ETIOLOGY OF MALOCCLUSION

CONTENT

• Introduction
• Orthodontic equation
• Primary etiological sites
• Systems of classification
• Specific cause of malocclusion
• Hereditary or genetic factors in malocclusion
• Environmental factors
• Abnormal Habits
• Roles of the muscles in producing Class I, II
& III malocclusion
• Conclusion
• References

2
 INTRODUCTION

 Malocclusion in most instances is a developmental

condition (rarely pathological) resulting from a complex
interaction among multiple factors that influence growth
and development, occasionally a single specific cause is
apparent. It is usually a clinically significant variation from
the normal range of growth and morphology.

 Etiology of malocclusion is the study of its cause or causes.

3
 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, though rarely one
site is involved alone.

 The different mechanisms of adaptation of the

primary etiologic tissue sites provide much of the
complexity and variability of malocclusions.

4
 ORTHODONTIC EQUATION (DOCKRELL R.
1952)

 It gives a brief expression of development of dentofacial

abnormalities.
 Certain original causes act for a time at a site and produce a
result.

5
 PRIMARY ETIOLOGICAL SITES

1. NEUROMUSCULAR SYSTEM
 It plays primary role in the etiology of dentofacial
deformity by the effects of reflex contractions on the bony
skeleton and dentition.
 Treatment of malocclusion must involve conditioning of
reflexes to bring about more favourable functional
environment for growing craniofacial skeleton and
developing dentition.
2. BONE
 Maxilla and mandible serve bases for dental arches.
 Aberrations in their morphology or growth may alter
occlusal relationship and functioning.
 Orthodontic treatment of skeletal disharmony must either
(a) alter the growing craniofacial skeleton or (b) camouflage
it by moving teeth to mask its disharmony.

6
3. TEETH
 The teeth may be a primary site in the etiology of
dentofacial deformity due to their gross variations in size,
shape, number, or position.
 Malpositions of teeth can induce malfunction and thus
alter the growth of the bones.
 Teeth may be moved in orthodontic treatment to correct
the malocclusion, camouflage a skeletal dysplasia, or aid
in the removal of neuromuscular dysfunction.

4. SOFT PARTS ( EXCLUDING MUSCLES)

 The role of the soft tissues is not as clearly discernible,
nor is it as important as that of the three other sites .
 Malocclusion can result from periodontal disease and loss
of the attachment apparatus and from a various soft-tissue
lesions including TMJ structures.

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 SYSTEM OF CLASSIFICATION

• Inherited or Congenital Causes & Acquired

causes
• Indirect or predisposing Causes & Direct or
determining causes

Various classifications proposed-

• Moyer’s Classification
• White and Gardiner’s Classification
• Graber’s Classification
• Salzmann’s Classification
• Proffit’s Classification

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 MOYER’S CLASSIFICATION (1972)

1. Hereditary
a) Neuromuscular system
b) Bone
c) Teeth
d) Soft parts
2. Diseases
a) Systemic disease
b) Post natal trauma
c) Local diseases:
(i) Nasopharyngeal Diseases
(ii) Gingival And Periodontal Diseases
(iii) Tumors
(iv) Caries

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3. Habit
a) Thumb and finger sucking
b) Tongue thrusting
c) Lip sucking and lip biting
d) Nail biting
4. Trauma
a) Prenatal trauma and birth injuries
b) Endocrine disorders
5. Developmental defect of unknown origin
6. Physical agent
a) Premature extraction of primary teeth
b) Nature of food
7. Malnutrition

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 WHITE AND GARDINER’S CLASSIFICATION

1. Dental base abnormalities

a) Anteroposterior malrelationship
b) Vertical malrelationship
c) Lateral malrelationship
d) Congenital abnormalities
e) Disproportion of size between teeth and basal bone
2. Pre-eruption abnormalities
a) Abnormalities in position of developing tooth germ
b) Supernumerary teeth and teeth abnormal in form
c) Missing teeth
d) Prolonged retention of deciduous teeth
e) Large labial frenum
f) Traumatic injury

11
3. Post eruption Abnormalities
a) Premature loss of deciduous teeth
b) Extraction of permanent teeth
c) Muscular:
(i) Active muscle force
(ii) Rest position of musculature
(iii) Sucking habits

4. Abnormalities in path of closure

a) Premature loss of deciduous teeth
b) Extraction of permanent teeth

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 GRABER’S CLASSIFICATION

1. General (extrinsic) factors

a) Hereditary
b) Congenital
c) Environment:
(i) Pre-natal
(ii) Post natal
d) Pre- disposing metabolic climate and disease:
(i) Endocrine imbalance
(ii) Metabolic disturbances
(iii) Infectious diseases
e) Dietary problems (nutritional deficiency)
f) Posture
g) Trauma and accidents
h) Abnormal pressure habits and functional aberrations:
(i) Abnormal sucking
(ii) thumb and finger sucking
(iii) tongue thrusting
(iv) lip and nail biting
(v) abnormal swallowing habits 13
(vi) Speech defects
(vii)Tonsils and adenoids
(viii) Respiratory abnormalities
(ix)Psychogenic tics and bruxism

2. Local (intrinsic) factors

a) Anomalies of number:
(i) Supernumerary teeth
(ii) Missing teeth
b) Prolonged retention of deciduous teeth
c) Anomalies of tooth size
d) Abnormal labial frenum
e) Dental caries
f) Abnormal eruptive pathway
g) Ankylosis
h) Anomalies of tooth shape
i) Improper dental restorations
j) Premature loss of deciduous teeth
k) Delayed eruption of permanent teeth 14
 SALZMANN CLASSIFICATION

• Salzmann’s diagrammatic representation of the etiologic

factors in malocclusion embodies prenatal and post natal
factors.

