Prof. Dr.

Hasham Khan
Head Deptt. of Paediatric Dentistry
Khyber College of Dentistry
Peshawar
 Tooth Abnormalities
1. Abnormalities of Number
2. Abnormalities of Form
3. Abnormalities of Size
4. Abnormalities of Structure
5. Abnormalities of Colour
6. Odontomes
7. Abnormalities of Eruption and Exfoliation
8. Chemical and Physical Injuries
9. Resorption
 Abnormalities of Tooth Number

• Human tooth formation begins in the 5th week of gestation.

• Tooth buds form at predetermined sites in the dental lamina,

corresponding to the future sites of the deciduous teeth.

• From the 20th week, further epithelial proliferation from the

dental lamina form the tooth buds of the permanent tooth
germs.

• Aberration in this pattern of development may result in

abnormalities in tooth number.
Abnormalities of Tooth Number

• Increase in number: Supernumerary teeth

• Decrease in number: Hypodontia

Variations in Root Number

• Increase in root number: Accessory roots

• Decrease in root number
 Supernumerary Teeth

Supernumerary teeth are those teeth which are

present in addition to the normal series of 20
deciduous teeth and 32 permanent teeth.
OR
May be defined as an excess number of teeth when
compared to the normal dental formula.
 Prevalence
The prevalence of supernumerary teeth varies between 0.1
and 3.8% and is more common in the permanent dentition.
 Prevalence in primary teeth: 0.2 – 1.9 %
 Prevalence in permanent teeth: 0.1 – 3.8 %
 Maxilla to Mandible ratio = 9:1
 Male to Female ratio = 2:1
 Most commonly occur in the pre-maxilla.
They may occur as single or multiple, unilateral or bilateral, in
isolation or associated with other conditions or syndromes.
 Associations

Supernumerary teeth may have association with:

• Invaginated teeth
• Megadonts
• Double teeth
Conditions / syndromes commonly associated with an
increased prevalence of supernumerary teeth include:
• Cleft lip and palate,
• Cleidocranial dysostosis
• Gardner syndrome
• Orofacial digital syndrome
Supernumerary Teeth in Primary Dentition
• Supernumeraries are usually supplemental in form in the
deciduous dentition. Frequently found adjacent to the maxillary
lateral incisors.

• Supernumerary teeth are almost always single in the deciduous

dentition.

• No predilection for sex.

• In 35 – 50 % of cases, supernumerary deciduous teeth are

followed by supernumerary permanent teeth.

• So careful follow up to prevent interference with the normal

development of occlusion by appropriate and correctly timed
surgical intervention.
 Classification

Classification based on morphology:

1. Conical
2. Tuberculate
3. Supplemental
4. Odontome
Classification based on location:
5. Mesiodens
6. Paramolar
7. Distomolar
8. Parapremolar
 Etiology of Supernumerary Teeth
The exact etiology of the supernumerary teeth is not completely
understood. Both genetic and environmental factors have been
considered. Several theories have been suggested to explain
their occurrence:

Atavism (phylogenetic theory)
(Reversion to extinct primates with three pairs of incisors –largely discounted).

Dichotomy theory
(Dichotomy of the tooth bud – discounted).

Dental lamina hyperactivity theory
(Localized, independent, conditioned hyperactivity of the dental lamina. According to this theory, a
supplemental form would develop from the lingual extension of an accessory tooth bud, whereas a
rudimentary form would develop from the proliferation of epithelial remnants of the dental lamina –
supported by literature).

Genetic factors
(Heredity may also play a role as supernumeraries are more common in the relatives of affected children
than in the general population. A sex-linked inheritance has been suggested by the observation that males
are affected approximately twice as often as females). Hypothetic existence of epithelial stem cells in
repeated teeth renewal has been recently proposed.
 Complications
Some supernumeraries are a chance radiographic discovery
but majority of them create some clinical problem. These
include:
• Delay or failure of eruption of permanent teeth
• Displacement or rotation of permanent teeth
• Crowding
• Root resorption of adjacent teeth
• Dilaceration
• Loss of vitality of adjacent teeth
• Incomplete space closure during orthodontic treatment
• Pathological problems such as dentigerous cyst formation
• Interfere in alveolar bone grafting
• Interference in implant placement
 Diagnosis and Assessment
• Unerupted supernumeraries (almost 75 %) are diagnosed on
radiographs.

• Localization of supernumerary teeth through radiographs is of

special importance if surgical intervention is required.

• Radiographic localization of supernumerary teeth can be done

easily by parallax technique (horizontal or vertical) and using
SLOB rule.

• Cone – beam computed tomography can also be used to evaluate

supernumerary teeth in all three dimensions.
 Removal
• Removal indicated if complications listed above are found during
examination. However prophylactic removal is debated when no
complication is present. Proponents of the prophylactic removal argue that:
1. Complications are likely if left untreated.

2. Supernumerary teeth serve no function.

3. Prognosis of surgical intervention is good (no recurrence).

• The surgical removal option must be affected by the conditions present.

Sometimes a prudent delay may provide easier and less traumatic
approach. On the other hand some supernumerary teeth will need early
removal, e.g; inverted conical form and tuberculate.

• Following removal of supernumerary teeth, the time taken for the

unerupted tooth to erupt can vary between 06 months - 03 years.
 Timing of Removal
• Highly controversial.
• The disadvantages of immediate intervention are:
1. Potential damage to the adjacent teeth resulting in devitalization.
2. Inability of a young child to psychologically tolerate the surgical procedure.
3. Performance of unnecessary surgery if future complications fail to develop.

• The disadvantages of delayed intervention are:

1. Loss of eruption potential of the central incisors.
2. Loss of anterior arch space or midline shift.
3. More extensive surgical and orthodontic treatment for correction.

• The timing of intervention not critical if the supernumerary is located beyond the apex or
has erupted.
• If the supernumerary tooth is not adversely affecting the developing occlusion or the
complication already developed would not worsen by delay, it is wise to delay surgical
intervention until the roots of the adjacent teeth develops fully.
• The tooth type is also critical in making the judgment when to surgically intervene.
• The timing of removal needs a prudent judgment after thoroughly evaluating the clinical
situation.
 Hypodontia

• Hypodontia: Congenital absence of some teeth.

• Anodontia: Total lack of one or both dentitions congenitally.

Usually only seen in cases of ectodermal
dysplasia.

• Oligodontia: Cases in which many, but not all, teeth are

congenitally missing.
 Clinical Features
• Initial sign may be spacing in the region of the missing tooth or prolonged retention
of a deciduous tooth or the defect may be revealed by only careful examination.

• Maxilla more often affected than the mandible in the deciduous dentition
(especially the maxillary lateral incisor region).

• Maxilla and mandible equally affected by hypodontia in the permanent dentition.

(3rd molar > mandibular 2nd premolar > maxillary lateral incisor).

• Hypodontia in deciduous teeth may be followed by agenesis of permanent teeth in

the same region in three-quarters of cases.

• Severe hypodontia sometimes associated with a relative lack of alveolar growth →

so increased freeway space → overclosure of mandible to achieve occlusion and
protrusion and eversion of the lips.

