Etiology of malocclusion 1/certified fixed orthodontic courses by Indian dental academy

ETIOLOGY OF ETIOLOGY OF MALOCCLUSIONMALOCCLUSION

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INDIAN DENTAL ACADEMYINDIAN DENTAL ACADEMY

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Etiology-Etiology- Etia – causeEtia – cause

Logy – ScienceLogy – Science

Scientific study of the causeScientific study of the cause

Malocclusion-Malocclusion- Malocclusion can be defined as a significant

deviation from what is defined as normal or ideal’s occlusion.

IntroductionIntroduction



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



Many components are involved in normal occlusion. Most important are

1. The size of maxilla2. The size of the mandible (both ramus and body)3. The factors which determine the relationship

between the two skeletal bases such as cranial base and environmental factors

4. Arch form5. Size and morphology of the teeth6. No. of teeth present7. Soft tissue morphology and behavior, lips, tongue

and peri-oral musculature


The understanding of a disease is incomplete The understanding of a disease is incomplete without total knowledge of its causation.without total knowledge of its causation.

Without knowledge of etiology neither Without knowledge of etiology neither prophylaxis nor specific treatment is possibleprophylaxis nor specific treatment is possible



Malocclusion is a major developmental problem.Malocclusion is a major developmental problem.

Kelly and Harvey report that only 9% of American Kelly and Harvey report that only 9% of American youths aged 12 to 17 years have virtually classic youths aged 12 to 17 years have virtually classic normal occlusion and that orthodontic treatment normal occlusion and that orthodontic treatment would measurably improve the occlusion of 55% would measurably improve the occlusion of 55% of the adolescent population.of the adolescent population.

The high prevalence is a major heath care The high prevalence is a major heath care concern, and it is only natural to be interested in concern, and it is only natural to be interested in the causes of malocclusion.the causes of malocclusion.



Epidemiology of Epidemiology of malocclusionmalocclusion

Proffit WR; 3rd ed.www.indiandentalacademy.comwww.indiandentalacademy.com

Prevalence of malocclusion is higher in developed Prevalence of malocclusion is higher in developed countries as compare to developing countries.countries as compare to developing countries.

Indians have more tendency for class II malocclusion.Indians have more tendency for class II malocclusion.

Netherlands, and Kenyans have more tendency for Netherlands, and Kenyans have more tendency for class III malocclusion.class III malocclusion.

Epidemiology of malocclusion Epidemiology of malocclusion



The prevalence of malocclusion among Indian The prevalence of malocclusion among Indian children has been reported to be as low as children has been reported to be as low as 19.6% 19.6% in Punjabin Punjab by Miglani D.S. et al in by Miglani D.S. et al in 19651965 and as high and as high as as 90% in Delhi90% in Delhi by Sidhu S.S. in by Sidhu S.S. in 1968.1968.

Epidemiology of Epidemiology of malocclusion in Indiamalocclusion in India


MALOCCLUSION STUDIES IN INDIA



The Orthodontic Equation:

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


Skeletal Crossbite

Occlusal relationship seems correct on the patients left side, crossbite on the right side.

Mandibular prognathism Patients face shows that the cross bite is

primarily the result of an osseous dysplasia.www.indiandentalacademy.comwww.indiandentalacademy.com

Muscular Or Functional Crossbite

Midline do not coincide, half the mandibular denture is outside the maxillary denture.

Removal of the occlusal interferences in the primary teeth enabled muscles to return the mandible to its proper position and to a proper occlusion.


Dental Type CrossbiteDental Type Crossbite

Mandibular and maxillary bases are harmonious with each other, midline coincide, crossbite is localized in the right central incisor region.

Due to tipping of individual teethwww.indiandentalacademy.comwww.indiandentalacademy.com

CLASSIFICATION OF ETIOLOGY OF MALOCCLUSION

Classification will help the clinician in identifying situation which they can either prevent or intervene, thus avoiding the severity of malocclusion.

The various classification proposed are:1. White and Gardiner’s classification.2. Salzmann’s classification.3. Moyer’s classification.4. Graber’s classification.


White & Gardiner’s Classification:

This was one of the first attempts to classify malocclusion.

A. Dental Base Abnormalities:

1. Anterio-posterior mal-relationship. 2. Vertical mal-relationship 3. Lateral mal-relationship 4. Disproportion of size between teeth and base

bone. 5. Congenital abnormalities.



B. PRE-ERUPTION ABNORMALITIES:

1. Abnormalities in position of developing tooth germs.

2. Missing teeth.3. Supernumerary teeth with teeth abnormal in

form.4. Prolonged retention of deciduous teeth.5. Large labial frenum.6. Traumatic injury.



C. POST-ERUPTIVE ABNORMALITIES:

1. Muscular:i. Rest position of musculature.ii. Active muscle force.iii. Sucking habits.iv. Abnormalities in path of closure.

2. Premature loss of deciduous teeth.3. Extraction of permanent teeth


A. PRENATAL:1. Genetic: malocclusion transmitted by genes, may or

may not be evidence at birth.

2. Differentiative: malocclusion that are inborn, engrafted on the body in the prefunctional embryonic developmental stage, can be subdivided into—

i. General or constitutional: effect the body as a whole.

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

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

Salzmann’s Classification:


B. POSTNATAL:

1. DEVELOPMENTAL:i. GENERAL DEVELOPMENTAL:

a. Abnormalities of relative rate of growth in dentofacial region

b. Hypo or hypertonicity of muscles which influence dentofacial development and function.

c. Childhood diseases, nutritional, endocrine, and other metabolic disturbances that affect dentofacial growth

d. Radiation and radiotherapy of mother or fetus which can produce orofacial clefts and cephalic and dental abnormalities in the offspring



B. POSTNATAL:

ii. LOCAL DENTOFACIAL:a. Birth injuries of the head, face, jaws

b. Micrognathia or macrognathia

c. Microglossia or macroglossia

d. Abnormal frenum labii

e. Facial hemiatrophy

f. Anomalies of tooth development and eruption



2. FUNCTIONAL:

i. GENERAL:

a. Muscular hyper or hypotonicityb. Neurotrophic disturbancesc. Postural defects of the tongue and jawsd. Masticatory and respiratory disturbances

ii. LOCAL:

a. Premature loss or prolonged retention of deciduous teeth

b. Loss of proximal contact following tooth lossc. Temporomandibular articulation disturbancesd. Muscular hypo or hyperactivity



3. ENVIRONMENTAL OR ACQUIRED:

i. GENERAL

a. Diseases can affect the dentofacial tissues directly or indirectlyb. Radiation

ii. LOCAL:

a. Eruption anomaliesb. Premature loss or prolonged retention of deciduous teethc. Loss of permanent teethd. Harmful dentofacial pressure habitse. Trauma f. Infectiong. Temporomandibular disturbances h. Periodontal disease



Prenatal

Postnatal

Genetic

Differentiative

congenital

Developmental

Functional

Environmental

Salzmann’sSalzmann’s diagrammatic representation of the diagrammatic representation of the interdependence of the interdependence of the

etiologic factors in malocclusionetiologic factors in malocclusionwww.indiandentalacademy.comwww.indiandentalacademy.com

MOYER’S CLASSIFICATION:

Moyer’s lists seven causes and clinical entities.

1. Heredity2. Development defect of unknown origin3. Trauma

a) Prenatal trauma and birth injuriesb) Post natal trauma

4. Physical agents5. Habits


6. Diseases a) Systemic diseaseb) Endocrine disorderc) Local diseasei. Nasopharyngeal diseases and disturbed

respiratory functionii. Gingival and periodontal diseasesiii. Tumorsiv. Caries

7. Malnutrition

MOYER’S CLASSIFICATION:


GRABER’S CLASSIFICATION:

Divide the etiologic factors into two groups:

General factor

Local factor


1. Heredity (the inherited pattern)

2. Congenital defect: cleft palate, torticollis, cleidocranial dysostosis, cerebral palsy, syphillis,etc.

3. Environment : -prenatal ( trauma, maternal diet, maternal

metabolism, German measles)

-postnatal ( birth injury, cerebral palsy, TMJ injury)

4. Predisposing metabolic climate and diseaseEndocrine imbalanceMetabolic disturbanceInfectious diseases

GRABER’S CLASSIFICATION:GRABER’S CLASSIFICATION:

GENERAL FACTORS


5. Dietary problem ( nutritional deficiency )6. Posture 7. Trauma and accident8. Habits

Abnormal suckling Thumb and finger sucking Tongue thrusting Lip and nail biting Abnormal swallowing habits (improper deglutition) Mouth breathing Speech defects Bruxism

GRABER’S CLASSIFICATION:GRABER’S CLASSIFICATION:

GENERAL FACTORS


1. Anomalies of number -supernumerary teeth -missing teeth2. Anomalies of tooth size3. Anomalies of tooth shape4. Abnormal labial frenum; mucosal barriers5. Premature loss of deciduous teeth6. Prolonged retention of deciduous teeth

GRABER’S CLASSIFICATION:GRABER’S CLASSIFICATION:LOCAL FACTORS

7. Delayed eruption of permanent teeth.8. Abnormal eruptive path.9. Ankylosis.10. Dental caries.11. Improper dental restoration


General FactorsHEREDITY:

Transmission of character from one generation to Transmission of character from one generation to the otherthe other

- Joseph Adam – 1847- Joseph Adam – 1847

There is a definite genetic determinant that influences the ultimate accomplishment of dentofacial morphology.