• The genetic, differentiative and congenital factors make

up the prenatal elements of causation, which can
influence one or all of the postnatal components-
developmental, functional, environmental.

15
• Prenatal Factors
1. Genetic: transmitted by genes. May or may not be
present at birth.
2. Differentiative:
a.General or Constitutional: whole body
b.Local or dentofacial: face, jaws & teeth
3.Congenital:hereditary or acquired . Exist at the
time of birth
• Postnatal Factors
A) Developmental
General factors
a. Abnormalities in relative rate of growth.

b. Hypo/hypertonicity of muscles.

c. Childhood diseases, nutritional,Endocrine,&

metabolic disturbance

d. Radiation/Radiotherapy
Local factors
16
a. Birth injuries
c. Micro/macroglossia.
d. Abnormal Labial Frenum
e. Facial hemiatrophy
f. Anomalies of tooth development & eruption

B) Functional
General factors
a. Muscular hyper or hypotonicity.
b. Neurotropic disturbances. c. Postural defects of the
tongue and jaws
d. Masticatory and respiratory disturbances
Local factors
a. Premature loss or prolonged retention of deciduous
teeth.
b. Loss of proximal contact.
c. Temporomandibular articulation disturbance.
d. Muscular hypo or hyperactivity

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C) Environmental or Acquired
General factors

Diseases can affect the dentofacial tissue directly or

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

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 PROFFIT’S CLASSIFICATION
1. Specific causes
a) Disturbances in embryological development
b) Skeletal growth disturbances
c) Muscle dysfunction
d) Acromegaly and Hemimandibular hypertrophy
e) Disturbances of dental development
2. Genetic influence
3. Environmental influence
a) Equilibrium theory and Development of dental
occlusion
b) Functional influences on dentofacial development

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 SPECIFIC CAUSES OF MALOCCLUSION

DISTURBANCES IN EMBRYOLOGICAL
DEVELOPMENT
 Defects in embryologic development usually result in death
of the embryo.
 Although most defects in embryos are of genetic origin,
effects from the environment also are important. Chemical
and other agents capable of producing embryologic defects
if given at the critical time are called teratogens.
 Teratogens typically cause specific defects if present at low
levels but, if given in higher doses, do have lethal effects.
 Teratogens can disturb jaw growth if introduced at the time
that the jaw is developing.
 It can also lead to cleft lip and palate leading to class III
skeletal pattern.

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Teratogens known to produce orthodontic problems such as

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 DEVELOPMENTAL DEFECTS OF UNKNOWN ORIGIN

 Developmental defects of unknown origin is a term applied to

gross defects of a rare type probably originating in failure of
differentiation at a critical period in embryonic development.

 Examples include congenital absence of some muscles,

micrognathia, facial clefts, and some instances of oligodontia
and anodontia
Malocclusion of
known etiology
5%

Normal Malocclusion
occlusion Of Unknown
35% etiology
60%

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 GROWTH DISTURBANCES IN FETAL AND PERINATAL
PERIOD
• Fetal moulding and birth injuries
• Injuries apparent at birth :
1.Intra uterine moulding [prenatal]
2.Trauma to mandible during the birth process [postnatal]
A) PRENATAL
Intrauterine moulding:
1. Pressure against the developing face prenatally can led to
distortion of rapidly growing areas.
2. An arm pressed against the face in utero can results in severe
maxillary deficiency
3. Fetus head flexed tightly against the chest in utero can prevent
mandible from growing forward normally.

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4. Decreased amount of amniotic fluid can lead to –
extremely small mandible at birth, accompanied with cleft
palate resulting in upward displacement of tongue
preventing normal closure of palatal shelves- Pierre Robin
sequence.
5. Catch-up growth occurs when pressure against the face
is released except when cartilage is affected like in
Stickler syndrome

B) POST-NATAL
Birth injuries
1. Trauma to mandible- Most mandibular deformities
are congenital anomalies but are thought to be due to birth
trauma.
2. Vogelgeschist: development ankylosis of TMJ, may be
due to birth injury like the forceps delivery

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 PROGRESSIVE DEFORMITIES IN CHILDHOOD

Childhood Fractures of the jaw

1. Mandible is more commonly affected than the maxilla.
2. Condylar neck is particularly vulnerable to frequent falls
and impacts of childhood.
3. In 75% of children with early fractures of mandibular
condylar process normal growth can be observed with no
further development of malocclusions.
4. Unilateral condylar fractures are more frequent than
bilateral fractures.
5. Asymmetric growth deficiency due to injury to the soft
tissue matrix produces scarring around the TMJ and
restricts the translation of condyle further restricting jaw
growth.

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5. Management of condylar fractures is very critical.
Conservative approach of early mobilization of jaw is followed
to minimize any restriction on movement.

Muscule Dysfunction
 The formation of bone at the point of muscle attachment
depends upon the activity of the muscle. The musculature is
the part of soft tissue matrix whose growth carries the jaw
downward and forward.
 Malocclusion can be caused by,
a) Decrease in tonic muscle activity caused due to muscular
dystrophy allows the mandible to drop downward resulting
in : increased facial height, distortion of facial proportions
and mandibular form, excessive eruption of posterior teeth,
narrowing of maxillary arch and anterior open bite.

