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

Etiology of malocclusion

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INDIAN DENTAL ACADEMY

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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


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.


• 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


Epidemiology of malocclusion


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 relationshipthan Africans (4.26% in Nigeria)

• Class III malocclusion is also less prevalent in Indiacompared to USA, Netherlands, and Kenya.


• 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.



MALOCCLUSION STUDIES IN INDIA



The orthodontic equation:

The orthodontic equation elaborated.(from Dockrell

R: classifying etiology of malocclusion. Dent Rec

1952; 72:25.) www.indiandentalacademy.com

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.


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.www.indiandentalacademy.co

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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 teethwww.indiandentalacademy.co

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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.


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.


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


Classification of etiology of malocclusion cont…

• Salzmann‘s diagrammatic representation of the etiologic factors in malocclusion

Genetic Environmental

Developmental

Congenital Functionalwww.indiandentalacademy.co

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Salzmann’s Classification

A. PRENATAL:

1. Genetic: malocclusion transmitted by genes, mayor may not be evidence at birth.

2. Differentiative: malocclusion that areinborn, engrafted on the body in the prefunctionalembryonic developmental stage, can besubdivided into—

i. General or constitutional: effect the body as awhole.

ii. Local: effect the face, jaws and teeth only.

3.. Congenital: can be hereditary or acquired but existing at birth.


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.


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


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 hyperactivitywww.indiandentalacademy.co

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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 malocclusionwww.indiandentalacademy.co

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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


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


GRABER’S CLASSIFICATION:

Divides 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

GENERAL FACTORS


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


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 restorationwww.indiandentalacademy.co

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General FactorsHEREDITY:

• Transmission of character from one generation to the other

- Joseph Adam – 1847

• There is a definite genetic determinant thatinfluences the ultimate accomplishment ofdentofacial morphology.

• These genetic determinants may be modifiedby prenatal and postnatal environment, byphysical entities, by pressures, abnormalhabits, nutritional disturbances and idiopathicphenomena.


Mode of inheritance-

Mendelian inheritance-

• Autosomal recessive

• Autosomal dominant

• X linked and Y linked conditions.

General Factors

HEREDITY:


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 FactorsHEREDITY:


• 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.


• 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.


• 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.


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


• 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


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


• 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


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


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


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 .


General Factors

HAPSBURG JAWwww.indiandentalacademy.co

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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


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 ofspecific 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. 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.


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


AchondroplasiaDeficient 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, 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


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.


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)


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 moresimilarities to their parents than girls. Facialskeletal structures were more frequentlytransmitted from mother to sons than frommother to daughters.

Hunter et. al. (1970) found genetic correlationto be strongest between father andchildren, especially in mandibular dimensions.There was a significant relation in facial heightbetween 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



GRABER’S CLASSIFICATION:

Divides 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

GENERAL FACTORS


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


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


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.


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



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:

• 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



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 highestfrequencies, 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.



• 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.



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




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:

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.



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

• 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)



Complete unilateral cleft lip and palate

Incomplete unilateral cleft lip and palate



Complete bilateral cleft lip and palate

Incomplete bilateral cleft lip and palate



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.



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:

1. DENTAL:

Multiple missing teeth (most commonly the maxillary lateral incisor).

Mobile premaxilla.

Anterior &/ posterior cross-bites.

Ectopically erupting teeth.



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.



2. ESTHETIC:

• Badly disfigured.

• Even following the closure of the cleft, themaxilla remains under-developed withcompromised esthetics.

• Deformity of the normal nasal architecture iscommonly seen in individuals with cleft lip.



3. PYSCHOLOGICAL:

• Psychological stress



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.



Predisposing factors

• Increased maternal age: increased risk

• Racial: Some races are more susceptible to clefts than others .

Mongoloid show the greatest percentage of incidence.


Mandibular cleft


Bilateral maxillary cleft lip


Oblique facial cleft


Median cleft lip


Lateral facial cleft


Median cleft lip and nose


Other Congenital Defects

Although cleft lip and palate is the most commoncongenital defects to be of concern to the dentist asfar as creation of malocclusion is concerned, butsome problems such as-

Cerebral palsy

Torticollis

Cleidocranial dysostosis

Congenital syphilis

Congenital Defects Cont..


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, ischaemic and other acquired etiology.

Cerebral palsy is often associated with epilepsy, abnormality with speech, vision and intellect.


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.


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.




Torticollis cont…

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

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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.


4.Cleidocranial Dysplasia

Congenital disease of unknown etiology which isoften but not always hereditary.

Transmitted as an autosomal dominant trait.

It is characterized by abnormalities of theskull, teeth, jaws and shoulder girdle as well asby occasional stunting of the long bones.



Delayed ossification of the skull, excessively largefontanelles and delayed closing of the sutures.

