Chapter one Developmental disorders of the teeth

Learning objectives

After studying this chapter should be able to:

 Understand the basis of the occurrence of developmental disorders of

the teeth.

 List & clinically differentiate different types of the developmental

disorders of the teeth.

Introduction:

In this chapter, several of the more common abnormalities & disturbances in

tooth morphology & formation will be discussed. These abnormalities may be
result of genetic factors, environmental factors, or a combination of the two.

Contents:

1. Alterations In Number
Anodontia
Supernumerary Teeth
2. Alterations In Size
Microdontia
Macrodontia
3. Alterations In Shape
Germination
Fusion
Concrescence
Dilacerations
Dens Invaginatus
Dens Evaginatus

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Chapter one Developmental disorders of the teeth

Taurodontism
Supernumerary Roots
Enamel Pearls
Shovel-shaped incisors
Congenital syphilis
4. Alterations in Structure
Defects of Enamel
Environmental Defects of Enamel
Amelogenesis Imperfect
Defects of Dentin
Dentinogenesis Imperfecta
Dentin Dysplasia
Defects of Enamel & Dentin
Regional Odontodysplasia
5. Alterations in Color
Exogenous Stains
Endogenous Stains
6. Alterations in Tooth Eruption
Early eruption
Delayed eruption
Dental anomalies are caused by complex multifactorial interactions
between genetic, epigenetic, and environmental factors during the long
process of dental development.

1. Alteration in number

Supernumerary teeth or hyperdontia

 This refers to a condition where extra teeth than normal are present.

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Chapter one Developmental disorders of the teeth

 Develop from

 Additional dental lamina near permanent tooth bud

 Splitting of the permanent tooth bud it self

 Present in Gardener’s syndrome & Cleidocranial dysplasia.

 Most common supernumerary tooth is mesiodens.

 Mesiodens is an extra tooth located between two maxillary incisors

(small conical tooth with a small root)

 Distomolar is the second most common supernumerary tooth. They

are situated distal to third molar.

 Paramolar are supernumerary teeth present either palatal or buccal to

molars.

 Natal teeth

 Rare event.

 Supernumerary teeth appearing at the time of birth.

 Commonly seen are prematurely erupted deciduous teeth.

 Usually mandibular central incisors.

 Natal teeth are teeth present at birth, and “neonatal teeth” are teeth
erupted within the first month of life. Premature eruption of a
tooth at the time of birth or too early is combined with many
misconceptions.

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Chapter one Developmental disorders of the teeth

Cleidocranial dysplasia

a. An autosomal-dominant of inheritance

b. Notable for aplasia or hypoplasia of clavicle (complete or partial

absence of clavicular calcification) responsible for long appearance
of the neck and narrow shoulder.

c. Craniofacial abnormalities.

d. The presence of numerous supernumerary & un-erupted teeth.

e. Maxillary hypoplastic gives the mandible prognathic appearance.

f. Un-erupted Supernumerary teeth.

g. Un-erupted teeth show:
 Hooked roots
 Enamel hypoplasia
 Conical crown
 Multiple dentigerous cysts
 Gemination
Gardner’s syndrome

a. Inherited as an autosomal-dominant disorder.

b. Characterized by intestinal polyposis, multiple osteomas, fibromas

of the skin, epidermal cysts, impacted permanent & supernumerary
teeth, & odontomas.

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Chapter one Developmental disorders of the teeth

Hypodontia or Anadontia

 Absence of all or some teeth.

 Most commonly missing tooth is third molars followed by maxillary

laterals and second premolars.

True Anodontia, classified as partial or total anodontia (Hereditary

Ectodermal Dysplasia) (ED , STREETER`S SYNDROME) resulting in lack of
hair (including eyebrows & eyelashes), toenails and fingernails can be
absent, thin, thick, grooved & poorly developed sweat glands.

Pseudo anodontia, when teeth are absent clinically because of impaction or

delayed eruption.

False anodontia, when teeth have been exfoliated or extracted.

2. Alteration in size
A. Microdontia
Generalized

All teeth in dentition appear smaller than normal.

Or teeth may be relatively small in comparison with large mandible and

maxilla.

Focal (localized)

Single tooth smaller than normal.

Seen in:

 Maxillary lateral incisor appears peg or cone (peg laterals).

An autosomal-dominant inheritance pattern.

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Chapter one Developmental disorders of the teeth

This disorder is often familial.