• Missing and deformed teeth together with the facial appearance may lead to
considerable psychological disturbance.
 Prevalence of Hypodontia

• Deciduous dentition = 0.1 – 0.9 %

• Permanent dentition = 3.5 – 6.5 %
( excluding 3rd molars)

In the deciduous dentition males and females are

equally affected. In the permanent dentition, it is
more frequent in girls in a ratio of 3:12.
 Associations

• Relationship between hypodontia and microdontia of

maxillary lateral incisors.

• May also be associated with a delay in the calcification and

eruption of teeth, as well as deficient alveolar growth.

• Some commonly known systemic conditions associated with

hypodontia are cleft lip and cleft palate, ectodermal dysplasia,
and Down’s syndrome.

• Many other conditions such as Block-Sulzberger, Ellis-van

Creveld, Books syndrome and thalidomide embryopathy may
also be associated with hypodontia.
 Aetiology
• Both genetic and environmental factors has been suggested.

• Genetic factors are suggested because of the many family case

reports and twin studies. May be polygenically determined.

• Environmental factors which may damage developing tooth

germs and cause hypodontia include local factors such as
osteomyelitis, neoplasms, trauma, irradiation, operative
procedures (ext. of primary teeth) and intrauterine systemic
factors such as rubella infection and thalidomide drug.

• A correlation between multiple births, low birthweight, maternal

age and the frequency of hypodontia has also been suggested.

• Genetic and environmental factors may work together to cause

the anomaly.
 Treatment

There will be many treatment options when a

patient with hypodontia is presented. Treat

according to the situation and the type of

tooth / teeth absent.

Increase in Root Number: Accessory Roots

An accessory root is one occurring in excess of

the usual number for that tooth.

The accessory root may follow the main root in size

and form.
 Clinical Features

• More difficult to treat a tooth with accessory roots (extraction,

endodontic and orthodontic treatment).

• Cannot be detected on clinical examination and may not

always be visible on radiographs.

• May occur on almost any tooth. Deciduous molars and

permanent molars (usually lower 1st permanent molars) may
show additional roots (usually distolingual or lingually
adjacent to the bifurcation and frequently fine, rounded,
tapering and curved in form).
 Prevalence

Overall prevalence = 05 per 1000 (0.5 %).

Accessory roots on lower deciduous molars = < 1 %

Accessory roots on lower 1st permanent molar = 1 – 45 %

 Associations

• Accessory roots have been found in association with:

• An increase in size of the cusp of carabelli.
• Paramolar tubercles in maxillary 2nd or 3rd permanent molars.
• Pulp-containing type of enamel pearl.

• May also be associated with:

• Abnormally large crowns.
• Supernumerary teeth.
 Aetiology

• Accessory roots may arise by division of normal roots,

possibly due to trauma.

• Rich vascularization of the dental papilla.

• Genetic factors.
 Decrease in Root Number

Confusion exists as to what constitutes ‘pyramidal’,

‘cuneiform’ and ‘fused’ roots.

Clinical Features:
• Occur in multi-rooted teeth.

• Any molar tooth may have single tapering root but more
frequent in 2nd and 3rd permanent molars.

• Reduced root surface area and tapering form - less resistant

to coronally applied displacing forces.
 Prevalence

Reduction in root number – a common root anomaly in the

permanent dentition.

• Prevalence in 1 permanent molar = 1 %

st

• Prevalence in 2 and 3 permanent molars = 15 -40 %.

nd rd

• Females more frequently have pyramidal roots than

males.
 Associations and Aetiology

Associations:
• Reduction in root number may occur together with
taurodont root forms.
• Reduction in root number is associated with
hypodontia.

Aetiology:
• May arise from a failure of the invagination of Hertwig’s
root sheath.
• Probably polygenic in nature.
Abnormalities of Tooth Form
– Invaginated teeth
– Evaginated teeth
– Double teeth
– Taurodontism
– Dilaceration
– Enamel projections and pearls
– Accessory cusps (Talon and Carabelli)
– Hutchinson’s incisors and Moon’s molar
 Invaginated Teeth
‘Dens in dente’ – Tooth within a tooth – a misconception.
Invagination in a tooth is also called ‘dens invaginatus’.
A developmental invagination of surface hard tissue
towards the pulp chamber.

Clinical Features:
• May occur in any tooth but the palatal surface of maxillary lateral
incisor is more commonly affected.

• Common in incisor teeth of ‘shovel ‘ form.

• May resemble a deep pit but the radiographic appearance is typical.

• Carious destruction of tooth tissue within the invagination may lead to

pulpal exposure, acute facial cellulitis or acute dentoalveolar abscess.
 Prevalence

• Deciduous teeth = Rare

• Permanent teeth = 0.4 – 6.8 %

depending on the ethnic group sampled.

• Boys more affected than girls in a ratio of 2 : 1

 Associations and Aetiology

Associations:
 Significant association between supernumerary and
invaginated teeth. So check radiograph for invagination
when a supernumerary is present or vice versa.

Aetiology:
 Arises as a result of an invagination of the enamel
epithelium into the dental papilla of the tooth germ.
Appears to be largely genetically determined.
 Clinical Implications and Treatment

• If an invagination is found in a tooth on one side, the same

tooth on the other side should be radiographed.

• Prophylactic sealing or restoration of invaginated teeth soon

after eruption should be done to prevent complications.

• If pulpal infection and degeneration has already occurred, the

advisability of endodontic treatment will depend on pulp
morphology and the restorability of the crown.
 Evaginated Teeth
Evagination – an outward projection of the tooth surface. A
teat-like enamel-covered tubercle projecting from the surface
of the tooth.

Clinical Features:

• Seen principally on the occlusal surface of premolars but

occasionally may affect any other tooth.

• A fine pulp horn usually extends into the dentine core.

• The condition is of clinical significance because the tubercle often

become worn or may fracture from the masticatory trauma of
opposing teeth. This may lead to pulpal infection, pulpal necrosis
and subsequent periapical infection.
 Prevalence, Associations and Aetiology

Prevalence:
• Prevalence in Mongoloid races – 4.8 % (southern
Chinese)
• Rare in Caucasians.
Associations:
• A peculiar idiopathic resorption of dentine may
sometimes be an associated feature.
Aetiology:
• This anomaly of tooth form is thought to result from an
outward folding, or evagination, of the enamel organ. It is
probably a largely genetically determined anomaly.
 Treatment
Treatment is directed at preventing the complications
associated with exposure and death of the pulp.
1. If no occlusal interference, seal the occlusal surface with a
filled composite resin and flow it around the tubercle and
over the adjacent fissures.

2. If occlusal interference, reduce the tubercle to relieve the

occlusal interference and examine:

a. If pulp is not exposed, proceed as 1.

b. If pulp is exposed, perform partial pulpotomy and seal the adjacent

fissures.
 Double Teeth
• Double teeth are known by a variety of names including
‘fusion’, ‘gemination’, ‘dichotomy’, ‘synodontia’, ‘schizodontia’,
and ‘connation’.
• May be formed either by fusion of two developing tooth
germs or by gemination (partial dichotomy) of one tooth
germ.
• When the double tooth is formed by two teeth of the normal
series, it is called fusion. In this case one tooth of the normal
dentition will be missing (counting the double tooth as one).
• The term ‘double tooth’ avoids the difficulty to decide
whether an abnormally large tooth is the result of fusion of a
normal and a supernumerary tooth, or of gemination.
 Clinical Features
• A large tooth may be identified as a double tooth by notching in its incisal
edge, or by a longitudinal groove in its crown, or by partial or complete
separation of its roots. The root canal and pulp chamber may be either
single or largely separate for each component.
• Deciduous double teeth with hypodontia are usually followed by
hypodontia in the permanent dentition, while deciduous double teeth
without hypodontia are often followed by permanent supernumeraries.
Permanent dentition may be normal (almost 50%).
• Double teeth in the primary dentition needs to be carefully followed as
physiological root resorption is sometimes retarded leading to delayed
eruption of the permanent successors.
• Double teeth are considerably more common in the deciduous than the
permanent dentition.
• May occur unilaterally or bilaterally. Double teeth in the permanent
maxillary central incisor region are frequently bilaterally symmetrical.
 Prevalence

• Double teeth are rare.