26
b) Damage to the motor nerve supply caused due to muscle
atrophy leading to loss of musculature and underdevelopment of
that part.
c) Excessive muscle contraction can restrict growth as seen in
scarring after an injury which can be seen clearly in torticollis
where excessive tonic contraction of neck muscles (SCM) on one
side

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Nutritional Deficiency-
1. Disturbances in the developmental timetable.
2. Rickets, scurvy and beriberi can produce severe
malocclusions.
3. Premature loss of teeth /Prolonged retention.
4. Abnormal eruptive path.
5. Poor tissue health.
6. Poor absorption-hormonal deficiency.
7. Decreased fluoride intake will be responsible for
loss of teeth due to caries which can cause
malocclusion.

Endocrine Imbalance-

1. Hypopituitarism

 Dwarfism- smaller teeth and jaws.

 Delayed eruption of permanent teeth and delayed
shedding of primary teeth. 28
 Crowding due to smaller arch size.
Mandibular growth is affected more
than maxilla.

2. Hyperpituitarism:

 Gigantism-large teeth and jaws.

 Acromegaly-occurs after growth and
ossification is complete.
 Lips are thick, tongue is enlarged
 Accelerated condylar growth will lead
to larger mandible.
 Teeth are tipped buccally due to
enlarged tongue.
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3. Hypothyroidism:

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

4. Hyperthyroidism:

 Early shedding and eruption.

 Atrophy of alveolar bone.

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 HEREDITARY / GENETIC FACTORS IN
MALOCCLUSION

 A strong influence of heredity on facial features is obvious

at a glance.

 GALTON’S LAW:
1. Sir Francis Galton did the first scientific analysis of twins
and concluded that it is possible to separate ‘Nurture’ from
‘Nature’.
2. The best method to find out about genetic basis in
malocclusion is by using-
• Familial studies – a) Parent child study b) Sibling study
(more comprehensive)
• Twin studies – difficult to obtain samples.
3. Twin studies:
a) Lundstrom (1963) - conducted a study on pair of twins , ½
were monozygotic and ½ were diazygotic. Both skeletal
and dental overjets were measured.
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• Conclusion: Greator variation was seen in dizygotic than
monozygotic twins; Larger genetic variation for skeletal
pattern was observed compared to dental indicating
dentoalveolar compensation.

b) Lauweryns et al (1993) – summarized a number of

twin studies and concluded that 40% of dental and skeletal
variations that lead to malocclusion can be attributed to
hereditary factors.

4. Familial studies:

a) Suzuki(1961) - studied Japanese families. If one parent

had the anomaly, 20% of children were affected. If both
parents had the anomaly then 40% of the children were
affected.

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b) Bolton and brush growth studies were conducted on
siblings between 1930s and 1970s. Harris and johnson
concluded that heritability of craniofacial characters was
relatively higher than dental occlusal characteristics.
Heritability estimates for skeletal characteristics increases
with age but for dental characteristics it decreases-
indicating environmental contribution to dental variation.

c) Litton et al ( 1970) – in their sibling study have reported

Class III malocclusion to be heritable trait that is polygenic
in nature.

d) Familial occurrence of class II div 2 has been documented

in several published reports including twin and triplet studies
– Korkhaus (1930) , Markovic (1992), Peck et al (1998).

e) Markovic (1992) – carried out cephalometric study of

Class II division 2 malocclusion.

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• For Class II division 2: 100% concordance of monozygotic;
90% discordance
• of dizygotic twins; suggesting strong evidence of genetics
as the main etiological factor.

 Genetic influence is probably autosomal dominant with

incomplete penetrance and variable expressivity. It can
also be explained by the POLYGENIC MODEL where
simultaneous expression of several genetically determined
morphological traits acts additively rather than being the
effect of a single controlling gene for entire occlusal
malformation.

 Hence appreciating the synergistic effects of genetics and

environment.

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f) Most famous example of genetic trait passing through
several generations in the pedigree of HAPSBURG
JAW (Hungarian/Australian dual monarchy).

STROHMAYER ( 1937) concluded from pedigree

analysis of the Hapsburg family line that the mandibular
prognathism was transmitted as an
AUTOSOMAL DOMINANT TRAIT.

Mandibular prognathism in the Hapsburg family became

known as the Hapsburg jaw as it recurred over multiple
generations in European royalty.

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 Malocclusion could be produced by inherited
characteristics in two major ways:
1. Disproportion between the size of the jaw and teeth
resulting in crowding or spacing of teeth.
2. Disproportion between size and shape of the upper and
lower jaw resulting in occlusal malrelationship either class
II or class III malocclusion.
 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.

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1. 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
 The study was misleading as many breeds of small
dogs carry genes for Achondroplasia.
2. Studies using out breeding in human population:
 In primitive human populations- malocclusion was
less frequent since it was characterized by genetic
isolation & uniformity.
 Tooth-size jaw-size discrepancies were infrequent.

37
 Whenever out breeding occurs incidence of malocclusion
is greatly increased.
 This seemed to show that the independent inheritance
could be a major cause of malocclusion.

3. Hawaiian melting-pot study, Chung et al:

 It was one of the best investigations to examine the
hypothesis of independent inheritance of tooth & jaw
characteristics.
 Hawaii-homogenous Polynesian population had large
stature, broad and well developed jaws and distinctive
form of lower jaw (ROCKER JAW)
 Large scale migration of Europeans, Chinese, Japanese
group resulted in Heterogeneous modern population.
 High prevalence of malocclusion would be expected in
this population but that was not seen.

38
 The prevalence of malocclusion though higher than in the
original population was only additive rather than
multiplicative.
 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 that Hereditary is significant in
determining :
• 1. Size, shape and number of teeth.
• 2. Size, shape of jaws and the palatal height.
• 3. Position and conformation of perioral musculature to
tongue size and shape
• 4. Soft tissue peculiarities (character and texture of
mucosa, frenum size, shape and position.)

