Etiology of malocclusion/certified fixed orthodontic courses by Indian dental academy

Etiology of
malocclusion
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INDIAN DENTAL ACADEMY
Leader in continuing dental education
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Introduction
• The origin of all science is the desire
to know causes; and origin of all false
causes rather than none; or, which is
the same thing, in the unwillingness
to acknowledge our own ignorance.
- “Burke and Edinburgh phrenologist.”
the atlas, February 15, 1829
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Etiology-
Etia – cause
Logy – Science
Scientific study of the cause.
Malocclusion-
Malocclusion can be defined as a
significant deviation from what is defined
as normal or ideal‘s occlusion.
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• Malocclusion is a major developmental problem.
• Kelly and Harvey report that only 9% of
American youths aged 12 to 17 years have
virtually classic normal occlusion and that
orthodontic treatment would measurably improve
the occlusion of 55% of the adolescent
population.
Introduction
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Epidemiology of
malocclusion
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Epidemiology of
malocclusion in India
• Prevalence of malocclusion is higher in developed
countries as compare to developing countries
• Disto-occlusion in India is very low as compare to
USA.(34% in whites and 15% in blacks) and Europe
29%.
• Indians have more tendency for class II relationship
than Africans (4.26% in Nigeria)
• Class III malocclusion is also less prevalent in India
compared to USA, Netherlands, and Kenya.
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• The prevalence of malocclusion among Indian
children has been reported to be as low as 19.6%
in Madras by Miglani D.S. et al in 1965 and as
high as 90% in Delhi by Sidhu S.S. in 1968.
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MALOCCLUSION STUDIES IN INDIA
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The orthodontic equation:
The orthodontic equation elaborated.(from Dockrell
R: classifying etiology of malocclusion. Dent Rec
1952; 72:25.) www.indiandentalacademy.co
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Skeletal crossbite
• Occlusal relationship seems correct on the patients left
side, crossbite on the right side.
• Mandibular prognathism.
• Patients face shows that the cross bite is primarily the
result of osseous dysplasia.
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Muscular or functional
crossbite
• Midline does not coincide, half the mandibular denture is
outside the maxillary denture.
• Removal of the occlusal interferences in the primary
teeth enabled muscles to return the mandible to its proper
position and to a proper occlusion.
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Dental type crossbite
• Mandibular and maxillary bases are harmonious with
each other, midline coincide, crossbite is localized in the
right central incisor region.
• Due to tipping of individual teeth
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CLASSIFICATION OF ETIOLOGY
OF MALOCCLUSION
• Classification will help the clinician in identifying
situation which they can either prevent or
intervene, thus avoiding the severity of
malocclusion.
• The various classification proposed are:
White and Gardiner‘s classification.
Salzmann‘s classification.
Moyer‘s classification.
Graber‘s classification.
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White & Gardiner’s
Classification:
This was one of the first attempts to classify
malocclusion.
A. Dental Base Abnormalities:
1. Antero-posterior mal-relationship.
2. Vertical mal-relationship
3. Lateral mal-relationship
4. Disproportion of size between teeth and
basal bone.
5. Congenital abnormalities.www.indiandentalacademy.co
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B. PRE-ERUPTION ABNORMALITIES:
1. Abnormalities in position of developing tooth
germs.
2. Missing teeth.
3. Supernumerary teeth with teeth abnormal in
form.
4. Prolonged retention of deciduous teeth.
5. Large labial frenum.
6. Traumatic injury.
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C. POST-ERUPTIVE ABNORMALITIES:
1. Muscular:
i. Rest position of musculature.
ii. Active muscle force.
iii. Sucking habits.
iv. Abnormalities in path of closure.
2. Premature loss of deciduous teeth.
3. Extraction of permanent teeth
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Classification of etiology of
malocclusion cont…
• Salzmann‘s diagrammatic representation of the
etiologic factors in malocclusion
Genetic Environmental
Developmental
Congenital Functional
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Salzmann’s
Classification
A. PRENATAL:
1. Genetic: malocclusion transmitted by genes, may
or may not be evidence at birth.
2. Differentiative: malocclusion that are
inborn, engrafted on the body in the prefunctional
embryonic developmental stage, can be
subdivided into—
i. General or constitutional: effect the body as a
whole.
ii. Local: effect the face, jaws and teeth only.
3.. Congenital: can be hereditary or acquired but
existing at birth.
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B. POSTNATAL:
DEVELOPMENTAL:
1.GENERAL DEVELOPMENTAL:
a) Abnormalities of relative rate of growth in
dentofacial region
b) Hypo or hypertonicity of muscles which
influence dentofacial development and function.
c) Childhood diseases, nutritional, endocrine, and
other metabolic disturbances that affect
dentofacial growth.
d) Radiation and radiotherapy of mother or fetus
which can produce orofacial clefts and cephalic and
dental abnormalities in the offspring.
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B. POSTNATAL:
2. LOCAL DENTOFACIAL:
• Birth injuries of the head, face, jaws
• Micrognathia or macrognathia
• Microglossia or macroglossia
• Abnormal frenum labii
• Facial hemiatrophy
• Anomalies of tooth development and eruption
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2. FUNCTIONAL:
– GENERAL:
• Muscular hyper or hypotonicity
• Neurotrophic disturbances
• Postural defects of the tongue and jaws
• Masticatory and respiratory disturbances
– LOCAL:
• Premature loss or prolonged retention of
deciduous teeth
• Loss of proximal contact following tooth
loss
• Temporomandibular articulation
disturbances
• Muscular hypo or hyperactivity
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3) ENVIRONMENTAL OR ACQUIRED:
– GENERAL
• Diseases can affect the dentofacial tissues directly or
indirectly
• Radiation
– LOCAL:
• Eruption anomalies
• Premature loss or prolonged retention of deciduous
teeth
• Loss of permanent teeth
• Harmful dentofacial pressure habits
• Trauma
• Infection
• Temporomandibular disturbances
• Periodontal diseasewww.indiandentalacademy.co
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Prenatal Postnatal
Genetic
Differentiative
congenital
Developmental
Functional
Environmental
Salzmann’s diagrammatic representation of the interdependence of the
etiologic factors in malocclusion
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MOYER’S CLASSIFICATION
Moyer’s lists seven causes and clinical entities.
1. Heredity
2. Development defect of unknown origin
3. Trauma
a) Prenatal trauma and birth injuries
b) Post natal trauma
4. Physical agents
5. Habits
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6. Diseases
a) Systemic disease
b) Endocrine disorder
c) Local disease
i. Nasopharyngeal diseases and disturbed
respiratory function
ii. Gingival and periodontal diseases
iii. Tumors
iv. Caries
7. Malnutrition
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GRABER’S CLASSIFICATION:
Divides the etiologic factors into two groups:
General factor
Local factor
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1. Heredity (the inherited pattern)
2. Congenital defect: cleft
palate, torticollis, cleidocranial
dysostosis, cerebral palsy, syphillis,etc.
3. Environment :
-prenatal ( trauma, maternal diet,
maternal metabolism, German measles)
-postnatal ( birth injury, cerebral palsy,
TMJ injury)
4. Predisposing metabolic climate and disease
Endocrine imbalance
Metabolic disturbance
Infectious diseases
GENERAL FACTORS
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5. Dietary problem ( nutritional deficiency )
6. Posture
7. Trauma and accident
8. Habits
 Abnormal suckling
 Thumb and finger sucking
 Tongue thrusting
 Abnormal swallowing habits (improper
deglutition)
 Mouth breathing
 Lip and nail biting
 Speech defects
 Bruxism
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1. Anomalies of number
-supernumerary teeth
-missing teeth
2. Anomalies of tooth size.
3. Anomalies of tooth shape.
4. Abnormal labial frenum; mucosal barriers.
5. Premature loss of deciduous teeth.
6. Prolonged retention of deciduous teeth.
LOCAL FACTORS
7. Delayed eruption of permanent teeth.
8. Abnormal eruptive path.
9. Ankylosis.
10.Dental caries.
11.Improper dental restoration
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General Factors
HEREDITY:
• Transmission of character from one
generation to the other
- Joseph Adam – 1847
• There is a definite genetic determinant that
influences the ultimate accomplishment of
dentofacial morphology.
• These genetic determinants may be modified
by prenatal and postnatal environment, by
physical entities, by pressures, abnormal
habits, nutritional disturbances and idiopathic
phenomena.
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Mode of inheritance-
Mendelian inheritance-
• Autosomal recessive
• Autosomal dominant
• X linked and Y linked conditions.
General Factors
HEREDITY:
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Autosomal recessive inheritance-
• Traits that are manifest only when mutations are
present in both copies of gene are recessive
traits.
• If a gene causing a recessive trait is on one of
the autosomes, the trait is autosomal recessive.
General Factors
HEREDITY:
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• Autosomal recessive trait tend to occur more
frequently in isolated populations or in cases of
consanguinity.
• The parents of affected individuals are usually
unaffected.
• Recurrences between siblings are common.
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• Seen in both males and females equally.
• The chance of having an affected child is 25% for
each pregnancy resulting from mating between two
heterozygous carriers of an autosomal recessive
condition.
• The other possibilities are 50% that a child will be a
carrier of a single copy of the mutation and 25% that
the child will be noncarrier.
because each parent has an approximately equal
probability of passing on either the normal or
abnormal allele.
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• On an average the ratio of affected, carrier, and
non affected is 1:2:1 in siblings.
• The recurrence risk in such family is 1 in 4 for
each birth.
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Autosomal dominant inheritance-
• In autosomal dominant disorders, heterozygous
individuals have a recognizable phenotype.
• Homozygous individuals also show the
phenotype, but may be more severely affected.
• Pedigrees will frequently show that parent is
affected.
General Factors
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• Trait is transmitted by an affected person to half
his children on an average
• The number of affected males and females is
approximately equal
• Two affected individuals may have affected and
unaffected children since each parent would have
one normal and one abnormal gene
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X-linked inheritance-
• Refers to conditions caused by genes on the X
chromosome.
• Many X-linked recessive conditions and a few X-
linked dominant conditions.
• If a mutation occurs in an X-linked recessive
gene, a female is likely to have mild or no
effects, because female inherit two copies of X
chromosome.
• A male who inherits the gene is likely to be more
severely affected because he has only one copy
of a gene
General Factors
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• Affected males pass the gene to 100% of their
daughters.
• There is no father-to-son transmission because
fathers do not give an X chromosome to their
sons.
General Factors
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X linked dominant inheritance-
• It is rare with a few disorders.
• Characterized by having all the daughters of
affected males inherit the disorder.
• Sons of affected males never inherit the
disorder, because they receive the Y chromosome
from the father.
• Affected females can transmit the disorder to
offspring of both sexes.
General Factors
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Multifactorial inheritance-
• Some human disorders result from an
interaction of multiple genes with
environmental influences.
• Cleft lip and palate demonstrate a multifactorial
inheritance.
General Factors
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General Factors
• A strong influence of inheritance on facial
features such as tilt of nose , shape of the jaw
and look of the smile are familial tendencies.
• Certain types of malocclusion run in families.
The HAPSBURG JAW , the prognathic
mandible of German royal family is the best
known example .
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General Factors
HAPSBURG JAW
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• Malocclusion could be produced by
inherited characteristics in two major ways
Disproportion between size of the teeth and the
size of the jaws
Disproportion between size and/ shape of the
upper and lower jaws
- Proffit
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Facial type of the offspring probably is heavily influenced by
heredity.
There are three general types of head shapes-
•Brachycephalic or broad round heads
•Dolichocephalic or long narrow heads
•Mesocephalic or a shape in between the brachycephalic
and the dolichocephalic
Hereditary Influence on Facial Type:
General Factors
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General Factors
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Hereditary influence on the growth and
developmental pattern:
 As ultimate morphogenetic pattern has a strong
hereditary component, the accomplishment of
that pattern is also at least partially under the
influence of heredity.
 For example, a child patient is very slow in
losing his deciduous teeth and the eruption of
permanent teeth is equally slow.
General Factors
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Heredity and specific dentofacial morphologic
characteristics:
• Heredity has role in the accomplishment of
specific dentofacial attributes.
• Lundstrom concluded that heredity could be
considered significant in determining the
following characteristics:
1.Tooth size.
2.Height of the palate.
3.Width and length of the arch.
4.Crowding and spacing of teeth.
5.Degree of sagittal overbite (overjet)
General Factors
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 Hereditary influence on Race:
• Facial and Dental characteristics of different races
is influenced by heredity.
• In homogenous racial groupings the incidence of
malocclusion seems relatively low.
• In certain areas of the world –for example, some
of the Philippine Islands –malocclusion is almost
nonexistent. Population groups there are relatively
pure genetically.
General Factors
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 Hereditary influence on Race:
• Where there has been a mixture of racial strains
the incidence of jaw size discrepancies and
occlusal disharmonies is significantly greater.
• Professor Stockard produced gross deformities
with his crossbreeding of dogs.
General Factors
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Breeding experiment with animal
by Professor Stockard
• Crossbred dogs (Boston terrier and collie) and
recorded the interesting effects on body
structure.
• Offspring might have the Collie‘s long, pointed
lower jaw and the terrier‘s diminutive upper
jaw. www.indiandentalacademy.co
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• Demonstrated that severe malocclusions could be
developed by crossing morphologically different