The fontanelles may remain open until adulthoodbut the sutures often close with interposition ofwormian bones.

Bossing of the frontal, parietal and occipitalregions give the skull a large globular shape withsmall face.

Characteristic skull abnormalities – ― ArnoldHead‖ .



Sagittal suture is characteristically sunken, givingthe skull a flat appearance.

Paranasal sinuses are underdeveloped andnarrow.

The head is brachycephalic.

Complete to partial absence or even a simplethinning of one or both clavicles is seen.



• 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



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



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



• Rhagades

• Pathognomonic of the disease is the occurrence of Hutchinson‘s triad

-Hypoplasia of the incisor and molar teeth.

-Eighth nerve deafness

-Interstitial keratitis



Environment

Prenatal Postnatal

(Intrauterine molding, maternal diet, maternal metabolism, Trauma, German measles etc.)

(Birth injury, TMJ injury etc).

General Factor


Prenatal Influence:

Small role.

Intrauterine molding pressure against thedeveloping face prenatally can lead todistortion of rapidly growing areas.

Eg. On rare occasions an arm is pressed acrossthe face in uterus, resulting in severe maxillarydeficiency at birth.

General Factor


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


Result – extremely small mandible atbirth, usually accompanied by the cleftpalate .

Intrauterine molding Distortion and Asymmetrywww.indiandentalacademy.com

Prenatal Influence:

Pierre Robin Syndrome considered a sporadicor non genetic condition with a very lowrecurrence risk in the family.

Extremes mandibular deficiency at birth .

General Factor


• 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.


Pierre Robin Syndrome (Robin Anomalad)

• Glossoptosis

• Micrognathia

• Cleft palate

The combination of micrognathia and glossoptosis can lead to

respiratory difficulty.www.indiandentalacademy.co

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Prenatal Influence

Severe mandibular deficiency in Pierre Robin Syndrome

General Factor


Prenatal Influence:

So, although abnormal fetal posture have causedmarked cranial or facial asymmetries that areapparent at birth, but after the first year of life mostof these have disappeared. Thus, the deformity istemporary.

Maternal nutritional disturbances such as folic aciddeficiency can produce malocclusions.

Minor injury to the mother is unlikely to affect thechild, since the fetus is well cushioned by the amnioticfluid.

German measles cause gross congenital deformitiesincluding malocclusion.

General Factor


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


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


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


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


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


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


5)Carbamazepine-

•It is an anticonvulsant drug.

•Exposure to carbamazepine produces malformations similar to those described with the foetal hydantoin syndrome.

General Factor


6)Alcohol-

•The fetal alcohol syndrome

General Factor


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


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.


Hypoplasia of facial

bones

Malformation of

external ear


High palate

Fistula

Birdlike or fishlike face


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 regionwww.indiandentalacademy.co

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Failure of closure

result in neural tube

defect


Encephalocele :

- Failure to complete

the neural tube

closure or membrane

fusion at closure

points within the

cranial region


Spina bifida cystica: -

neural tube defect at

spinal cord and at

covering at various level.


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


Postnatal influence

• High forceps delivery

• Temporomandibular joint has been damaged.


• 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


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.


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


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


Predisposing metabolic climate and disease

Endocrine Imbalance Metabolic disturbances Infectious Diseases(Poliomyelitis etc.)

General Factor


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.


General FactorENDOCRINE DISTURBANCES:

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

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General Factor

ENDOCRINE DISTURBANCES:PITUITARY PROBLEMS:

HYPOPITUITARISM

Two basic manifestations of hypopituitarism-

• Dwarfism in children

• Simmonds‘ disease in adults


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.


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.


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.


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.


General Factor

THYROID PROBLEMS

HYPOTHYROIDISM:

If hypothyroidism occurs in infancy and childhood, cretinism results.

If it occurs in the adult, myxedema results.


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.


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.


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.


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 teethoccurs earlier than normal.

Eruption of the permanent teeth is greatlyaccelerated.

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.

General FactorPARATHYROID 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 symptomof 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


General Factor

HYPOPARATHYROIDISM

Caused by elimination of parathyroid glands which may bedue to surgical removal or rarely due to congenital absence.

Blood chemistry shows a low concentration of serum calciumand a high concentration of serum phosphorus.

When serum calcium level falls to 6 to 7 mg/dl, tetanydevelops

Aplasia or hypoplasia of the teeth when hypoparathyroidismdeveloped before the teeth were entirely formed.


SEX HORMONES

•Sex hormones (oestrogen and androgen) play an importantrole in maintenance of bone volume, a reduction causes osteoporosis.

•Sex hormones affect craniofacial bone development.