39
• Heredity also plays an important role in-
1. Congenital deformities.
2. Cleft-lip/palate.
3. Facial asymmetries.
4. Diastemas.
5. Macro/micrognathia.
6. Deep overbites.
7. Macro/microdontia
8. Crowding & rotation of teeth.
9. Oligodontia & anodontia.
10. Mandibular prognathism/ retrusion
11.Tooth shape variations.

40
Genetically the growth of mandible and maxilla is independent of
one another since the genes predetermines the structural pattern
of maxilla which differs from that of mandible.

• Clinical implications:
Heredity can affect orthodontic treatment as:

1. Class II malocclusion caused due to habit is much more 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 is for
a successful outcome by means of orthodontic intervention.

41
• Congenital malformations
1. Single gene abnormality
2. Chromosomal disorders
3. Multifactorial disorder
4. Disorder cause by Teratogens
5. Disorders of unknown etiology

• Autosomal Dominant Disorder

1. Treacher collins syndrome
2. Achondroplasia
3. Crouzon Disease [cranio facial dysostosis]
4. Cleido cranial dysostosis
5. Marfan syndrome
6. Dentinogenesis imperfecta
7. Hemifacial microsomia [Goldenhar syndrome]
8. Basal cell nevus syndrome

42
• Autosomal Recessive Disorders
1. Cerebro-Costo-mandibular syndrome [micrognathia with
Pierre Robin Syndrome]
2. Bloom syndrome [with Skin lesion]- Maxillary hyperplasia
3. Stickler syndrome
4. Nagar Acrofacial dysostosis

• Multi Factorial Inheritance

1. Cleft Lip and Palate
2. Disease which is dealt with malocclusion, Dental Caries,
Periodontal disease with multifactorial traits

43
 1. 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 live births, depending on geographic
origin, racial & ethnic background & socioeconomic
status.
 Both dental & skeletal components are affected.
 More commonly seen in maxilla causing damage to
profile due to maxillary deficiency.
 Etiology of cleft:
 Fogh & Anderson – Genetic in origin
 Bhatia – Either by single mutant gene or by number of
genes.

44
 Bixler – 1. Probably polygenic.
2. Monogenic or syndromic.
Various environmental factors.
- Alcohol
-Maternal illness & smoking

• Problems associated with CL & CP

1.Dental
2.Esthetics.
3.Speech & hearing.
4.Psychology.

45
Dental problem:

1.Congenitally missing teeth

2.Multiple decayed teeth

3.Mobile premaxilla

4.Periodontal complications
5.Anterior & posterior cross bite

6.Enamel hypoplasia & microdontia

7.Ectopically erupting teeth

8.Protruding premaxilla
9.Impacted teeth

10.Deep bite
11.Supernumerary teeth
46
12.Spacing/crowding
 2. Cliedocranial
dysplasia

 Hereditary is an 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

47
3. Ectodermal Dysplasia

 This syndrome is characterized by a congenital

dysplasia of one or more ectodermal structures
manifested primarily by hypohydrosis,
hypotricosis & hypodontia.
 X-linked recessive mendelian disorder.
 EDSs may manifest in association with
midfacial defect- CL &CP.
 Clinical manifestations:
1. Underdeveloped eyebrows, broad nose,
Anodontia or oligodontia, normal growth of
jaw.
2. Ridge-like lip configuration, pronounced
mentolabial sulcus, frontal bossing & Sparce
hair on the Scalp
3. Underdevelopment of middle face & lower
facial height, Alveolar process do not develop-
reduced vertical dimension-protuberant lip and
high Palatal arch, Collapsed middle third of48
face.
 4. Mandibulofacial Dysostosis
 Encompasses a group of closely related defects of the head &
face.
 Hereditary or familial in pattern.
 Clinical manifestations:
1. Antimongoloid palpebral fissures with a coloboma of the outer
portion of the lower lids & deficiency of the eyelashes.
2. Hypoplasia of facial bone.
3. Malformation of the external ear.
4. Macrostomia, high palate & abnormal position & malocclusion
of teeth.
5. Blind fistulas between the angle of the ears & angle of mouth.
6. Facial cleft and deformity .
7. Characteristic facies of patient-Birdlike or Fishlike

49
 6. Craniofacial Dysostosis [Crouzon Disease]

 Autosomal dominant pattern with the mutation of FGFR-2 gene is

seen. There occurs early synostosis of the sutures.
 Clinical manifestations :
1. Facial deformities observed at birth. Mimicks frog face. Upper lip
is shortened & cleaved.
2. Anteroposterior diameter is smaller than transverse diameter.
3. Deviation of nasal septum, narrowed anterior nares & wide beaked
nose.
4. Impaired vision & hearing.

50
1. Malocclusion, malposed teeth & dysplasia is seen . Cranial
& facial deformities, mandibular prognathism, high-arched
palates & clefts, is seen.
2. Wide face & hypoplastic maxilla producing pseudo
prognathism.

7. Pierre Robin Syndrome

 May/may not be genetic in origin

 Characterised by- Cleft Palate, Micrognathia, Glossoptosis.
 It is a primary defect seen in mandible.
 U or V-shaped hard & soft palate are seen.
 Respiratory difficulty can be observed due to epiglottic
obstruction.

51
 8. Achondroplasia

 Caused by mutations in the gene for FGFR-3

[fibroblast growth factor receptor]
 It is a characteristic form of dwarfism.
 The disease begins in utero and 80% of affected infants
are stillborn.
 Clinical manifestations:
1. Maxillary retrusion & mandibular prognathism.
2. Midfacial hypoplasia & prominent forehead.