breeds, more from jaw discrepancies than from tooth
size – jaw size imbalances.
• He confirms that independent inheritance of facial
characteristics could be the major cause of
malocclusion and the rapid increase in malocclusion
was probably the result of increased outbreeding.
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 These dog experiments turned out to be
misleading, because many breeds of small dogs carry
the gene for achondroplasia.
Most of the malocclusions produced in Stockard’s
breeding experiments can be explained not on the
basis of inherited jaw size but by the extent to which
achondroplasia was expressed in that animal.
So these experiments have been severely criticized
on the basis that the gene for achondroplasia is likely to
have contributed.
General Factors
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Achondroplasia
Deficient growth of cartilage in the cranial base
Autosomal dominant trait
Rare in humans
In humans; short limbs, deficient maxillary
translation, relative midface deficiency
General Factors
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• Results of out breeding in human populations
casts doubt on the hypothesis that independently
inherited tooth and jaw characteristics are a
major cause of malocclusion.
• The best data are from investigations carried out
in Hawaii by Chung et al.
• Hawaii had a homogenous Polynesian population
– large scale migration to the islands by
European, Chinese, Japanese and many other
racial and ethnic group resulted in heterogeneous
modern population.
General Factors
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• Tooth size, jaw size and jaw proportions were all
rather different for the
Polynesian, Oriental, European contributors.
• If tooth and jaw characteristics were inherited
independently, a high prevalence of severe
malocclusion would be expected in this
population.
• The prevalence and the types of malocclusion in
the current Hawaiian population, though greater
than the prevalence of malocclusion in the
original population, do not support this concept.
• The effect of interracial crosses appear to be
additive than the multiplicative.
General Factors
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Twin Study
 The classic way to determine to what extent a
characteristic is determined by inheritance is to
compare monozygotic twins (identical) with
dizygotic twins (fraternal).
 Studies of this type are limited because it is
difficult to establish zygosity and confirm that
environments were in fact the same for both
members of a twin pair.
 Lauweryns et al ; concluded that 40% of dental
and facial variation that lead to malocclusion can
be attributed to hereditary factor.
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Classical Method Is To Study
Family Members:
 The other classic method of estimating the
influence of heredity is to study family
members by observing similarity and
differences between father-child, mother-
child, and sibling pairs.
 For most measurements of facial skeletal
dimensions (i.e. length of the
mandible), correlation coefficients for parent-
child pairs are about 0.5 .
 For dental characteristics, the parent – child
correlations are lower, ranging from a
maximum of nearly 0.5 for overjet to a
minimum of 0.15 for overbite.www.indiandentalacademy.co
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Classical Method Is To Study
Family Members:
 When parent-child correlation are used to
assist in predicting facial growth, errors are
reduced
 It indicates hereditary influence on these
dimensions.
- Suzuki A, Takahama
Y, 1991(AJODO,99:1991)
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Heritability of craniofacial characteristics
between parents and offspring
Nakasima et al. found high correlation co-
efficient values between parents and their
offspring in the class II and class III malocclusion
groups suggesting a strong familial tendency in
the development of these malocclusions.
 The genetic effects of determining the
craniofacial form of offspring by the father were
equivalent to those by the mother, but daughters
were more affected by parents than were sons
because of this finding they suggested a major
influence of X-linked genes from 0.5 to 0.9.
(By BerglindJohanndottir et al.)
AJODO Vol. 127, Feb 2005)
General Factors
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Heritability of craniofacial characteristics
between parents and offspring cont…
 Fernex et. al.(1967) found boys to show more
similarities to their parents than girls. Facial
skeletal structures were more frequently
transmitted from mother to sons than from
mother to daughters.
Hunter et. al. (1970) found genetic correlation
to be strongest between father and
children, especially in mandibular dimensions.
There was a significant relation in facial height
between mother and their offspring's.
(BJO Vol.26 NO.3, Sep. 1999)
General Factors
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• For skeletal characteristics, the heritability
estimates increased with increasing age, for
dental characteristics, the heritability estimates
decreased, indicating an increase in
environmental contribution to the dental
variation.
( Harris EF, Johnson MG, AJO vol.99,1991)
General Factors
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• The influence of inherited tendencies is
particularly strong for mandibular prognathism
• The one third of the group of children who
presented with severe class III malocclusion had
a parent with the same problem
(Litton SF, Ackerman LV, Isaacson RJ,AJO Vol.
58, 1970)
• The long face pattern seems to be the second
most likely type of deformity to run in families.
General Factors
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• It is logical to assume that heredity plays a part in
the following conditions.
1. Congenital deformities.
2. Facial asymmetries.
3. Macrognathia and micrognathia.
4. Macrodontia and microdontia.
5. Oligodontia and anodontia.
6. Tooth shape variations (peg-shaped lateral incisors,
carabelli’s cusps, mamelons etc).
General Factors
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7. Cleft palate and harelip.
8. Frenum diastemas.
9. Deep overbite.
10.Growing and rotation of teeth.
11.Mandibular retrusion
12.Mandibular prognathism.
General Factors
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Congenital Defects
1. CLEFT LIP & PALATE
Cleft lip and palate can be
defined as a ―a furrow in
the lip and palatal vault‖.
It may be defined as a
―breach in continuity of lip
and palate‖.
General Factors
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Etiology-
Heredity
 According to Bhatia the possible modes of transmission are either by
a single mutant gene producing a large effect, or by a number of
gene (polygenic inheritance) each producing a small effect together,
create this condition.
 According to Fogh-Andersen slightly less than 40% of the cleft lip
cases with or without cleft palate are genetic in origin whereas
slightly less than 20% of the isolated cleft palate cases appear to
be genetically derived.
Cleft lip & Palate Cont..
• Clefts usually have a strong genetic relationship.
• About 1/3 or 1/2 of all cleft palate children have a
familial history.
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Environment: Teratogens, radiation, dietary
deficiency
• Teratogens are:
• Aspirin – cleft lip and palate
• Cigarette smoke (hypoxia) – cleft lip and
palate
• Dilantin – cleft lip and palate
• Valium- cleft lip and palate
• Rubella virus
Etiology
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Environment
Radiations such as X-rays, gamma rays are capable
of producing clefts in fetus during pregnancy.
Dietary deficiency- such as folic acid deficiency can
produce clefts.
Etiology
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Etiology
MULTIFACTORIAL ETIOLOGY:
• Multi-factorial inheritance theory implies that
many contributory risk genes interact with one
another and the environment, resulting in a
defect in the developing fetus
• Unless a person is genetically susceptible, the
environmental factors may not by themselves
cause clefts
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Incidence:
Common.
• The reported incidence of clefts of the lip and
palate from 1 in 500 to 1 in 2500 live births
depending on geographic origin, racial and ethnic
backgrounds and socioeconomic status.
• Asian populations have the highest
frequencies, often at 1 in 500 or higher, with
Caucasian populations intermediate, and African-
derived populations the lowest at 1 in 2500
• In the USA, one child in every 700 live births is
afflicted.
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• Unilateral cleft accounts for nearly 80% of all cleft
seen.
• While bilateral clefts account for remaining 20%.
• Among the unilateral clefts, clefts involving the
left side are more common.
• Male patients show a higher incidence of cleft lip
with and without palate.
• Female patients suffer from isolated cleft palate
more.
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Epidemiology of cleft lip and palate
• In India – 1 in every 600-1000 birth.
• Negroid have the least incidence – 1 in every
2000 birth.
• Mongoloids have the highest incidence.
• Cleft lip is common in male
• Cleft palate is common in female
• 80% incidence of unilateral cleft (70% on left
side)
• 20% incidence of bilateral cleft
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Categories of Clefts:
4 general categories
1. Involving the lip and alveolus.
2. Involving the lip and palate.
3. Palate alone is affected .
4. Submucous cleft palate.
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Clefts of the lip and alveolus:
 May be complete, extending from the vermilion
border to the floor of the nose or it may be
incomplete.
 May be unilateral or bilateral.
 Drillien, estimated that the incidence of
bilateral clefts of the lip is 3.6%, while that of
unilateral clefts of the lip is 96.4%.
 According to Fogh-Anderson, the incidence of
complete bilateral cleft of the lip is only 1% of
all individuals with cleft lip with or without a
cleft palate. (AJODO,1985,JULY)
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 The effect of the cleft of the lip and alveolus on
the growth of the premaxilla varies.
 With cleft lip only and no alveolar clefts, the
continuity of the palatal bone helps maintain the
maxillary arch form and relationship.
 When the cleft of the lip extends to involve the
primary palate, the premaxilla protrudes to
different degrees because of absence of the
restraining influence of the lip and the lack of
continuity of the bony palate.
(AJODO,1985,JULY)
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 Nasal alar cartilage on the side of the cleft is
displaced and flattened.
 The tip of the nose is deviated towards the non
cleft side.
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Unilateral Cleft of the
lip and alveolus
Bilateral Cleft of the lip
and alveolus
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Cleft lip and cleft palate:
 Complete or incomplete.
 Unilateral or bilateral.
 In a complete unilateral cleft of the lip and
palate, a direct communication exists between
the oral and nasal cavities on the side of the
palate where the cleft is situated.
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Cleft lip and cleft palate
• In a complete bilateral cleft lip and palate both
nasal chambers are in direct communication with
the oral cavity.
• Premaxilla projects considerably forward from the
facial aspect of the maxilla.
• Anteriorly progressive constriction of the upper
dental arch (Omar Gabriel da Silva Filho and et
al,1998 Aug, AJODO)
• Significantly longer maxillary dental arch, which is
attributed to the premaxillary anterior projection.
(Omar Gabriel da Silva Filho and et al,1998
Aug, AJODO)
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BCLP patients tend to have
• Smaller mandibles
• Mandible showed a vertical growth pattern, with
an increased mandibular plane inclination.
• Increase in lower anterior facial height.
• These are mandibular morphologic
characteristics that are also found in unilateral
CLP and isolated CP.
(AJODO,1998,AUG)
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Complete unilateral
cleft lip and palate
Incomplete unilateral
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Complete bilateral
Incomplete bilateral
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Isolated Cleft palate:
 Neither the lip nor the alveolar process is
involved.
 The cleft may involve only the soft palate or
both the soft and hard palates but never the
hard palate alone.
 In some cases, cleft is limited to the uvula or to
the uvula and soft palate.
 In others it may extend into the hard palate.
 In the extreme form, the cleft palate may
extend anteriorly as far as the nasopalatine
foramen.
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 When the cleft involves a considerable portion of the
hard palate, the nasal chambers are in direct
communication with the oral cavity.
 The outline of the cleft may be wide or
narrow, pyriform or V- shaped.
 With wide cleft that extend to a considerable degree
into the hard palate– excessively wide dental arches
result.
 In such instances the mandibular dental arch may
be in complete lingual relation to the maxillary arch.
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Cleft of the uvulae Cleft of the soft
palate and uvulae
Isolated cleft of the
hard and soft palate
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Submucous Cleft palate:
The classic triad of diagnostic signs is the
1. Bifid uvula.
2. Partial muscle separation in the midline with
an intact mucosal surface.
3. Midline notch in the posterior edge of bony
palate.
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Submucous Cleft palate
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The problems associated with cleft lip and/ palate
patients:
1. DENTAL:
 Multiple missing teeth (most commonly the
maxillary lateral incisor).
 Mobile premaxilla.
 Anterior &/ posterior cross-bites.
 Ectopically erupting teeth.
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 Impacted teeth.
 Supernumerary teeth.
 Poor alignment of the teeth often predisposes to
poor oral hygiene.
 Multiple decayed tooth.
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Cleft palate with congenital absence of lateral incisor
in cleft area and three missing second premolars.
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2. ESTHETIC:
• Badly disfigured.
• Even following the closure of the cleft, the
maxilla remains under-developed with
compromised esthetics.
• Deformity of the normal nasal architecture is
commonly seen in individuals with cleft lip.
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3. PYSCHOLOGICAL:
• Psychological stress
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4. SPEECH & HEARING:
• Cleft lip and palate are sometimes associated
with disorders of the middle ear which may affect
hearing.
• Since speech is learnt by the art of imitation, if
hearing is compromised so is the speech.
• Also if the maxilla is underdeveloped the space
for the tongue gets decreased and the speech is
likely to get affected.
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Predisposing factors
• Increased maternal age: increased risk
• Racial: Some races are more susceptible to clefts
than others .
Mongoloid show the greatest percentage of
incidence.
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Mandibular cleft
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Bilateral maxillary cleft lip
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Oblique facial cleft
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Median cleft lip
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Lateral facial cleft
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Median cleft lip and nose
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Other Congenital Defects
Although cleft lip and palate is the most common
congenital defects to be of concern to the dentist as
far as creation of malocclusion is concerned, but
some problems such as-
Cerebral palsy
Torticollis
Cleidocranial dysostosis
Congenital syphilis
Congenital Defects Cont..
m