• Prevalence in primary teeth: 0.5 – 1.6 %

• Prevalence in permanent teeth: 0.1 – 1.0 %

• No difference in prevalence in males and females.

 Aetiology and Associations
Aetiology:
• Exact aetiology is unclear.
• There is some evidence that the anomaly may be
genetically determined.
• Of the possible environmental factors, trauma can damage
developing teeth in such a way that the mature tooth
resembles a double formation.
Associations:
• Double and megadont teeth may sometimes occur
together, as do double and supernumerary teeth.
• Double teeth may also be part of syndromes such as
achondrodysplasia and chondroectodermal dysplasia.
 Complications and treatment
Complications:
• Caries, periodontal disease, aesthetic problems and malocclusions
have been reported.
Treatment:
• No treatment for primary double teeth.
• Treatment alternatives suggested for perm teeth include:
Acceptance with prevention, selective grinding to reduce width
and occlusal interference, placement of composite restoration,
surgical division, endodontics and extraction. In addition
orthodontic treatment is often beneficial.
• Patient’s expectations and cooperation must be assessed before
determining suitable management.
• It is advisable to defer the treatment until apical closure and
some recession of the pulp horns has occurred.
 Taurodontism

Taurodontism describes teeth (molars) in which the

body of the tooth containing the pulp chamber is
vertically enlarged at the expense of the roots.
 Clinical Features

• The anomaly is essentially diagnosed on radiographs.

• The normal constriction of a tooth at the level of the amelo-
cemental junction is frequently reduced or absent.
• Depending on the increasing degree of severity, the taurodont
teeth have been classified as hypotaurodont, mesotaurodont
and hypertaurodont.
• Deciduous molars has been seen with taurodontism.
• In permanent dentition, taurodontism is diagnosed most
often in molars and occasionally in premolars.
 Prevalence and Aetiology
Prevalence:
The prevalence for taurodontism ranges from 0.25 – 11.3
%. This wide range is due to wide variations in both
sampling methods and diagnostic criteria.
Aetiology:
• Taurodontism is thought to originate from a delay or
failure of invagination of Hertwig’s epithelial root sheath
which maps out the shape of the root.
• May be inherited as an autosomal dominant trait with
variable expressivity but more likely to be polygenically
determined.
 Associations

• Association has been reported with amelogenesis imperfecta.

Taurodontism is found in about 20 % of patients AI.

• Other associations include:

• Trico-dento-osseous syndrome
• Ectodermal dysplasia
• Ellis-van Creveld syndrome
• Achondroplasia
• Hemifacial hypoplasia
• Klinefelter’s syndrome (XXY)
 Clinical Consideration

Clinical consideration in the management of

taurodont teeth are:
• Endodontic treatment is difficult.
• Susceptibility to root resorption during orthodontic
treatment.

• Extraction may be more difficult.

• Anchorage value of teeth may be reduced.
 Dilaceration

A dilacerated tooth is one that has a distorted crown or root or

an abnormal bend of the root or crown or crown-root during
its development is called dilaceration.
Types:
1. Labial dilaceration or vestibular dilaceration
2. Palatal or lingual dilaceration
3. Lateral dilaceration

Dilaceration is most commonly associated with maxillary permanent

central incisors. A dilacerated tooth usually fails to erupt, but may
sometimes erupt into an abnormal position and cause displacement of
adjacent teeth.
 Etiology

1. Severe trauma to primary incisors is a common cause

of dilaceration.
2. Some cases are not associated with trauma and are
due to abnormal development of the tooth (Stewart
1978).
Severe injury to a maxillary primary incisor may cause dilaceration of
either the crown or the root (or crown-root) of the permanent successor,
depending on the stage of development of the permanent tooth and its
relationship to the root of the primary incisor at the time of injury.
Maxillary permanent incisors develop palatal to and very near to the root
apices of the primary incisors; as they erupt they move over the roots of
the primary teeth.
Etiology continues:

• Intrusion or displacement of the primary incisor in infancy is most likely to

displace the permanent tooth crown palatally – hence palatal dilaceration
of the crown. It also has hypoplasia of the enamel in the area of the
distortion.

• After about 4.5 years of age, when the roots of the permanent incisors are
forming and the teeth are moving over the primary incisor roots, injury to
the primary incisors will most likely cause labial dilaceration (of root) and
there will be no enamel hypoplasia.

• Dilaceration of the apical third of a permanent incisor root is caused by

injury to the tooth itself at the age of 8 – 10 years. Intrusion or gross
displacement of the tooth are the most likely causes.

• Dilacerated teeth not associated with trauma are gently curved from
crown to root; the crown is bent labially from the crown-root junction and
there is no enamel hypoplasia.
 Treatment

• Unerupted dilacerated teeth must be extracted if it is not

possible to bring the tooth into the arch by a combination of
surgery and orthodontics.

• Erupted teeth with root dilaceration are also usually extracted

if they are in an abnormal position because it is difficult to
move them orthodontically.

• After extraction, the space must either be maintained with a

prosthesis (to restore esthetics and to prevent tilting of
adjacent teeth) or closed orthodontically.
 Enamel Projections and Pearls
Enamel Projections:
These are irregularities of the enamel margin in molars in the
furcation area.
• Seen on deciduous second molars and all permanent molars.
• Occur more often on mandibular than maxillary teeth and more
common on the buccal aspect of tooth. May be predisposing factor
to periodontal disease.

• Prevalence range is from 6 – 24 %. Higher in Mongoloids.

• Enamel projections and enamel pearls tend to occur together.
• Often occurs bilaterally, suggests it is due to systemic rather than
localized factors.
Enamel Pearls:
Enamel pearls are isolated round or oval deposits called enamel
pearls, drops, nodules or exostoses. These may be composed of
enamel only or contain a dentine core, which may also enclose
an extension of pulpal tissue.
• Pearls composed of enamel only are very small (about 0.3mm) and difficult to
be detected macroscopically.
• Pearls containing dentine vary greatly in size. Enamel pearls may be extradental
or intradental (included in dentine).
• Enamel pearls are not seen in deciduous dentition.
• In permanent dentition, molars are most often involved, often bilaterally
symmetrical and the enamel is poorly mineralized.
• Prevalence range from 1 – 7 % (teeth examined macroscopically).
• Enamel projections and enamel pearls tend to occur together.
• Enamel pearls are probably indicative of some disturbance in the function of
Hertwig’s root sheath. Some pearls may be due to trauma.
 Accessory Cusps

Many teeth may have additional cusps. People with

large teeth tend to have more cusps.