•It has been reported, that the suppression of sex hormonesecretion during the pubertal growth phase inhibits craniofacialgrowth, particulary mandibular growth, and results in reducedcraniofacial development

European Journal of Orthodontics 28 (2006)


METABOLIC DISTURBANCES

Acute febrile diseases are capable of affecting notonly the general health of the child but might alsoaffect the dentition and its surrounding hard and thesoft tissues.

Temporarily they are capable of slowing downgrowth and may cause delayed tooth eruption.

Usually if the severity and duration is not prolongedthe child is able to recoup lost time and catch upgrowth is possible.

General Factor


INFECTIOUS DISEASES

Disease with paralytic effect, such aspoliomyelitis are capable of producingmalocclusions.

Osteomyelitis

The adult afflicted with acute suppurativeosteomyelitis is usually in severe pain.

The teeth in the area of involvement are looseand sore.

General Factor


INFECTIOUS DISEASES

German Measles: (Rubella)

Enamel hypoplasia

A high caries incidence

Delayed eruption of deciduous teeth


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


Dietary Problems

Vitamin A deficiencies

In the developing tooth that is deficient in vitamin A, theodontogenic epithelium fails to undergo normalhistodifferentiation and morphodifferentiation, resulting inthe distortion of the shape of the teeth.

Since the enamel forming cells are disturbed, enamelmatrix is arrested &/or poorly defined so that calcification isdisturbed and enamel hypoplasia results.


Vitamin A deficiencies

Eruption rate is retarded and in prolonged deficiencieseruption ceases.

The alveolar bone is retarded in its rate of formation.

The gingival epithelium becomes hyperplastic & inprolonged deficiencies shows keratinization. This tissue iseasily invaded by bacteria that may cause periodontaldisease.


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.


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 HABITS

General Factor


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)


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.


Classification of Habits

Habits in relation to malocclusion perhaps should be classified as:

1.Useful2.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.



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.


• Intentional

• Unintentional

Intrinsic

Extrinsic



• 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



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


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.


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‖


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.


THUMB SUCKING AND DIGIT SUCKING

According to GellinThumb sucking is defined as the placement of the thumb or one or more fingers in varying depths into the mouth.

According to MoyersThumb sucking is defined as the repeated and forceful sucking of thumb with associated strong buccal and lip contractions.


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.



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.


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.


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.


During the very first weeks of life, thumbsucking are typically related to feedingproblems.

Some children suck their thumb

as a teething device during the difficulteruption of a primary molar.

for the release of emotional tensions withwhat they are unable to cope.

as an attention-seeking weapon.


• 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.


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 suckingduration also had detectable differences fromthose with minimal habit duration.

•Implications: It may be prudent to revisitsuggestions that sucking habits continued to aslate 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 B37www.indiandentalacademy.co

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There are 2 forms of sucking:

• Nutritive form

• Non-nutritive form



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.



• 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 disappearduring 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.



•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


• 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.



Nonphysiological nursing with aconventional 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.


• 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.



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.


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


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.



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



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.



Intensity

In some children the sucking can be heard in thenext room. The perioral muscle function andfacial contortions are easily visible.

In others the thumb habit is little more than apassive insertion of the finger in the mouth withno apparent buccinator activity.



OTHER FACTORS

1. Position of thumb or fingers in the mouth.

2. Associated contraction of the muscles of the lips and cheeks.


“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.


EXCESSIVE digit sucking can set up abnormal

forces on the oral cavity and surrounding structures.


Clinical manifestation

• Anterior open bite

• Proclination of maxillary anteriors

• Increased overjet

• Posterior crossbite

• Hypotonic upper lipand hypertonic mentalis activity.



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.



Anterior Open Bite: (Cozza P et al, Am J Orthod Dentofacial

Orthop. 2005 Oct)

• It is associated by a combination of interferencewith normal eruption of incisors and excessiveeruption of posterior teeth.

• When a thumb or finger is placed between theanterior teeth, the mandible must be positioneddownward to accommodate it.

• The interposed thumb directly impedes incisoreruption.

• At the same time, the separation of jaws alter thevertical equilibrium on the posterior teeth and as aresult, there is more eruption of posterior teeth.


Anterior Open Bite:

• Because of the geometry of jaw, 1mm ofelongation posteriorly opens the bite about 2mm anteriorly, so this can be a powerfulcontributor to the development of anterioropen bite


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

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Unilateral and bilateral cross bites areoften associated with finger habits.

( Warren JJ et al.Pediatr Dent. 2005 Nov-Dec)



Retardation of deglutitional maturation

• Increase in over-jet makes normal swallowingprocedures increasingly difficult.

• Instead of the lips containing thedentition, during deglutition, the lower lipcushions to the lingual of the maxillaryincisors, forcing them farther forward.

• Lip muscle aberrations are often assisted by acompensatory tongue thrust during theswallowing act.

• So the infantile suckle-swallow continues, or thetransitional period is greatly prolonged with amixture of infantile and mature swallowingcycle.