2.Cerebral palsy
• Paralysis or lack of muscular coordination
attributed to an intracranial lesion.
• Most commonly caused by –birth injury
Cerebral palsy is also caused by a broad group of
development, genetics, metabolic, infectious, ischa
emic and other acquired etiology.
Cerebral palsy is often associated with
epilepsy, abnormality with speech, vision and
intellect.
m

Cerebral palsy cont…
• Cerebral palsy is chronic motor disability that
begins in childhood with a prevalence of 2/1000.
• Effects of this neuromuscular disorder may be
seen in the integrity of the occlusion.
• Electromyographic studies on cerebral palsied
children show a significant difference in the level
of activity even when muscles are not in active
function.
m

3. Torticollis:
Twisting of the head caused by excessive tonic
contraction of the neck muscles on one side (primary
sternocleidomastoid).
The fore-shortening of the sternocleidomastoid muscle
can cause profound changes in the bony morphology of
the cranium and face.
m

Torticollis cont…
• Facial asymmetries with uncorrectable dental
malocclusions may be created if this problem
is not treated early.www.indiandentalacademy.co
m

Other physical features of Torticollis
1. Plagiocephaly (generally visible as a
mild flattening of the occiput on one
side and the forehead on the opposite
side).
2. Misalignment of the eyes.
3. Asymmetry of the ears.
4. Depression on the side of the neck
under the ear.
5. Flattening of the mandible.
6. Upward tilting of the lower jaw and
gum line.
7. Limited movement of the neck.
m

4.Cleidocranial Dysplasia
 Congenital disease of unknown etiology which is
often but not always hereditary.
 Transmitted as an autosomal dominant trait.
 It is characterized by abnormalities of the
skull, teeth, jaws and shoulder girdle as well as
by occasional stunting of the long bones.
m

 Delayed ossification of the skull, excessively large
fontanelles and delayed closing of the sutures.
 The fontanelles may remain open until adulthood
but the sutures often close with interposition of
wormian bones.
 Bossing of the frontal, parietal and occipital
regions give the skull a large globular shape with
small face.
 Characteristic skull abnormalities – ― Arnold
Head‖ .
m