These genetic determinants may be modified by prenatal and postnatal environment, by physical entities, by pressures, abnormal habits, nutritional disturbances and idiopathic phenomena.


Mode of inheritance-Mode of inheritance-

Mendelian inheritance-Mendelian inheritance- Autosomal recessiveAutosomal recessive Autosomal dominantAutosomal dominant X linked and Y linked conditions.X linked and Y linked conditions.

General Factors

HEREDITY:


Autosomal recessive inheritance-Autosomal recessive inheritance-

Traits that are manifest only when mutations are present in Traits that are manifest only when mutations are present in both copies of gene are recessive traits.both copies of gene are recessive traits.

If a gene causing a recessive trait is on one of the If a gene causing a recessive trait is on one of the autosomes, the trait is autosomal recessive.autosomes, the trait is autosomal recessive.

Autosomal recessive trait tend to occur more frequently in Autosomal recessive trait tend to occur more frequently in isolated populations or in cases of consanguinity.isolated populations or in cases of consanguinity.

The parents of affected individuals are usually unaffected.The parents of affected individuals are usually unaffected.

Recurrences between siblings are common.Recurrences between siblings are common.



Seen in both males and females in equal numbers.Seen in both males and females in equal numbers.

The chance of having an affected child is 25% for each The chance of having an affected child is 25% for each pregnancy resulting from mating between two pregnancy resulting from mating between two heterozygous carriers of an autosomal recessive heterozygous carriers of an autosomal recessive condition.condition.

The other possibilities are 50%that a child will be a The other possibilities are 50%that a child will be a carrier of a single copy of the mutation and 25% that carrier of a single copy of the mutation and 25% that the child will be noncarrier.the child will be noncarrier.

This is because each parent has an approximately equal This is because each parent has an approximately equal probability of passing on either the normal or abnormal probability of passing on either the normal or abnormal allele.allele.

General Factors

HEREDITY:


Autosomal dominant inheritance-Autosomal dominant inheritance-

In autosomal dominant disorders, heterozygous individuals have a In autosomal dominant disorders, heterozygous individuals have a recognizable phenotype.recognizable phenotype.

Homozygous individuals also show the phenotype, but may be more Homozygous individuals also show the phenotype, but may be more severely affected.severely affected.

Pedigrees will frequently show that parent is affected. Pedigrees will frequently show that parent is affected.

Trait is transmitted by an affected person to half his children on an Trait is transmitted by an affected person to half his children on an averageaverage

The number of affected males and females is approximately equalThe number of affected males and females is approximately equal

Two affected individuals may have affected and unaffected children Two affected individuals may have affected and unaffected children since each parent would have one normal and one abnormal genesince each parent would have one normal and one abnormal gene



X-linked inheritance-X-linked inheritance-

Refers to conditions caused by genes on the X Refers to conditions caused by genes on the X chromosome.chromosome.

Many X-linked recessive conditions and a few X-linked Many X-linked recessive conditions and a few X-linked dominant conditions.dominant conditions.

If a mutation occurs in an X-linked recessive gene, a If a mutation occurs in an X-linked recessive gene, a female is likely to have mild or no effects, because female is likely to have mild or no effects, because female inherit two copies of X chromosome.female inherit two copies of X chromosome.

A male who inherits the gene is likely to be more A male who inherits the gene is likely to be more severely affected because he has only one copy of a severely affected because he has only one copy of a genegene



Affected males pass the gene to 100% of their Affected males pass the gene to 100% of their daughters.daughters.

There is no father-to-son transmission because There is no father-to-son transmission because fathers do not give an X chromosome to their fathers do not give an X chromosome to their sons.sons.



X linked dominant inheritance-X linked dominant inheritance-

It is rare with a few disorders.It is rare with a few disorders.

Characterized by having all the daughters of Characterized by having all the daughters of affected males inherit the disorder.affected males inherit the disorder.

Sons of affected males never inherit the disorder, Sons of affected males never inherit the disorder, because they receive the Y chromosome from the because they receive the Y chromosome from the father.father.

Affected females can transmit the disorder to Affected females can transmit the disorder to offspring of both sexes.offspring of both sexes.



Multifactorial inheritance-Multifactorial inheritance-

Some human disorders result from an Some human disorders result from an interaction of multiple genes with interaction of multiple genes with environmental influences.environmental influences.

Cleft lip and palate demonstrate a multifactorial Cleft lip and palate demonstrate a multifactorial inheritance.inheritance.

General Factors

HEREDITY:


General Factors

HEREDITY:

A strong influence of inheritance on facial features such as tilt of nose , shape of the jaw and look of the smile are familial tendencies.

Certain types of malocclusion run in families. The HAPSBURG JAW , the prognathic mandible of German royal family is the best known example


General Factors

HAPSBURG JAWHAPSBURG JAW


Facial type of the offspring probably is heavily influenced by heredity.

There are three general types of head shapes-

•Brachycephalic or broad round heads

•Dolichocephalic or long narrow heads •Mesocephalic or a shape in between the brachycephalic and the dolichocephalic

Hereditary Influence on Facial Type:

General Factors


General Factors


Hereditary influence on the growth and developmental pattern:

As ultimate morphogenetic pattern has a strong hereditary component, the accomplishment of that pattern is also at least partially under the influence of heredity.

For example, a child patient is very slow in losing his deciduous teeth and the eruption of permanent teeth is equally slow.

General Factors


Heredity and specific dentofacial morphologic characteristics:

Heredity has role in the accomplishment of specific dentofacial attributes.

Lundstrom concluded that heredity could be considered significant in determining the following characteristics:

1.Tooth size.2.Height of the palate.3.Width and length of the arch.4.Crowding and spacing of teeth.5.Degree of sagittal overbite (overjet)

General Factors


Hereditary influence on Race:

Facial and Dental characteristics of different races is influenced by heredity.

In homogenous racial groupings the incidence of

malocclusion seems relatively low.

In certain areas of the world –for example, some of the Philippine Islands –malocclusion is almost nonexistent. Population groups there are relatively pure genetically.

General Factors


Hereditary influence on Race: Where there has been a mixture of racial strains

the incidence of jaw size discrepancies and occlusal disharmonies is significantly greater.

Professor Stockard produced gross deformities with his crossbreeding of dogs.

General Factors


Breeding experiment with animal by Professor Stockard

Crossbred dogs (Boston terrier and collie) and recorded the interesting effects on body structure.

Offspring might have the Collie’s long, pointed lower jaw and the terrier’s diminutive upper jaw.


Breeding experiment with animal by Professor Stockard

Demonstrated that severe malocclusions could be developed by crossing morphologically different breeds, more from jaw discrepancies than from tooth size – jaw size imbalances.

Confirm that independent inheritance of facial characteristics could be the major cause of malocclusion and the rapid increase in malocclusion was probably the result of increased outbreeding.


These dog experiments turned out to be misleading, because many breeds of small dogs carry the gene for achondroplasia.

Most of the malocclusions produced in Stockard’s breeding experiments can be explained not on the basis of inherited jaw size but by the extent to which achondroplasia was expressed in that animal.

So these experiments have been severely criticized on the basis that the gene for achondroplasia is likely to have contributed.

General Factors


AchondroplasiaDeficient growth of cartilage in the cranial baseAutosomal dominant traitRare in humansIn humans; short limbs, deficient maxillary translation, relative midface deficiency

General Factors


Results of out breeding in human populations casts doubt on the hypothesis that independently inherited tooth and jaw characteristics are a major cause of malocclusion.

The best data are from investigations carried out in Hawaii by Chung et al.

Hawaii had a homogenous Polynesian population – large scale migration to the islands by European, Chinese, Japanese and many other racial and ethnic group resulted in heterogeneous modern population.

General Factors


Tooth size, jaw size and jaw proportions were all rather different for the Polynesian, Oriental, European contributors.

If tooth and jaw characteristics were inherited independently, a high prevalence of severe malocclusion would be expected in this population.

The prevalence and the types of malocclusion in the current Hawaiian population, thought greater than the prevalence of malocclusion in the original population, do not support this concept.

The effect of interracial crosses appear to be additive than the multiplicative.

General Factors


Twin Study

The classic way to determine to what extent a characteristic is determined by inheritance is to compare monozygotic twins (identical) with dizygotic twins (fraternal).