Are of no significance other than cosmetic.

 Maxillary third molar.

 Supernumerary tooth.

B. Macrodontia
Generalized

Enlarged teeth throughout dentition this may be seen in pituitary gigantism.

Or it may be owing to disproportionately small mandible and maxilla.

Focal (localized)

Abnormal large tooth or group of teeth.

This relatively uncommon condition is usually seen with mandibular third

molar.

Hemifacial hypertrophy, teeth in affected side are abnormally large compare

with unaffected side.

Is rare congenital disease characterized by unilateral enlargement of the head

and teeth.

Multiple etiologic factors, including anatomic & functional vascular or

lymphatic abnormalities, endocrine dysfunction, central nervous system
disturbances, chromosome disturbances, & asymmetric cell division.

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Chapter one Developmental disorders of the teeth

Craniofacial findings:

 Asymmetry of the frontal bone, maxilla, palate, mandible, alveolar

process, condyles, & associated overlying soft tissue.

 The skin may be thickened, with excessive secretions by sebaceous &

sweat glands & hypertrichosis.

 Unilateral enlargement of one the cerebral hemispheres may be

responsible for mental retardation in 15% to 20% of patients &
occurrence of seizure disorders.

The oral findings:

 Tongue is unilaterally hyperplastic.

 The fungiform papillae are usually enlarged & resemble soft polypoid
excrescences.

 Dysgeusia (A bad taste in the mouth) has been reported.

 Intraoral soft tissues are thickened & anatomically enlarged.

Dental findings

 Include abnormalities in crown size & root size & shape, as well as
precocious development & eruption.

 The permanent canines, premolars, & first molars are oft enlarged.

 When the primary dentition is affected, abnormalities are limited to

second molars &, less commonly, the canines.

 Unilateral macrodontia.

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Chapter one Developmental disorders of the teeth

 Root size & shape are proportionately enlarged or uncommonly

shortened, & premature apical development is usual.

 The primary teeth on the affected side calcify, erupt. & exfoliate sooner
than the contralateral teeth.

 Eruption of the affected permanent teeth by age 4 or 5 years.

Dental malocclusions
 Midline deviations, severely canted occlusal planes, & open bites are
common.

3. Alteration in shape

Gemination

 This is a developmental anomaly affecting shape of tooth in which a

single tooth germ is attempting to divide, by an invagination, resulting
in incomplete formation of two teeth.

 The permanent maxillary incisors the primary mandibular incisors are

most often affected.

 So affected tooth has a bifid crown (completely or incompletely

separated crown) with a single root.

 These teeth may be cosmetically unacceptable & may cause crowding.

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Chapter one Developmental disorders of the teeth

Fusion

 In this anomaly two normally separated tooth germs fuse (join) together
to form a single tooth.

 Depending on time of fusion the resulting tooth may be a completely

fused tooth with single crown and root or separated crown with single
root.

 Trauma may be suggested.

Germination of teeth may be distinguished from fusion by the fact that in

germination a full complement of teeth is present while in fusion a tooth is
usually missing when the anomalous tooth is counted as one. This rule is
compromised if a normal tooth fuses with a supernumerary tooth.

Concrescence
 Fusion of two teeth occurs by the deposition of cementum.

 Cause complication at the time of extraction.

 This may take place before or after eruption of teeth &n believed to be
related to trauma or overcrowding.

 Most commonly seen in association with maxillary second & third

molars.

 Surgical sectioning may be required to save the other tooth.

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Chapter one Developmental disorders of the teeth

Dilacerations

 Any sharp bend or curve in the root or crown of the tooth.

 This occurs due to trauma to the developing tooth.

 Difficult in extraction.

Taurodontism “bull-shaped” tooth

 Body of the tooth is enlarged at the expense of root.

 Due to failure of HERS to invaginate at the proper horizontal level.

 Appears rectangular without cervical constriction and the bifurcation of

the root is shifted more apical than normal.

 X-ray pulp chamber appears to be extremely enlarged with increased

apico-occlusal height.

 May be seen as an isolated incident & in association with syndromes

such as Down’s syndrome & Klinefelter’s syndrome.

Dens Invaginatus (Dens in dente)

 Invagination of enamel organ into the dental papilla during

odontogenesis.

 Varies from slightly accentuated lingual pit to a deep folding reaching

the root of the tooth.

 X-ray: Pear shaped radiolucency in enamel and dentin with a narrow

constriction at the opening surface.