 Sagittal suture is characteristically sunken, giving
the skull a flat appearance.
 Paranasal sinuses are underdeveloped and
narrow.
 The head is brachycephalic.
 Complete to partial absence or even a simple
thinning of one or both clavicles is seen.
m

• High, narrow, arched palate, and actual cleft palate
appears to be common.
•The maxilla is underdeveloped in relation to the mandible.
•Prolonged retention of the deciduous teeth and subsequent
delay in eruption of the permanent teeth.
•The roots of the teeth are often somewhat short and
thinner than usual and may be deformed
m

 There is absence or paucity of cellular cementum
on the roots of the permanent teeth and this may
be related to the failure of eruption so frequently
seen.
 Unerupted supernumerary teeth are common.
These are most prevalent in the mandibular
premolar and incisor areas.
 Partial anodontia has also been recorded but is
rare.
m

Cleidocranial dysplasia
m

Prolonged retention of deciduous teeth. Supernumerary Teeth
m

Highly vaulted and narrow palate
m

5. Congenital (Prenatal) Syphilis
 It is transmitted to the offspring only by an
infected mother and is not inherited.
 Persons with congenital syphilis manifest a great
variety of lesions, including-
• frontal bossing
• Short maxilla
• High palatal arch
• Saddle nose
• Mulberry molars
• Relative protuberance of mandible
m

• Rhagades
• Pathognomonic of the
disease is the occurrence
of Hutchinson‘s triad
-Hypoplasia of the
incisor and molar teeth.
-Eighth nerve deafness
-Interstitial keratitis
m

Environment
Prenatal Postnatal
(Intrauterine molding,
maternal diet, maternal
metabolism, Trauma,
German measles etc.)
(Birth injury, TMJ injury etc).
General Factor
m

Prenatal Influence:
 Small role.
 Intrauterine molding pressure against the
developing face prenatally can lead to
distortion of rapidly growing areas.
 Eg. On rare occasions an arm is pressed across
the face in uterus, resulting in severe maxillary
deficiency at birth.
General Factor
m

Prenatal influence
• Uterine posture, fibroids of the mother, amniotic
lesion have been blamed for malocclusion.
• After the 1st year of life most of these facial
asymmetries disappear.
• Occasionally a fetus head is flexed tightly against
the chest in uterus, preventing the mandible from
growing forward normally
m

 Result – extremely small mandible at
birth, usually accompanied by the cleft
palate .
Intrauterine molding Distortion and Asymmetrywww.indiandentalacademy.co
m

Prenatal Influence:
 Pierre Robin Syndrome considered a sporadic
or non genetic condition with a very low
recurrence risk in the family.
 Extremes mandibular deficiency at birth .
General Factor
m

• Because the pressure against the face that
caused the growth problem would not be
present after birth, one would predict normal
growth thereafter.
• So early aggressive treatment to lengthen the
mandible should be avoided.
m

Pierre Robin Syndrome (Robin
Anomalad)
• Glossoptosis
• Micrognathia
• Cleft palate
The combination of micrognathia and glossoptosis can lead to
respiratory difficulty.www.indiandentalacademy.co
m

Prenatal Influence
Severe mandibular deficiency in Pierre Robin
Syndrome
General Factor
m

Prenatal Influence:
 So, although abnormal fetal posture have caused
marked cranial or facial asymmetries that are
apparent at birth, but after the first year of life most
of these have disappeared. Thus, the deformity is
temporary.
 Maternal nutritional disturbances such as folic acid
deficiency can produce malocclusions.
 Minor injury to the mother is unlikely to affect the
child, since the fetus is well cushioned by the amniotic
fluid.
 German measles cause gross congenital deformities
including malocclusion.
General Factor
m

Prenatal Influence:
 Certain chemical (teratogens) , taken during
pregnancy, causes gross congenital deformities
including malocclusion.
 The time of exposure is important concept for
teratogen, as certain stages of embryonic & fetal
development are more vulnerable than others.
 In general, the embryonic stage (first trimester)
is more vulnerable than the fetal period (second &
third trimester).
General Factor
m

The critical period of exposure is during organogenesis
from the 35th-48th day after the last menstrual period.
The malformations is linked to the time of exposure:
35-37 days- no ears
39-41 days- no arms
41-43 days- no uterus
45-47 days- no tibia
47-49 days- triphalangeal thumbs.
Prenatal Influence:
General Factor
m

Some of the known teratogens are-
1)Thalidomide-
Embryo is most vulnerable in the first trimester.
It was use to treat morning sickness but is not used
anymore.
Thalidomide produced malformations limited to limbs, ears,
cardiovascular system & gut musculature.
 Abnormal development of long bones, typically the upper
limbs were more severely involved than the lower limbs.
 Phocomelia, polydactyly, syndactyly, oligodactyly were all
reported.
 Cleft palate could be a complication.
General Factor
m

2)Hydantoins(Phenytoin & Trimethadione)-
It is anticonvulsant drug.
Hydantions have been associated with Foetal hydantoin
syndrome.
The clinical features include wide anterior fontanelle, ocular
hypertelorism, depressed nasal bridge, cleft lip & cleft palate.
General Factor
m

3)Folic acid antagonists(Aminopterin & Methotrexate)-
•Aminopterin is an antifolic drug,is used as a abortifacient.
•Surviving fetuses of such abortion attempts are grossly
malformed.
•Malformation include facial anomalies(cleft palate,high arched
palate, micrognathia, ocular hypertelorism, external ear
anomalies), intrauterine growth retardation & mental
retardation.
General Factor
m

4)Isotretinoin(13-cis-retinoic acid)-
It is a synthetic vitamin A derivative,prescribed for severe
cystic acne.
A pattern of anomalies termed Retinoic acid
embryopathy has been associated with isotretinoin exposure
in pregnancy.
The clinical features include craniofacial anomalies
micrognathia, flat nasal bridge, cleft lip& palate.
General Factor
m

5)Carbamazepine-
•It is an anticonvulsant drug.
•Exposure to carbamazepine produces malformations similar
to those described with the foetal hydantoin syndrome.
General Factor
m

6)Alcohol-
•The fetal alcohol syndrome
General Factor
m

Full expression of this syndrome occurs with chronic daily
ingestion of at least 2 grams alcohol / kg (eight drinks /
day).
Alcohol is teratogen that affects the central nervous
system.
So alcohol,at any time during pregnancy,has the potential
to cause birth defects.
Alcohol consumption should be avoided entirely
during pregnancy.
General Factor
m

Treacher Collins Syndrome
• Drug induced deformity
• Affect the formation and migration of neural crest
cell.
• Clinical manifestations:
Antimongoloid
palpebral fissure with
coloboma of lower
lid.
m

Hypoplasia of facial
bones
Malformation of
external ear
m

High palate
Fistula
Birdlike or fishlike face
m

Anencephaly
• Etiology: Deficiency of nutritional folic acid, a
water soluble vitamin
• Neural tube closure at several sites:
Site 1: Future hind brain
and spinal cord
Site 2,3,4: Three distinct
site at cranial region
Site5: Canalization occur
in the caudal region
m

Failure of closure
result in neural tube
defect
m

Encephalocele :
- Failure to complete
the neural tube
closure or membrane
fusion at closure
points within the
cranial region
m

Spina bifida cystica: -
neural tube defect at
spinal cord and at
covering at various level.
m

Birth Injury:
• In some diffficult birth, the use of forceps to the head
to assist in delivery might damage either or both the
temporomandibular joints.
• At one time this was a common explanation for
mandibular deficiency.
• But, in light of contemporary understanding, the
condylar cartilage is not as easy to blame
underdevelopment of the mandible.
• So injury to the mandible during a traumatic delivery
appears to be rare and unusual cause of facial
deformity.
General Factor
Postnatal Influence
m

Postnatal influence
• High forceps delivery
• Temporomandibular joint has been damaged.
m

• Another possibility, is the delivery induced
deformation of the upper jaw.
• Obstetricians frequently insert the forefinger and
middle finger into the baby‘s mouth to ease
passage through the birth canal.
• Due to the plasticity of the maxillary and
premaxillary region, temporary deformation is
quite likely and permanent damage may result.
General Factor
Postnatal Influence
m

Postnatal influence cont…
• Delivery induced deformation of the upper jaw.
• Extensive scarring of neck and lower face as a
result of severe burns during infancy has
restricted mandibular growth.
m

General Factor
Accidents:
• The falls and impacts of childhood can fracture
jaws just like other parts of the body.
• The condylar neck of the mandible is particularly
vulnerable.
• When a problem does arise following condylar
fracture, it usually is asymmetric growth, with
the previously injured side lagging behind.
Postnatal Influence
m

Deficient growth on the affected side after fracture of the
left condylar process
m

Predisposing metabolic climate and disease
Endocrine Imbalance Metabolic disturbances Infectious Diseases
(Poliomyelitis etc.)
General Factor
m

General Factor
ENDOCRINE DISTURBANCES:
PITUITARY PROBLEMS:
• A few workers have studied the relation of the pituitary
gland to dental development, notably Schour and Van
Dyke and Baume, Becks and associates. Working with
rats, they found that after hypophysectomy there was a
– progressive retardation of eruption of the incisor
tooth which eventually ceases to erupt.
– The tooth attained only about 2/3rd normal size and
showed a distortion of form.
– When an extract of the anterior lobe of the pituitary
was injected into the hypophysectomized rats, the
eruption rate of the incisor tooth returned to normal.
m