• Talon cusps

• Shovel-shaped incisors

• Cusp of Carabelli
 Talon Cusp
The talon cusp (resemble an eagle’s talon) projects lingually
from the cingulum area of a maxillary or mandibular
permanent incisor.
• There is a deep developmental groove in which caries may develop
where the cusp blends with the sloping lingual surface.
• Talon cusp is composed of normal enamel and dentine and
contains a horn of pulp tissue.
• Talon cusp present problems because of its:
» Appearance
» Caries developing in the grooves
» Interference with occlusion
 Treatment

1. Soon after the tooth erupts, seal the developmental groove

at the junction between the cusp and the tooth if it is plaque
retentive.
2. If the cusp is causing occlusal interference or has caused
tooth displacement, either:
a. Selectively grind away much of the cusp over a period of time
(1mm at monthly intervals), encouraging obliteration of the pulp
horn with secondary dentine stimulated by the grinding.

b. If immediate treatment is required, administer LA, isolate the

tooth with rubber dam and remove the cusp. If pulp is exposed,
perform a conservative partial pulpotomy.
 Shovel-shaped incisors

• Shovel-shaped incisors with prominent lateral borders on the

lingual surfaces are found most frequently in mongoloid
races.

• The opposite variation in form, vertical ridges, marginal

cristae on the labial surface of incisors, is termed rugae
adamantinae and is rare.

• Very occasionally, the shovel shape is associated with rugae

adamantinae to give a ‘double shovel’ shape.
 Cusp of Carabelli

The maxillary first permanent molar frequently has an

additional cusp, the cusp or tubercle of Carabelli, located
mesiopalatally.

• Usually the cusp occurs bilaterally.

• Its prevalence ranges from approximately 10 – 60 % in
different populations.

• This may be of clinical importance when fitting bands on

these molars for orthodontic treatment.
Hutchinson’s incisors and Moon’s molars

Hutchinson described a triad of interstitial keratitis,

disease of the otic labyrinth and abnormal tooth
morphology of the permanent maxillary central
incisor in patients with congenital syphilis.

It has since been recognized that other teeth may be

involved.
 Clinical Features
Hutchinson’s Incisor:
The term ‘barrel-shaped’ is often applied to the typical
Hutchinson’s incisor. It is narrower at the incisal edge than at the
cervix, has rounded incisal angles and may have a notch of the
incisal edge.
Moon’s Molars:
Moon and Lus described the characteristic first permanent molar
defect, with a reduction of the crown form towards the occlusal
surface.
Mulberry Molar:
The so-called ‘mulberry molar’ of congenital syphilis is due to a
marked enamel hypoplasia affecting the first permanent molar.
-------------------------------------------------------------------------------------
Dental changes are seen in approximately 40 – 70 % of patients
with congenital syphilis (caused by spirochaete, Treponema
Pallidum).
 Abnormalities of Tooth Size

– Crown size
• Megadontia
• Microdontia

– Variations in Root Size

• Large root size
• Small root size
 Megadontia
Teeth larger than the range of normal variation for a given
population are called megadonts or macrodonts.

Clinical Features:

• Sometimes associated with increased complexity of form.

• Megadont upper incisors can be distinguished from double teeth by an

absence of notching of the incisal edge and the radiographic appearance
of the root and pulp.

• Localized megadontia may be bilaterally symmetrical and is found most

frequently in the permanent maxillary incisor and mandibular second
premolar regions.
Prevalence, Associations & Etiology

Prevalence: 1.1 % in the permanent dentition.

Associations:
• Generalized megadontia may occur in association with pituitary gigantism.
• Unilateral hyperplasia of the face is associated with megadontia of teeth
on the affected side.
• Megadont teeth may also be found in patients with hypertrichosis and
hereditary gingival hyperplasia.
Etiology:
The etiology of isolated megadontia is not known. It may be multifactorial,
with a polygenic hereditary component.
 Microdontia

Microdontia is defined as having small teeth.

Clinical Features:

• Microdont teeth may be small but of normal form or may be both of small
dimensions and of tapering (conical or peg) form.

• The commonest affected teeth are the permanent maxillary lateral incisor
and the third molar.

• Generalized microdontia is uncommon.

Prevalence, Associations & Etiology
Prevalence:
 Prevalence in primary dentition: 0.2 – 0.5 %
 Prevalence in permanent dentition:2.5 %
 Prevalence of generalized microdontia: 0.2 %
 Females are more frequently affected than males.
Associations:
 Microdontia may be associated with hypodontia of maxillary lateral
incisors.
 Microdontia is frequent in patients with Down’s syndrome and
ectodermal dysplasia.
Etiology:
 Twin and family studies show that etiology of microdontia has a
genetic component.
 Etiology may be multifactorial with the involvement of environmental
factors as well.
Abnormalities of Tooth Structure

 All tissues
 Enamel defects
 Dentine defects
 Cementum defects
 Discolourations
All Tissues

– Arrest of development of a tooth germ

– Odontodysplasia
 Arrest of Development of a Tooth Germ

• Arrested development of tooth germs may occur as a

complication of osteomyelitis or irradiation .

• May also occur as a rare sequel to either severe trauma or

infection spreading from carious deciduous teeth.

• In approximately 20 – 30 % of cases, infection of primary

teeth may spread to the follicular tissues of the underlying
permanent tooth germ.

• Eventually the tooth germ may be expelled or sequestrated.

 Odontodysplasia
Odontodysplasia is a rare developmental anomaly principally
affecting the coronal odontogenic tissues or a localized arrest in
tooth development. Also called ghost teeth or odontogenic
dysplasia.
Clinical Features:
 Occurs with equal frequency in both sexes. Seen twice as often in the
maxilla as in the mandible. Teeth of either dentition may be involved.
 Patient may present with delayed eruption of teeth. Teeth are affected in a
segmental or regional pattern, although the abnormality may cross the
midline, especially in the maxilla.
 Affected teeth have thin layers of poorly calcified enamel and dentin with
large, diffusely calcified pulp chambers and shortened, poorly defined
roots. Teeth are dysmorphic in overall appearance. If the teeth erupts,
may be mistakenly diagnosed as grossly carious.
 The ‘ghost-like’ radiographic appearance is characteristic of the condition.
 Etiology

No conclusive etiologic factor or inheritance pattern has been identified.

Suggested Etiology:
Disturbance of vascular supply to the area of the jaw either during
prenatal or early postnatal life.

Other Possible Causes:

 Radiation
 Osteomyelitis

Treatment:
Removal of the affected teeth and replacement.
 Enamel defects
• Genetically determined enamel defects
– Enamel defects confined to the dentition
• Amelogenesis Imperfecta
– Enamel defects associated with generalized defects
• Epidermolysis bullosa
• Pseudohypoparathyroidism
• Tricho-dento-osseous syndrome
• And so many other syndromes
• Environmentally determined enamel defects
– Localized
– generalized
 Amelogenesis Imperfecta

o Amelogenesis Imperfecta (AI) is a hereditary disorder which

primarily affects enamel formation.

o Major enamel matrix proteins (amelogenin, enamelin and

ameloblastin) are secreted during the process of amelogenesis.
The defects are a result of gene mutations associated with
these proteins. They follow an autosomal dominant, autosomal
recessive or x-linked pattern of inheritance.
o In AI the enamel in both the primary and the permanent
dentition will be affected.
Prevalence

The prevalence of AI is very varied:

 In US, the prevalence is: 1 : 14000
 In Europe, the prevalence is: 1 : 700

Varied prevalence of AI is thought to be due to:

1. Diagnosis
2. Gene Pooling
3. Racial differences (not sure)
Classification

• Several classifications.