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Chapter one Developmental disorders of the teeth

 Because the defect cannot kept free of plaque & bacteria, dens
invaginatus predisposes tooth to early decay & subsequent pulpitis.

 Prophylactic filling of pit is recommended.

Dens Evaginatus (Leung’s premolar)

 Evagination of IEE and dental papilla into the enamel organ.

 The presence of a globule of enamel or an extra cusp on the occlusal

aspect between the buccal and lingual cusp.

Enameloma (enamel preal)

 Globule of enamel seen on the root near cemento enamel junction or

close to furcation area.

 These structure may have a central core of pulp covered by dentin and
enamel.

Hypercementosis

 Deposition of excessive cementum that is continuous with the normal

cementum.

Talon cusp (resembles eagle’s talon)

 This is an anomalous cusp like structure projecting from the lingual

aspect, in the region of cingulum of maxillary and mandibular incisors.

 With Sturge-Weber syndrome, a red or pink birthmark called a port-

wine birthmark.

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Chapter one Developmental disorders of the teeth

Supernumerary roots

 Commonly seen in mandibular canines, premolars, & molars

(especially third molars).

Shovel shaped incisor

 Morphological anomaly of the crowns of incisor teeth.

 Prominence of the mesial & distal marginal ridges which encloses a

central fossa on the lingual surface of incisor teeth.

 Common in maxillary teeth than in the mandibular teeth.

Congenital syphilis

 Etiology: Treponema pallidum (a spirochete).

 Identified by silver stains (Warthin-Starry, Steiner or Leveditti).

 Transmission:

Sexual intercourse with infected partner.

Contact with open wound (e.g. dentists).

 Acquired in-utero from infected mother.

 Rare today because of routine serologic tests.

Features:

1. Frontal bossing of skull.

2. Short maxilla with high palatal vault.

3. Saddle nose.

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Chapter one Developmental disorders of the teeth

4. Hypoplastic teeth (Hutchinson’s incisors and Mulberry molars).

5. Rhagades: fissures around mouth.

Hutchinson’s triad:

A. Mulberry molars + Hutchinson’s incisors.

B. Interstitial keratitis (scarred cornea).

C. 8th cranial nerve affection leading to deafness.

4. Alterations in Structure:

Defects of Enamel
a) Environmental Defects of Enamel:

During enamel formation, ameloblasts are susceptible to various external

factors that may be reflected in erupted teeth.
1. Quantitatively defective enamel, when of normal hardness, is known as
enamel hypoplasia.
2. Qualitatively defective enamel, in which normal amounts of enamel are
produced but hypomineralized, is known as enamel hypocalcification.
Etiologic factors may occur locally, affecting only a single tooth, or they
may act systemically, affecting all teeth in which enamel is being formed.

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Chapter one Developmental disorders of the teeth

Turner’s tooth (Acquired):

Local trauma or abscess formation can adversely affect the ameloblasts
overlying developing crown, resulting in enamel hypocalcification or
hypoplasia.
Affected teeth may have areas of coronal discoloration, or they may have
actual pits & irregularities.
Most commonly seen in permanent dentition in which the overlying
deciduous tooth become abscessed or is physical forced into enamel organ
of permanent tooth.
Dental fluorosis (Systemic):
Fluorosis occurs if the level of fluoride ions reaches 1.5 ppm or more.
Mild to moderate fluorosis ranges clinically from white enamel spots to
mottled brown-and-white discolorations.

Severe fluorosis appears as pitted, irregular, & discolored enamel.

Although fluoride-induced enamel hypoplasia or hypocalcification is

caries resistant, it may be cosmetically objectionable, making aesthetics
dental restorations.

Very Mild Small, opaque, paper white areas scattered irregularly over the
tooth but not involving as much as approximately 25% of the
tooth surface.

Mild The white opaque areas in the enamel of the teeth are more
extensive but do involve as much as 50% of the tooth.

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Chapter one Developmental disorders of the teeth

Moderate Chalky and discolored areas involving the whole surface.

Severe Enamel is opaque, pitted, brown, brittle and easily chipped away.

b) Amelogenesis imperfecta:
Mutations in 5 genes have been associated with amelogenesis imperfecta.