52
 9. Down’s Syndrome

 First described by John Langdon Down in 1866.

 It is somatic abnormality that occurs due to a number of
chromosomal aberrations.
 Three Cytogenetic variants:
Trisomy-21, Trisomy-18, Trisomy-13
 Clinical manifestations:
1. Small head, flat face, depressed nasal bridge, flat occiput
& broad short neck.
2. Small slanting eyes with epicanthal folds, open mouth,
frequent prognathism & sexual underdevelopment.
3. Protrusion of tongue [macroglossia] with difficulty in
eating & speaking, scrotal tongue, hypoplasia of maxilla.

53
 5. Delayed tooth eruption, partial anodontia,
enamel hypoplasia, juvenile periodontitis &
Cleft lip or palate.
6. Fissuring & thickening of lips & angular
Cheilitis are frequent

10. Stickler Syndrome

 Stickler Syndrome was first described by Dr.

Gunnar Stickler in the year 1965. It was
originally termed as hereditary progressive
arthro-ophthalmopathy because it
predominantly affects the eyes and the joints.
 Autosomal dominant connective tissue
disorder.
 It is greater between the families rather than
within families.
 At birth only features of Pierre Robin sequence
is observed.
 The facial appearance at birth –mid-face
hypoplasia, flat nasal bridge, anteverted nares 54
& prominent eyes.
 11. Syphillis

 Caused by Treponema palladium.

 Classified as Congenital & Acquired.
 Congenital syphilis is transmitted to offspring only by an
infected mother.
 Manifests as a variety of lesions including frontal bossing,
short maxilla, high palatal arch, saddle nose, mulberry
molars, protuberance of the mandible Higoumenakis’s sign [
irregular thickening of the sternoclavicular portion of
clavicle].
 Hutchinson’s triad:
1. Hypoplasia of incisor & molar teeth
2. Eighth nerve deafness
3. Interstitial Keratitis.
 Malocclusion frequently observed is open bite & lack of
development of maxilla.
55
 12. Rubella [German Measles]
 Caused by Togavirus which spreads 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.

13. Cerebral palsy

 Cerebral palsy is a paralysis or lack of muscular

coordination attributed to an intracranial lesion.
 Most commonly considered to be a result of birth injuries.
The 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.
The uncontrolled aberrant activity upsets the muscle
balance necessary for establishment and maintenance of
normal occlusion. 56
 ENVIRONMENTAL INFLUENCES

EQUILIBRIUM CONSIDERATION
 Equilibrium theory was first given by WEINSTEIN.S et al
A.C. 1963 and revisited by WILLIAM R. PROFFIT in 1978.
 Equilibrium theory, as applied in engineering, states 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.
 Hence it can be concluded that:
1. Dentition is in equilibrium.
2. Movement occurs when equilibrium is disturbed. 57
 EQUILLIBRIUM COMPONENTS:
 Four major primary factors are:
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 and Lips.
 Duration of force is of greater importance than the
magnitude. Heavy but intermittent forces result in no
change in tooth position
 Periodontal ligament acts as a shock absorber but if the
forces are maintained for a longer duration pain is felt.

58
The chewing force is heavy. The forces from lips, cheek, and
tongue are lighter but if they act for a longer duration they are
capable of causing tooth movement. Since no tooth movement
occurs forces are in equilibrium.

 Study by Walter Straub (1950)- clinically observed:

 Tongue and lip pressures during swallowing varied among
individuals and did not correlate with the position of the teeth.
 The tongue and lip pressures were never balanced, and the
tongue pressure was several times higher during swallowing.
 It was thought that lip pressure acted for a longer duration
which was later disapproved.
 Hence it was concluded that incorrect swallowing was the
major cause of anterior open bite & incisor protrusion.

59
 Lear & Moorrees –
 They studied tongue and lip pressures measured over a 4-
hour period and projected over 24 hours.
 In the 24 hour period, summary of tongue and lip pressures
were close to the equilibrium but the total tongue and lip
pressures were still imbalanced.
 They concluded that other forces must be considered if
equilibrium is to be explained.
2. Extrinsic forces: Pressure habits & orthodontic
appliances.
 Orthodontic treatment causing tooth movement interferes
with the equilibrium. The same can be concluded about
habits.
 Extrinsic forces are effective only when the duration exceeds
6 hours.
3. Factors affecting equilibrium in the vertical direction:
1.Tongue & lips.
2.Forces of occlusion.
3.Forces of eruption
60
 Studies by Wallen- to find if tongue pressure leads to
anterior open bite:
1. Tongue pressure in patients with anterior open bite was less
than in persons with normal vertical relationships.
2. Due to relatively high position of the incisors the tongue
doesn’t contact them during swallowing

The occlusal forces influence vertical position of teeth.

Vertical position of teeth, when changed, can alter the rest
position of the mandible.
Extrusion of molar teeth rotates the mandible downward &
backward and the intrusion causes the mandible to move to a
closed position.
These changes are mediated by proprioceptors in the
periodontal ligament.

61
• Forces of eruption:
 Eruptive force moves the tooth through the bone and
they remain active till tooth has come into occlusion.
 Extraction of the antagonist teeth restarts the eruption
process again.
 Studies show that eruptive force are generated in the
periodontal membrane rather than the root apex.

• Biting forces & Eruption:

Patients with deep / open bite show infra/supra eruptive
posterior teeth – concluding that the amount of tooth
eruption depends on the amount of force placed on it.
Studies to find if long faced persons have lower
maximum biting force & short faced persons have high
biting forces were also done.