Studies of this type are limited because it is difficult to established zygosity and confirm that environments were in fact the same for both members of a twin pair.

Lauweryns et al ; concluded that 40% of dental and facial variation that lead to malocclusion can be attributed to hereditary factor.


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


Classical Method Is To Study Classical Method Is To Study Family Members: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 more similarities to their parents than girls. Facial skeletal structures were more frequently transmitted from mother to sons than from mother to daughters.

Hunter et. al. (1970) found genetic correlation to be strongest between father and children, especially in mandibular dimensions. There was a significant relation in facial height between mother and their offspring's.

(BJO Vol.26 NO.3, Sep. 1999)

General Factors


For skeletal characteristics, the heritability estimates increased with increasing age, for dental characteristics, the heritability estimates decreased, indicating an increase in environmental contribution to the dental variation.

( Harris EF, Johnson MG, AJO vol.99,1991)

General Factors


The influence of inherited tendencies is particularly strong for mandibular prognathism

The one third of the group of children who presented with severe class III malocclusion had a parent with the same problem

(Litton SF, Ackerman LV, Isaacson RJ,AJO Vol. 58, 1970)

The long face pattern seems to be the second most likely type of deformity to run in families.

General Factors


It is logical to assume that heredity plays a part in the following conditions.

1. Congenital deformities.

2. Facial asymmetries.

3. Macrognathia and micrognathia.

4. Macrodontia and microdontia.

5. Oligodontia and anodontia.

6. Tooth shape variations (peg-shaped lateral incisors, carabelli’s cusps, mamelons etc).

General Factors


7. Cleft palate and harelip.

8. Frenum diastemas.

9. Deep overbite.

10.Growing and rotation of teeth.

11.Mandibular retrusion

12.Mandibular prognathism.

General Factors


Congenital Defects

Cleft lip & Palate-Cleft lip and palate can be

defined as a “a furrow in the lip and palatal vault”. It may be defined as a “breach in continuity of lip and palate

General Factors


Etiology-Heredity

According to Bhatia the possible modes of transmission are either by a single mutant gene producing a large effect, or by a number of gene (polygenic inheritance) each producing a small effect together, create this condition.

According to Fogh-Andersen slightly less than 40 % of the cleft lip cases with or without cleft palate are genetic in origin where as slightly less than 20% of the isolated cleft palate cases appear to be genetically derived.

Cleft lip & Palate Cont..

Clefts usually have a strong genetic relationship.

About 1/3 or 1/2 of all cleft palate children have a familiar history of this deformity.


Environment: Teratogens, radiation, dietary deficiency

Teratogens are: Aspirin – cleft lip and palate Cigarette smoke (hypoxia) – cleft lip and

palate Dilantin – cleft lip and palate Valium- cleft lip and palat Rubella virus

Etiology



EnvironmentRadiations such as X-rays, gamma rays are capable of

producing clefts in fetus during pregnancy.

Dietary deficiency- such as folic acid deficiency can produce clefts

Etiology



Etiology

MULTIFACTORIAL ETIOLOGY: Recent studies have shown that the etiology of cleft

lip and palate cannot be attributed solely to either genetic or environmental factors. It seems to involve more than one factor.

Multi-factorial inheritance theory implies that many contributory risk genes interact with one another and the environment, resulting in a defect in the developing fetus

Unless a person is genetically susceptible, the environment factors may not by themselves cause clefts



Incidence:

Cleft lip & palate are common congenital malformations.

The reported incidence of clefts of the lip and palate from 1 in 500 to 1 in 2500 live births depending on geographic origin, racial and ethnic backgrounds and socioeconomic status.

Asian populations have the highest frequencies, often at 1 in 500 or higher, with Caucasian populations intermediate, and African-derived populations the lowest at 1 in2500

In the USA, one child in every 700 live births is afflicted.



Incidence:

Unilateral cleft accounts for nearly 80% of all cleft seen.

While bilateral clefts account for remaining 20%.

Among the unilateral clefts, clefts involving the left side are more common.

Male patients show a higher incidence of cleft lip with and without palate.

Female patients suffer from isolated cleft palate more.





Categories of Clefts: 4 general categories1. Involving the lip and alveolus.2. Involving the lip and palate.3. Palate alone is affected .4. Submucous cleft palate.



Clefts of the lip and alveolus:

May be complete, extending from the vermilion border to the floor of the nose or it may be incomplete.

May be unilateral or bilateral.

Drillien, estimated that the incidence of bilateral clefts of the lip is 3.6%, while that of unilateral clefts of the lip is 96.4%.

According to Fogh-Anderson, the incidence of complete bilateral cleft of the lip is only 1% of all individuals with cleft lip with or without a cleft palate. . (AJODO,1985,JULY)




The effect of the cleft of the lip and alveolus on the growth of the premaxilla varies.

With cleft lip only and no alveolar clefts, the continuity of the palatal bone helps maintain the maxillary arch form and relationship.

When the cleft of the lip extends to involve the primary palate, the premaxilla protrudes to different degrees because of absence of the restraining influence of the lip and the lack of continuity of the bony palate.

(AJODO,1985,JULY)




Nasal alar cartilage on the side of the cleft is displaced and flattened.

The tip of the nose is deviated towards the non cleft side.



Unilateral Cleft of the lip and alveolus

Bilateral Cleft of the lip and alveolus



Cleft lip and cleft palate:

May be complete or incomplete.

May be unilateral or bilateral.

In a complete unilateral cleft of the lip and palate, a direct communication exists between the oral and nasal cavities on the side of the palate where the cleft is situated.



Cleft lip and cleft palate

In a complete bilateral cleft lip and palate both nasal chambers are in direct communication with the oral cavity.

Premaxilla projects considerably forward from the facial aspect of the maxilla.

Anteriorly progressive constriction of the upper dental arch (Omar Gabriel da Silva Filho and et al,1998 Aug, AJODO)

Significantly longer maxillary dental arch, which is attributed to the premaxillary anterior projection.

(Omar Gabriel da Silva Filho and et al,1998 Aug, AJODO)



BCLP patients tend to have-BCLP patients tend to have-

Smaller mandibles Smaller mandibles

Mandible showed a vertical growth pattern, with an Mandible showed a vertical growth pattern, with an increased mandibular plane inclinationincreased mandibular plane inclination

Increase in lower anterior facial height. Increase in lower anterior facial height.

These are mandibular morphologic characteristics that These are mandibular morphologic characteristics that

are also found in unilateral CLP and isolated CP. are also found in unilateral CLP and isolated CP. (AJODO,1998,AUG)



Complete unilateral cleft lip and palate

Incomplete unilateral 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, cleft is limited to the uvula or to the uvula and soft palate.

In others it may extend into the hard palate.

In the extreme form, the cleft palate may extend anteriorly as far as the nasopalatine foramen.



Isolated Cleft palate: When the cleft involves a considerable portion of the

hard palate, the nasal chambers are in direct communication with the oral cavity.

The outline of the cleft may be wide or narrow, pyriform or V- shaped.

With wide cleft that extend to a considerable degree into the hard palate– excessively wide dental arches result.

In such instances the mandibular dental arch may be in complete lingual relation to the maxillary arch.



Cleft of the uvulae

Cleft of the soft palate and uvulae

Isolated cleft of the hard and soft palate



Submucous Cleft palate:

The classic triad of diagnostic signs is the1. Bifid uvula

2. Partial muscle separation in the midline with an intact mucosal surface.

3. Midline notch in the posterior edge of bony palate.



Submucous Cleft palate



The problems associated with cleft lip and/ palate patients:

DENTAL:

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

Mobile premaxilla.

Anterior &/ posterior cross-bites.

Ectopically erupting teeth.




DENTAL:

Impacted teeth.

Supernumerary teeth.

Poor alignment of the teeth often predisposes to poor oral hygiene.

Multiple decayed tooth.



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




ESTHETIC:

The patients with un-repaired clefts are badly disfigured.

Even following the closure of the cleft, the maxilla remains under-developed with compromised esthetics.

Deformity of the normal nasal architecture is commonly seen in individuals with cleft lips.



The problems associated with cleft lip and/ palate-

PYSCHOLOGICAL:

The disfigurement caused by the condition is enough to cause psychological stress for the patient and the family.




SPEECH & HEARING:

Cleft lip and palate are sometimes associated with disorders of the middle ear which may affect hearing.

Since speech is learnt by the art of imitation, if hearing is compromised so it the speech.

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



Other Congenital DefectsAlthough cleft lip and palate is the most common congenital defects to be of concern to the dentist as far as creation of malocclusion is concerned, but some problems such as-

Cerebral palsy

Torticollis

Cleidocranial dysostosis

Congenital syphilis

Congenital Defects Cont..