Thumb sucking habit can create a class IImalocclusion.

Thumb-suckers may be found to have anarrower nasal floor and high palatal vault.

The maxillary lip becomes hypotonic and themandibular lip becomes hyperactive.



Anterior Open BiteNarrow Constricted maxillary arch

Posterior Cross Bite



Tell-tale callus on the back of the fingeror thumb are often present.



TONGUE THRUSTING

• Definition:-

placement of the tongue tip forward between the incisors during swallowing.


Tongue Thrusting Habit

The term tongue thrust is a misnomer.

Since it implies that the tongue is forcefullythrust forward.

But individuals who place the tongue tip forwardwhen they swallow usually do not have moretongue force against the teeth than those whokeep the tongue tip back.


Swallowing is not a learned behavior, but isintegrated and controlled physiologically atsubconscious levels.

Individuals with an anterior open bite place thetongue between the anterior teeth when they swallowwhile those who have a normal incisor relationshipusually do not and it is tempting to blame the openbite on this pattern of tongue activity.



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 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.


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


NORMAL SWALLOWING

•Incisors are momentarily in contact

•Tip of the tongue touches the lingualinterdental 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, theupper 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


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.


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



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


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.


FLETCHER has classified etiological factors as:

1. Genetic factors

2. Learned behavior

3. Maturational

4. Mechanical restrictions

5. Neurological disturbance

6. Psychogenic factors


Classification

1. Simple Tongue Thrust

2. Complex Tongue Thrust



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

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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


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


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.


•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.


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 protracted 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



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


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.


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.


MOUTH BREATHING HABITS

ETIOLOGY• Humans are primarily nasal breathers but everyone

breathes partially through the mouth underphysiologic conditions.

• The most prominent being an increased need for airduring exercise.

• At rest, minimum airflow is 20-25 L per minute, butheavy mental concentration or even normalconversation lead to increased airflow and transitionto partial mouth breathing.

• For the average individual there is a transition topartial oral breathing when ventillatory exchangerates above 40-45L/min are reached.

• At maximum effort 80 or more L/min of airneeded, about half of which is obtained through themouth.


• Nasopharyngeal Obstruction

• Allergies

• Chronic respiratory infection

• Enlarged tonsils &adenoids

• Nasal polyp or tumor

• Any mechanical obstruction anywhere within thenasorespiratory system

• Deviated nasal septum



• Hypertrophy

• Anatomic-short upper lip

• Abnormal development of nasal cavity

• Localized benign tumor

• Narrow nasal passage associated with narrow maxilla

• Fibrous dysplasia


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 whocontinually breathes through his mouth by forceof habit, although the abnormal obstruction hasbeen removed.

Anatomical mouth breather is one whose shortupper lip does not permit complete closurewithout undue effort.



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-facialequilibrium. There is an unrestricted buccinator activity These postural changes influence the position of the teeth & also the growth the jaws.



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 bitewww.indiandentalacademy.co

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• 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.


•Narrower maxillary dental arch(J Clin Pediatr Dent. 2004

Summer;28(4)



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 ofmouth breathing is to establish how much of thetotal airflow goes through the nose and howmuch through the mouth, which requires specialinstrumentation to simultaneously measuresnasal and oral airflow.


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 overthe upper lip below nostrils.

• If the cotton flutters down, it is a sign of nasalbreathing.

• This test can be used to determining unilateralnasal blockage.

Other methods of diagnosis


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.


BRUXISM

Bruxism is the habitual grinding of the teeth

either during sleep or as an unconscious habit

during waking hours.


ETIOLOGY

Nadler (1957) gave the following causes of bruxism-

•Local

•Systemic

•Psychologic

•Occupational

BRUXISM


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


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


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


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.


In skeletal CLASS II the lower lip tends to be further back than upper lip.

If the skeletal discrepancy is not severe, the lower lip may procline the upper incisor so that the occlusal relationship is more severely CLASS II than the skeletal discrepancy .

In other instances, with skeletal CLASS II, the lower lip functions entirely in front of the upper incisors

causing them to be retroclined into

CLASS II division 2 incisor relationship.


The Lip Biting habit is as follows:

• The first motion of the act consists of wetting the lips with the tongue.

• The lower lip is turned inward and the tongue goes back into the mouth.

• As the tip of the tongue passes the incisal edges of the maxillary incisors, the lower lip is caught between the maxillary and mandibular teeth and pressure is exerted as the lip slowly returns to its normal position.


• The force produced by the lip as it slides around the teeth moves the maxillary incisor labially and mandibular incisors lingually.

• The deformity reaches its maximum when the discrepancy between the maxillary and mandibular incisors becomes equal to the thickness of the lower lip.