General Factor
PITUITARY PROBLEMS
Baume and his associates injected thyroxin into
hypophysectomized animals, either alone or with
purified growth hormones. Their findings led them to
the following explanation.
– The pituitary gland influence eruption not only with
its thyrotropin but also with its growth hormones.
– The effect of thyroxin on dental growth and
development are different from those of the pituitary
growth hormone.
– Thyroxin is the factor which stimulates the eruption
movements and tooth size but it has little influence
on alveolar growth.
– Growth hormones on the other hand spur dental as
well as alveolar growth.www.indiandentalacademy.co
m

General Factor
PITUITARY PROBLEMS:
HYPOPITUITARISM
Two basic manifestations of hypopituitarism-
• Dwarfism in children
• Simmonds‘ disease in adults
m

General Factor
Hypopituitarism
 Under-secretion of growth hormone before
epiphyseal plate closure resulting in Pituitary
Dwarfism.
 In pituitary dwarfism, there is diminutive but
well-proportioned body.
 Supporting structures are retarded in growth.
 The osseous development of mandible is more
retarded than maxilla.
m

Hypopituitarism:
 The dental arch is smaller than normal and
therefore cannot accommodate all the teeth, so
that a malocclusion develops.
 In pituitary dwarfs the eruption rate and
shedding time of the teeth are delayed.
 Clinical crown appears smaller than normal
because even though eruption does occur, it is
not complete.
 The roots of teeth are shorter than normal in
dwarfism.
m

General Factor
HYPERPITUITARISM
 An increase in the number of granules in the
acidophilic cells or an adenoma of the anterior lobe of
the pituitary is associated with gigantism or acromegaly
 If the increase occurs before the epiphyses of the long
bones are closed, gigantism results.
 If the increase occurs later in life i.e. after epiphyseal
closure, acromegaly develops.
m

Hyperpituitarism
 Gigantism is characterized by a general symmetric
overgrowth of the body.
 Some persons with this disturbance attaining a
height of over 8 feet.
 The teeth in gigantism are proportional to the size
of the jaws and rest of the body.
 The roots may be longer than normal.
m

Hyperpituitarism:
 Acromegaly, results in enlarged hands, feet, an
enlarged skull and mandible along with soft tissue
enlargement.
 Excessive growth of mandible, creating a skeletal
class III malocclusion.
m

Hyperpituitarism:
 The lips become thick.
 The tongue also becomes enlarged and shows
indentations on the sides from pressure against
the teeth.
 The teeth in the mandible are usually tipped to the
buccal or labial side, owing to the enlargement of
the tongue.
m

Hyperpituitarism:
 Multiple root resorptions may be seen.
m

General Factor
THYROID PROBLEMS
HYPOTHYROIDISM:
 If hypothyroidism occurs in infancy and
childhood, cretinism results.
 If it occurs in the adult, myxedema results.
m

General Factor
Hypothyroidism:
 The cretinism leads to mental defects, retarded
somatic growth, generalized edema.
 Skeletal growth in the cretin is characteristically more
inhibited than the soft tissue growth.
 As a result of this disproportionate rate of
growth, the soft tissues are likely to enlarge
excessively, giving the cretin the appearance of an
obese and short child.
m

Hypothyroidism:
 The cretin or acutely hypothyroid dwarf has -
-Thick neck
-Shorter extremities
-Thick lips
-Large protruding tongue
 But the pituitary dwarf is harmoniously
proportioned.
 In both intances dentition is delayed, with deciduous
teeth still present
m

Hypothyroidism
m

Large tongue in cretinism, may contribute to the development of
mandibular prognathism by causing the mandible to be positioned
forward at all times.
Hypothyroidism
m

` Hypothyroidism:
Myxedema is characterized by
• Lower metabolic rate
• Slowed heart rate
• Decreased cardiac output
• Decreased mental activity
• Increased weakness
• Increased weight
• Depressed growth of hair and scaliness of skin
• Facial edema
• Increase blood cholesterol
m

Hypothyroidism:
 The orofacial findings in myxedematous patients are
apparently limited to the soft tissues of the face and
mouth.
 Lips, nose, eyelids are edematous and swollen.
 The tongue is large and edematous, frequently
interfering with speech.
m

General Factor
THYROID PROBLEMS
HYPERTHYROIDISM:
Boothby and Plummer described two
fundamental different type of hyperthyroidism
– Exophthalmic goiter (Grave‘s disease)
characterized by diffused hyperplasia of the
thyroid and by eye signs.
– Toxic adenoma, in which hyperfunction
originates in a benign tumor of the thyroid
gland.
m

Hyperthyroidism
This is usually manifested as
• Increased basal metabolic rate
• Increased blood pressure
• Increase heart rate
• Increased weakness
• Intolerance to heat
• Increased appetite
• Increased weight loss
• Nervousness and tremors to the hands
• Increased sweating
m

Hyperthyroidism:
 In hyperthyroidism shedding of deciduous teeth
occurs earlier than normal.
 Eruption of the permanent teeth is greatly
accelerated.
 Alveolar atrophy occurs in advanced cases.
m

 Increased activity is usually due to an adenoma of
one or more of the four parathyroid glands.
 Almost all patients with hyperparathyroidism have
skeletal lesions, some of which may occur in the skull
or jaws.
 The skeletal disturbances in hyperparathyroidism vary
from vague to roentgenographically characteristic
lesions and even gross clinical evidence of bone
lesions.
General Factor
PARATHYROID HORMONE PROBLEMS
PRIMARY HYPERPARATHYROIDISM:
m

Primary Hyperparathyroidism
– Three times more common in females than
males.
– Usually affects people of middle age.
– Pathological fracture may be the first symptom
of the disease.
– Bone pain and joint stiffness are frequent early
symptoms.
– Occasionally the first sign of the disease may
be a giant cell tumor or a cyst of the jaw.
– Loss of phosphorus and calcium in this
disturbance results in a generalized
osteoporosis.
– Malocclusion caused by sudden drifting with
definite spacing of teeth.
m

Primary Hyperparathyroidism
Roentgenographic feature
– Bones of the affected person shows a
general radiolucency as compared with
those of normal people.
– Later, sharply defined round and oval
radiolucent areas develop, which may be
lobulated.
– In the jaws it has been described as having
a ―ground-glass appearance‖
– Lamina dura around the teeth may be
partially lost.
– Pulp calcification
m

PRIMARY HYPERPARATHYROIDISM
Numerous mandibular radiolucencies
m

• Hyperparathyroidism can also occur secondary
to other disorder, the most common being end
stage renal disease.
• Roentgenographic evidence of bone disease
involving the jaws shows Brown tumor and loss
of lamina dura.
Secondary Hyperparathyroidism
m

SECONDARY HYPERPARATHYROIDISM
“BROWN” GIANT CELL TUMOR ON THE PALATE
m

SECONDARY HYPERPARATHYROIDISM
“BROWN” GIANT CELL TUMOR
m

General Factor
HYPOPARATHYROIDISM
 Caused by elimination of parathyroid glands which may be
due to surgical removal or rarely due to congenital absence.
 Blood chemistry shows a low concentration of serum calcium
and a high concentration of serum phosphorus.
 When serum calcium level falls to 6 to 7 mg/dl, tetany
develops
 Aplasia or hypoplasia of the teeth when hypoparathyroidism
developed before the teeth were entirely formed.
m

SEX HORMONES
•Sex hormones (oestrogen and androgen) play an important
role in maintenance of bone volume, a reduction causes
osteoporosis.
•Sex hormones affect craniofacial bone development.
•It has been reported, that the suppression of sex hormone
secretion during the pubertal growth phase inhibits craniofacial
growth, particulary mandibular growth, and results in reduced
craniofacial development
European Journal of Orthodontics 28 (2006)
m

METABOLIC DISTURBANCES
 Acute febrile diseases are capable of affecting not
only the general health of the child but might also
affect the dentition and its surrounding hard and the
soft tissues.
 Temporarily they are capable of slowing down
growth and may cause delayed tooth eruption.
 Usually if the severity and duration is not prolonged
the child is able to recoup lost time and catch up
growth is possible.
General Factor
m

INFECTIOUS DISEASES
 Disease with paralytic effect, such as
poliomyelitis are capable of producing
malocclusions.
Osteomyelitis
 The adult afflicted with acute suppurative
osteomyelitis is usually in severe pain.
 The teeth in the area of involvement are loose
and sore.
General Factor
m

INFECTIOUS DISEASES
German Measles: (Rubella)
 Enamel hypoplasia
 A high caries incidence
 Delayed eruption of deciduous teeth
m

Dietary problems ( Nutritional
deficiency)
• Rickets, Scurvy, Beriberi can produce severe
malocclusion
• Main problem is upsetting the dental
development timetables
Premature loss
Prolonged retention
Poor tissue health and abnormal eruptive paths
m

Dietary Problems
Vitamin A deficiencies
 In the developing tooth that is deficient in vitamin A, the
odontogenic epithelium fails to undergo normal
histodifferentiation and morphodifferentiation, resulting in
the distortion of the shape of the teeth.
 Since the enamel forming cells are disturbed, enamel
matrix is arrested &/or poorly defined so that calcification is
disturbed and enamel hypoplasia results.
m

Vitamin A deficiencies
 Eruption rate is retarded and in prolonged deficiencies
eruption ceases.
 The alveolar bone is retarded in its rate of formation.
 The gingival epithelium becomes hyperplastic & in
prolonged deficiencies shows keratinization. This tissue is
easily invaded by bacteria that may cause periodontal
disease.
m

