DEVELOPMENTAL DISORDER OF

SIZE AND SHAPE OF THE TEETH

1
 INTRODUCTION
Disorders of development of teeth

Disorders of development of teeth may be

prenatal or postnatal in origin and may be inherited
or acquired.

Their recognition and evaluation require a

thorough knowledge of the normal chronology of
the human dentition and of the normal development
and structure of the teeth.

2
Disorders of development of teeth may be due to
abnormalities in the differentiation of the dental
lamina and the tooth germs, causing anomalies in
the number, size, and form of teeth (abnormalities
of morphological differentiation)
or to abnormalities in the formation of the dental
hard tissues resulting in disturbances in tooth
structure (abnormalities of histo differentiation).

3
 Developmental Anomalies
Hypodontia
Alteration of
number
Hyperdontia
Alteration of
size
Developmental
anomalies
Alteration in
shape

Alteration in
structure

Amelogenesis
imperfecta
Gemination Taurodontism Dilaceration

Dentinogenesis
imperfecta Fusion Talons cuap

Dens
Regional Concresence
evaginatus 4
odontodysplasia
 Developmental alteration in number
Hypodontia

Definition
The developmental absence of multiple teeth usually in association with
systemic manifestations

Etilogy

Autosomal dominant with incomplete penetrance,trauma , infection of the

developing tooth bud ,radiation overdose ,glandular dysfunction ,
Systemic conditions-rickets , syphillis, german measles during pregnancy
and severe intrauterine disturbances .
Absence of appropriate dental lamina.

5
Clinical features

Missing tooth:
Primary or permanent.

Other abnormalities
-fusion,ankylosis and short roots.

Syndromes-hereditary ectodermal dysplasia.

Treatment-orthodontic closure of the space or a prosthesis.

control of caries
crown recontouring

6
 Hyperdontia

An excess number of teeth when compared to the normal dental formula

Etiology

Recessive, autosomal or sex linked

Cleft lip and palate-28%
Cleidocranial dysplasia
Gardiners syndrome
Continued activity of the dental lamina after the formation of the normal number of
tooth buds.

Clinical features
Types include- mesiodens, supplumental tooth, paramolar and distomolar

Treatment
Surgical removal
Orthodontic alignment if needed.

7
 ANOMALIES AFFECTING SIZE OF TEETH
MICRODONTIA:
• Microdontia is a common disease of teeth.
• This is the disease in which all or some teeth of a person are smaller
than the normal size. ,
• Which occurs because of the genetic disorders.

TYPES OF MICRODONTIA

• TRUE GENERALIZED
• RELATIVE GENERALIZED
• LOCALIZED

8
 TRUE GENERALIZED
• All the teeth are smaller than normal(fig:1)
• Occurs in pituitary dwarfism, down’s
syndrome and congenital heart disease

Fig : 1

9
 RELATIVE GENERALIZED

Normal-sized teeth may appear small when widely spaced

within jaws that are larger than normal, this appearance has
been historically termed relative microdontia (fig:2)
It is hereditary.
It often exhibits spacing between the teeth.

Fig:2
10
 LOCALIZED
• It involves only single tooth.
• It occurs with congenital heart disease, down syndrome
CLINICAL FEATURES:
Maxillary lateral incisors(peg shaped laterals) fig:3
and 3rd molars

11
 MACRODONTIA
• Also called as megadontia fig:4
• It is of three types
TRUE MACRODONTIA:(fig :4)
• All the teeth are larger than normal.
• It is commonly associated with pituitary gigantism
RELATIVE GENERALIZED: (fig :5)
Teeth normal or slightly larger than normal teeth, but present
in small jaw

Fig:5
LOCALIZED: one or more large teeth
exits in relation to an normal dentition
12
Clinical features :
 Crowding results in malocclusion
• Space is less
• Impaction of teeth

13
 ANOMALIES AFFECTING SHAPE OF TEETH
GEMINTION:
Defined as a single enlarged tooth or joined
tooth in which the tooth count is normal when the
anomalous tooth is counted as one.(fig:6&7)
Fig:6 Fig:7

14
CLINICAL FEATURES
• The commonly affected teeth are deciduous mandibular
incisors and permanent incisors.
• Bifid crown on single root (fig:8 &9)
• It does not increase or decrease the number of teeth present
• Enamel or dentin of crown of geminated teeth may be
hypoplastic or hypocalcified fig:9
• fig: 8