LIP SUCKING AND LIP BITING

CLINICAL FEATURES

• Labioversion of upper incisors

• Open bite

• Linguoversion of mandibular incisors

• Cracking of lips


Lip biting most often involves the lower lip which is turned

inwards and pressure is exerted on the lingual surfaces of the

maxillary anteriors.

LIP SUCKING AND LIP BITING


NAIL BITING

Minor tooth irregularities such as rotation, wear of

incisal edge and minor crowding.


CHIN PROPPING HABIT

• Extrinsic pressure, unintentional habit

• Causes deep anterior closed bite

• Mandibular retraction


FACE LEANING HABIT

• Extrinsic pressure, unintentional pressure habit

• Lateral pressure from face leaning cause a lingual movement of maxillary teeth on that side mandible being less affected


CONCLUSION

• Mechanical orthodontists may have the ability to move the teeth , but their success in retaining them and preventing relapse is not nearly so great as that of orthodontist who not only are mechanical but also understand the laws and principles of growth and development.

• Teeth and jaws are into functional occlusion by removing interferences , and then has a greater success in retaining them, reducing the number of relapses by eliminating the factors which contribute to the cause of malocclusion.


THANK

YOU!!!


• One of the major causes of malocclusion is size discrepancy between the arch & the teeth.

• Anomalies in tooth size - Microdontia

Macrodontia

LOCAL FACTORS

ANOMALIES OF TOOTH SIZE:


MICRODONTIA: Teeth which are smaller than normal.

True generalized microdontia: All the teeth are smaller than normal.

Relative generalized microdontia: Normal or slightly smallerthan normal teeth are present in the jaws that are somewhat

larger than normal and therefore is an illusion of truemicrodontia.

Microdontia involving only a single tooth is a rather commoncondition.

It affects most often the maxillary lateral incisor (peg lateral)and the 3rd molar.


MACRODONTIA:

It refers to teeth that are larger than normal

True generalized macrodontia: The condition in which all teeth are larger than normal.

Relative generalized macrodontia: presence of normal or slightly larger than normal teeth in smaller jaws which give the illusion of macrodontia.

Macrodontia of single teeth


Occasionally the cingulum is quite pronounced andparticularly with the Japanese, the marginal ridges canbe sharp and well defined, bounding the lingual fossa.

The presence of an exaggerated cingulum or heavymarginal ridges can force the involved teeth labiallyand prevent the establishment of a normal overjet-overbite relationship.

The mandibular 2nd premolar also shows greatvariation in shape and size. It may have an extralingual cusp, which usually increases the mesiodistaldimension.


The size of teeth in largely determined by heredity.

We might assume that there is a greater tendency towards crowding with large teeth than with the smaller teeth. From various research studies, this does not seem to follow.

In the dentition of growing child by Moorrees, severalobservations were made on the size of teeth andmalocclusion. There does not seem to be any correlationbetween tooth size and between spacing and crowdingof teeth.

There may be a variation in tooth size within the sameindividual. Often one maxillary lateral incisor will be ofnormal size and configuration while the other isdiminutive.


SUPERNUMERARY TEETH

Extra teeth above the normal number of 32.

Is usually a supernumerary tooth which erupts at an advanced age that is responsible for what the Newspaper dub, ―a third set of teeth‖.

A frequently seen supernumerary tooth is the mesiodens, palatal to the maxillary incisors, conical in shape and which is one of the main causes of malocclusion.


• Various theories have been advanced to explain the additional teeth.

1. They have been attributed to excessive growth of dental lamina as a result of which an additional tooth germ is given off from the prolongation of the lamina.

Additional teeth have sometimes been regarded as an ―Atavistic Tendency‖ for the typical mammalian dentition is 3 4 1 3 3 1 4 3

3 4 1 3 3 1 4 3


This is now present amongst others in pig, horse etc.

Thus in man and many mammals some of the teeth have been lost especially 4 incisors and 8 premolars.

• If an incisor is lost, it is the more distal one.

• When premolars are lost the loss occurs from before backwards and the reverse order is found if molars are missing.


2. Another explanation of additional teeth is that tooth germ of the normal series has undergone dicotomy. If the division is equal the result is a supernumerary which resembles its neighbour.

If the dicotomy is unequal the additional tooth is malformed and usually conical.

3. The third possibility of the origin of malformed teeth is that they are derived from clumps of epithelium that remain after the breaking up of the tooth band and become activated to tooth formation.


ANODONTIATOTAL ANODONTIA

Total anodontia denotes complete developmental absence of teeth in both dentitions .

Rare condition

Associated with Ectodermal dysplasia of the anhidrotic type

Total anodontia is rare in females, but it is not always recessive and Dahberg states that, it appears in females when one X chromosome is affected.


• In total anodontia of both dentitions there is complete aplasia of the dental lamina.