• These classifications are based predominantly on the clinical

and radiographic appearance of the enamel defect OR are
based on the predominant clinical and radiographic
appearance of the enamel defect and the mode of
inheritance of the trait.

• The term AI was introduced by Weinmann, Svoboda and

Woods (1945) who divided the defects into two types, i.e;
hypoplasia and hypocalcification of the enamel.
Classification
The following classification is based on the predominant clinical
and radiographic appearance of the enamel defect.

Four main types of Amelogenesis Imperfecta:

1. Hypoplasia
2. Hypocalcification
3. Hypomaturation
4. Hypomaturation – hypoplastic with taurodontism.
( Fifteen genetically distinct types have been described by Winter & Brook 1975,
Witkop 1988).
Hypoplastic Amelogenesis Imperfecta

• Defect in the formation of the enamel matrix and therefore

the enamel does not develop to normal thickness.

• Enamel is randomly pitted, grooved or very thin.

• Enamel is hard and translucent.

• Autosomal dominant, autosomal recessive and x-linked

inheritance.

• Radiographically enamel contrasts normally from dentine.

Hypocalcified Amelogenesis Imperfecta

• Defect in the calcification of the enamel.

• Enamel is normal in thickness but is weak and opaque or

chalky in appearance.

• Teeth become stained and rapidly wear down to the dentine.

• Autosomal dominant and autosomal recessive inheritance.

• Radiographically enamel is less radio-opaque than the

dentine.
Hypomaturation Amelogenesis Imperfecta

• Enamel is of normal thickness but appears mottled in

appearance.

• Enamel is slightly softer than normal and is vulnerable to

attrition but not as severely as the hypocalcified type.

• Autosomal dominant, autosomal recessive and x-linked

inheritance.

• Radiographically enamel has similar radiodensity as dentine.

Hypomaturation – hypoplastic with
taurodontism

• Mixed hypomaturation / hypoplastic appearance.

• Taurodontism common feature.

• Autosomal dominant inheritance.

• Radiographically enamel has approximately the same or

slightly greater radiodensity than dentine.
 Treatment
 Because of the wide range in the severity of the clinical
problems in AI, it is not possible to give precise
recommendations for treatment. Only guidelines may be
provided.

 It is important to reassure and encourage the child and the

parent by telling them that treatment is possible but it will
need your interest and cooperation.

 Three principles of treatment in common with other

restorative treatment cases:
 Alleviation of pain.
 Restoration and maintenance of the remaining dentition.
 Maintenance / restoration of the occlusal vertical height.
Continues:

The management of young patients with amelogenesis

imperfecta is carried out in three stages:

 Temporary phase: Undertaken during the primary or mixed

dentition.

 Transitional phase: When all the permanent teeth have erupted

and continues till adulthood.

 Permanent phase: Occurs in adulthood.

Treatment for Primary Teeth with AI

Posterior Teeth:
• Stainless steel crowns (conservation of the primary molars ensure that
the 1st permanent molars erupt in their normal positions and normal height).

Anterior Teeth:
• Strip crowns
• In severe cases extraction is justified.
Treatment for Permanent Teeth with AI
Anterior Teeth:
 Small areas of hypomineralized labial enamel do not require
treatment because it may not be of concern to the child and
parent.

 Small areas of localized discolourations or hypoplasia may be

treated with composite resin.

 Severely hypoplastic teeth require extensive treatment because

the teeth are not only unsightly but also sensitive as a result of
exposed dentine. Porcelain jacket crowns not suitable for children
(large pulp chambers & passive eruption). Therefore:
 Composite veneers
 Porcelain veneers
 In adults, porcelain jacket crowns.
Continues:

Posterior Teeth:

 Small areas of hypoplastic enamel in posterior teeth can be

restored with amalgam, composite resin or glass-ionomer
cement.

 Stainless steel crowns for more severely affected molar teeth.

Cast veneers for premolars (SS crowns for premolars not
available).

 In adults, bonded porcelain crowns for posterior teeth

(premolars & molars).
Environmentally determined enamel defects
Localized & Generalized

Localized:
1. Infection
2. Trauma
i. Mechanical trauma
ii. Extraction of deciduous teeth
iii. Fracture of the jaw
iv. Cleft lip / palate ( defects attributed to surgical repair)

3. idiopathic
Generalized
Environmental influences may be:
 Prenatally
 Endocrine disturbances (e.g; hypoparathyroidism)
 Infections (e.g; rubella)
 Drugs ( e.g; thalidomide)
 Nutritional deficiencies (e.g; rickets)
 Haematological and metabolic disorders (e.g; hyperbilirubinaemia
associated with Rhesus incompatibility and erythroblastosis fetalis)
 Perinatally
 Early childhood
 Viral exanthematous diseases (common in early childhood) suggested (not
proved), if these can than what about gastroenteritis and pneumonia?
 Excessive chronic ingestion of fluoride in the drinking water.
 Tetracycline chelates calcium to form a tetracycline – calcium
orthophosphate complex.
 Hypothyroidism
 Idiopathic hypoparathyroidism
 Nephrotic syndrome
 Idiopathic
 Dentine defects
– Genetically determined dentine defects
• Confined to the dentition
• Hereditary opalescent dentine
• Coronal dentine dysplasia
• Radicular dentine dysplasia
• Fibrous dysplasia of dentine
• Shell teeth
• Associated with generalized conditions
• Osteogenesis imperfecta with dentinogenesis imperfecta
• Ehlers- Danlos syndrome
• Vitamin D-resistant rickets
• Vitamin D-dependant rickets
• Marfan’s syndrome
– Environmentally determined dentine defects
• Localized
• generalized
Dentinogenesis Imperfecta
Dentinogenesis Imperfecta (DI) is a hereditary disorder that
primarily affects dentine formation.

Incidence:
• Type I DI: 1 : 20,000

• Type II & III DI: 1 : 8000

• Type I DI appears in 20 – 40 % of patients with Osteogenesis

Imperfecta.

• Both sexes are equally affected.

• Both the primary and the permanent dentitions are affected.

Classification

Shields et al proposed the following classification of DI, which is

based upon the clinical appearance of various forms of DI:

Type - I DI that occurs in conjunction with Osteogenesis

Imperfecta (OI).
Type – II DI not associated with OI.
( Hereditary Opalescent Dentine)
Type – III Brandywine Isolate.
Only found in the tri-racial in-bred population of
Maryland, USA.
Type I DI: Associated with Osteogenesis
Imperfecta
• Autosomal dominant or recessive inheritance.
• Opalescent teeth, features similar to DI type – II.
• Defect in type-I collagen synthesis.
• Brittle bones.
• Blue sclera and impairment of hearing.
• Mainly affects primary dentition – features similar to DI type II.
• Variable expression in permanent dentition, usually affecting
lower incisors and canines.
• Similar radiographic appearance to type – II.
Type – II DI: Hereditary opalescent dentine
(Teeth only Affected)
• Autosomal dominant inheritance.

• All teeth in both the dentitions are usually affected.

• Defect in the mineralization of dentine.

• Enamel is normal but the ADJ is weak and cracking within

enamel / at ADJ can occur.