15
 FUSION
Defined as a single enlarged tooth or joined tooth
in which the tooth count reveals a missing tooth when the
anomalous tooth is counted as one.(fig:10)

fig:10

ETIOLOGY:
• Autosomal dominant trait
• Two separate developing tooth germ being initially close
together as they grow and expand they contact with each
other and the germs fuse to varying degree

16
 CLASSIFICATION
COMPLETE:
• If fusion take place before calcification, the two teeth may be
completely united to form a single large tooth
INCOMPLETE:
• When the portion of crown has completed its formation ,
then there is union of root only.
CLINICAL FEATURES:
• Most common in anterior teeth(fig:11 & 12)

• Fig:11 Fig:12

17
• Deciduous dentition(fig:13)
fig:13

• Between a normal tooth and supernumerary tooth

Fig:14

• If deciduous teeth fuse , the corresponding permanent

teeth may be absent
• Dental caries is common in fused teeth
• Reduce number of teeth in jaws
• Treatment-surgical division and selective shaping of the
crown.
18
CONCRESCENCE:
Concrescence is the union of two teeth by cementum without
confluence of the dentin(fig:15,16&17)

Fig:15
Fig:16 Fig:17

19
ETIOLOGY:
Occur due to traumatic injury
Over crowding of teeth with resorption and
interdental bone loss.
Distal inclination of crown of molar,
Space restriction during development
Excessive occlusal trauma and local infection after
development .

20
TYPES
• True concrescence: if roots are bound
during development
• Acquired concrescence: if the condition
occurs after development

21
CLINICAL FEATURES:

• Common in maxillary 2d and 3rd molar(Fig:18)

• Either primary or secondary teeth

are affected
Fig:18
• Usually involved are only two teeth, roots are fused
by cementum

• Teeth may fail to erupt or incompletely erupt

• There may be malocclusion or teeth may be
impacted

22
• The developmental pattern often involves a second
molar tooth in which its roots closely approx the
adjacent impacted third molar

• The post inflammatory pattern frequently involves

carious molar in which the apices overlie the roots of
horizontally or distal angulated third molars.

• This latter pattern most frequently arises in a carious

tooth that exhibits large coronal tooth loss

23
• The resultant large pulpal exposure often permits pulpal
drainage, leading to a resolution of a portion of the intra bony
pathosis
• Cemental repair then occurs(fig:19)

Fig:19

24
TALON’S CUSP:
• It project lingually from cingulum area , of maxillary and
mandibular teeth or it is an anomalous hyperplasia of cingulum
on the lingual of maxillary and mandibular incisors, resulting in
the formation of supernumerary cusp (fig:20&21)
Fig:20 Fig:21

25
PATHOGENESIS
• A focal proliferation of tissue during development and
excuberant development of the fourth lobe (cingulum)
leads to development of talon cusp

CLINICAL FEATURES:
• common in both dentition
• Resembles like an eagle’s talon(fig:22)
• Cusp blends with the sloping lingual tooth Surface
• Talon cusp on mandibular lateral incisor
fig:22

26
• It composed of normal enamel, dentin and contains a form of
pulp tissue
• It is usually ‘T’ shaped(fig:23)
• Patient face problem with high incidence of caries.
• It is associated with RUBINSTEIN –TAYBI SYNDROME.

Fig:23

27
• Because many of these cusps contain pulp , rapid
removal often results in pulpal exposure

• Removal without the loss of vitality may be

accomplished through periodic grinding of the
cusp , with time allowed for tertiary dentin
deposition and pulpal recession.

• After successful removal , the exposed dentin is

covered with calcium hydroxide , the peripheral
enamel is etched , and composite resin is placed.

28
• On eruption , the affected tooth should be inspected for
the presence of a deep fissure at the junction between
the Talon’s cusp and surface of the tooth.

• If a fissure is present , it should be restored to avoid

early carious extension into the nearby dental pulp.

29
DILACERATION
The term dilaceration refers to an angulation or a
sharp bend or curve, in the root or crown of a formed
teeth(fig:24)

Fig:24

ETIOLOGY:
• Injury that displaces the calcified portion of the tooth
germ, and the remainder of the tooth is formed at an
abnormal angle
The damage frequently follows avulsion or intrusion of
the overlying primary predecessor.
30
• Bend develops secondary to the presence of an adjacent
cyst,tumor or odontogenic hamartoma

CLINICAL FEATURES:
• It is commonly formed in maxillary incisors
• The curve or bend may occur anywhere along the length of
the tooth, sometimes at cervical portion or midway along the
root or even just at the apex of root(F ig25&26)