62
Swallowing, chewing & maximum biting forces were
evaluated.
3 groups measured were- children with long faces,
children with normal faces & long faced adults. It was
concluded that all 3 groups had less biting forces than
normal adults.
 The difference in occlusal forces arises at puberty when
the normal faced individual gains muscle strength.
 The tendency towards long face develop long before the
difference in force appears.
4. Forces from the periodontal membrane:
 Periodontal membrane forms an important part in
stabilization of the teeth.

63
 Although the tongue & lip pressure are unequal it is observed
that periodontal ligament maintains teeth in stable position.
 Pathological migration can cause break down of the
periodontal ligament.
 Final position of teeth is influenced by two factors-
1. Resting positions of lip, cheek & tongue.
2. Metabolic activity within the periodontal membrane.

64
 ABNORMAL HABITS

 All habits are learned patterns of muscle contraction

of a very complex nature.
 Habits such as normal lip action and mastication are
stimulants for the normal growth while the
undesirable habits produces malocclusion

65
 The trident of habit factors:
1. Duration
2. Frequency
3. Intensity

 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.

66
 1. Thumb/Digit sucking

 One of the most important factors in producing and

maintaining malocclusion is thumb or digit sucking.
 It begins at birth and is outgrown by 3-4 years.
 Finger sucking from birth to 4 years:
 Suckling mechanism is the most important exchange with the
outside world.
 Through suckling the child obtains- nutrients, feelings of
euphoria, a sense of security, and feeling of warmth.
 Time of appearance of digital sucking-
 First few weeks- feeding problems.
 During the eruption of teeth- Teething device
 Older children- it is a form of release of emotional tensions

67
CLASSIFICATION OF SUCKING HABITS
1. 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.

68
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.

2. O’Brien (1996)
• Nutritive sucking habit – breast feeding/bottle
feeding.
• Non-nutritive sucking habit – thumb / finger
sucking, pacifier sucking.

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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.
• It agrees with the Freudien theory that suckling increases the
erotogenesis of the mouth.

70
 Studies done to evaluate psychological aspects reveal
that :
Thumb sucking results in inadequate attention and is a
manifestation of feeling of insecurity.
Children should be screened for underlying psychological
disturbances.

 Studies done to evaluate feeding patterns:

 Children who were adequately fed had less thumb-sucking
habit than children whose feedings were widely separated.
 Non-thumb suckering individuals took a longer time to feed.
 Digital sucking is 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 was less.
 Psychological consultation is needed when trying to break the
habit.

71
 Studies in the university of Alberta disproved the above
facts.
This study was done with 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.
The results supported the theory that digital sucking is a
simple learned habit. No support was found for the
interpretation of thumb sucking as a symptom of
psychological disturbance.

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Orthodontic intervention failed to produce any increase in
alternative or substitute undesirable behavior.
Palatal crib with spurs was most effective and associated
habits like hair-twisting, and fondling, disappeared with
finger habits.
Thumb-sucking arises out of a progressive stimulus &
reward reaction and spontaneously disappears unless it
becomes an attention getting mechanism.
Various theories of non-nutritive digit sucking are not
completely incompatible. The findings support the learning
theory – associated with prolonged nutritive sucking.

Digit Sucking & Malocclusion

 Large percentage of children practicing digit sucking had
little correlation with malocclusion.
 Sucking habits in primary dentition has little or no long
term effects.

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 But if the habit persists beyond the time the permanent
.
teeth erupt - malocclusion occurs.
 Characterized by: flared & spaced maxillary incisors,
lingually positioned lower incisors, anterior open bite, and
narrow upper arch.
 It is rarely due to finger pressure alone but also occurs with
the assistance from perioral musculature.
• How does malocclusion actually occur?
When thumb/finger is placed between the teeth it is
positioned at an angle and presses lingually against the
lower incisors & labially against the upper incisors.

74
There can be variation depending on which teeth are
contacted.
Duration of the sucking is most important factor.
 Child who sucks vigorously but intermittently does not
displace incisors but when continuous light pressure is
applied – malocclusion results.
 Anterior open bite is a combination of thumb sucking &
interference with normal eruption.
 The mandible is positioned in a downward manner to
accommodate the interposed thumb- causing increased
eruption of posterior teeth.
 Excessive eruption of posterior teeth causes direct
impediment of incisor eruption.

75
 Maxillary constriction occurs- due to an imbalance between
tongue & cheek pressure. The tongue is lowered which
decreases the pressure on the upper posterior teeth. Cheek
pressure is increased as the buccinator muscle contracts during
suckling.
 Constricted maxillary arch is least likely to correct
spontaneously.
 When the maxillary arch is expanded, incisor protrusion &
anterior open bite improves spontaneously.
 Orthodontic therapy is not started till the habit is corrected.

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 2. Tongue Thrusting

 Normal swallow – the teeth are in occlusion, lips are lightly

closed, and the tongue is held against the palate behind the
anterior teeth.
 Tongue thrust is the forward placement of the tongue between
the anterior teeth & against the lower lip during swallowing-
Schneider (1982).
 It is often associated with thumb sucking habit.
• CLASSIFICATION OF TONGUE THRUST SWALLOW:
1. Simple tongue-thrust swallow –
• Normal teeth together swallow.
• It is associated with previous history of digit sucking .
• Mandible is stabilized by muscles of mastication
• Facial muscle contraction during swallowing is not seen
• Well defined open bite. Proper, secure, posterior occlusal fit
is seen.