Cerebral Palsy:

Cerebral palsy is a paralysis or lack of muscular co-ordination attributed to an intracranial lesion.

It is most commonly considered to be the result of a birth injury.

CP is also caused by a broad group of development, genetics, metabolic, infectious, ischemic and other acquired etiology.

CP is often associated with epilepsy, abnormality with speech, vision.



Cerebral Palsy:

Effects of this neuromuscular disorder may be seen in the integrity of the occlusion.

The uncontrolled or aberrant activities upset the muscle balance that is necessary for the establishment and maintenance of the normal occlusion.



Torticollis:

Twisting of the head caused by excessive tonic contraction of the neck muscles on one side (primary sternocleidomastoid).

The fore-shortening of the sternocleidomastoid muscle can cause profound changes in the bony morphology of the cranium and face.



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

Preoperative Preoperative TorticollisTorticollis

Postoperative Postoperative TorticollisTorticollis



Torticollis:

Other physical pictures of Torticollis1. Plagiocephaly (generally visible as

a mild flattening of the occiput on one side and the forehead on the opposite side).

2. Misalignment of the eyes.3. Asymmetry of the ears.4. Depression on the side of the

neck under the ear.5. Flattening of the mandible.6. Upward tilting of the lower jaw

and gum line.7. Limited movement of the neck.



Cleidocranial Dysplasia:

Congenital disease of unknown etiology which is often but not always hereditary.

Transmitted as an autosomal dominant trait.

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




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

The fontanelles may remain open until adulthood but the sutures often close with interposition of wormian bones.

Bossing of the frontal, parietal and occipital regions give the skull a large globular shape with small face.

Characteristic skull abnormalities – “ Arnold Head” .




Sagittal suture is characteristically sunken, giving the skull a flat appearance.

Paranasal sinuses are underdeveloped and narrow.

The head is brachycephalic.

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



Cleidocranial dysplasia:

• High, narrow, arched palate, and actual cleft palate appears to be common.

•The maxilla is underdeveloped in relation to the mandible.

•Prolonged retention of the deciduous teeth and subsequent delay in eruption of the permanent teeth.

•The roots of the teeth are often somewhat short and thinner than usual and may be deformed



Cleidocranial dysplasia:

There is absence or paucity of cellular cementum on the roots of the permanent teeth and this may be related to the failure of eruption so frequently seen.

Unerupted supernumerary teeth are common. These are most prevalent in the mandibular premolar and incisor areas.

Partial anodontia has also been recorded but is rare.



Cleidocranial dysplasia


Prolonged retention of deciduous teeth. Supernumerary Teeth



Highly vaulted and narrow palate



Congenital (Prenatal) Syphilis: It is transmitted to the offspring only by an infected

mother and is not inherited.

Persons with congenital syphilis manifest a great variety of lesions, including

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



• Rhagades

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

-Hypoplasia of the incisor and molar teeth.

-Eighth nerve deafness -Interstitial keratitis

Congenital (Prenatal) Syphilis:



Environment

Prenatal Postnatal

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

(Birth injury, TMJ injury etc).

General FactorGeneral Factor


Prenatal Influence:

The role of prenatal influences on malocclusion is probably very small.

Intrauterine molding pressure against the developing

face prenatally can lead to distortion of rapidly growing areas.

Eg. On rare occasions an arm is pressed across the face in uterus, resulting in severe maxillary

deficiency at birth.



Prenatal Influence:

Occasionally a fetus head is flexed tightly against the chest in uterus, preventing the mandible from growing forward normally.

The result is an extremely small mandible at birth, usually accompanied by the cleft palate because the restriction on the displacement of the mandible forces the tongue upwards and prevents normal closure of the palatal shelves.

Intrauterine molding Distortion and Asymmetry



Prenatal Influence: Extremes mandibular deficiency at birth is the Pierre Robin

syndrome.

Characterized by 1. Cleft palate2. Micrognathia3. Glossoptoptosis


The combination of micrognathia and glossoptosis can lead to respiratory difficulty.

Because the pressure against the face that caused the growth problem would not be present after birth, one would predict normal growth thereafter.

So early aggressive treatment to lengthen the mandible should be avoided.www.indiandentalacademy.comwww.indiandentalacademy.com

Prenatal Influence:

Severe mandibular deficiency in Pierre Robin Syndrome



Prenatal Influence:

So, although abnormal fetal posture have caused marked cranial or facial asymmetries that are apparent at birth, but after the first year of life most of these have disappeared. Thus, the deformity is temporary.

Maternal nutritional disturbances such as folic acid deficiency

can produce malocclusions.

Minor injury to the mother is unlikely to affect the child, since the fetus is well cushioned by the amniotic fluid.

German measles cause gross congenital deformities including malocclusion.



Prenatal Influence:

Certain chemical (teratogens) , taken during pregnancy, causes gross congenital deformities including malocclusion.

The time of exposure is important concept for teratogen, as certain stages of embryonic & fetal development are more vulnerable than others.

In general, the embryonic stage (first trimester) is more vulnerable than the fetal period (second & third trimester).



Thalidomide provides a classic example.

The critical period of exposure is during organogenesis from the

35th-48th day after the last menstrual period.

The malformations is linked to the time of exposure:35-37

days-no ears,39-41 days-no arms,41-43days-

no uterus,45-47 days-no tibia,47-49 days-triphalangeal

thumbs.

Prenatal Influence:



Some of the known teratogens are-

1)Thalidomide-

Embryo is most vulnerable in the first trimester.

It was use to treat morning sickness but is not used anymore.

Thalidomide produced malformations limited to limbs, ears, cardiovascular system,& gut musculature.

Abnormal development of long bones, typically the upper limbs were more severely involved than the lower limbs.

Phocomelia, polydactyly, syndactyly, oligodactyly were all reported.

Cleft palate could be a complication.



2)Hydantoins(Phenytoin & Trimethadione)-

It is anticonvulsant drug.

Hydantions have been associated with Foetal hydantoin syndrome.

The clinical features include wide anterior fontanelle, ocular hypertelorism, depressed nasal bridge, cleft lip & cleft palate.



3)Folic acid antagonists(Aminopterin & Methotrexate)-

•Aminopterin is an antifolic drug,is used as a abortifacient.

•Surviving fetuses of such abortion attempts are grossly malformed.

•Malformation include facial anomalies(cleft palate,high arched palate, micrognathia, ocular hypertelorism, external ear anomalies), intrauterine growth retardation & mental retardation.



4)Isotretinoin(13-cis-retinoic acid)-

It is a synthetic vitamin A derivative,prescribed for severe cystic acne.

A pattern of anomalies termed Retinoic acid embryopathy has been associated with isotretinoin exposure in pregnancy.

The clinical features include craniofacial anomalies micrognathia, flat nasal bridge, cleft lip& palate).



5)Carbamazepine-

•It is a anticonvulsant drug.

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



6)Alcohol-

•The fetal alcohol syndrome



Full expression of this syndrome occurs with chronic daily ingestion of at least 2 grams alcohol / kg(eight drinks / day).

Alcohol is teratogen that affects the central nervous system& central nervous system is sensitive to teratogens throughout the entire pregnancy.

So alcohol,at any time during the pregnancy,has the potential to cause birth defects. This is why alcohol consumption should be avoided entirely during pregnancy.

General FactorGeneral Factor6)Alcohol-


Birth Injury:

In some diffficult birth, the use of forceps to the head to assist in delivery might damage either or both the temporomandibular joints.

At one time this was a common explanation for mandibular deficiency.

But, in light of contemporary understanding, the condylar cartilage is not as easy to blame underdevelopment of the mandible.

So injury to the mandible during a traumatic delivery appears to be rare and unusual cause of facial deformity.

General FactorGeneral FactorPostnatal Influence


Birth Injury:

Another possibility, is the delivery induced deformation of the upper jaw.

Obstetricians frequently insert the forefinger and middle finger into the baby’s mouth to ease passage through the birth canal.

Due to the plasticity of the maxillary and premaxillary region, temporary deformation is quite likely and permanent damage may result.

General FactorGeneral FactorPostnatal Influence



Accidents:

The falls and impacts of childhood can fracture jaws just like other parts of the body.

The condylar neck of the mandible is particularly vulnerable.

Fortunately, the condylar process tends to regenerate well after early fractures. 75% of children with early fractures of the mandibular condylar process have normal mandibular growth, therefore do not develop malocclusions.

When a problem does arise following condylar fracture, it usually is asymmetric growth, with the previously injured side lagging behind.

Postnatal Influence


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



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

Postnatal Influence


Predisposing metabolic climate and disease

Endocrine Imbalance Metabolic disturbances Infectious Diseases(Poliomyelitis etc.)