Fig :25 Fig :26

31
DENS IN DENTE
• It is also called as dens invaginatus ,ordilated composite
odontome or gestant odontome
• It is a developmental variation which arises as a result of an
invagination in the surface of tooth crown before
calcification has occurred(Fig :27)

Fig :27

32
DENS EVAGINATUS

• Dens evaginatus appears clinically as an accessory cusp

or globule of enamel on occlusal surface, between buccal
and lingual cusp of premolar(Fig35)

Fig35

33
CLINICAL FEATURES:
• It occur on premolar and molar teeth and usually occur
unilaterally and bilaterally
• It consists of all three dental tissue, ie enamel, dentin and pulp
• It appears as a tubercle of enamel on occlusal surface of the
affected tooth
• Polyp like protuberance in central groove, on lingual groove, on
lingual ridge of buccal cusp is seen(Fig36)

Fig36

34
ETIOLOGY:
• Due to an increased localized external pressure.
• Focal growth retardation and focal growth stimulation in certain
areas of the tooth bud(Fig 28)

CLASSIFICATION:
• Coronal dens invaginatus (Fig 28)
• Radicular dens invaginatus

35
CLINICAL FEATURES:
CORONAL DENS INVAGINATUS:
• Commonly affected tooth is permanent maxillary lateral
incisor(Fig:29)
• It is more common in female
• This condition is frequently bilateral
Fig:29

36
• In mild type form there is a deep pit cingulum(fig 31)

• In moderate type pocket of enamel is formed within tooth, with

dentin at periphery(fig 31)

• In severe type it may exhibit an invagination extending nearly to

the apex of the root.(fig31)

fig:31

37
• The crown may or may not be enlarged.
The shape of the crown may be conical or
it may be of irregular shape(Fig32)

• The labial surface of the tooth is often bulbous.

Fig 32

Maxillary cuspid exhibiting an enamel invagination that parallels

the pulp canal and perforates the lateral root surface
38
RADICULAR DENS INVAGINATUS :

• Arise secondary to a proliferation of Hertwig’s root

sheath, with the formation of a strip of enamel that
extends along the surface of the root.(Fig33)

Fig 33

39
• It is more common in mandibular 1st premolar, upper lateral
incisor and second molar
• It is usually unilateral
• Crown is small, short and conical with small orifice at the
extreme summit of the convexity(Fig34)
• Lingual marginal ridge is prominent

Fig :34

Radicular dens invaginatous

40
TAURODONTISM

• Taurodontism is an enlargement of the body and pulp chamber

of the multi rooted teeth with apical displacement of the pulpal
floor and bifurcation of the roots.(Fig37)

Fig37

41
CLASSIFICATION BY SHAW(Fig:38)

• HYPOTAURODONT:(mild): Bi or trifurcation is near the

cervical area of the root .This is mild form.
• MESOTAURODONT:(moderate) bi or trifurcation occur at
the middle area of the root
• HYPERTURODONT:(severe)In this condition bi or
trifurcation occur at the apices of the root

Fig:38

42
CLINICAL FEATURES:
• It affects permanent teeth more frequently than deciduous
teeth.
• It may be unilateral or bilateral
• The first molars is usually affected least , with increasing
severity noted in the second and third molars.(Fig:39)
• Involved teeth tend to be rectangle shape.
• Increased frequency of taurodontism - cleft lip and cleft palate
patients.
• It may occur as an isolated trait or as a component of a specific
syndrome.

43
•It may associate with certain dermatological
condition like epidermolysis bullosa,and
dyskeratosis congenita.

•Syndromes associated with this disease are

klinefelter’s syndrome, and tricho dento osseous
syndrome

44
 SUPERNUMERARY ROOTS

• The term supernumerary roots refers to the development of an

increased number of roots.(Fig40)
• Involves both deciduous and permanent dentition.
• Any tooth may develop accessory roots.

Fig40

45
• The most frequently affected teeth are permanent
molars(especially third molars) from either arch and
mandibular cuspids and premolars
• In some instance the supernumerary roots are divergent
• In some cases additional root is small(Fig41)

Fig41

46
Ectopic enamel:
It is also called as enameloma
• Ectopic enamel refers to the presence of enamel in
unusual locations, mainly the tooth root, known as
enamel pearls.