77
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.
 Mandible is stabilized by muscles of lips and cheeks
( facial muscles)
 Facial muscle contraction can be seen during swallowing
 Reflex drop of mandible – separates 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.
Hence adequate airway.
 Jaws are held apart during swallow – tongue remains in
a protracted position.

78
 Studies by Melsen et al. showed tongue thrust
swallow & teeth apart swallow favor development of
distocclusion, maxillary overjet & open bite.
Swallowing is not a learnt behavior but is integrated
& controlled physiologically at subconscious levels.
 Tongue thrusting results due to
1. TONGUE POSTURE:
• Tongue thrust swallowing of shorter duration doesn’t
have any impact on tooth position. But if posture of
tongue is forward resting for a longer duration it
effects tooth position.
2. 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
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Tongue thrusting is seen in two circumstances-
1.Children with normal occlusion passing through the
transition stage.
2.Where there is an anterior open bite or protracted
anterior teeth.
 Mature adult swallow develops at 3 years of age, in
majority of people seen by the age of 6 yrs.

80
• Transition stage is characterized by muscular activity which
brings the lips together, separates the posterior teeth & there is
forward protrusion of the tongue. Delayed normal swallow
transition is associated with previous history of sucking habit.
• Upper incisor protrusion or anterior open bite is observed with
tongue thrusting . Hence it is difficult to seal the mouth by
bringing lips together. So bringing the tongue forward is a
successful maneuver to form an anterior seal.

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 3. Respiratory Pattern

 Respiratory needs are the primary determinants of the jaw &

tongue.
 Breathing through the mouth alters equilibrium of the jaws &
teeth.
 Lowering of the mandible & tongue and 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 and Increase in overjet.
-Pressures from stretched cheeks ,narrow maxillary arch,
Posterior crossbite & class II malocclusion.

82
 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
 Methods to evaluate nasal obstruction:
1. Clinical tests- fogging of mirror, movement of cotton
wisps.
2. Cephalometric Radiographs.
3. Rhinomanometric tests- It measures Total airflow through
mouth and nose and % of nasal and oral respiration . Less
than 40% nasal breathing is seen in most adenoid facies

 Studies to Find Association of Respiratory Pattern &

Craniofacial Growth.

83
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. Children with nasal obstruction have downward &
backward rotation of mandible and the subsequent
growth increases lower facial height.
b. Howard reviewed 500 patients with a history of
tonsil problems out of which 159 patients were
classified as mouth breathers.
59% - normal occlusion.
14% with Class II malocclusion.
27% with Class III / Class I malocclusion.

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c. Linder – Aronson & Backstrom compared facial
types & type of occlusion in nose breathers and mouth
breathers.
Greater nasal resistance was seen in children with long
narrow faces & high narrow palate.
No direct correlation between mouth breathing & type
of occlusion was seen particularly overbite / overjet.
d. James A. McNamara Jr. – performed preliminary
analysis of skeletal & dental characteristics on 40
subjects from Tonsilar & adenoid study (children’s
hospital Pittsburgh).
• Each subject met 1 criterion for adenoidectomy:
1. Recurrent otitis media.
2. Nasal obstruction due to large adenoids.
3. Both

85
 Each was randomly assigned as surgical/non-surgical
groups.
 Lateral radiographs were analyzed indicating-
 77% - Class I molar relation.
 13% - Class II molar relation.
 10% - Class III molar relation.
 On average this group was characterized by excessive
anterior facial height & steep mandibular plane
(31.5°). Four of the patients had steep mandibular
plane and 4 fell within normal limits.
 Results indicated craniofacial relationships with mouth
breathing are variable & associated with no. of facial
patterns.
e. Fields et al- compared respiratory modes of normal
and long-faced subjects using respirometric studies. He
observed -
86
• 1/3rd of the long-faced individuals had less than 50% nasal
respiration and none of the normal-faced individuals had such
low values.
• Most of the long-faced individuals were predominantly nasal
breathers. Nasal impairment may have contributed to long –face
but was not the sole and major cause. A multifactoral nature of
association between nasal obstruction and facial growth was
seen.
• 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.

87
2. EXPERIMENTAL STUDIES OF RESPIRATORY
OBSTRUCTION:
• a) James Mcnamara-
• Caused complete nasal obstruction in primates using silicon
plugs and found downward & backward rotation of mandible
& increased lower facial height.
• b. Harvold Miller – conducted classical studies in young
rhesus monkeys. Latex plugs were inserted into the nasal
passages forcing them to breathe through the mouth. Gradual
adaptation from nasal to oral respiration was observed-
1. Lower border of the mandible became steeper and increased
gonial angle was observed.
2. The ramus height maintained its normal relation –
masticatory muscles attaching the ramus to the skull are
unaffected.

88
Conclusions:
 Every animal adapted to the environmental insult with unique
neuromuscular adaptation.
 Occlusal effects varied-
 Those animals who rotated the mandible in a posteroinferior
direction developed Class I skeletal open bite or Class II
malocclusion.
 Those who maintained a more anterior position of mandible
developed Class III malocclusion.
 Total nasal obstruction- rare in human beings.

89
3. STUDIES FOR ADAPTATIONS FOLLOWING
REMOVAL OF NASAL OBSTRUCTIONS:
• Linder- Aronson studied 41 children who underwent
adenoidectomies for 5 years postoperatively.
 34 children who switched to oral respiration were
compared with 54 normal children.
 Significant group mean difference was found initially.
Mouth breathers had more retroclined upper and lower
incisors with lower tongue positions.
 The greatest change occurred in the dentition and the
sagittal depth of the nasopharynx in the first postoperative
year. Mandibular plane angle diminished by 4 degrees
(gradual change).
 Results were statistically significant but no large
measurement differences was observed. Facial height was
only 3 mm larger in the adenoidectomy group.