Inheritance Phenotype Related gene

Autosomal dominant Generalized pitted

Autosomal dominant Localised hypoplastic ENAM (enamelin)

Autosomal dominant Generalized thin ENAM

Autosomal dominant Hypocalcification

Autosomal dominant With taurodontism DLX3

Autosomal recessive Localized hypoplastic

Autosomal recessive Generalized thin

Autosomal recessive Pigmented MMP20, KLK4

hypomaturation (enamelysin, kallikrein-
4)

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Chapter one Developmental disorders of the teeth

Autosomal recessive Hypocalcification

X-linked Generalized thin AMELX (amelogenin)

X-linked Diffuse hypomaturation AMELX

X-linked Snow–capped
hypomaturation

The formation of enamel is a multistep process, and problem may arise in any
one of the steps.
Development of enamel (3 major stages):
1. Elaboration of the organic matrix
2. Mineralization of the matrix
3. Maturation of the enamel
The hereditary defects of the formation of enamel also divided along these
lines:
1. Hypoplastic
2. Hypoclacified
3. Hypomaturation
 Hypoplastic amelogenesis imperfecta
In the generalized pattern,
Pinpoint-to-pinhead-sized pits are scattered across the surface of the teeth.
The buccal surfaces of the teeth are affected more severely.

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Chapter one Developmental disorders of the teeth

The pits may be arranged in rows or columns.

Staining of the pits may occur.
The enamel between the pits is of normal thickness, hardness, & coloration.
In localized pattern,
The affected teeth demonstrate horizontal rows of pits, a linear depression, or
one large area of hypoplastic enamel surrounded by a zone of
hypocalcification.
The altered area is located in the middle third of the buccal surfaces of the
teeth.
The incisal edge or occlusal surfaces usually is not affected.
Both dentitions (and only primary teeth) may be affected.

In the autosomal dominant smooth pattern (generalized thin pattern), the

enamel of all teeth exhibits a smooth surface and is thin, hard, & glossy.
The absence of appropriate enamel thickness results in teeth that are shaped
like crown preparation & demonstrate open contact points and anterior open
bite.
The color of the teeth varies from opaque white to translucent brown.
Radiograph demonstrate thin peripheral outline of radiopaque enamel.
Unerupted teeth may undergo resorption.

X-linked amelogenesis subdivision

X-linked smooth pattern
In males
◦ Exhibit diffuse thin, smooth, & shiny enamel in both dentitions.

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Chapter one Developmental disorders of the teeth

◦ The teeth oft have the shape of crown preparation & demonstrate open
contact points.
◦ The color varies from brown to yellow-brown.
◦ Radiograph demonstrate thin peripheral outline of radiopaque enamel.
◦ Unerupted teeth may undergo resorption.
In females
◦ Exhibit vertical furrows (grooves) of thin hypoplastic enamel, alternating
between bands of normal thickness.
◦ The females are mosaics, with mixture of cells, some with active maternal
X chromosomes & others with parental X chromosomes. Usually the mix
is of approximately equal proportions. If one X were to direct the formation
of defective enamel and the other X were to form normal enamel, then the
teeth exhibit alternating zone of normal and abnormal enamel in females.
◦ The banding oft is detectable with dental radiographs.
◦ An open bite is seen in almost all males & in minority of females.

In the rough pattern (generalized thin pattern), the enamel is thin, hard, &
rough-surfaced,
As in the smooth forms, the teeth taper toward the incisal-occlusal surface &
demonstrate open contact points.
The color varies from white to yellow white.
The enamel is denser than that seen in the smooth patterns, & the teeth are
less exposed to attrition.
Radiograph demonstrate thin peripheral outline of radiopaque enamel.
Unerupted teeth oft undergo resorption.
An anterior open bite.

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Chapter one Developmental disorders of the teeth

Enamel agenesis:
Total lack of enamel formation.
The teeth are the shape & color of dentin, with a yellow-brown hue, open
contact points, & crowns taper toward the incisal-occlusal surface.
The surface of dentin is rough, & an anterior open bite.
Radiographs demonstrate no peripheral enamel overlying dentin.
A lack of eruption of many teeth with significant resorption.
In autosomal recessive pattern amelogenesis imperfecta termed enamel
agenesis, the presence of a thin band of enamel has been confirmed.
 Hypocalcified amelogenesis imperfecta
In this type the enamel matrix is laid down appropriately but no significant
mineralization.
Types are autosomal dominant & recessive.
The teeth are appropriately shaped on eruption, but enamel is very soft &
easily lost.
On eruption the enamel is yellow-brown to black exhibits rapid calculus
apposition.
With years of function much of the coronal enamel is removed, except for the
cervical portion that is occasionally calcified better.
Unerupted teeth & anterior open bite are not rare.
Both patterns are similar, but the autosomal recessive examples are generally
more severe than the autosomal dominant.
 Hypomaturation amlogenesis imperfecta
The enamel matrix is laid down appropriately & begins to mineralize;
however, there is a defect in the maturation of the enamel’s crystal structure.
Affected teeth are normal in shape but exhibit a mottled, opaque white-brown-
yellow discoloration.