• In those cases in which the deciduous dentition is present or partially so, the dental lamina has developed and given off the enamel organ for the dentition but furthur development has been interrupted.


PARTIAL ANODONTIA (OLIGODONTIA OR HYPODONTIA)

When one or a number of teeth are absent.

• Hereditary factor

According to a study by Keeler Ten, pedigrees were collected in which there were 23 marriages between normal individuals and individual with one or maxillary first incisors missing or underdeveloped.

In the offspring 38 were normal and 45 had some defect. This defect was inherited as a unit dominant characteristic, even though there was not an exact equality between the normal and affected individuals.


• Some investigators believe cases of missing third molars to be evidence of an evolutionary trend towards fewer teeth.

• Hereditary ectodermal dysplasia may be associated with partial anodontia and in these instances the few teeth that are present may be deformed or misshapen, frequently cone shaped.


• Sperber suggests that viral diseases such as Rubella during the first 6 months of pregnancy may be a causative factor.

• Dower has shown that partial anodontia occurs more frequently in glandular dysfunction and particularly hypothyroidism.

• Occasionally children may have teeth missing in one quadrant or both quadrants on the same side due to X-ray radiation of the face at an early stage.

• Tooth buds are extremely sensitive to X-ray radiation and may be destroyed completely by relatively low dosages.

• Teeth already forming and partially calcified may be stunted by X-ray radiation.


Abnormalities Of Tooth Shape

Fusion:

Fused teeth arise through union of two normally separated toothgerms.

Some physical force or pressure produces contact of thedeveloping teeth and their subsequent fusion.

In some cases the condition has been reported to show ahereditary tendency.

If this contact occurs early, before calcification begins, the twoteeth may be completely united to form a single large tooth.

If the contact of teeth occurs later, when a portion of the toothcrown has completed its formation, there may be union of rootsonly.

The possible clinical problems related to appearance, spacing andperiodontal conditions brought about by fused teeth.


FUSIONwww.indiandentalacademy.co

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Concrescence

• A form of fusion which occurs after root formation has been completed.

• Teeth are united by cementum only.

• Thought to arise as a result of treatment injury or crowding of teeth with resorption of interdental bone so that the two roots are in approximation and become fused by the deposition of cementum between them.


Gemination

Arise from division of single tooth germ by aninvagination with resultant incomplete formation of twoteeth.

The differentiation between gemination and fusion canbe difficult and is usually confirmed by counting thenumber of teeth in an area.

If the bifurcated central incisor is present but the othercentral and both incisors are also present, a bifurcatedcentral incisor is a result of either gemination or lessprobably, fusion with a supernumerary incisor.

Whereas, if the lateral incisor on affected side ismissing, the problem mostly is fusion of the central andlateral incisor buds.


GEMINATION


Twinning

• This term has sometimes been used to designate the production of equivalent structure by division resulting in one normal and one supernumerary tooth.


Talons cusp

• An anomalous structure resembling an eagle's talon, projects lingually from the cingulum area of a maxillary or mandibular permanent incisor.

• It blends smoothly with the tooth except that there is a deep developmental groove where the cusp blends with the sloping lingual tooth surface.

• Composed of normal enamel, dentin and contains a horn of pulp tissue.

• Problems of occlusal accomodation.


• Dilaceration refers to an angulation or a sharp bend or curve, in the root or crown of a formed tooth.

• The condition is thought to be due to trauma during the period in which the tooth is forming, with the result that the position of the calcified portion of the tooth is formed at an angle.

• If distortion of root position is severe enough, it is almost impossible for the crown to assume its proper position for this reason, it may be necessary to extract a severely dilacerated tooth.

Dilaceration


Dens evaginatus: (Leong‘s premolar, occlusal

enamel pearl, evaginated odontoma)

It appears clinically as an accessory cusp or a globuleof enamel on the occlusal surface between the buccaland lingual cusps of premolars

Unilaterally or bilaterally.

Pathogenesis:

Proliferation and evagination of an area of the innerenamel epithelium and subjacent odontogenicmesenchyme into the dental organ during early toothdevelopment.


Dens evaginatus:

Clinical Significance

This extra cusp may contribute to -

- incomplete eruption

- displacement of teeth

-and/or pulp exposure with subsequent infectionfollowing occlusal wear or fracture.


At birth the frenum is attached to the alveolar ridge, with fibres actually running into the lingual interdental papilla.

As the teeth erupt and as alveolar bone is deposited, the frenum attachment migrates superiorly with respect to the alveolar ridge.

Fibers may persist between the maxillary central incisors and in the V-shaped intermaxillary suture.

LOCAL FACTORS

ABNORMAL LABIAL FRENUM


This attachment may well interfere with the normal developmental closure of the spacing in ‗ugly duckling‘ stage.

