Etiology of Malocclusion: Understanding the Causes

ETIOLOGY OFETIOLOGY OF
MALOCCLUSIONMALOCCLUSION
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Etiology-Etiology-
Etia – causeEtia – cause
Logy – ScienceLogy – Science
Scientific study of the causeScientific study of the cause
Malocclusion-Malocclusion-
Malocclusion can be defined as a significant deviation
from what is defined as normal or ideal’s occlusion.
IntroductionIntroduction

 The term “ NORMAL OCCLUSION “ is arbitrary but is
generally accepted to be class I molar relationship with
good alignment of all teeth.

 Many components are involved in normal occlusion.
Most important are
1. The size of maxilla
2. The size of the mandible (both ramus and body)
3. The factors which determine the relationship between
the two skeletal bases such as cranial base and
environmental factors
4. Arch form
5. Size and morphology of the teeth
6. No. of teeth present
7. Soft tissue morphology and behavior, lips, tongue and
peri-oral musculature

 The understanding of a disease is incompleteThe understanding of a disease is incomplete
without total knowledge of its causation.without total knowledge of its causation.
 Without knowledge of etiology neither prophylaxis norWithout knowledge of etiology neither prophylaxis nor
specific treatment is possiblespecific treatment is possible

 Malocclusion is a major developmental problem.Malocclusion is a major developmental problem.
 Kelly and Harvey report that only 9% of American youthsKelly and Harvey report that only 9% of American youths
aged 12 to 17 years have virtually classic normalaged 12 to 17 years have virtually classic normal
occlusion and that orthodontic treatment wouldocclusion and that orthodontic treatment would
measurably improve the occlusion of 55% of themeasurably improve the occlusion of 55% of the
adolescent population.adolescent population.
 The high prevalence is a major heath care concern, andThe high prevalence is a major heath care concern, and
it is only natural to be interested in the causes ofit is only natural to be interested in the causes of
malocclusion.malocclusion.

Epidemiology of malocclusionEpidemiology of malocclusion
Proffit WR; 3rd
ed.

 Prevalence of malocclusion is higher in developed countriesPrevalence of malocclusion is higher in developed countries
as compare to developing countries.as compare to developing countries.
 Indians have more tendency for class II malocclusion.Indians have more tendency for class II malocclusion.
 Netherlands, and Kenyans have more tendency for class IIINetherlands, and Kenyans have more tendency for class III
malocclusion.malocclusion.
Epidemiology of malocclusionEpidemiology of malocclusion

 The prevalence of malocclusion among Indian childrenThe prevalence of malocclusion among Indian children
has been reported to be as low ashas been reported to be as low as 19.6% in Punjab19.6% in Punjab byby
Miglani D.S. et al inMiglani D.S. et al in 19651965 and as high asand as high as 90% in Delhi90% in Delhi byby
Sidhu S.S. inSidhu S.S. in 1968.1968.
Epidemiology of malocclusion inEpidemiology of malocclusion in
IndiaIndia

MALOCCLUSION STUDIES IN INDIA

The Orthodontic Equation:
 The orthodontic equation elaborated.(from Dockrell R:
classifying etiology of malocclusion. Dent Rec 1952;
72:25.)

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 an osseous dysplasia.

Muscular Or Functional Crossbite
 Midline do 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.

Dental Type CrossbiteDental 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

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:
1. White and Gardiner’s classification.
2. Salzmann’s classification.
3. Moyer’s classification.
4. Graber’s classification.

White & Gardiner’s Classification:
This was one of the first attempts to classify malocclusion.
A. Dental Base Abnormalities:
1. Anterio-posterior mal-relationship.
2. Vertical mal-relationship
3. Lateral mal-relationship
4. Disproportion of size between teeth and base
bone.
5. Congenital abnormalities.

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.