90
 ROLES OF THE MUSCLES IN PRODUCING
CLASS I, II & III MALOCCLUSION
 Class I malocclusion –
 Muscle function is usually normal & in a state of balance.
 Class I open bite – is an 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 and
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.
 Mentalis activity increases and puckering of the skin with
each swallow occurs.
 Tongue drops lower in the mouth and no longer
approximates the palate

91
 Disturbance of the equilibrium causes narrowing of the
maxillary arch.
 Over eruption of the posterior teeth occurs because lateral
portion of tongue does not overlay occlusal surfaces of the
posterior teeth.
 Interocclusal space is eliminated. Crossbite occurs –
leading to mandibular displacement.
 Though the finger habit did not entirely cause
malocclusion, it was the first assault on the integrity of the
dentition. Compensatory tongue & lip activity resulted in a
significant deforming mechanism.
 Class II Div. 1 malocclusion:
 Change in muscle function is a requisite.
 Proclination of anterior teeth leads to excessive overjet.

92
 Lip sucking habit develops – hypertrophic lower lip.
 Incisors move further labially – no resistance from
hypotonic functionless upper lip.
 Lower incisors are pushed lingually by abnormal mentalis
activity and the lower tongue position produces a narrow
maxillary arch.
 Class II Div. 2 malocclusion:
 Muscle function is usually normal.
 Tongue occupies the interocclusal space increasing
interocclusal clearance and interfering with eruption
accentuating the curve of spee.
 Due to lingual inclination, excessive interocclusal
clearance & infra occlusion of posterior teeth forced
retrusion of the mandible occurs.

93
 TMJ problems can arise.
 ‘Forced retrusion’- controversial.
 Swann (1954)- functional
displacement of mandible occurred
when teeth are occluded.
 Ricketts (1955), Jarabak (1963), and
Graber(1969)-also agreed that there
was a displacement of the mandible
posteriorly and superiorly.
 Recent studies have challenged this
concept.
 Gianelly (1989)-studied 19
asymptomatic subjects with no
overjet, deep bite, and upright
incisors against Class II subjects with
normal overbite, overjet, and
interincisal angulations of less than
145 degree.

94
 Concluded that condylar positions in both groups were essentially
centered.
 Demisch- concluded that if there is distal positioning of the
mandible, it would spontaneously reposition anteriorly on
treatment. As this phenomenon is not noticed-mandible not
displaced posteriorly.
 Assessment of the condylar position in class II div 2, using the
mandibular position indicator.
• Conclusions:
• 1.Although no particular predisposition to condylar retrusion, it is
seen in (uni/bilaterally) 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.

95
 Class III malocclusion
 Abnormal muscle function is seen.
 Upper lip is short but not hypotonic, shows greater activity
during swallowing
 Lower lip hypertrophic & redundant – passive during
deglutition.
 Tongue lies low in the floor of the mouth with constricted
maxillary arch.
 Interocclusal space is small or absent

96
 CONCLUSION
• The recognition and reporting of a malocclusion or a
condition that could lead to a malocclusion is the most
important service that a dentist can provide to his patients.
Malocclusion has an important impact on the function and
esthetics of the entire dentition with detrimental effects on
the self-esteem of many children, adolescents, and adults.

• Comprehensive orthodontic management includes various

interceptive and preventive orthodontic procedures involved
in identifying possible etiological factors to eliminate the
same.

• A sound knowledge of the various etiological factors that

lead to malocclusion, will help in rendering excellent
treatment for patients with good retention and stability.
97
 REFERENCES
 Salzmann. J. A- Orthodontics in daily practice- 4th ed
 T. C. White, J. H. Gardiner, B. C. Leighton- Orthodontics
for dental students.
 Shafer, Hine and Levy- A textbook of oral pathology- 4th
ed
 Graber T M – Orthodontics, principle and practice-3 rd
edition.
 William R. Proffit, Henry W. Fields, David M. Sarver.-
Contemporary orthodontics. 4th edition -2007
 Robert E.Moyers- Handbook of Orthodontics-4th edition
 Samire Bishara- Text book of Orthodontics
 Nasir Al-Hamlan -The Nature of Orthodontic Problems:
Known Causes of Malocclusion
 Alok Ranjan , Pravin Shetty, Amol patil -Craniofacial
growth theories
 Gianelly AA, Petras JC, Boffa J. 1989, ‘Condylar
position and Class II deep-bite, no-overjet
malocclusions’, Am J Orthod Dentofacial Orthop. Vol.
96, no.5, pp. 428-432.
98
• Lauweryns, I et al. 1993,“The use of twins in dentofacial
genetic research.” American journal of orthodontics and
dentofacial orthopedics : official publication of the
American Association of Orthodontists, its constituent
societies, and the American Board of Orthodontics vol. 103,
no. 1
• Harris, E F, and M G Johnson 1991, “Heritability of
craniometric and occlusal variables: a longitudinal sib
analysis.” American journal of orthodontics and dentofacial
orthopedics : official publication of the American
Association of Orthodontists, its constituent societies, and
the American Board of Orthodontics vol. 99, no. 3, pp.258-
68.
• Litton, S F et al. 1970, “A genetic study of Class 3
malocclusion.” American journal of orthodontics vol. 58, no
6, pp. 565-77
• McNamara, JA 1981, “Influence of respiratory pattern on
craniofacial growth.” The Angle orthodontist vol. 51, no. 4,
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