But existence of a heavy fibrous frenum does not always mean that spacing is present


Spacing between the maxillary central incisors and thepresence of the fibrous tissue attachment such as the labialfrenum provide an excellent ―chicken egg‖ routine forcontroversy which came first?

Fibrous attachment is causative or resultant.

The hereditary component is a major factor in persistantdiastemas. Therefore a check of parents and siblings isadvisable.

Diastema may be due to other factors asMicrodontia, macrognathia, supernumerary teeth (especiallymesiodens), peg laterals, missing lateral incisors, habitssuch as thumb sucking, tongue thrust, and midline cyst.


• In past, thousands of labial frena have been clipped to allow space to close.

• In a large percentage to these cases it is likely that closure would have occurred autonomously with the eruption of the permanent canines.

• In many other instances, due to the lack of recognition of habit problems, tooth size discrepancy, congenitally missing teeth or midline supernumerary teeth, the clipping of the frenum has done little to close the space.

It is sufficient to say here that the mere clipping of the frenum attachment will not solve the diastema problem.

So a thorough examination and differential diagnosis are imperative before the dentist sets out to clip the frenum to confirm whether diastema is present due to abnormal labial frenum or may be due to other factors.


• Frequently during the course of orthodontic therapy the interposed fibres will atrophy, making frenectomy unnecessary.

• Interincisor spacing will close in most cases without any interference is confirmed by Taylor who noted the following figures.

AGE INCIDENCE OF DIASTEMA

6 97%

6-7 88%

10-11 48%

12-18 7%


One diagnostic adjunct that helps to determine the fibrous attachment is the ―Blanche Test‖.

Ordinarily the frenum has migrated sufficiently superiorly by 10 to 12 years of age so that a tug on the upper lip causes no demonstrable change at the maxillary central interdental papilla.

But when a heavy fibrous frenum is present, however a ‗blanching‘ of the tissue just lingual to the maxillary central incisors can be noted. This usually means that fibrous attachment still remains in this area.


PREMATURE LOSS OF DECIDUOUS TEETH

Deciduous teeth serve not only as organs of mastication, but as ‗space savers‘ for the permanent teeth.

Assist in maintaining the opposing teeth at the proper occlusal level.

When a unit within the dental arch is lost, the arch tends to contract and the space close.

Premature extraction of a deciduous second molar will very likely lead to mesial drift of the first permanent molar and blocking of the erupting second premolars.




When a primary 1st molar or canine is lost prematurely, there is also a tendency for the space to close.

This occurs primarily by distal drift of incisors, not up mesial drift of posterior teeth.

If a primary canine or first molar is lost prematurely on only one side, the permanent teeth drift distally only on that side, leading to an asymmetry in the occlusion as well as a tendency toward crowding.



In the maxillary or mandibular anteriorareas, space maintenance for deciduous teeth isseldom necessary in a normal occlusion but withan arch length deficiency or overjetproblem, however, spaces can close rapidly.

The early loss of permanent teeth should beconsidered just as severe a ‗malocclusion maker‘as the loss of deciduous teeth.

The result is shortening of arch length on the sideof the loss, tipping of the contiguousteeth, overeruption of opposing teeth.


Over retained deciduous teeth cause buccal/labial or palatal/lingual deflection in the path of eruption of permanent successors.

A palatally deflected permanent tooth might lead to a cross bite.

The method of control is removal of the deciduous tooth according to the timetable established by the same tooth in the remaining quadrants of the mouth and creating a tract, for the permanent tooth to erupt toward its normal position in the mouth.

LOCAL FACTORS

PROLONGED RETENTION AND ABNORMAL RESORPTION OF DECIDUOUS TEETH


Prolonged retention of deciduous teeth is one of the characteristic signs in a history of hypothyroidism.

Another possible factor is Ankylosis.

Frequently fragments of deciduous roots are retained in the alveolar process.

These fragments, if not resorbed may deflect the permanent tooth in the eruptive path.

Such fragments should be removed, if possible without endangering the adjoining teeth.


DELAYED ERUPTION OF PERMANENT TEETH

Possibility of delayed eruption of permanent teeth may be seen because of :-

Endocrine disorder (such as hypothyroidism).

Presence of a supernumerary tooth or deciduous root (Road block).

Ankylosed deciduous teeth.

Presence of cysts and odontomas.


There is the relative chance of a ―mucosal barrier‖. The heavy mucosa usually deteriorates before the advancing tooth.

Since root formation and eruption go hand-in-hand, the delay in root formation further reduces the eruptive force.

Frequently early loss of the deciduous tooth means early eruption of the permanent tooth.

But occasionally a bony crypt forms in the line of eruption of the permanent tooth, like the mucosal barriers, it effectively bars the eruption of the tooth.