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

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.
Salzmann’s Classification:

B. POSTNATAL:
1. DEVELOPMENTAL:
i. 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

B. POSTNATAL:
ii. LOCAL DENTOFACIAL:
a. Birth injuries of the head, face, jaws
b. Micrognathia or macrognathia
c. Microglossia or macroglossia
d. Abnormal frenum labii
e. Facial hemiatrophy
f. Anomalies of tooth development and eruption

2. FUNCTIONAL:
i. GENERAL:
a. Muscular hyper or hypotonicity
b. Neurotrophic disturbances
c. Postural defects of the tongue and jaws
d. Masticatory and respiratory disturbances
ii. LOCAL:
a. Premature loss or prolonged retention of deciduous
teeth
b. Loss of proximal contact following tooth loss
c. Temporomandibular articulation disturbances
d. Muscular hypo or hyperactivity

3. ENVIRONMENTAL OR ACQUIRED:
i. GENERAL
a. Diseases can affect the dentofacial tissues directly or indirectly
b. Radiation
ii. LOCAL:
a. Eruption anomalies
b. Premature loss or prolonged retention of deciduous teeth
c. Loss of permanent teeth
d. Harmful dentofacial pressure habits
e. Trauma
f. Infection
g. Temporomandibular disturbances
h. Periodontal disease

Prenatal Postnatal
Genetic
Differentiative
congenital
Developmental
Functional
Environmental
Salzmann’sSalzmann’s diagrammatic representation of the interdependence of thediagrammatic representation of the interdependence of the
etiologic factors in malocclusionetiologic factors in malocclusionwww.indiandentalacademy.comwww.indiandentalacademy.com

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

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
MOYER’S CLASSIFICATION:

GRABER’S CLASSIFICATION:
Divide the etiologic factors into two groups:
General factor
Local factor

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
GRABER’S CLASSIFICATION:GRABER’S CLASSIFICATION:
GENERAL FACTORS

5. Dietary problem ( nutritional deficiency )
6. Posture
7. Trauma and accident
8. Habits
 Abnormal suckling
 Thumb and finger sucking
 Tongue thrusting
 Lip and nail biting
 Abnormal swallowing habits (improper deglutition)
 Mouth breathing
 Speech defects
 Bruxism
GENERAL FACTORS

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

General Factors
HEREDITY:
 Transmission of character from one generation to theTransmission of character from one generation to the
otherother
- Joseph Adam – 1847- 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.

Mode of inheritance-Mode of inheritance-
Mendelian inheritance-Mendelian inheritance-
 Autosomal recessiveAutosomal recessive
 Autosomal dominantAutosomal dominant
 X linked and Y linked conditions.X linked and Y linked conditions.
General Factors
HEREDITY:

Autosomal recessive inheritance-Autosomal recessive inheritance-
 Traits that are manifest only when mutations are present in bothTraits that are manifest only when mutations are present in both
copies of gene are recessive traits.copies of gene are recessive traits.
 If a gene causing a recessive trait is on one of the autosomes, theIf a gene causing a recessive trait is on one of the autosomes, the
trait is autosomal recessive.trait is autosomal recessive.
 Autosomal recessive trait tend to occur more frequently in isolatedAutosomal recessive trait tend to occur more frequently in isolated
populations or in cases of consanguinity.populations or in cases of consanguinity.
 The parents of affected individuals are usually unaffected.The parents of affected individuals are usually unaffected.
 Recurrences between siblings are common.Recurrences between siblings are common.
General Factors
HEREDITY:

 Seen in both males and females in equal numbers.Seen in both males and females in equal numbers.
 The chance of having an affected child is 25% for eachThe chance of having an affected child is 25% for each
pregnancy resulting from mating between two heterozygouspregnancy resulting from mating between two heterozygous
carriers of an autosomal recessive condition.carriers of an autosomal recessive condition.
 The other possibilities are 50%that a child will be a carrier of aThe other possibilities are 50%that a child will be a carrier of a
single copy of the mutation and 25% that the child will besingle copy of the mutation and 25% that the child will be
noncarrier.noncarrier.
 This is because each parent has an approximately equalThis is because each parent has an approximately equal
probability of passing on either the normal or abnormal allele.probability of passing on either the normal or abnormal allele.
General Factors
HEREDITY:

Autosomal dominant inheritance-Autosomal dominant inheritance-
 In autosomal dominant disorders, heterozygous individuals have aIn autosomal dominant disorders, heterozygous individuals have a
recognizable phenotype.recognizable phenotype.
 Homozygous individuals also show the phenotype, but may be moreHomozygous individuals also show the phenotype, but may be more
severely affected.severely affected.
 Pedigrees will frequently show that parent is affected.Pedigrees will frequently show that parent is affected.
 Trait is transmitted by an affected person to half his children on anTrait is transmitted by an affected person to half his children on an
averageaverage
 The number of affected males and females is approximately equalThe number of affected males and females is approximately equal
 Two affected individuals may have affected and unaffected childrenTwo affected individuals may have affected and unaffected children
since each parent would have one normal and one abnormal genesince each parent would have one normal and one abnormal gene
General Factors
HEREDITY:

X-linked inheritance-X-linked inheritance-
 Refers to conditions caused by genes on the X chromosome.Refers to conditions caused by genes on the X chromosome.
 Many X-linked recessive conditions and a few X-linkedMany X-linked recessive conditions and a few X-linked
dominant conditions.dominant conditions.
 If a mutation occurs in an X-linked recessive gene, a female isIf a mutation occurs in an X-linked recessive gene, a female is
likely to have mild or no effects, because female inherit twolikely to have mild or no effects, because female inherit two
copies of X chromosome.copies of X chromosome.
 A male who inherits the gene is likely to be more severelyA male who inherits the gene is likely to be more severely
affected because he has only one copy of a geneaffected because he has only one copy of a gene
General Factors
HEREDITY:

 Affected males pass the gene to 100% of theirAffected males pass the gene to 100% of their
daughters.daughters.
 There is no father-to-son transmission because fathersThere is no father-to-son transmission because fathers
do not give an X chromosome to their sons.do not give an X chromosome to their sons.
General Factors
HEREDITY:

X linked dominant inheritance-X linked dominant inheritance-
 It is rare with a few disorders.It is rare with a few disorders.
 Characterized by having all the daughters of affectedCharacterized by having all the daughters of affected
males inherit the disorder.males inherit the disorder.
 Sons of affected males never inherit the disorder,Sons of affected males never inherit the disorder,
because they receive the Y chromosome from the father.because they receive the Y chromosome from the father.
 Affected females can transmit the disorder to offspring ofAffected females can transmit the disorder to offspring of
both sexes.both sexes.
General Factors
HEREDITY:

Multifactorial inheritance-Multifactorial inheritance-
 Some human disorders result from an interaction ofSome human disorders result from an interaction of
multiple genes with environmental influences.multiple genes with environmental influences.
 Cleft lip and palate demonstrate a multifactorialCleft lip and palate demonstrate a multifactorial
inheritance.inheritance.
General Factors
HEREDITY:

General Factors
HEREDITY:
 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

General Factors
HAPSBURG JAWHAPSBURG JAW

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

General Factors

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

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

 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

 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

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.

Breeding experiment with animal by
Professor Stockard
 Demonstrated that severe malocclusions could be developed by
crossing morphologically different breeds, more from jaw
discrepancies than from tooth size – jaw size imbalances.
 Confirm 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.

 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

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

 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

 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, thought 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

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
established 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.

Classical Method Is To Study FamilyClassical Method Is To Study Family
Members: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.

Classical Method Is To Study FamilyClassical Method Is To Study Family
Members: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)

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

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

 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

 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

 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

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

Congenital Defects
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

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 where as
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 familiar history of this
deformity.

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 palat
 Rubella virus
Etiology

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

Etiology
MULTIFACTORIAL ETIOLOGY:
 Recent studies have shown that the etiology of cleft lip and
palate cannot be attributed solely to either genetic or
environmental factors. It seems to involve more than one
factor.
 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 environment
factors may not by themselves cause clefts

Incidence:
 Cleft lip & palate are common congenital malformations.
 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 in2500
 In the USA, one child in every 700 live births is afflicted.

Incidence:
 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.

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.

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)

 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)

 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.

Unilateral Cleft of the
lip and alveolus
Bilateral Cleft of the
lip and alveolus

Cleft lip and cleft palate:
 May be complete or incomplete.
 May be 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.