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Chapter one Developmental disorders of the teeth

The enamel is softer than normal & tends to chip from underlying dentin.
Radiographically, the affected enamel exhibits a radiodensity that is similar
to dentin.
Types:
1. Pigmented pattern
2. X-linked pattern
3. Snow-capped patterns
Pigmented pattern
Surface enamel mottled & agar-brown.
Enamel oft fractures from the underlying dentin & is soft enough to be
punctured by a dental explorer.
Surface enamel may be affected severely & be similar in softness to that of
hypocalcified. These cases often demonstrate extensive calculus deposition.
X-linked pattern
Affected male:
Exhibit different patterns in deciduous & permanent dentitions.
The deciduous teeth are opaque white with translucent mottling.
The permanent teeth are opaque yellow-white & may be darken with age.
Enamel tends to chip & oft can be punctured with a dental explorer point.
The degree of enamel loss is more rapid than that in normal teeth but not that
seen in hypocalcified forms.
Focal areas of discoloration may develop within the white opaque enamel.
Radiographically, the contrast between enamel & dentin is reduced.
Affected females:
Exhibit similar pattern in both dentitions.

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Chapter one Developmental disorders of the teeth

The teeth demonstrate vertical bands of white opaque enamel & translucent
enamel.
Radiographically, the bands are not visible, & the contrast between enamel &
dentin is within normal limits.
Snow-capped patterns
Exhibit a zone of white opaque enamel on the incisal or occlusal one quarter
to one third of the crown.
Both dentitions are affected.
Most cases demonstrate an X-linked pattern of inheritance.
Defects of Dentin
A. Dentinogenesis imperfect (hereditary opalescent dentin; Capdepont’s
teeth)
Dentin defects associated with osteogenesis imperfect are termed
(osteogenesis imperfecta with opalescent teeth).
All teeth in both dentitions are affected. The severity of the dental alterations
varies with the age at which the tooth developed.
Deciduous teeth are affected most severely, followed by the permanent
incisors & first molars, with the second & third molars being least altered.
The dentitions have a blue-to-brown discoloration oft with a distinctive
translucence.
The enamel frequently separates easily from underlying defective dentin.
Once exposed, the dentin demonstrates significantly accelerated attrition.
Radiographically, the teeth have bulbous crowns, cervical constriction, thin
roots, & early obliteration of the root canals & pulp chambers.

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 Chapter one Developmental disorders of the teeth

Dentinogenesis imperfecta III (Shell teeth):

Demonstrate normal-thickness enamel in association with extremely thin
dentin & enlarged pulps.
The thin dentin may involve the entire tooth or be isolated to the root.
Most frequently in deciduous teeth in presence of dentinogenesis imperfect.

Shields Clinical Witkop system Inheritance Gene

presentation
Dentinogenesis Osteogenesis Dentinogenesis Autosomal COL1A1,
imperfecta I imperfecta imperfecta dominant or COL1A2
with recessive
Encodes
opalescent
production of
teeth
type I
collagen
Dentinogenesis Isolated Hereditary Autosomal DSPP
imperfecta II opalescent opalescent teeth dominant
(dentin
teeth
sialophospho
protein)
Dentinogenesis Isolated Brandywine Autosomal DSPP
imperfecta III opalescent isolate known dominant
teeth as shell teeth

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Chapter one Developmental disorders of the teeth

Histopathology:
Coronal dentin exhibiting short misshapen tubules within atypical granular
dentin matrix.
B. Dentin dysplasia
Types
Dentin dysplasia I (radicular type)
Dentin dysplasia II (coronal type)
Autosomal dominant
DSPP gene mutated
In dentin dysplasia type II, the color of primary dentition is opalescent & the
permanent dentition is normal; in type I both dentitions are of normal color.
The coronal pulps in type II are usually large (thistle tube appearance).
Periapical lesions are not a regular feature of type II, as they are of type I.
Crowns appear normal in color & shape in dentin dysplasia I.
Premature loss may occur because of short roots or periapical inflammatory
lesions.
Teeth show greater resistance to caries than do normal teeth.