Vitamin D deficiency
 It is required for normal development of bones and teeth.
 Necessary for the absorption of calcium and phosphorus from
food in the small intestine.
 Deficiency leads to rickets.
 Rickets refers to any disorder in the vitamin D –calcium
phosphorus axis which results in hypomineralized bone matrix.
 Children with rickets shows bowing of the legs.
m

Effects on teeth
• Delayed eruption
• Misalignment of teeth
• Disturbed calcification of teeth
• Higher caries index.
Vitamin D deficiency
m

Dietary Problems
Vitamin C
 Vitamin C is important for normal development of
intercellular ground substances in bone, dentition, and
other connective tissues so deficiency of ascorbic acid are
associated with disturbances in these tissues.
 The characteristic change in the teeth is atrophy and
disorganization of the odontoblasts resulting in the
production of irregularly laid down dentine with
few, irregularly arranged tubules.
m

Vitamin C
 Interdental and marginal gingiva is bright red with a
swollen, smooth, shiny surface. In fully developed
scurvy the gingiva becomes boggy, ulcerates and
bleeds
 In severe, chronic cases of scurvy, hemorrhages into
and swelling of periodontal membranes
occur, followed by loss of bone & loosening of
teeth, which eventually exfoliate.
m

Dietary Problems
Protein Deficiency
 Overall growth and growth of the jaws were
decreased.
 Delayed eruption.
 The gingiva and periodontal membranes exhibited
varying degrees of degeneration.
m

ORAL HABITS
General Factor
m

HABITS
• Definition:- A habit can be defined as the
tendency towards an act that has become a
repeated performance, relatively fixed, consistent
and easy to perform by an individual.
OR
• Definition:- Learned patterns of muscle
contraction of very complex nature.(MOYERS)
m

Finn says that habits cause concern as they
cause:
•Oral structural changes: Harmful,
unbalanced pressures bear upon the
immature, highly malleable alveolar
ridges and bring about potential changes
in position of teeth and occlusion.
•Behavioral problems
•Socially unacceptable act.
m

Classification of Habits
 Habits in relation to malocclusion perhaps should
be classified as:
1.Useful
2.Harmful
 Useful Habits: Should include the habits of
normal function, such as correct tongue
position, proper respiration, deglutition and
normal use of the lips in speaking.
 Harmful Habits: include all that exert perverted
stresses against the teeth and dental arches such
as lip biting, lip sucking, thumb sucking.
m

According to Finn & Sim
1. Compulsive oral habits
2. Non-compulsive oral habits
m

1. Compulsive oral habits:
• When it has acquired a fixation in the child to
the extent that he retreats to the practice of
this habit whenever his security is threatened
by events which occur in his world.
• They express deep-seated emotional needs.
• Attempt to correct them may cause increased
anxiety.
m

2. Non-compulsive oral habits:
Habits which are easily added or dropped from
the child‘s behavior pattern as he matures.
m

• Intentional
• Unintentional
Intrinsic
Extrinsic
m

• Intentional : intentional are planned
pressures.
Orthodontic treatment appliance
Myofunctional therapy
Intentional head deformation
Giraffe-necks of the Padaung women
Chinese custom of foot binding
Reshaping horns of cattle
m

Unintentional: abnormal pressure habits
Intrinsic pressure habits (within the mouth)
-Thumb and finger sucking
-Tongue thrust and tongue sucking
-Lip and nail biting
-Mouth breathing
Extrinsic pressure habits
-Chin propping
-Face leaning on hand
-Abnormal pillowing, leaning on forearm or hand
m

Intentional head deformation
• Skull of the Pueblo Indian square head.
• Flathead Indian tied their papooses to boards to
produce the flat head which they admired.
m

Giraffe necks of the Padaung women
• The Padaung women live in Burma
• Etiology:- Amount of brass wire used for
coiling around their necks
- They begin with 5coils as thick as little
finger and add more as the neck stretches
until twenty one coils.
 C/F:- An elongation of individual neck to
become ―giraffe necked‖
m

Chinese custom of foot binding
• Foot binding was prohibited by the new laws of
Chinese republic in 1921.
• It was originated from the desire of men to keep
their women from running away.
m

THUMB SUCKING AND DIGIT
SUCKING
According to Gellin
Thumb sucking is defined
as the placement of the
thumb or one or more
fingers in varying depths
into the mouth.
According to Moyers
Thumb sucking is defined
as the repeated and
forceful sucking of thumb
with associated strong
buccal and lip
contractions.
m

BASIC PHYSIOLOGY OF SUCKING REFLEX:
 At birth, the child has a reflex pattern of
neuromuscular functions as sucking.
 The habit of sucking is a reflex occurring in the
oral stage of development and disappears during
normal growth between 1 to 31/2 years.
 Even before birth, oral contraction have been
observed.
THUMB SUCKING AND DIGIT SUCKING
m

According to Traisman and Traisman 2650 infants
and children were screened from birth to
16years. 46% sucked their thumb at some time
during this period. Of these, 26% began during
the later part of their first year.
On an average most stopped by the age 4.
There were some who continued the habit as late
as 12 – 15 years.
m

ETIOLOGY
PSYCHOLOGY
FREUD and his contemporaries have proposed that a
child goes through various distinct phases of
psychological development of which oral phase and
anal phase are in the first 3 years of age.
In the oral phase it is believed that the mouth is the
center of attraction of oro-erotic zone. During this
phase the child takes anything and everything to the
oral cavity.
m

At birth, the child has developed a reflex pattern of
neuromuscular function called the ―SUCKLING
REFLEX‖.
The reflex influences the child in his early bearing
situations and contributes to his body and the
relief from hunger which follows the sucking.
m

 During the very first weeks of life, thumb
sucking are typically related to feeding
problems.
 Some children suck their thumb
 as a teething device during the difficult
eruption of a primary molar.
 for the release of emotional tensions with
what they are unable to cope.
 as an attention-seeking weapon.
m

• Almost all normal children engage in non
nutritive sucking, prolonged sucking habit can
lead to malocclusion
• Sucking during the primary dentition years have
little if any long term effect
• Habit is considered normal till the age of 3-4
years. Persistence of the habit beyond this age
can lead to malocclusion.
m

Oral habits and primary dentition
• While continuous nonnutritive sucking habits of
48 months or longer produced the greatest
changes in dental arch and occlusal
characteristics, children with shorter sucking
duration also had detectable differences from
those with minimal habit duration.
•Implications: It may be prudent to revisit
suggestions that sucking habits continued to as
late as 5 to 8 years of age are of little concern.
Warren J et al. Effects of oral habits’ duration on dental
characteristics in the primary dentition. JADA
2001( Dec); 132: 1685- 93 B37
m

There are 2 forms of sucking:
• Nutritive form
• Non-nutritive form
m

Nutritive form
Breast & bottle feeding which provides essential
nutrients.
Breast feeding-
• Accomplished by 2 maneuvers-suckling and
swallowing.
• The milk of lactating mammals are surrounded by
smooth muscles, which contracts to force out the
milk.
• Suckling stimulates the smooth muscle to
contract and squirt milk into his mouth.
m

• Suckling consist of small nibbling movements of the lips.
• When the milk is squirted into the mouth, it is only
necessary for the infant to groove the tongue & allow the milk
to flow posteriorly into the pharynx and esophagus.
• The tongue, however, must be placed anteriorly in contact
with the lower lip, so that milk is deposited on the tongue.
• This sequence of events defines as infantile swallow.
• The suckling reflex and the infantile swallow normally disappear
during the first year of life.
m

Bottle feeding
• Nipple manufactures have ignored the basic
physiology of suckling.
• The conventional nipple contacts only the mucous
membrane of the lips.
• The warmth of association conferred by the
breast & the mother‘s body is largely lacking &
the physiology of suckling is not duplicated.
m

•Because of poor design, the mouth is held open more
widely & greater demand is made on the buccinator
mechanism.
•The pumping action of the tongue, the raising &
lowering & the rhythmic backward & forward movement
of the mandible are reduced.
•Suckling becomes sucking.
BOTTLE FEEDING
m

• Breast-feeding practices contribute in the
prevention of malocclusion in addition to
decreasing the practice of parafunctional habits.
(P R Health Sci J. 2006 Mar)
• To provide as close a duplicate of the human
breast as possible, a nipple was designed which
incited the same functional activity as breast
feeding.
• The functionally designed latex nipple largely
eliminate the objectionable features of previous
non-physiologic counterparts.
m

Nonphysiological nursing with a
conventional nipple
•Mouth is propped open unduly.
•Lip seal difficult.
•Abnormal muscle pressure are
exerted because of excessive
opening movement.
Nursing action of nuk sauger nipple
•Closely simulates natural activity.
•Entire perioral areas is able to contact
the warm nipple base.
m

• A minimum of half an hour per nursing interval is
recommended.
• Weaning to the cup should be postponed until at least
the first birthday.
• If nursing is done with the physiologically designed
nipple in conjunction with fondling & maternal
contact, there is reason to believe that the incidence
of prolonged sucking habits will be significantly
reduced.
m

NON NUTRITIVE FORM:
• Children who neither receive unrestricted breast
feeding nor have access to a pacifier may satisfy
their need with habits like thumb sucking which
ensures a feeling of warmth & sense of security
but may be detrimental to their dentofacial
development.
• Nearly all modern infants engage in some sort of
habitual non nutritive sucking- sucking of the
thumb, finger or a similarly shaped objects.
• Vast majority of infants do so from 6 months to 2
years or later.
m