• Amber-brown or blue-grey discolouration of teeth with an

opalescent sheen.
• Radiographically crowns are bulbous with marked cervical
constriction and short, blunt roots are seen with partial or total
obliteration of the pulp chambers and root canals by dentine.
Type – III DI: Brandywine Isolate

• Rare autosomal dominant inheritance.

• Variant of Type – II DI.

• First described in tri-racial isolate in Maryland, USA.

• Similar radiographic appearance to Type – II DI.

Dentine dysplasia

• Dentine dysplasia has a similar clinical appearance to DI and

may be misdiagnosed.

• Dentine dysplasia is a hereditary disorder of both the primary

and permanent teeth.

• Shields et al described two types of dentine dysplasia:

• Coronal dentine dysplasia
• Radicular dentine dysplasia
Coronal Dentine Dysplasia

• Affects the primary and permanent teeth differently.

• Coronal dentine dysplasia in the primary dentition may be

difficult to differentiate clinically and radiographically from
hereditary opalescent dentine.

• The permanent dentition appear normal in colour but the

teeth characteristically exhibit thistle or flame-shaped pulp
chambers, with narrow or obliterated root canals upon
radiographic examination.
Radicular Dentine Dysplasia

• All teeth of both dentitions are involved.

• The colour of teeth varies from normal to having a slight

brown or blue tinge.

• On radiograph, the crowns have a normal outline but the

roots are short and blunt. The pulp chambers are small or
obliterated and no root canal is visible. The teeth may be lost
earlier because of short roots.
Fibrous Dysplasia of Dentine

• The permanent teeth have a normal form and

colour.

• Radiographs show the position of the pulp

chambers and canals only to be represented by
occasional radiolucent areas.
Shell Teeth

• Very rare variety of dentine defect, in which the teeth show

very large pulp spaces and little dentine formation.

• Histological examination show normal dentine for 1-2 mm

from the amelodentinal junction, then an abrupt change in
tubule direction and morphology in the remaining thin
dentine. Further dentine deposition appear to be completely
arrested.

• Described by Rushton. He traced them back and found to be

related to DI – II.
Treatment
• Unless teeth are crowned (especially posterior), they will be worn
down by attrition and have to be extracted. However, the teeth
may be unsuitable for crowning because they are poorly
supported by short, thin roots.

• In addition to the assessment of teeth for their suitability for

crowning, much depends on whether the patient is keen to have
the extensive treatment despite the uncertain prognosis.

• It should be noted that periapical radiolucencies and

spontaneous abscesses may occur in the absence of any
pathology in DI. The treatment is not affected by the form of DI
the patient has.
Continues:

Primary Dentition:
• Stainless steel crowns for primary molars.
• Anterior teeth may be restored with composite (strip crowns).

Permanent Dentition:
• In children, stainless steel crowns for molar teeth. Cast veneers for
premolars (SS crowns for premolars not available).
• Anterior teeth may be restored with composite (strip crowns).
• In adults, bonded porcelain crowns for posterior teeth and jacket
crowns for anterior teeth.
Continues:

• If it is decided not to undergo extensive conservative

treatment (because of poor prognosis), the teeth should be
retained for as long as possible though provision of dentures
will eventually be necessary.

• For a young patient, it is preferable to make over-dentures to

ensure the maintenance of alveolar ridges but eventually
normal dentures have to be provided.
Treatment of Osteogenesis Imperfecta (OI) with
Bisphosphonate Therapy
• Bisphosphonates are now a days used for the treatment of certain bone
disorders including Osteogenesis Imperfecta.
• Bisphosphonates affect bone metabolism by inhibiting osteoclast function and
hence bone resorption and, in doing so, reduce the turnover of bone.
• In children with OI, they have been shown to lower the risk of fractures and
reduce bone pain, amongst other beneficial effects.
• The relevance of these drugs to paediatric dentists is the potential risk of
bisphosphonate - associated osteonecrosis of the jaws (BONJ).
• The risks are low. The mandible, owing to its limited blood supply , is twice as
frequently affected as the maxilla.
• 60 % of BONJ cases in patients with myeloma or breast cancer have occurred
following a dental surgical procedure (e.g; extraction). So therapy after dental
fitness.
• At present, no known long-term side-effects of bisphosphonates in children,
and no known cases of BONJ have been reported.
• Bisphosphonates have a long half-life. So risk of developing BONJ many years
after the therapy.
 Environmentally determined dentine defects
Localized & generalized

Localized
• Injury to the developing permanent tooth germ via the
deciduous tooth interferes with dentine formation:
• A hypoplastic area in the enamel may show a corresponding zone
of interglobular dentine beneath.
• In cases of crown dilaceration and root angulation, the dentine is
always involved.
• Direct trauma to an erupted tooth may result in gradual
pulpal calcification.
• In some cases, post-traumatic irregular dentine formation has
been observed.
• Where a root fracture occurs, a calcific union with tissue
resembling osteodentine may sometimes follow.
Generalized:
• Generalized environmental insults which affect enamel
formation may also affect dentine. Therefore, in dentine,
there is a neonatal line corresponding to that in enamel.
• Factors retarding dentinogenesis in children:
• Tetracycline discolouration of dentine and delay in
dentinogenesis.
• Irradiation.
• Lathyrism.
• Hypothyroidism.

• Nutritional deficiencies of minerals, proteins and vitamins

may cause increased formation of interglobular dentine,
predentine and osteoid.
 Cementum defects

 Genetically determined
 Associated with generalized
defects

 Environmentally determined
Genetically Determined Cementum Defects
Associated with Generalized Defects:
Cleidocranial dysostosis
 Aplasia or hypoplasia of clavicles.
 Brachycephalic skull with pronounced frontal and parietal bossing.
 Delayed closure of the cranial fontanelles and sutures.
 Numerous wormian bones are formed in the suture lines, especially
lambdoidal sutures.
 Presence of large numbers of supernumerary teeth, especially in
the anterior segments of the jaws.
 Eruption of many deciduous and permanent teeth may be delayed
or fail completely.
 Histologically, there is hypoplasia of cementum, especially affecting
the cellular cementum.
Hypophosphatasia

• Low levels of serum alkaline phosphatase.

• Phosphoethanolamine in urine and plasma.

• Skeletal changes resembling rickets.

• Teeth may be affected by aplasia or hypoplasia of cementum

with the resultant lack of periodontal attachment and early
loss from the jaws.

• Best documented for the deciduous dentition, but may also

occur in permanent teeth.
Environmentally Determined Cementum Defect

• The formation of cementum on permanent teeth may

continue throughout life.

• Hypercementosis, stimulated by heavy occlusal loads or

chronic inflammation, may affect any tooth. Such excessive
cementum formation can lead to concrescence, the
pathological union of the roots of two or more teeth.
 Abnormalities of Colour
• The colour of a tooth depends 0n the amounts, quality
and relations of the different tissues forming the tooth.
• Teeth tends to darken in colour as the age advances.
• Therefore, there is a considerable variation between
individuals in what is ‘normal’ tooth colour.
• Classified into:
• Intrinsic (Internal)
• Extrinsic (External)
• A third category of ‘stain internalization’ has recently
been described where extrinsic stain enters the tooth
through defects in the tooth structure.
 Abnormalities of Colour
Internal
Generalized
•Developmental
•Hereditary
•Dentinogenesis Imperfecta
•Amelogenesis Imperfecta
•Environmental
•Fluorosis • Tetracycline antibiotics
•Erythroblastosis fetalis • Neonatal hepatitis
•Congenital malformations of the bile duct • Congenital erythropoietic porphyria
•Acquired
•Changes in colour with age
Localized
•Developmental
•Trauma (Enamel and dentine defects)
•Infection (Enamel and dentine defects)
•Acquired
•Early and extensive carious lesions • Effects of amalgam
•Some root canal filling materials • Pulpal hemorrhage.
•Pulpal necrosis • Pulpal calcification
•Internal (pink spot) resorption
.