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)

BCLP patients tend to have-BCLP patients tend to have-
 Smaller mandiblesSmaller mandibles
 Mandible showed a vertical growth pattern, with anMandible showed a vertical growth pattern, with an
increased mandibular plane inclinationincreased mandibular plane inclination
 Increase in lower anterior facial height.Increase in lower anterior facial height.
 These are mandibular morphologic characteristics thatThese are mandibular morphologic characteristics that
are also found in unilateral CLP and isolated CP.are also found in unilateral CLP and isolated CP.
(AJODO,1998,AUG)

Complete unilateral
cleft lip and palate
Incomplete unilateral

Complete bilateral
Incomplete bilateral

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, 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.

Isolated Cleft palate:
 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.

Cleft of the uvulae Cleft of the soft
palate and uvulae
Isolated cleft of the
hard and soft
palate

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.

Submucous Cleft palate

The problems associated with cleft lip and/ palate patients:
DENTAL:
 Multiple missing teeth (most commonly the maxillary lateral
incisor).
 Mobile premaxilla.
 Anterior &/ posterior cross-bites.
 Ectopically erupting teeth.

DENTAL:
 Impacted teeth.
 Supernumerary teeth.
 Poor alignment of the teeth often predisposes to poor oral
hygiene.
 Multiple decayed tooth.

Cleft palate with congenital absence of lateral
incisor in cleft area and three missing second
premolars.

ESTHETIC:
 The patients with un-repaired clefts are 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 lips.

The problems associated with cleft lip and/ palate-
PYSCHOLOGICAL:
 The disfigurement caused by the condition is enough to
cause psychological stress for the patient and the family.

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 it the speech.
 Also if the maxilla is underdeveloped the space for the tongue
gets decreased and the speech is likely to get affected.

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..

Cerebral Palsy:
 Cerebral palsy is a paralysis or lack of muscular co-
ordination attributed to an intracranial lesion.
 It is most commonly considered to be the result of a birth
injury.
 CP is also caused by a broad group of development,
genetics, metabolic, infectious, ischemic and other
acquired etiology.
 CP is often associated with epilepsy, abnormality with
speech, vision.

Cerebral Palsy:
 Effects of this neuromuscular disorder may be seen in
the integrity of the occlusion.
 The uncontrolled or aberrant activities upset the muscle
balance that is necessary for the establishment and
maintenance of the normal occlusion.

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.

 Bizarre facial asymmetries with uncorrectable dental
malocclusion because of growth restriction on the
affected side, may be created if this problem is not
treated fairly early.
Preoperative TorticollisPreoperative Torticollis Postoperative TorticollisPostoperative Torticollis

Torticollis:
Other physical pictures 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.

 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.

 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” .

 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.

 Cleidocranial dysplasia:
• 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

 Cleidocranial dysplasia:
 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.

Cleidocranial dysplasia

Prolonged retention of deciduous teeth. Supernumerary Teeth

Highly vaulted and narrow palate

 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 bossae
• Short maxilla
• High palatal arch
• Saddle nose
• Mulberry molars
• Relative protuberance of mandible

• Rhagades
• Pathognomonic of the disease is
the occurrence of Hutchinson’s
triad
-Hypoplasia of the incisor and
molar teeth.
-Eighth nerve deafness
-Interstitial keratitis
Congenital (Prenatal) Syphilis:

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

Prenatal Influence:
 The role of prenatal influences on malocclusion is
probably very small.
 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.

Prenatal Influence:
 Occasionally a fetus head is flexed tightly against the chest in
uterus, preventing the mandible from growing forward
normally.
 The result is an extremely small mandible at birth, usually
accompanied by the cleft palate because the restriction on the
displacement of the mandible forces the tongue upwards and
prevents normal closure of the palatal shelves.
Intrauterine molding Distortion and Asymmetry

Prenatal Influence:
 Extremes mandibular deficiency at birth is the Pierre Robin
syndrome.
 Characterized by
1. Cleft palate
2. Micrognathia
3. Glossoptoptosis
 The combination of micrognathia and glossoptosis can lead to
respiratory difficulty.
 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. www.indiandentalacademy.comwww.indiandentalacademy.com

Prenatal Influence:
Severe mandibular deficiency in Pierre Robin Syndrome

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.