• After the eruption of the primary molars during
the second year, drinking from a cup replaces
drinking from a bottle or continued nursing at the
mother‘s breast, the number of children who
engage in non nutritive sucking diminishes.
• Some fetuses have been reported to suck their
thumbs in utero.
m

• Recent studies shown that thumb sucking may be
practiced even during intra uterine life.
m

Almost all normal children who engage in
non-nutritive sucking, can lead to
malocclusion.
As a general rule, sucking habits during the
primary dentition years have little if any long
term effect.
 If these habits persist beyond the time that
the permanent teeth begin to
erupt, malocclusion occurs.
m

TRIDENT OF FACTORS
Damage to the teeth and investing tissues is
dependant on trident of factors that must be
recognized and evaluated.
i. Duration
ii. Frequency
iii. Intensity
m

 Equally important.
 The frequency of the habit during the day and
night affects the end result.
The child who sucks sporadically or just when going
to sleep is much less likely to do any damage
than one who constantly has his finger in his
mouth.
m

 Intensity
 In some children the sucking can be heard in the
next room. The perioral muscle function and
facial contortions are easily visible.
 In others the thumb habit is little more than a
passive insertion of the finger in the mouth with
no apparent buccinator activity.
m

OTHER FACTORS
1. Position of thumb or fingers in the mouth.
2. Associated contraction of the muscles of the lips
and cheeks.
m

“COWBAR EFFECT”
Flattening of the mandibular incisor segment, which
causes mild crowding.
As a result shallow and open bite relationship of the
anterior teeth develops.
Flattened mandibular anterior segment
Abnormal mentalis muscle function and
lower lip activity serve to flatten the mandibular
anterior segment.
m

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

Clinical manifestation
• Anterior open bite
• Proclination of
maxillary anteriors
• Increased overjet
• Posterior crossbite
• Hypotonic upper lip
and hypertonic
mentalis activity.
m

Malocclusion characterized by
 Flared and spaced maxillary incisors and
lingually positioned lower incisors.
 The labially posed upper permanent incisors are
particularly vulnerable to accidental fractures.
m

Afzelius-Alm A, et al, (Swed Dent J. 2004;28)
found that the majority of children with
prolonged thumb-sucking have proclined lower
incisors rather than retroclined lower incisors.
In retroclined lower incisors groups
– the angle between the thumb and the lower
incisors was significantly smaller.
– the thickness of the lower lip significantly
thinner than in the group with proclined
incisors.
– A higher frequency of early loss of deciduous
molars was also observed in the group with
retroclined incisors.
m

Anterior Open Bite: (Cozza P et al, Am J Orthod Dentofacial
Orthop. 2005 Oct)
• It is associated by a combination of interference
with normal eruption of incisors and excessive
eruption of posterior teeth.
• When a thumb or finger is placed between the
anterior teeth, the mandible must be positioned
downward to accommodate it.
• The interposed thumb directly impedes incisor
eruption.
• At the same time, the separation of jaws alter the
vertical equilibrium on the posterior teeth and as a
result, there is more eruption of posterior teeth.
m

Anterior Open Bite:
• Because of the geometry of jaw, 1mm of
elongation posteriorly opens the bite about 2
mm anteriorly, so this can be a powerful
contributor to the development of anterior
open bite
m

 Narrow upper arch:
• Although negative pressure is created within the
mouth during sucking, but this is not responsible
for the constriction of the maxillary arch.
• When the thumb is placed between the teeth the
tongue must be lowered, which decreases
pressure by the tongue against the lingual of
upper posterior teeth.
• At the same time cheek pressure against these
teeth is increased as the buccinator muscle
contracts during sucking.
• Cheek pressures are greatest at the corners of
the mouth, and this probably explains why the
maxillary arch tends to become V-shaped, with
more constriction across the canines than the
molars. www.indiandentalacademy.co
m

 Unilateral and bilateral cross bites are
often associated with finger habits.
( Warren JJ et al.
Pediatr Dent. 2005 Nov-Dec)
m

 Retardation of deglutitional maturation
• Increase in over-jet makes normal swallowing
procedures increasingly difficult.
• Instead of the lips containing the
dentition, during deglutition, the lower lip
cushions to the lingual of the maxillary
incisors, forcing them farther forward.
• Lip muscle aberrations are often assisted by a
compensatory tongue thrust during the
swallowing act.
• So the infantile suckle-swallow continues, or the
transitional period is greatly prolonged with a
mixture of infantile and mature swallowing
cycle.
m

 Thumb sucking habit can create a class II
malocclusion.
 Thumb-suckers may be found to have a
narrower nasal floor and high palatal vault.
 The maxillary lip becomes hypotonic and the
mandibular lip becomes hyperactive.
m

Anterior Open Bite
Narrow Constricted
maxillary arch
Posterior Cross Bite
m

 Tell-tale callus on the back of the finger
or thumb are often present.
m

TONGUE THRUSTING
• Definition:-
placement of the
tongue tip forward
between the
incisors during
swallowing.
m

Tongue Thrusting Habit
 The term tongue thrust is a misnomer.
 Since it implies that the tongue is forcefully
thrust forward.
 But individuals who place the tongue tip forward
when they swallow usually do not have more
tongue force against the teeth than those who
keep the tongue tip back.
m

 Swallowing is not a learned behavior, but is
integrated and controlled physiologically at
subconscious levels.
 Individuals with an anterior open bite place the
tongue between the anterior teeth when they swallow
while those who have a normal incisor relationship
usually do not and it is tempting to blame the open
bite on this pattern of tongue activity.
m

Humans show 2 types of swallow pattern:
Infantile and neonates swallow
Mature/Adult swallow
m

Infantile visceral swallow
• Jaws apart, tongue
between gum pads
• Mandible stabilized by
contraction of facial
muscles and interposed
tongue
• Swallow is guided and
controlled by sensory
interchange between lip
and tongue
m

• Active contractions of the musculature of the lips.
• Tongue tip is brought forward into contact with
the lower lip.
• Little activity of the posterior tongue or
pharyngeal musculature.
• Forward position of mandible and tongue.
• Tongue grooved (depressed central position) to
steer the liquid into pharynx and oesophagus.
m

Mature somatic swallow
• Teeth – together
(momentarily)
• Mandible stabilized by
contraction of mandibular
elevator muscles
• Tongue tip- against
palate, above and behind the
incisors
• Minimum contraction of lips
• Appears between 2-4 years in
normal pattern
m

NORMAL SWALLOWING
•Incisors are momentarily in contact
•Tip of the tongue touches the lingual
interdental papillae of maillary arch
•Lips are tightly closed together
•Dorsum of the tongue closely
approximates the palate during
swallowing
ABNORMAL SWALLOWING
•Teeth are often separated
•Tongue thrusts forward into the
excessive overjet
•Instead of the lips creating firm seal, the
upper lips remains relatively functionless
•Dorsum of the tongue drops away from
the palatal vault
•Mentalis exerts strong forward and upward
thrust of lower lip against lingual surfaces
of maxillary incisors
m

Retained Infantile Swallow
Is defined as a predominant persistance of the
infantile swallowing reflex after the arrival of
permanent teeth.
• Contraction of lips, facial muscles (Buccinator)
Patients may have inexpressive faces, since the 7th
cranial nerve muscles are not used for the
delicate purpose of facial expression but rather
for the massive effort of stabilizing the mandible
during swallow.
m

Predisposing factors
• Associated with history of finger sucking
• Maintain an anterior seal
• Associated chronic naso respiratory distress
• Mouth breathing
• Tonsillitis or pharyngitis
• Improper bottle feeding
• Macroglossia
• Constricted dental arches
• Retained infantile swallow
m

ETIOLOGY OF TONGUE THRUST
1. Bottle feeding
2. Genetic influence
• A tendency towards allergies and upper respiratory
congestion.
• An extremely high or narrow palatal arch.
• An unusually large tongue.
• Restricted nasal pathway.
• Imbalance between number or size of teeth and
oral cavity.
3. Thumb sucking
4. Open spaces during dentition
m

5. Gap-filling tendency
6.Tonsils and adenoids
7. Allergies, affecting the upper respiratory tract
8. Macroglossia in which the tongue is inadequate
to fill the oral space resulting in a forward
thrusting tongue.
m

FLETCHER has classified etiological
factors as:
1. Genetic factors
2. Learned behavior
3. Maturational
4. Mechanical restrictions
5. Neurological disturbance
6. Psychogenic factors
m

Classification
1. Simple Tongue Thrust
2. Complex Tongue Thrust
m

Simple tongue thrust
(Teeth together
swallow)
• Teeth are in occlusion
as tongue protrudes
into open bite
• Tongue thrust is
present to seal open
bite
• Well circumscribed
open bite
• Secure intercuspation
• History of digit sucking
• Displays contractions of
lips, mentalis and
mandibular elevators .www.indiandentalacademy.co
m

Simple tongue thrust
• This particular tongue thrust is simply an
adaptive mechanism to maintain an open bite
created by some other cause.
Ex - Thumb sucking
m

Complex tongue thrust
(Teeth apart swallow)
• Teeth apart during tongue
thrust
• More diffuse open bite
• Poor occlusal fit
• History of breathing or
chronic nasorespiratory
diseases
• Combined contractions of
lip, facial and mentalis
muscles.
• Lack of contraction of
mandibular elevators
m