External
• Generalized
• Localized
 Numerous external staining agents.
 More staining if hypomineralization of enamel, pits or
grooves, or marginal leakage of restorations.
 External staining agents include:
 Tobacco, betel nuts and medicaments such as iron, iodine,
and silver nitrate.
 The stannous ion of topical stannous fluoride preparations
may cause dark staining, particularly of demineralized area.
 The products of some of the bacteria found in oral flora may
cause staining in plaque which varies from brown and black to
green.
Odontomes
Odontomes are developmental malformations or tumors
containing enamel, dentine and pulp.
Types:
• Compound odontome
• Complex odontome

Etiology: Not known but the hypothesis are:

1. Hereditary
2. Hamartoma
3. Neoplasm
4. Local trauma & infection has also been proposed
Clinical Features:
• No sex predilection.
• Usually affect children and young adults.
• Occur more in maxilla than mandible.
• Compound odontomes have predilection for pre-maxilla (right side)
while complex odontomes occur mostly in posterior region of the
jaws.
• Presentation is usually as an asymptomatic bony swelling. Rarely
swelling become cystic.
• Commonly a tooth / teeth missing or unerupted. May cause localized
malocclusion.
• Usually discovered on routine radiographs or sometimes the
odontome get infected and cause problem.
• Sometimes surrounded by a thin radiolucent zone caused by the
fibrous capsule.
Compound Odontome

• A malformation in which all the dental tissues are represented in

an orderly pattern and hence the lesion consists of many tooth-
like structures.

• May present with the failure of permanent tooth eruption, jaw

swelling, or be diagnosed on routine radiography, usually
between 10 and 30 years of age.

• Most common in the anterior regions of the jaws.

• Compound odontomes are four times more common than

complex odontomes.
Complex Odontome
• A malformation in which all the dental tissues are represented
but occurring in a more or less disorderly pattern.
• There are usually no morphologically recognizable teeth
present radiographically, but histological examination will
reveal tooth- like structures.
• The quantity of each tissue and the degree of differentiation
varies between patients.
• Diagnosis is usually made radiographically in the 10 to 30-year
age group, occasionally because teeth are missing from the
arch.
• Most common in the posterior regions of the jaws (right side).
Similar distribution in the maxilla and mandible.
 Treatment of Odontomes

• Surgical enucleation of the hamartomatous mass ad

fibrous capsule.

• Recurrence very rare.

• Do histopathology because if ameloblastic odontoma,

may recur.

• Early diagnosis and treatment is of benefit to children.

Abnormalities of Eruption and Exfoliation
 Normal eruption
• Control
 Disturbances in Eruption
• Premature eruption
 Natal and neonatal teeth
• Retarded eruption
 Disturbances in Exfoliation
• Premature exfoliation
• Delayed exfoliation
 Infraocclusion
 Deciduous double teeth
 Hypodontia

 Impaction
 Normal eruption
• The time of eruption of a given tooth in a population is
influenced by both genetic and environmental factors.
• The first tooth to emerge in the majority of children is a lower
central incisor.
• There are a number of factors which influence the eruption
times of the permanent dentition:
• Sex: Permanent teeth erupt in females several months before
males.
• Race: Negroids erupt their permanent dentition earlier than
Mongoloids who in turn are in advance of Caucasians.
• Socioeconomic factors:
Possibly acting through nutrition, influence eruption times.
Children from higher socioeconomic groups erupt their teeth
earlier.
Disturbances in Eruption
 Premature Eruption

 There is often a family history of early eruption times.

 Children with a high birthweight tend to erupt their

deciduous teeth early.

 Precocious eruption of the permanent dentition is seen

in those who have precocious puberty and those with
excessive secretion of growth or thyroid hormones.
Natal and Neonatal Teeth
Teeth which are present in the mouth at birth are called natal
teeth while teeth which erupt during the 30 days following birth
are called neonatal teeth.
Clinical Features:

 Approximate prevalence is 1 in 3000.

 The teeth involved are usually lower central incisors of the

normal deciduous series.

 Usually there is excessive mobility of the teeth due to lack of

root development. The surrounding soft tissues are often
inflamed.
Etiology and Treatment
Etiology:
 Not known.
 It has been suggested that the tooth germs develop in an
abnormally superficial position.
 It may be hereditary as a familial pattern is often reported.
Treatment:
• Difficult to decide to retain or extract as they will not be
replaced by other deciduous teeth.
• Extraction is indicated :
• If the degree of mobility gives concern that the tooth may
become detached and inhaled.
• If there is excessive bleeding from the tooth attachment.
• If the teeth are interfering with feeding.
 Retarded Eruption

 Deviations of eruption times of up to 6 months for the

deciduous, and up to 18 months for the permanent,
dentition should not be considered abnormal.

 Delayed eruption of the deciduous dentition occurs in

children born pre-term with a low birth weight.
Localized Causes of Delayed Eruption
• Ectopic crypt positions
• Supernumeraries or Odontomes
• Early loss of deciduous teeth
• Space loss
• Impaction
• Crowding
• Dentigerous cyst
• Retained deciduous teeth
• Dilaceration
• Local bone or soft tissue pathology
Generalized Causes of Delayed Eruption
• Rickets
• Hypothyroidism (Cretinism)
• Fibrous dysplasia
• Down’s Syndrome and Turner’s Syndrome
• Cleidocranial dysostosis
• Gross nutritional deficiency
• Decreased growth hormone secretion
• Congenital heart defects
• Radiotherapy
Disturbances in Exfoliation
 Premature Exfoliation
• Extraction is the commonest cause of early tooth loss.
• Occasionally a disorder affecting the periodontium or a
systemic disorder may give rise to premature exfoliation.
These are:
• Aggressive periodontitis (juvenile periodontitis)
• Hypophosphatasia
• Papillon Lefevre syndrome
• Vitamin D-resistant rickets
• Diabetes mellitus
• Cyclic neutropenia and other immune defects
• Osteolytic lesions of the jaws
• Acrodynia
• Histiocytosis X
• Leukemia
 Delayed Exfoliation
Conditions leading to delayed exfoliation include:
 Infraocclusion
 Deciduous double teeth
 Hypodontia
 Other local causes of abnormal resorption and persistence
of deciduous teeth include:
 Ectopically placed permanent tooth germs
 Trauma
 Severe periradicular infection of deciduous teeth
Infraocclusion
An infraoccluded tooth is one that has failed to maintain its
occlusal relation to the adjacent and opposing teeth.
Clinical Features:
 Infraocclusion is usually associated with primary molars but
permanent molars are occasionally affected.

 The reported prevalence ranges from 1 – 9% with no difference in

frequency between boys and girls.