General FactorGeneral FactorENDOCRINE 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 FactorGeneral 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.comwww.indiandentalacademy.com

General FactorGeneral FactorENDOCRINE DISTURBANCES:

PITUITARY PROBLEMS:

Hypopituitarism:

Two basic manifestations of hypopituitarism-

Dwarfism in children

Simmonds’ disease in adults



Hypopituitarism:

Under-secretion of growth hormone before epiphyseal plate closure resulting in Pituitary Dwarfism.

In pituitary dwarfism, there is diminutive but well-proportioned body.

Supporting structures are retarded in growth.

The osseous development of mandible is more retarded than maxilla.



Hypopituitarism:

The dental arch is smaller than normal and therefore cannot accommodate all the teeth, so that a malocclusion develops.

In pituitary dwarfs the eruption rate and shedding time of the teeth are delayed.

Clinical crown appears smaller than normal because even though eruption does occur, it is not complete.

The roots of teeth are shorter than normal in dwarfism.



Hyperpituitarism:

An increase in the number of granules in the acidophilic cells or an adenoma of the anterior lobe of the pituitary is associated with gigantism or acromegaly

If the increase occurs before the epiphyses of the long

bones are closed, gigantism results.

If the increase occurs later in life i.e. after epiphyseal closure, acromegaly develops.


General FactorGeneral Factor 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.



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.



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.



Multiple root resorptions may be seen.


General FactorGeneral FactorTHYROID PROBLEMS:

Hypothyroidism:

If hypothyroidism occurs in infancy and childhood, cretinism results.

If it occurs in the adult, myxedema results.


General FactorGeneral 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.


General FactorGeneral Factor 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 presentwww.indiandentalacademy.comwww.indiandentalacademy.com

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 FactorGeneral FactorTHYROID 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.


General FactorGeneral FactorHyperthyroidism:

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


General FactorGeneral FactorHyperthyroidism:

In hyperthyroidism shedding of deciduous teeth occurs earlier than normal.

Eruption of the permanent teeth is greatly accelerated.

Alveolar atrophy occurs in advanced cases.


Increased activity is usually due to an adenoma of one or more of the four parathyroid glands.

Almost all patients with hyperparathyroidism have skeletal lesions, some of which may occur in the skull or jaws.

The skeletal disturbances in hyperparathyroidism vary from vague to roentgenographically characteristic lesions and even gross clinical evidence of bone lesions.

General FactorGeneral FactorParathyroid Hormone Problems:

Primary Hyperparathyroidism:


General FactorGeneral Factor Primary Hyperparathyroidism

– Three times more common in females than males.– Usually affects people of middle age.– Pathological fracture may be the first symptom of

the disease.– Bone pain and joint stiffness are frequent early

symptoms.– Occasionally the first sign of the disease may be a

giant cell tumor or a cyst of the jaw.– Loss of phosphorus and calcium in this disturbance

results in a generalized osteoporosis.– Malocclusion caused by sudden drifting with definite

spacing of teeth.


General FactorGeneral Factor 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 FactorGeneral Factor Hypoparathyroidism:

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

Blood chemistry shows a low concentration of serum calcium and a high concentration of serum phosphorus.

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

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



Sex hormones-

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

•Sex hormones affect craniofacial bone development.

•It has been reported, that the suppression of sex 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 not only the general health of the child but might also affect the dentition and its surrounding hard and the soft tissues.

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

Usually if the severity and duration is not prolonged the child is able to recoup lost time and catch up growth is possible.



INFECTIOUS DISEASES:

Disease with paralytic effect, such as poliomyelitis are capable of producing malocclusions.

Osteomyelitis

The adult afflicted with acute suppurative osteomyelitis is usually in severe pain.

The teeth in the area of involvement are loose

and sore.



INFECTIOUS DISEASES:


German Measles: (Rubella)

Enamel hypoplasia

A high caries incidence

Delayed eruption of deciduous teeth


Dietary Problems:


Vitamin A deficiencies-

In the developing tooth that is deficient in vitamin A, the odontogenic epithelium fails to undergo normal histodifferentiation and morphodifferentiation, resulting in the distortion of the shape of the teeth.

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



Vitamin A deficiencies-

Eruption rate is retarded and in prolonged deficiencies eruption ceases.

The alveolar bone is retarded in its rate of formation.

The gingival epithelium becomes hyperplastic & in prolonged deficiencies shows keratinization. This tissue is easily invaded by bacteria that may cause periodontal disease.



Vitamin D deficiency:

It is required for normal development of bones and teeth.

Necessary for the absorption of calcium and phosphorus from food in the small intestine.

Deficiency leads to rickets.

Rickets refers to any disorder in the vitamin D –calcium phosphorus axis which results in hypomineralized bone matrix.

Children with rickets shows bowing of the legs.



Effects on teeth:

• Delayed eruption

• Misalignment of teeth

• Disturbed calcification of teeth

• Higher caries index.

Vitamin D deficiency:


Dietary Problems


Vitamin C

Vitamin C is important for normal development of intercellular ground substances in bone, dentition, and other connective tissues so deficiency of ascorbic acid are associated with disturbances in these tissues.

The characteristic change in the teeth is atrophy and disorganization of the odontoblasts resulting in the production of irregularly laid down dentine with few, irregularly arranged tubules.


Dietary Problems


Vitamin C

Interdental and marginal gingiva is bright red with a swollen, smooth, shiny surface. In fully developed scurvy the gingiva becomes boggy, ulcerates and bleeds

In severe, chronic cases of scurvy, hemorrhages into and swelling of periodontal membranes occur, followed by loss of bone & loosening of teeth, which eventually exfoliate.


Dietary Problems


Protein Deficiency:

Overall growth and growth of the jaws were decreased.

Delayed eruption.

The gingiva and periodontal membranes exhibited varying degrees of degeneration.


ORAL HABITSORAL HABITS


DEFINATIONDEFINATION It is defined as tendency towards an act

that has become a repeated performance, relatively fixed, consistent and easy to perform by an individual.


DEFINATIONDEFINATION

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


Fins says that habits cause concern because they cause:

Oral structural changes: Harm, unbalanced pressures bear upon the immature, highly malleable alveolar ridges and bring about potential changes in position of teeth and occlusion.

Behavioral problems

Socially unacceptable act.


Classification of Habits 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 and deglutition and normal use of the lips in speaking.

Harmful Habits: include all that exert perverted stresses against the teeth and dental arches such as lip biting, lip sucking, thumb sucking.


Classification of HabitsClassification of HabitsAccording to Finn & Sim

1. Compulsive oral habits

2. Non-compulsive oral habits


Classification of Habits Classification of 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.


Classification of HabitsClassification of Habits

2. Non-compulsive oral habits:

Habits which are easily added or dropped from the child’s behavior pattern as he matures.


THUMB SUCKING THUMB SUCKING AND DIGIT SUCKINGAND DIGIT SUCKING


BASIC PHYSIOLOGY OF SUCKING REFLEX:BASIC PHYSIOLOGY OF SUCKING REFLEX:

At birth, the child has a reflex pattern of neuromuscular functions as sucking.

The habit of sucking is a reflex occurring in the oral stage of development and disappears during normal growth between 1 to 31/2 years.

Even before birth, oral contraction have been observed.

THUMB SUCKING AND DIGIT THUMB SUCKING AND DIGIT SUCKINGSUCKING


There are 2 forms of sucking:

• Nutritive form

• Non-nutritive form



The nutritive form-Breast & bottle feeding which provides essential nutrients.

Breast feeding-• Accomplished by 2 maneuvers-suckling and swallowing.

• The milk of lactating mammals are surrounded by smooth muscles, which contracts to force out the milk.

• Suckling stimulate the smooth muscle to contract and squirt milk into his mouth.



• Suckling consist of small nibbling movements of the lips.

• When the milk is squirted into the mouth, it is only necessary for the infant to groove the tongue & allow the milk to flow posteriorly into the pharynx and esophagus.

• The tongue, however, must be placed anteriorly in contact with the lower lip, so that milk is deposited on the tongue.

• This sequence of events defines as infantile swallow.


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


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.




BOTTLE FEEDING:

•Because of poor design, the mouth is held open more widely & greater demand is made on the buccinator mechanism.

•The pumping action of the tongue, the raising & lowering & the rhythmic backward & forward movement of the mandible are reduced.

•Suckling becomes sucking.


Breast-feeding practices contribute in the prevention of malocclusion in addition to decreasing the practice of parafunctional habits. (P R Health Sci J. 2006 Mar)

To provide as close a duplicate of the human breast as possible, a nipple was designed which incited the same functional activity as breast feeding.

The functionally designed latex nipple largely eliminate the objectionable features of previous non-physiologic counterparts.



Nonphysiological nursing with aconventional nipple•Mouth is propped open unduly.

•Lips seal difficult.

•Abnormal muscle pressure are exerted because of excessive opening movement.

Nursing action of nuk sauger nipple

•Closely simulates natural activity.

•Entire perioral areas is able to contact the warm nipple base.


A minimum of a half hour per nursing interval is recommended.

