retrusion.

Class III malocclusion:
Abnormal muscle function is seen.
Upper lip – short but not hypotonic.
Lower lip hypertrophic & redundant –
passive during deglutition.
Upper lip shows greater activity during
swallowing.
Tongue lies low in the floor of the mouth –
constricted maxillary arch.
Interocclusal space – small or absent

Lip-Sucking & Lip-Biting
May be seen on its own or associated
with thumb sucking.
Mandibular lip mostly involved.
Results in labioversion of maxillary
teeth.
Open bite & linguoversion of
mandibular incisors.

Nail-Biting
Seen in high strung & nervous children.
Symptom of social & psychologic
maladjustment.
Often mentioned to cause malposition but
rarely does.
Marked increase in children after 6 year of
age.
Clinical examination of the incisor teeth in
finger-nail biters indicate that the habits is
responsible for openbite & rotation of the
mandibular incisor.

Clenching & Bruxism
Is rhythmic contraction of the
masticatory muscle – side to side
grinding & gnashing of teeth during
sleep.
Imp factor psycological or emotional
tension.
Initiated local factors-cusp interference
loose teeth, high filling…

Effect on Dentition
Reduction in the length of the crown.
Esthetic concern arises from
excessive wear in anterior region.
Wear in posteriors-Inter proximal
spacing & food impaction.
Generalised wear of teeth-reduced
facial vertical dimension or
mandibular overclosure.

Posture
 Frequently suggested that poor posture
can lead to malocclusion.
 Stooping with chin on the chestmandibular retrusion.
 Child resting head on hand or sleeping on
arm or fist- possible development of
malocclusion.
 May accentuate existing malocclusion.
 Role as primary etiological factor to be
proved conclusively.

Appliances Leading to Malocclusion
Milwaukee Brace –
Given in the treatment of
scoliosis.
Holds the head in
extended position.
Constant pressure on
the mandible – causes
malocclusion.

Plaster castsUsed to stabilize
cervical vertebrae can
produce similar effects.

Accident or Trauma
Undiscovered traumatic experiencessignificant in malocclusion.
Eruptive abnormalities.
Abnormal resorption.
Loss of vitality.
Both prenatal trauma & postnatal
injuries- Dentofacial deformity:

Prenatal trauma
Intrauterine pressure or trauma during
delivery-Hypoplasia of mandible.
Asymmetry

Postnatal Trauma
Fracture of jaws &teeth.
Habits may produce „microtrauma‟.
TMJ-impaired growth & functionasymmetry & TMD.

REFERENCES
Robert E. Moyers- Handbook of Orthodontics- 4th
ed
Salzmann. J. A- Orthodontics in daily practice- 4th
ed
William R. Proffit- Contemporary Orthodontics- 3rd
ed
T. M. Graber- Orthodontics- Principles and
practice
T. C. White, J. H. Gardiner, B. C. LeightonOrthodontics for dental students.
Shobha Tandon- Text book of pedodontics
Shafer, Hine and Levy- A text book of oral
pathology- 4th ed

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