Bony crypt Mucosal barrier


In some cases it may be associated with systemic conditions,

• Rickets

• Cretinism

• Cleidocranial dysplasia


ABNORMAL ERUPTIVE PATH


In the case of inadequate space to accommodate all the teeth, deflection of the erupting tooth may occur.

Presence of a supernumerary tooth.

Retained deciduous tooth or root fragment.

Possible bony barrier.

Ankylosed tooth


A blow to the tooth: Because of blow to the tooth, deciduous incisor may be driven into the alveolar process, it may turn the developing successor in an abnormal direction.

Coronal cysts can also cause abnormal eruptive paths.

Some abnormal eruptive paths are of idiopathic(unknown) origin. A canine or premolar will erupt buccally, lingually, or transposed, with no apparent cause.


• Mechanical interference by orthodontic treatment also can cause a change in eruptive path.

• Early Class II therapy against the maxillary arch to move the maxillary dentition posteriorly can cause abnormal eruption of the upper second permanent molars to erupt into crossbite.



Another form of abnormal eruption is referred to as Ectopic eruption.

Ectopic eruption may generally be considered a manifestation of arch length deficiency.

Frequently the maxillary 1st permanent molar is the offending tooth, causing abnormal resorption of the maxillary second deciduous molar as it erupts beneath the distal convexity of this tooth.


Resorption of central incisor root due to abnormal canine eruption path

A permanent tooth erupting through the alveolar process causes resorption on a contiguous deciduous tooth or permanent tooth, rather than its predecessor.


ANKYLOSIS

Ankylosis is a phenomenon in which a tooth is fixed inits surrounding bone while the contiguous teethcontinue to erupt and shift with growth anddevelopment.

Ankylosis or partial ankylosis is encountered relativelyfrequently during the 6 to 12 years of age.

Ankylosis is probably due to an injury of some sort, asa result of which a part of the periodontal membraneis perforated and a bony ―bridge‖ forms, joining thelamina dura and cementum.


Other causes for ankylosis: Infection, disturbedlocal metabolism or a genetic influence, certainendocrine conditions and congenital diseases likecleidocranial dyostosis.

Clinically the observant sees what appears to bea ‗submerging‘ of the offending teeth. If leftalone, ankylosed teeth can actually be coveredover again by the ever-growing mucosa, and thecontiguous teeth often migrate into thespace, effectively locking the tooth in theprocess.

‗Submerged‘ teeth are deciduous teeth, mostcommonly mandibular 2nd molars.

It prevents their exfoliation and subsequentreplacement by permanent teeth.

.


• Many ankylosed deciduous teeth do not have permanent successors. When the succedaneous tooth is present, it may become impacted and its emergence may be prevented.

• Tooth ankylosis is important to the Orthodontist because the malocclusion associated with it becomes progressively worse.


ANKYLOSED DECIDUOUS SECOND MOLARSSECOND PREMOLAR DEFLECTED TO DISTAL


The diagnosis of ankylosis of a tooth is usuallysuspected clinically and confirmed byroentogenographic examination.

The affected tooth lack mobility even though rootresorption is far advanced.

Upon percussion, an ankylosed tooth imparts acharacteristic solid sound in contrast to thedull, cushioned sound of a normal tooth.

Roentogenographically, at least partial absence of theperiodontal ligament is seen with areas of apparentblending between the tooth root and bone.


• Dr. Biedurman did a study on ankylosis and came up with the following:

1. There seems to be a specificity as to site. Nearly all ankylosed teeth are molars, both deciduous and permanent.

2. There seems to be a specificity as to physiologic time. Most ankyloses take place in the deciduous and mixed dentition.

3. Deciduous teeth become ankylosed far more frequently than do permanent teeth, the ratio being better than 10:1.

4. Lower teeth are ankylosed more frequently than upper teeth more than twice as often.

William Biederman .AJO 1962.www.indiandentalacademy.co

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DENTAL CARIES

Most common local causes of malocclusion.

Caries leads to premature loss of a deciduous orpermanent tooth so that subsequent drifting ofcontinuous teeth, abnormal axialinclination, overeruption, bone loss occurs.

Because of proximal carious lesions that areunrepaired, there is actual loss of arch length.

So it is basic that carious lesions should be repairednot only to prevent infection and loss of teeth but tomaintain the integrity of the dental arches.



IMPROPER DENTAL RESTORATION

An increase in arch length through improperrestoration of one or more carious proximal surfacesmay result in the creation of brokencontacts, rotations.

Poor contacts encourage food packing.

Lack of anatomic detail in restoration of cuspal area ofa tooth can permit elongation of opposing teeth orcreate functional prematurities.

Lack of anatomic detail in restoration of cuspalareas`of a tooth can permit supraeruption of opposingteeth or at the very least, create functionalprematurities and possible tooth guidance foci formandibular shifts


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Date post:	11-Jul-2015
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