But no hard & fast rule can be established because some children demand more attention & time, some less depending on individual make up.

Weaning to the cup should be postponed until at least the first birthday.

If nursing is done with the physiologically designed nipple in conjunction with fondling & maternal contact, there is reason to believe that the incidence of prolonged sucking habits will be significantly reduced.



NON NUTRITIVE FORM:

Children who neither receive unrestricted breast feeding nor have access to a pacifier may satisfy their need with habits like thumb sucking which ensures a feeling of warmth & sense of security but may be detrimental to their dentofacial development.

Nearly all modern infants engage in some sort of habitual non nutritive suckingsucking of the thumb, finger or a similarly shaped objects.

Vast majority of infants do so during from 6 months to 2 years or later.

After the eruption of the primary molars during the second year, drinking from a cup replaces drinking from a bottle or continued nursing at the mother’s breast, the number of children who engage in non nutritive sucking diminishes.

Some fetuses have been reported to suck their thumbs in utero.


Recent studiesRecent studies shown that shown that thumb suckingthumb sucking may be may be

practiced even during practiced even during intra uterineintra uterine life. life.www.indiandentalacademy.comwww.indiandentalacademy.com

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

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

THUMB SUCKING AND THUMB SUCKING AND DIGIT SUCKINGDIGIT SUCKING


Almost all normal children engage in non-nutritive sucking, can lead to malocclusion.

As a general rule, sucking habits during the primary dentition years have little if any long term effect.

If these habits persist beyond the time that the permanent teeth began to erupt, however malocclusion occurs.



It is during the transition from the deciduous to the permanent arch that much of the damage takes place.

So during this transition stage that the avoidance of all abnormal pressure habits is of the utmost importance.

If a child’s sucking habits persist by the time he/she is 36 to 48 months of age, professionalassistance may be warranted to minimize the risk of malocclusion



Oral habits and primary dentition

Warren J et al. (JADA 2001,dec) concluded that continuous nonnutritive sucking habits of 48 months or longer produced the greatest changes in dental arch and occlusal characteristics, children with shorter sucking duration also had detectable differences 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.



ETIOLOGY

During the very first weeks of life, thumb sucking are typically related to feeding problems.

To meet the primitive demands like hunger.

Some children suck their thumb as a teething device during the difficult eruption of a primary molar.

Some children use digital sucking for the release of emotional tensions with what they are unable to cope.

Some children suck their thumb as an attention-seeking weapon



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



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

The frequency of the habit during the day and night affects the end result.

The child who sucks sporadically or just when going to sleep is much less likely to do any damage than one who constantly has his finger in

his mouth.www.indiandentalacademy.comwww.indiandentalacademy.com


The intensity of the habit is important.

In some children the sucking can be heard in the next room. The perioral muscle function and facial contortions are easily visible.

In others the thumb habit is little more than a passive insertion of the finger in the mouth with no apparent buccinator activity.


EXCESSIVE digit sucking can set up abnormalforces on the oral cavity and surrounding

structures.www.indiandentalacademy.comwww.indiandentalacademy.com

THUMB SUCKING AND DIGIT THUMB SUCKING AND DIGIT SUCKINGCSUCKINGC

Malocclusion characterized by:

Flared and spaced maxillary incisors and lingually positioned lower incisors.

The labially posed upper permanent incisors are particularly vulnerable to accidental fractures.


Afzelius-Alm A,et al, (Swed Dent J. 2004;28)-

found that the majority of children with prolonged thumb-sucking have proclined lower incisors rather than retroclined lower incisors.

In retroclined lower incisors groups– the angle between the thumb and the lower incisors

was significantly smaller.

– the thickness of the lower lip significantly thinner than in the group with proclined incisors.

– A higher frequency of early loss of deciduous molars was also observed in the group with retroclined incisors.

THUMB SUCKING AND DIGIT THUMB SUCKING AND DIGIT CKINGCKING



Anterior Open Bite: (Cozza P et al, Am J Orthod Dentofacial Orthop. 2005 Oct)

• It is associated by a combination of interference with normal eruption of incisors and excessive eruption of posterior teeth.

• When a thumb or finger is placed between the anterior teeth, the mandible must be positioned downward to accommodate it.

• The interposed thumb directly impedes incisor eruption.

• At the same time, the separation of jaws alters the vertical equilibrium on the posterior teeth and as a result, there is more eruption of posterior teeth than might otherwise have occurred. www.indiandentalacademy.comwww.indiandentalacademy.com

Anterior Open Bite:

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



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.





Unilateral and bilateral cross bites are often associated with finger habits. ( Warren JJ et al.

Pediatr Dent. 2005 Nov-Dec))

Flattened mandibular anterior segment: Abnormal mentalis muscle function and

lower lip activity serve to flatten the mandibular anterior segment.



Retardation of deglutitional maturation:

• Increase in over-jet makes normal swallowing procedures increasingly difficult.

• Instead of the lips containing the dentition, during deglutition, the lower lip cushions to the lingual of the maxillary incisors, forcing them farther forward.

• Lip muscle aberrations are often assisted by a compensatory tongue thrust during the swallowing act.

• So the infantile suckle-swallow continues, or the transitional period is greatly prolonged with a mixture of infantile and mature swallowing cycle



Thumb sucking habit can create a class II malocclusion:.

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

The maxillary lip becomes hypotonic and the mandibular lip becomes hyperactive.



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



Anterior Open Bite Narrow

Constricted maxillary arch

Posterior Cross Bitewww.indiandentalacademy.comwww.indiandentalacademy.com

Tongue Thrusting HabitTongue Thrusting Habit

Tongue thrust swallowing defined as placement of the

tongue tip forward between the incisors during swallowing.



The term tongue thrust is something a misnomer.

Since it implies that the tongue is forcefully thrust forward.

But individuals who place the tongue tip forward when they swallow usually do not have more tongue force against the teeth than those who keep the tongue tip back.


Tongue Thrusting HabitTongue Thrusting Habit Swallowing is not a learned behavior, but is

integrated and controlled physiologically at subconscious levels.

So whatever the pattern of swallow, it cannot be considered a habit in the usual sense.

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



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


Humans show 2 types of swallow pattern:

Infantile and neonates swallow

Mature/Adult swallow



Infantile visceral swallow

• Jaws apart, tongue between gum pads

• Mandible stabilized by contraction of facial muscles and interposed tongue

• Swallow is guided and controlled by sensory interchange between lip and tongue

• Active contractions of the musculature of the lips.

• Tongue tip brought forward into contact with the lower lip.

• Little activity of the posterior tongue or pharyngeal musculature

• Forward position of mandible and tongue

• Tongue grooved(depressed central position) to steer the liquid into pharynx and esophagus www.indiandentalacademy.comwww.indiandentalacademy.com

Mature somatic swallow

Teeth – together (momentarily)

Mandible stabilized by contraction of mandibular elevator muscles

Tongue tip- against palate, above and behind the incisors

Minimum contraction of lips

Appears between 2-4 years in normal patternwww.indiandentalacademy.comwww.indiandentalacademy.com

NORMAL SWALLOWING

•Incisors are momentarily in contact

•Tip of the tongue touches the 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

•Dorsum of the tongue drops away from the palatal vault

•Instead of the lips creating firm seal,theupper lips remains relative functionless

•Mentalis exerts strong forward and upward thrust of lower lip against lingual surfaces of maxillary incisorswww.indiandentalacademy.comwww.indiandentalacademy.com


Classification

1. Simple Tongue Thrust

2. Complex Tongue Thrust



Simple tongue thrust swallow (Teeth together swallow)• Teeth are in occlusion as

tongue protrudes into open bite

• Tongue thrust is present to seal open bite

• Well circumscribed open bite

• Secure intercuspation• History of digit sucking• Displays contractions of

lips, mentalis and mandibular elevators



Complex tongue thrust Swallow (Teeth apart swallow)• Teeth apart during tongue

thrust• More diffuse open bite• Poor occlusal fit• History of breathing or

chronic nasorespiratory diseases

• Combined contractions of lip, facial and mentalis muscles.

• Lack of contraction of mandibular elevators


Clinical Feature:

If the postural position is normal, the tongue thrust swallow has

no clinical significance because tongue thrust swallowing simply

has too short a duration to have an impact on tooth position.

• Pressure by the tongue against the teeth during a typical swallow lasts for approximately 1 second.

• A typical individual swallows about 800 times/day while awake but has only a few swallows /hour while asleep. The total/day therefore is usually under 1000.

• One thousand seconds of pressure, of course, totals only a few minutes, not nearly enough to effect the equilibrium.



On the other hand, if a patient has a altered resting posture of the tongue, the duration of this pressure, even if very light, could effect tooth position, vertically or horizontally.

Two significant variations from the normal tongue posture can be seen.