Radiographically,
Type I:
Obliterated pulps, short roots, & periapical lesions.
Horizontal ribbons (chevrons/ residual fragments) of dental pulp.
Type II:
Deciduous teeth as type I.

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Chapter one Developmental disorders of the teeth

Permanent teeth exhibit enlarged pulp chambers (thistle tube appearance/

flame-shaped), & numerous pulp stones.
Defects of enamel & dentin:
Regional odontodysplasia (Ghost teeth):
Involves the hard tissues that are derived from both epithelial (enamel) &
mesenchymal (dentin & cementum) components of the tooth-forming
apparatus.
Causes: trauma, nutritional differences, infections, metabolic abnormalities,
systemic diseases, local vascular compromise, & genetic influences.
The teeth in a region or quadrant of the maxilla or mandible are affected to
the extent that they exhibit short roots, open apical foramina, & enlarged pulp
chambers.
The thinness & poor mineralization quality of enamel & dentin layers.
One or both dentitions may be affected. The permanent more than deciduous,
& maxillary anterior more than other teeth.
Eruption of affected teeth may be delayed or not occur.
Treatment: poor quality of affected teeth; removal is indicated & resorted by
implant or a prosthesis.
Histopathological features:
Follicular tissue contains scattered collection of enameloid conglomerates
(focal collection of basophilic enamel-like calcifications) & islands of
odontogenic epithelium.
Lesions associated with regional odontodysplasia:
Ectodermal dysplasia
Neurofibrmatosis
Rh factor incompatibility
Vascular nevi

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Chapter one Developmental disorders of the teeth

5. Alterations in Color

Extrinsic Intrinsic

Bacterial stains Amelogenesis imperfect

Iron Dentinogenesis imperfect
Tobacco Dental fluorosis
Food and beverages Erythropoietic porphyria
Gingival hemorrhage Hyperbilirubinemia
Restorative materials Trauma
Medications Medications

Tobacco discoloration = extrinsic brown stains of the enamel on the lingual

surfaces of the anterior mandibular dentition.
Use products of high amounts of iron or iodine = black pigmentations of
the teeth
Chlorhexidine = yellow-brown stain that predominantly involves the
interproximal surfaces near the gingival margins
Erythropoietic porphyria (pink teeth, lavender teeth):
Resulting in the accumulation of protoporphyrins in red blood cells.
One of several inborn errors of porphyrin metabolism.
Autosomal-recessive trait.
Also associated with photosensitivity, vesiculobullous skin eruptions, red
urine, & splenomegaly.
Teeth may appear red to brown because of deposition of porphyrin in the
developing tooth.
Affected teeth fluoresce bright red under UV light.

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Chapter one Developmental disorders of the teeth

Rh incompatibility (erythroblastosis fetalis):

Endogenous staining in primary teeth.
Because of red blood cell hemolysis resulting from maternal antibody
destruction of fetal red blood cells, blood breakdown products (BILIRUBIN)
are deposited in developing primary teeth (green to brown).
Tetracycline stain
Tetracycline stain yellow color of the posterior teeth and grey color of anterior
teeth.
Can cross placenta, it may stain primary teeth.
If it administered between birth and age 6 or 7 years, permanent teeth may be
affected.

6. Alterations in Tooth Eruption

Early eruption:
Usually affects deciduous teeth.
Occurs in hemifacial hypertrophy.
Of no clinical significance.
Delayed eruption:
1. Impaction:
Most often affects third molars and maxillary canines.
Impaction occurs because of obstruction from crowding or from other
physical barrier.
It may be due to an abnormal eruption path, because of unusual orientation of
the tooth germ.
Eruption squestrum: Small spicule of non-vital bone may be seen
radiographically or clinically overlying the crown of partially erupted
permanent posterior tooth.

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Chapter one Developmental disorders of the teeth

2. Ankylosis:
The fusion of a tooth to surrounding bone, is another cause of impaction.
This usually occurs in association with erupted molars. It may result in
impaction of a subjacent permanent tooth.
The reason is unknown, but it believed to be related to periapical inflammation
and subsequent repair. With the focal loss of the periodontal ligament, bone
and cementum become mixed, causing fusion of the tooth to alveolar bone.

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