Complex tongue thrust
• Combine contractions of the lips, facial, and
mentalis muscles, lack of contraction of the
elevators.
• The open bite associated with it is more diffuse
and difficult to define than that seen with a
simple tongue thrust.
• Examination of the dental casts reveals a poor
occlusal fit and instability of intercuspation, since
a persistent teeth apart swallow does not
stabilize the occlusion.
m

•Complex tongue thrust are more likely to be associated with chronic
nasorespiratory distress, mouth breathing, tonsillitis, or pharyngitis.
•When the tonsils are inflamed, the root of the tongue may encroach
on the enlarged facial pillars.
•To avoid this encroachment, the mandible reflexly drops, separating
the teeth and providing more room for the tongue to be thrust forward
during swallowing to a more comfortable position.
•Pain and lessening of space in the throat precipitate a new forward
tongue posture and swallowing reflex.
•Melsen et al state that both tongue thrust swallow favor the
development of distoocclusion, extreme maxillary overjet and open
bite.
m

Clinical Feature:
If the postural position is normal, the tongue thrust swallow has
no clinical significance because tongue thrust swallowing simply
has too short a duration to have an impact on tooth position.
• Pressure by the tongue against the teeth during a typical
swallow lasts for approximately 1 second.
• A typical individual swallows about 800 times/day while
awake but has only a few swallows /hour while asleep. The
total/day therefore is usually under 1000.
• One thousand seconds of pressure, of course, totals only a
few minutes, not nearly enough to effect the equilibrium.
m

 On the other hand, if a patient has a altered resting
posture of the tongue, the duration of this
pressure, even if very light, could effect tooth
position, vertically or horizontally.
 Two significant variations from the normal tongue
posture can be seen.
• Protracted Tongue posture
• Retracted Tongue posture
m

There are two forms of protracted tongue
posture
• Endogenous protracted tongue posture.
• Acquired protracted tongue posture.
m

Endogenous protracted tongue posture:
• May be a retention of infantile postural pattern.
• Some persons, reasons not yet clear, do not change their
tongue posture during the arrival of the primary incisors and
the tongue tip persists between the incisors.
• For the great majority of patients with endogenous
protracted tongue posture, the open bite is mild and not a
serious clinical problem, but on rare occasions, quite serious
open bites are present.
m

Acquired protracted tongue posture
• Usually it is the adaptation to enlarged tonsils,
pharyngitis, or tonsilitis.
• When the acutely inflamed throat (pharyngitis or
tonsilitis) is anesthetized, the adaptive protracted posture
of the tongue may spontaneously correct to a more
normal position.
• As long as the precipitating pain mechanism is present,
the tongue will posture itself forward, and repositioning
of the incisors will not be stable. Therefore, it is best to
refer such patients to a physician for correlative therapy.
m

The protracted tongue posture usually results in
Anterior open bite
Proclination of anterior teeth
Contracted upper arch
m

MOUTH BREATHING HABIT
Incidence
• Common in children between 5 and 15 years of
age
• 80% mouth breathers suffer from nasal
obstruction
• 20% habitual mouth breathers
• Condition is self correcting after puberty
m

As the child grows older and the laryngeal skeleton
descends in the neck, air can be taken in through the
mouth, but this is normally prevented by 3 sphincter
mechanism:
Anterior sphincter : formed by lips.
Intermediate : formed by tongue and hard palate
Posterior : formed by soft palate and dorsum of tongue
Failure of these barriers causes mouth
breathing, which is mostly intermittent and more
common at night.
m

ROBERT MOYERS (1988) says that enlarged
adenoids obstruct the airway causing mouth
breathing which neccesitates changes in tongue, lip
and mandibular posture.
These changes upset the soft tissue balance and lead
to alterations in craniofacial form and to
malocclusion, including increased anterior face
height, narrow and high palate, increased lower face
height, anterior open bite and a tendency for
crossbite.
These changes are thought to be brought about by
compression, disuse atrophy and alternate air
pressure.
m

MOUTH BREATHING HABITS
ETIOLOGY
• Humans are primarily nasal breathers but everyone
breathes partially through the mouth under
physiologic conditions.
• The most prominent being an increased need for air
during exercise.
• At rest, minimum airflow is 20-25 L per minute, but
heavy mental concentration or even normal
conversation lead to increased airflow and transition
to partial mouth breathing.
• For the average individual there is a transition to
partial oral breathing when ventillatory exchange
rates above 40-45L/min are reached.
• At maximum effort 80 or more L/min of air
needed, about half of which is obtained through the
mouth.
m

• Nasopharyngeal Obstruction
• Allergies
• Chronic respiratory infection
• Enlarged tonsils &adenoids
• Nasal polyp or tumor
• Any mechanical obstruction anywhere within the
nasorespiratory system
• Deviated nasal septum
m

• Hypertrophy
• Anatomic-short upper lip
• Abnormal development of nasal cavity
• Localized benign tumor
• Narrow nasal passage associated with narrow
maxilla
• Fibrous dysplasia
m

Classification of mouth breathing:
Obstructive
Habitual
Anatomical
m

OBSTRUCTIVE MOUTH BREATHERS: Those who have
– Increased resistance to or a complete obstruction of the
normal flow of air through the nasal passages.
– Because of the difficulty of inspiring and expiring air
through the nasal passages, the individual is forced to
breathe through his mouth.
– Obstructive mouth breathing is frequently observed in
ectomorphic children who possess long, narrow
faces, and nasopharyngeal spaces.
m

Habitual mouth breather is an individual who
continually breathes through his mouth by force
of habit, although the abnormal obstruction has
been removed.
Anatomical mouth breather is one whose short
upper lip does not permit complete closure
without undue effort.
m

PATHOPHYSIOLOGY
During oral respiration the following 3 changes in the
posture occur-
a) Lowering of the mandible.
b) Lowering of the tongue.
c) Tipping back of the head.
Lowering of the mandible & tongue upsets the oro-facial
equilibrium.
There is an unrestricted buccinator activity
These postural changes influence the position of the teeth
& also the growth the jaws.
m

CLINICAL FEATURES
• Long face syndrome or
adenoid facies
• Expression-less face
• Increased over jet
• Contracted upper arch
• Posterior cross bite
• Increase dental caries
• Narrow nasal passage
• Anterior open bite
m

• Because of the lowering of the
mandible and tongue and
extend (tip-back) the
head, face height would
increase.
• Posterior teeth would super-
erupt.
• The mandible would rotate
down and back.
• Opening the bite anteriorly.
m

•Narrower maxillary dental arch
(J Clin Pediatr Dent. 2004
Summer;28(4)
m

Diagnosis
• Observers tend to equate lip separation at rest
with mouth breathing, but this is simply not
correct.
• It is perfectly possible for an individual to breathe
through the nose while the lips are apart.
• The only reliable way to quantify the extent of
mouth breathing is to establish how much of the
total airflow goes through the nose and how
much through the mouth, which requires special
instrumentation to simultaneously measures
nasal and oral airflow.
m

 Mirror Test: A double-sided mirror is held between
the mouth and nose.
• Fogging on the nasal side of the mirror indicates
nasal breathing while fogging on oral side
indicates mouth breathing.
 Cotton Test or Massler’s Butterfly Test:
• Butterfly shaped cotton strands are placed over
the upper lip below nostrils.
• If the cotton flutters down, it is a sign of nasal
breathing.
• This test can be used to determining unilateral
nasal blockage.
Other methods of diagnosis
m

Water Test:
• The patient is asked to fill the mouth with water
and retain for a period of time.
• Mouth breathers find this task difficult.
m

BRUXISM
Bruxism is the habitual grinding of the teeth
either during sleep or as an unconscious habit
during waking hours.
m

ETIOLOGY
Nadler (1957) gave the following causes of bruxism-
•Local
•Systemic
•Psychologic
•Occupational
BRUXISM
m

LOCAL FACTORS
•Generally associated with some form of mild occlusal
disturbance.
SYSTEMIC FACTORS
•Gastrointestinal disturbances
•Sub-clinical nutritional deficiencies
•Allergy
•Endocrine disturbances
•A hereditary background has been described in some
cases.
BRUXISM
m

PSYCHOLOGIC FACTOR
Certain psychic traits are present in bruxers, while occlusal
factors are not useful parameters to discern bruxers from
non-bruxers.
Manfredini et al. (Aust Dent J. 2004 Jun;49(2):849)
OCCUPATIONAL
•Occupations in which the work must be unusually
precise, such as that of the watchmaker, are prone to
cause bruxism.
•Athletes engaged in physical activities often develop
bruxism, although the exact reason for this is uncertain.
BRUXISM
m

CLINICAL FEATURES
•Attrition of the teeth may occur.
• Loss of integrity of the periodontal structures, resulting in
loosening or drifting of teeth or even gingival recession with
alveolar bone loss.
•Temporomandibular joint disturbances.
•Hypertrophy of the masticatory muscles, particularly the
masseter muscle.
•Bruxism may give rise to facial pain and headache.
BRUXISM
m

LIP BITING
Normally the lower lip at rest covers the lower 1/3 or
¼ of the crowns of upper incisors .
When the upper lip is short, habitual lip closure is
difficult and may contribute to functional
chewing, swallowing, speech etc. and non functional
contacts between upper teeth and lower lip.
Instead of exerting a light continuous force on the
labial segments of upper anterior teeth, the lower lip
cushions against the lingual surfaces and is often
implicated as the principle etiological factor in
labially tipped upper incisor.
m

Etiology of malocclusion/certified fixed orthodontic courses by Indian dental academy

Etiology of malocclusion/certified fixed orthodontic courses by Indian dental academy

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