• Protracted Tongue posture

• Retracted Tongue posture



There are two forms of protracted tongue posture

Endogenous protracted tongue posture.

Acquired adaptive tongue posture



Endogenous protracted tongue posture:

• May be a retention of infantile postural pattern.

• Some persons, reasons not yet clear, do not change their tongue posture during the arrival of the primary incisors and the tongue tip persists between the incisors.

• For the great majority of patients with endogenous protracted tongue posture, the open bite is mild and not a serious clinical problem, but on rare occasions, quite serious open bites are present.



Acquired protracted tongue posture

• Usually it is the adaptation to enlarged tonsils, pharyngitis, or tonsilitis.

• When the acutely inflamed throat (pharyngitis or tonsilitis) is anesthetized, the adaptive protracted posture of the tongue may spontaneously correct to a more normal position.

• As long as the precipitating pain mechanism is present, the tongue will posture itself forward, and repositioning of the incisors will not be stable. Therefore, it is best to refer such patients to a physician for correlative therapy.



The protracted tongue posture usually results in

• Anterior open bite

• Proclination of anterior teeth

• Contracted upper arch



Complex tongue thrust-

•Defined as a tongue thrust with a teeth apart swallow.

•Combine contractions of the lips, facial, and mentalis muscles, lack of contraction of the elevators.

•The open bite associated with it is more diffuse and difficult to define than that seen with a simple tongue thrust.

•Indeed, on occasion, complex tongue thrust-thrusters have no open bite at all.

•Examination of occlusal casts typically reveals a poor occlusal fit and instability of intercuspation.

•The incidence of complex tongue thrusting does not diminish as much with age as does the simple tongue thrust.



•Complex tongue thrust are more likely to be associated with chronic nasorespiratory distress, mouth breathing, tonsillitis, or pharyngitis.

•When the tonsils are inflamed, the root of the tongue may encroach on the enlarged facial pillars.

•To avoid this encroachment, the mandible reflexly drops, separating the teeth and providing more room for the tongue to be thrust forward during swallowing to a more comfortable position.

•Pain and lessening of space in the throat precipitate a new forward tongue posture and swallowing reflex.

•Melsen et al state that both tongue thrust swallow favor the development of distoocclusion, extreme maxillary overjet and open bite.



MOUTH BREATHING HABITSMOUTH BREATHING HABITSETIOLOGY:• Humans are primarily nasal breathers but everyone breathes

partially through the mouth under physiologic conditions.

• The most prominent being an increased need for air during exercise.

• A rest, minimum airflow is 20-25 L per minute, but heavy mental concentration or even normal conversation lead to increased airflow and transition to partial mouth breathing.

• For the average individual there is a transition to partial oral breathing when ventillatory exchange rates above 40-45L/min are reached.

• At maximum effort 80 or more L/min of air needed, about half of which is obtained through the mouth.


MOUTH BREATHING HABITSMOUTH BREATHING HABITS• Nasopharyngeal Obstruction if a nose is obstructed, the work associated with nasal breathing increases and at a 3.5-4 cm H-2-0/l/min resistance to

nasal airflow, the individual switches to partial mouth breathing. Chronic respiratory infection Enlarged tonsils &adenoids Nasal polyp or tumor Any mechanical obstruction anywhere within the nasorespiratory system

• Anatomic- -short upper lip

•


MOUTH BREATHING HABITSMOUTH BREATHING HABITS

Classification of mouth breathing:

Obstructive Habitual

Anatomical



OBSTRUCTIVE MOUTH BREATHERS: Those who have

– Increased resistance to or a complete obstruction of the normal flow of air through the nasal passages.

– Because of the difficulty of inspiring and expiring air through the nasal passages, the individual is forced to breathe through his mouth.

– Obstructive mouth breathing is frequently observed in ectomorphic children who possess long, narrow faces, and nasopharyngeal spaces.



Habitual mouth breather is an individual who continually

breathes through his mouth by force of habit, although the

abnormal obstruction has been removed.

Anatomical mouth breather is one whose short upper lip

does not permit complete closure without undue effort.



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 that influences the position of the teeth & also the growth the jaws.



CLINICAL FEATURES:• 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.www.indiandentalacademy.comwww.indiandentalacademy.com


•Increasing overjet

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

•These types of faces are called as adenoid faces or long face syndrome.


Diagnosis

• Observers tend to equate lip separation at rest with mouth breathing, but this is simply not correct.

• It is perfectly possible for an individual to breathe through the nose while the lips are apart.

• The only reliable way to quantify the extent of mouth breathing is to establish how much of the total airflow goes through the nose and how much through the mouth, which requires special instrumentation to simultaneously measures nasal and oral airflow.

• Certain percentage of oral respiration, maintained for a certain percentage of time, should be the definition of significant mouth breathing, but a definition has not been produced.


Mirror Test: A double-sided mirror is held between the mouth and nose.• Fogging on the nasal side of the mirror indicates

nasal breathing while fogging on oral side indicates mouth breathing.

Cotton Test or Massler’s Butterfly Test:• Butterfly shaped cotton strands are placed over

the upper lip below nostrils.• If the cotton flutters down it is a sign of nasal

breathing.• This test can be used to determining unilateral

nasal blockage.

Other methods of diagnosis


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):84-9)

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 most often involves the lower lip which is turned inwards and pressure is exerted on the lingual surfaces of the maxillary anteriors.

LIP BITING


Etiology:• Psychological : May appear due to forced discontinuation of thumb or finger sucking

• Morphological : Class II div I Cases

Clinical Feature:

•Proclination of upper anterior, Retroclination of lower ant.

•Increased overjet

•Cracking of lips.

LIP BITING


NAIL BITING

Minor tooth irregularities such as rotation, wear of incisal edge and minor crowding.


1. Anomalies of tooth number2. Anomalies of tooth size 3. Anomalies of tooth shape4. Abnormal labial frenum5. Premature loss of deciduous teeth6. Prolonged retention of deciduous teeth7. Delayed eruption of permanent teeth8. Abnormal eruptive path9. Ankylosis10. Dental caries11. Improper dental restoration

LOCAL FACTORSLOCAL FACTORS


1.Anomalies in number of 1.Anomalies in number of teethteeth

SUPERNUMERARY TEETHSUPERNUMERARY TEETH MISSING TEETHMISSING TEETH


LOCAL FACTORSLOCAL FACTORS ANOMALIES IN NUMBER OF TEETH:

ETIOLOGY: Several theories have been advanced to explain supernumerary or congenitally absent teeth

Heredity plays an important & a strong part in many cases.

There is a relatively high frequency of extra or missing teeth associated with congenital deformities such as cleft lip and cleft palate.

Generalized pathoses, such as ectodermal dysplasia, cleidocranial dysostosis and others may also affect the number of teeth in the dental arches.www.indiandentalacademy.comwww.indiandentalacademy.com

Supernumerary teeth-

Teeth that are extra to the normalcomplement are termed assupernumerary teeth. Supernumerary teeth can cause

Non eruption of the adjacent teeth Delayed eruption of adjacent teeth Deflect the erupting teeth into abnormal position Crowding in the dental arch


Noneruption of canine



So early intervention to remove it, is usually required to obtain reasonable alignment and occlusal relationship.

But if such teeth are completely out of line of occlusion and have no effect on the dental arches they should be left alone because removal endangers the apical regions of contiguous permanent teeth.


There is no definite time when supernumerary teeth may develop. They may form prior to birth or as late as 10 to 12 years of age.

Approximately 90% of all supernumerary teeth occur in the maxilla, although, they may erupt in any area of the mouth.

Supernumerary teeth in the deciduous dentition are less common than in the permanent dentition.

When this situation does occur in the deciduous dentition, the supernumerary tooth is usually a maxillary lateral incisor, although both supernumerary maxillary & mandibular deciduous cuspids have also been seen.



A supernumerary tooth may closely resemble the teeth of the group to which it belongs i.e. molars, premolars, or anterior teeth, or it may bear little resemblance in size or shape to the teeth with which it is associated.

Supernumerary teeth develop from a third tooth bud arising from the dental lamina near the permanent tooth bud, or possibly from splitting of the permanent bud itself.



Although these teeth may be found in any location, they have an apparent predilection for certain sites.

The most common supernumerary teeth is the “mesiodens” between the maxillary central incisors occurring singly or paired, erupted or impacted



The maxillary fourth molar is the second most common supernumerary tooth and is situated distal to the 3rd molar.

Supernumerary lateral incisors, extra premolars also occurs

LOCAL FACTORSLOCAL FACTORSSUPERNUMERARY TEETH: (CONT..)


Any supernumerary tooth may be erupted or impacted.

Multiple supernumerary teeth, many of them impacted are characteristically found in Cleidocranial dysplasia, Gardner’s syndrome.