 The lower first deciduous molar is the most commonly affected tooth
although some studies reported it to be the second primary molar.

 The second molar tends to become grossly submerged more

frequently than does the first molar.
Etiology
• The etiology of Infraocclusion is not clear.

• Ankylosis may result from an imbalance of the normal pattern

of resorption and repair (excessive deposition of bone)that
characterize normal root resorption of primary teeth.

• It may follow infection or trauma, but the teeth involved are

often not infected and may not have an opponent.

• Also it has been suggested that the ankylosis is secondary to a

failure of the continued eruption of the tooth and vertical
growth of the alveolus.

• Genetic factors could be important.

Treatment

Many infraoccluded primary teeth (especially the first

primary molars) exfoliate normally and do not interfere
with the eruption of premolars. However, some form of
treatment becomes necessary:

• If there are radiological signs of interference with premolar

eruption.

• If there is a possibility of adjacent teeth tilting over the

submerged tooth.

• If there is a danger that the tooth may become submerged

below gingival level.
The type of treatment required depends on the degree of
infraocclusion:
• Minimal infraocclusion (marginal ridge of submerged tooth
occlusal to adjacent contact areas):
• Monitor to asses whether the condition worsens.
• Take radiographs every 6 – 12 months to determine whether premolar
eruption is being affected.
• Moderate infraocclusion (marginal ridge of submerged tooth just
cervical to adjacent contact areas). Two options:
• Retain the submerged tooth.
– Retain the tooth if no interference with premolar eruption.
– Restore normal contacts with adjacent teeth by fitting SS crown or by
building up the occlusal surface with composite resin.
• Extract the submerged tooth.
– Because of ankylosis the tooth will be more difficult to extract.
– Fitting of space maintainer may or may not be needed.
• Severe infraocclusion (marginal ridge at gingival level):
• Extract the submerged tooth.
• Consideration should be given to space maintenance.
Deciduous Double Teeth

• Deciduous double teeth may not exfoliate normally.

• The delayed resorption of deciduous double teeth may be

due to their greater mass of root dentine and the increased
area of root surface relative to the size of the permanent
successor’s crown.

• Delayed or ectopic eruption of the permanent tooth can be

prevented by careful follow up and surgical intervention at
the appropriate time.
Hypodontia

• A deciduous tooth without a permanent successor is

usually retained after the normal time of exfoliation.

• Resorption of the deciduous tooth usually does occur, but

it is slower.

• The retained tooth may be subject to excessive attrition.

 Impaction
An impacted tooth is one which remains unerupted because it is
impeded in its normal path of eruption.
• Impaction of deciduous teeth is rare, but it is quite common in the
permanent dentition.
• The teeth most frequently impacted are the third molars, the
maxillary canines and the premolars.
Etiological Factors:
• Supernumeraries can either impede the eruption of teeth of the normal
series or themselves become impacted.
• Crowding due to a discrepancy between arch size and tooth size may lead
to impaction.
• Dentigerous cysts and tumors may also cause displacement and
impaction of the teeth they involve
• Patients with Cleidocranial dysostosis may have many impacted teeth.
 Chemical and Physical Injuries

• Erosion
• Attrition
• Abrasion
• Irradiation
• Secondary Dentine
• Pulpal Calcification
• Hypercementosis
 Tooth Wear

Tooth wear may be caused by attrition, abrasion or erosion, or by

any combination of the three processes.

Attrition: Loss of dental hard tissue caused by tooth-to-tooth

contact.

Abrasion: Loss of dental hard tissue caused by object-to-tooth

contact (e.g; toothbrushing).

Erosion: Loss of dental hard tissue primarily caused by a

chemical process other than that which is involved in dental
caries.
Erosion

Dental erosion may be caused by:

 Extrinsic factors
 Intrinsic factors
Extrinsic factors:
• Include consumption of acidic foods and drinks, especially fruit
drinks and carbonated beverages.
• Excessive consumption of acidic foods and drinks is especially
hazardous in the primary dentition because the enamel and
dentine are thinner than in the permanent dentition.
• Certain medicinal preparations may also be highly acidic and will
cause erosion unless used carefully.
• Some occupations, e.g; battery construction, involve contact
with acidic substances. The workers may suffer from erosion of
the labial surfaces of the incisors.
Intrinsic Factors:
• Include recurrent vomiting resulting from an abnormality of the
GIT or from psychological disorders such as anorexia or bulimia
nervosa. Erosion will occur on palatal or lingual surfaces of teeth.
Treatment
We have to be vigilant to detect minor changes in enamel
indicative of erosion so that appropriate intervention can be
made:
1. Take a careful social, dental and medical history, and ask the parent to
complete a 3-day diet record.

2. If dietary factors are identified, ask the patient to reduce the frequency
of intake of erosive food and drink, to confine drinks to mealtimes, and
use a straw to reduce the erosive effect on anterior teeth (the most
affected).

3. Give OHI. Advise against brushing immediately after taking an acid

food or drink as this is likely to accelerate loss of enamel by abrasion.
4. In case of gastric regurgitation, advise the patient to use an alkaline
mouthwash immediately after regurgitation to neutralize the gastric acid.
Alternatively, make a mouthguard, to be worn at times of high risk, which
can be loaded with an alkali such as magnesium hydroxide or sodium
bicarbonate. The mouthguard can also be used for self-application of
fluoride gel.

5. If teeth are sensitive, advise use of a fluoride mouthrinse and a

toothpaste containing strontium chloride and fluoride, and apply topical
fluoride varnish.

6. The arrest or progress of erosion can be monitored using standardized

photographs and study models cast from silicone impressions.

7. The affected teeth should be restored only when the cause has been
identified and removed, otherwise erosion will continue around the
restorations. For restoration of anterior teeth composite resin or
porcelain veneers may be used. However, if buccal and lingual surfaces of
teeth are affected full coverage crowns may be indicated.
Resorption

• Aetiology of resorption

• External resorption

• Internal resorption
Aetiology of resorption
1. Acute mechanical trauma to the tooth, such as avulsion, subluxation or
root fracture.

2. Chronic trauma such as excessive occlusal load.

3. Some forms of orthodontic treatment.

4. Periapical inflammation and infection due to pulpal disease.

5. Teeth which remain completely embedded in the jaws are more prone
than others to undergo resorption.

6. Resorption of the roots of adjacent teeth may be caused by impacted

teeth.

7. The tumors that produce resorption of the roots of teeth are those with
moderate growth and expansion rates such as ameloblastomas.

8. Cause of the external resorption may remain obscure.

External Resorption
• More common than internal resorption.
• May affect different parts of the root surface and possibly
several areas at the same time.
• The prevalence of external root resorption increases with age
and there is no sex difference in frequency.
• Usually diagnosed by chance on radiograph although
occasionally the affected tooth may become mobile due to
severe resorption.
• Radiographic appearance varies with the area of the root
affected. In the apical region, the periodontal membrane may
remain of normal thickness and the apex may have a rounded
appearance.
Internal resorption

• Internal resorption has its origin on the pulpal wall of dentine.

• Occurs more often in anterior than posterior teeth.
• With increase in size of internal resorption, the color of the
clinical crown changes and is called ‘pink spot’.

• May be halted by root canal therapy, if there is no direct

communication of the internal (central) resorption with the
periodontal membrane.

• In primary teeth internal resorption may occur due to pulpal

inflammation.