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).

Thalidomide provides a classic example.
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,41-43days-
no uterus,45-47 days-no tibia,47-49 days-triphalangeal
thumbs.
Prenatal Influence:

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.

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.

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.

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).

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

6)Alcohol-
•The fetal alcohol syndrome

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&
central nervous system is sensitive to teratogens throughout the
entire pregnancy.
So alcohol,at any time during the pregnancy,has the potential to
cause birth defects. This is why alcohol consumption should be
avoided entirely during pregnancy.
6)Alcohol-

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.
Postnatal Influence

Birth Injury:
 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.
Postnatal Influence

 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.
 Fortunately, the condylar process tends to regenerate well
after early fractures. 75% of children with early fractures of the
mandibular condylar process have normal mandibular growth,
therefore do not develop malocclusions.
 When a problem does arise following condylar fracture, it
usually is asymmetric growth, with the previously injured side
lagging behind.
Postnatal Influence

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

 Extensive Scar tissue: Eg. From a burn, may also
produce malocclusions.
Postnatal Influence

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

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.

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.

PITUITARY PROBLEMS:
Hypopituitarism:
Two basic manifestations of hypopituitarism-
 Dwarfism in children
 Simmonds’ disease in adults

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.

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.

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.

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.

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.

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.

Hyperpituitarism:
 Multiple root resorptions may be seen.

THYROID PROBLEMS:
Hypothyroidism:
 If hypothyroidism occurs in infancy and childhood, cretinism
results.
 If it occurs in the adult, myxedema results.

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.

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

Hypothyroidism

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

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

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.

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.

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

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.

 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.
Parathyroid Hormone Problems:
Primary Hyperparathyroidism:

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.

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

PRIMARY HYPERPARATHYROIDISM
Numerous mandibular radiolucencies

 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

SECONDARY HYPERPARATHYROIDISM
“BROWN” GIANT CELL TUMOR ON THE PALATE

SECONDARY HYPERPARATHYROIDISM
“BROWN” GIANT CELL TUMOR

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, tenany develops
 Aplasia or hypoplasia of the teeth when hypoparathyroidism developed
before the teeth were entirely formed.

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)

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.

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.

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

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.

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.

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.

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

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.

Dietary Problems
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.

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.

ORAL HABITSORAL HABITS

DEFINATIONDEFINATION
It is defined as tendency towards an act that has
become a repeated performance, relatively
fixed, consistent and easy to perform by an
individual.

DEFINATIONDEFINATION
According to Moyers, “All habits are
learned patterns of muscle contraction of a
very complex nature”.

Fins says that habits cause concern because they
cause:
Oral structural changes: Harm, 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.

Classification of HabitsClassification 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 and 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.

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

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.

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

THUMB SUCKING ANDTHUMB SUCKING AND
DIGIT SUCKINGDIGIT SUCKING

BASIC PHYSIOLOGY OF SUCKING REFLEX: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 DIGITTHUMB SUCKING AND DIGIT
SUCKINGSUCKING

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

The 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 stimulate the smooth muscle to contract and squirt
milk into his mouth.
SUCKINGSUCKING

• 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.
SUCKINGSUCKING
• The suckling reflex and the infantile swallow normally disappear
during the first year of life.

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.
SUCKINGSUCKING

SUCKINGSUCKING
BOTTLE FEEDING:
•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.

 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.
SUCKINGSUCKING

Nonphysiological nursing with a
conventional nipple
•Mouth is propped open unduly.
•Lips 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.

 A minimum of a half hour per nursing interval is
recommended.
 But no hard & fast rule can be established because some
children demand more attention & time, some less depending
on individual make up.
 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.
SUCKINGSUCKING

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 suckingsucking of the thumb, finger or a similarly shaped
objects.
 Vast majority of infants do so during from 6 months to 2 years or
later.
 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.

Recent studiesRecent studies shown thatshown that thumb suckingthumb sucking may bemay be
practiced even duringpracticed even during intra uterineintra uterine life.life.

 According to Gellin -Thumb sucking is defined as
placement of 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.

Almost all normal children 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 began to erupt, however
malocclusion occurs.