MISSING TEETH True anodontia or congenital absence of teeth may be of 2

types Total and partial

Total anodontia, in which all the teeth are missing, may involve both the deciduous and the permanent dentition

This is rare condition, eg. hereditary ectodermal dysplasia



MISSING TEETH Partial anodontia (Hypodontia or oligodontia) involves

one or more teeth and is a rather common condition.

Induced or false anodontia occurs as a result of extraction of all teeth.

While the term ‘Psuedoanodontia’ is sometimes applied to multiple unerupted teeth



MISSING TEETH

Although any tooth may be congenitally missing, there is a tendency for certain teeth to be missing more frequently than others.

The order of frequency of absence is

1. Maxillary & Mandibular 3rd molar 2. Maxillary lateral incisors 3. Mandibular 2nd Premolar 4. Mandibular incisors 5. Maxillary 2nd Premolar



Congenitally missing deciduous teeth are uncommon but when occurring, usually involve the maxillary lateral incisors, mandibular incisors & mandibular cuspids may also be missing.


MISSING TEETH(CONT..)

Congenitally missing teeth are many times more frequently found than supernumerary teeth.

Supernumerary teeth are usually found in the maxilla, missing teeth are frequent in both jaws.

Congenital absence problems are more likely to be bilateral than are supernumerary teeth.


Congenitally missing teeth can lead to

Gaps between teeth Abnormal swallowing pattern Abnormal tilting of adjacent teeth

LOCAL FACTORSLOCAL FACTORSMISSING TEETH(CONT..)

CONGENITAL ABSENCE OF MAXILLARY LATERAL INCISORS WITH GENERALIZED SPACINGwww.indiandentalacademy.comwww.indiandentalacademy.com

VARYING POSITIONS OF PERMANENT CANINES IN CASES OF CONGENITAL ABSENCES OF LATERAL INCISORS

CANINE IN CONTACT WITH CENTRAL INCISORS DIASTEMA BETWEEN INCISOR

CANINE IN CONTACT WITH FIRST PREMOLAR


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

Anomalies in tooth size - Microdontia Macrodontia


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 smaller than normal teeth are present in jaws that are somewhat

larger than normal and there is an illusion of true microdontia.

Microdontia involving only a single tooth is a rather common condition.

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 small jaw give the illusion of macrodontia.

Macrodontia of single teeth


The size of teeth in largely determined by heredity.

It might be assumed 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, several observations were made on the size of teeth and malocclusion. There does not seem to be any correlation between tooth size and between spacing and crowding of teeth.

There may be a variation in tooth size within the same individual often one maxillary lateral incisor will be of normal size and configuration while the other is diminutive. www.indiandentalacademy.comwww.indiandentalacademy.com

Sometimes a tooth size discrepancy can be noted when comparing maxillary and mandibular dental arches.

Anomalies of size are relatively frequent in the mandibular premolar area.

Unless the teeth are match for size, normal occlusion is impossible.

As might be expected the most variable teeth, the maxillary lateral incisors are major culprits.


Occasionally the cingulum is quite pronounced and particularly with the Japanese, the marginal ridges can be sharp and well defined, bounding the lingual fossa.

The presence of an exaggerated cingulum or heavy marginal ridges can force the involved teeth labially and prevent the establishment of a normal overjet-overbite relationship.

The mandibular 2nd premolar also shows great variation in shape and size. It may have an extra lingual cusp, which usually serves to increase the mesiodistal dimension.


Abnormalities Of Tooth Shape (Contd)

Fusion:

Fused teeth arise through union of two normally separated tooth germs.

It has been thought that some physical force or pressure produces contact of the developing teeth and their subsequent fusion.

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

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

If the contact of teeth occurs later, when a portion of the tooth crown has completed its formation, there may be union of roots only.

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


FUSION


Abnormalities Of Tooth Shape (Contd)

Gemination:

Geminated teeth arise from division of single tooth germ by an invagination with resultant incomplete formation of two teeth.

The differentiation between gemination and fusion can be difficult and is usually confirmed by counting the number of teeth in an area.

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

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

Normal occlusion, of course, is all but impossible in the presence of geminated, fused or otherwise malformed teeth.


GEMINATION


Other Developmental Anomalies in Tooth Shape(Cont..)

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 globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars, unilaterally or bilaterally.

This extra cusp may contribute to incomplete eruption, displacement of teeth and/or pulp exposure with subsequent infection following 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 incisor and in the V-shaped intermaxillary suture.


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

ABNORMAL LABIAL FRENUM(CONT..)


Spacing between the maxillary central incisors and the presence of the fibrous tissue attachment such as the labial frenum provide an excellent “chicken egg” routine for controversy which came first?

The difficulty lies in establishing whether this fibrous attachment is causative or resultant.

The hereditary component is a major factor in persistant diastemas. Therefore a check of parents and siblings is advisable whenever a diastema is observed.

Diastema may be due to other factors any and all of the following list should be eliminated as possible causative factors: Microdontia, macrognathia, supernumerary teeth (especially mesiodens), peg laterals, missing lateral incisors, habits such as thumb sucking, tongue thrust, and midline cyst.


In the 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 a frenectomy unnecessary.

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

AGEAGE INCIDENCE OF DIASTEMAINCIDENCE OF DIASTEMA

66 97%97%

6-76-7 88%88%

10-1110-11 48%48%

12-1812-18 7%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.

They also 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.

Even when the premolar erupts, it is deflected buccally or lingually into a position of malocclusion.




PREMATURE LOSS OF DECIDUOUS TEETH(CONT..)

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.


PREMATURE LOSS OF DECIDUOUS TEETH (CONT..)

In the maxillary or mandibular anterior areas, space maintenance for deciduous teeth seldom necessary in a normal occlusion but with an arch length deficiency or overjet problem, however, spaces can close rapidly.

The early loss of permanent teeth should be considered just as severe a ‘malocclusion maker’ as the loss of deciduous teeth.

If the loss occurs before the dentition is complete, the disturbance is likely to be particularly marked.

The resultant shortening of arch length on the side of the loss, tipping of the contiguous teeth, overeuption of opposing teeth occurs.


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 FACTORSLOCAL FACTORSPROLONGED 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 in prolonged retention of deciduous teeth is Ankylosis.

Even when the deciduous teeth appear to be lost on time, the patient should be observed until the permanent teeth erupt.

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 this is 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 cryptBony crypt Mucosal barrierMucosal barrierwww.indiandentalacademy.comwww.indiandentalacademy.com

ABNORMAL ERUPTIVE PATH

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

Because of the 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.


ABNORMAL ERUPTIVE PATH(CONT..) Another form of abnormal eruption is referred to as ectopic

eruption.

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

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.

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

Resorption of central incisor root due to abnormal canine eruption pathwww.indiandentalacademy.comwww.indiandentalacademy.com

ANKYLOSIS

Ankylosis is a phenomenon in which a tooth is fixed in its surrounding bone while the contiguous teeth continue to erupt and shift with growth and development.

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

Ankylosis is probably due to an injury of some sort, as a result of which a part of the periodontal membrane is perforated and a bony “bridge” form joining the lamina dura and cementum.

The process is basically one of resorption of tooth substance and bony repair with the result that the tooth is locked in bone.



Other causes for ankylosis: Infection, disturbed local metabolism or a genetic influence, certain endocrine conditions and congenital diseases like cleidocranial dyostosis.

Clinically ‘submerging’ of the offending teeth.

‘Submerged’ teeth are deciduous teeth, most commonly mandibular 2nd molars.

It prevents their exfoliation and subsequent replacement by permanent teeth.

If left alone, ankylosed teeth can actually be covered over again by the ever-growing mucosa, and the contiguous teeth often migrate into the space, effectively locking the tooth in the process.

Permanent teeth may also be ankylosed.


ANKYLOSED DECIDUOUS SECOND MOLARS.SECOND PREMOLAR DEFLECTED TO DISTAL


The diagnosis of ankylosis of a tooth is usually suspected clinically and confirmed by roentogenographic examination.

The affected tooth lack mobility even though root resorption is far advanced.

Upon percussion, an ankylosed tooth imparts a characteristic solid sound in contrast to the dull, cushioned sound of a normal tooth.

Roentogenographically, at least partial absence of the periodontal ligament is seen with areas of apparent blending between the tooth root and bone.


DENTAL CARIES

Dental caries may be considered the local causes of malocclusion.

Caries leads to premature loss of a deciduous or permanent tooth so that subsequent drifting of continuous teeth, abnormal axial inclination, overeruption, bone loss occurs.

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

So it is basic that carious lesions should be repaired not only to prevent infection and loss of teeth but to maintain the integrity of the dental arches.




IMPROPER DENTAL RESTORATION

An increase in arch length through improper restoration of one or more carious proximal surfaces may result in the creation of broken contacts, rotations.

Poor contacts encourage food packing.

Lack of anatomic detail in restoration of cuspal area of a tooth can permit elongation of opposing teeth or create functional prematurities.



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