It is during the transition from the deciduous to the
permanent arch that much of the damage takes place.
 So during this transition stage that the avoidance of all
abnormal pressure habits is of the utmost importance.
If a child’s sucking habits persist by the time he/she is
36 to 48 months of age, professional
assistance may be warranted to minimize the risk of
malocclusion

Oral habits and primary dentition
Warren J et al. (JADA 2001,dec) concluded that
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.

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

SUCKINGSUCKING
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

SUCKINGSUCKING
 Duration of the habit beyond early childhood is not the
only determinant. Frequency of the habit and intensity
of the habit are 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.

SUCKINGSUCKING
 The intensity of the habit is important.
 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.

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

SUCKINGCSUCKINGC
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.

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.
CKINGCKING

SUCKINGSUCKING
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 alters the
vertical equilibrium on the posterior teeth and as a
result, there is more eruption of posterior teeth than
might otherwise have occurred.www.indiandentalacademy.comwww.indiandentalacademy.com

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

SUCKINGSUCKING
 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.comwww.indiandentalacademy.com

SUCKINGSUCKING

SUCKINGSUCKING
 Unilateral and bilateral cross bites are often
associated with finger habits. ( Warren JJ et al.
Pediatr Dent. 2005 Nov-Dec))
 Flattened mandibular anterior segment:
Abnormal mentalis muscle function and lower lip
activity serve to flatten the mandibular anterior
segment.

SUCKINGSUCKING
 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 cyclewww.indiandentalacademy.comwww.indiandentalacademy.com

SUCKINGSUCKING
 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.

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

SUCKINGSUCKING
Anterior Open
Bite Narrow Constricted
maxillary arch
Posterior Cross Bite

Tongue Thrusting HabitTongue Thrusting Habit
Tongue thrust swallowing defined as placement of the
tongue tip forward between the incisors during swallowing.

 The term tongue thrust is something 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.

 Swallowing is not a learned behavior, but is integrated and
controlled physiologically at subconscious levels.
 So whatever the pattern of swallow, it cannot be considered a
habit in the usual sense.
 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.

Predisposing factors
– Associated with history of finger sucking
– Associated chronic naso respiratory distress
– Mouth breathing
– Tonsillitis or pharyngitis
– Improper bottle feeding
– Macroglossia
– Constricted dental arches

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

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
• Active contractions of the
musculature of the lips.
• Tongue tip 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 esophagus www.indiandentalacademy.comwww.indiandentalacademy.com

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 patternwww.indiandentalacademy.comwww.indiandentalacademy.com

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
•Dorsum of the tongue drops away from
the palatal vault
•Instead of the lips creating firm seal,the
upper lips remains relative functionless
•Mentalis exerts strong forward and upward
thrust of lower lip against lingual surfaces
of maxillary incisors

Classification
1. Simple Tongue Thrust
2. Complex Tongue Thrust

Simple tongue thrust
swallow
(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

Complex tongue thrust
Swallow (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

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.

 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

There are two forms of protracted tongue posture
 Endogenous protracted tongue posture.
 Acquired adaptive tongue posture

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.

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.

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

Complex tongue thrust-
•Defined as a tongue thrust with a teeth apart swallow.
•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.
•Indeed, on occasion, complex tongue thrust-thrusters have no open
bite at all.
•Examination of occlusal casts typically reveals a poor occlusal fit
and instability of intercuspation.
•The incidence of complex tongue thrusting does not diminish as
much with age as does the simple tongue thrust.

•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.

MOUTH BREATHING HABITSMOUTH 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.
• A 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.

• Nasopharyngeal Obstruction
if a nose is obstructed, the work associated with nasal
breathing increases and at a 3.5-4 cm H-2-0/l/min resistance
to nasal airflow, the individual switches to partial mouth
breathing.
 Chronic respiratory infection
 Enlarged tonsils &adenoids
 Nasal polyp or tumor
 Any mechanical obstruction anywhere within the
nasorespiratory system
• Anatomic-
-short upper lip

Classification of mouth breathing:
Obstructive
Habitual
Anatomical

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.

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.

Etiology of Malocclusion: Understanding the Causes

Etiology of Malocclusion: Understanding the Causes

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