• These are hemispheric structures that consist entirely

of enamel or contain underlying dentin and pulp tissue

47
• Usually 1mm or 2mm in diameter,
that form on the root, or at bifurcation or trifurcation
of multi rooted teeth (fig42)

Fig:42

48
ETIOLOGY:
• It arises from local activity of remnants of Hertwig’s
epithelium, before it reduces to rests of malassez

• It may form due to proliferation of group of displaced

ameloblasts or localized activity of odontoblastic layer
located between the hertwig’s root sheath and developing
dentin which also induces enamel formation

49
CERVICAL ENAMEL EXTENSION:
• Occurs along the surface of dental roots,
these extensions represent a dipping of the
enamel from the cemento - enamel junction
toward the bifurcation of molar teeth.

• This pattern of ectopic enamel forms a

triangular extension of the coronal enamel that
develops on the buccal surface of the molar
teeth directly overlying the bifurcation.

50
• The base of the triangle is continuous with the inferior
portion of the coronal enamel, these areas of ectopic
enamel have been called cervical enamel
projections.(Fig43)
• Tiny nodule may be sufficiently close to gingival
margin to become involved in the periodontal problems

Fig43

51
• Involvement of deciduous molars is not rare

• In addition to periodontal furcation involvement,

cervical enamel extensions have been
associated with development of inflammatory
cysts.

• The cysts develop along the buccal surface

over the bifurcation and most appropriately are
called buccal bifurcation cysts

52
 GLOBODONTIA
• It is common in crown of premolar and molar teeth.(Fig46)
 Teeth have a round globular or clove leaf appearance.(Fig47)

Fig 46 Fig 47

53
MULBERRY MOLAR/ MOON’S MOLAR /
FOURNIER MOLAR’S

 It is a characteristic syphilitic lesion of posterior teeth in which

hypoplastic enamel develops its spherical aggregates or
globules on the occlusal surface(Fig48)

(Fig48)

54
• 1st molar is commonly involved.
• Cusp of teeth show exaggerated rounded or nodular
shapes.(Fig49)

Fig49

55
HUTCHINSON’S INCISOR
• Exhibit crowns that are shaped like straight-edge screw
drivers, with the greatest circumference present in the middle
one third of the crown and a constricted incisal edge often
demonstrates a central hypoplastic notch.(Fig50)

Fig 50

56
 SHOVEL SHAPED INCISOR
• It is morphologically an anomally of the crowns of incisor teeth.
• It is more common in the maxillary lateral and central incisors most
frequently affected(Fig51)

Fig51

• The shovel shape is manifested by the prominence of the mesial

and distal marginal ridges which encloses a central fossa on the
lingual surface of incisor teeth
57
 DEVELOPMENTAL
DISTURBANCES IN
STRUCTURE OF TEETH

58
 SYNOPSIS
AMELOGENESIS IMPERFECTA.

ENAMEL HYPOPLASIA

DENTINOGENESIS IMPERFECTA

DENTINE DYSPLASIA

REGIONAL ODONTODYSPLASIA

DENTINE HYPOCALCIFICATION
59
AMELOGENESIS IMPERFECTA (AI) :
Hereditary brown opalescent teeth, hereditary enamel dysplasia).

Teeth affected with amelogenesis imperfecta

A complex inheritance pattern due to structural defect of the tooth enamel.

SUBGROUPS:
• Hypoplastic (HP)
• Hypocalcified (HC)
• Hypomaturation (HM)
PREVALENCE:
1 in 718 to 1 in 14,000- depending upon the population studied.
o Hypoplastic type- 60-73% of all cases.
o Hypomaturation type- 20-40%
o Hypocalcificatin type- 7%. 60
CLASSIFICATION OF AMELOGENESIS IMPERFECTA: (witkop-1989)

Type I Hypoplastic:

•I A –Hypoplastic, pitted autosomal dominant.

•1 B- Hypoplastic, local autosomal dominant.
•1C- Hypoplastic, local autosomal recessive.
•1D- Hypoplastic, smooth, autosomal dominant.
•1E- Hypoplastic,smooth,x-linked.
•1F- Hypoplastic ,rough, autosomal dominant.
•1G-Enamel agenesis ,autosomal dominant.

Type11: Hypomaturation:

•11A- Hypomaturation ,pigmented autosomal recessive.

•11B- Hypomaturation, x-linked recessive.
•11C- Snow-capped teeth, autosomal dominant.

Type 111: hypocalcified:

•111A- Autosomal dominant.

•111B-Autosomal recessive. 61
Enamel defects of basic types.

62
Type 1V Hypomaturation-hypoplastic with taurodontism:

1V A- Hypomaturation-hypoplasatic with taurodontium ,autosomal dominant.

1V-B-Hypoplastic-hypomaturation with taurodontism ,autosomal dominant.

RADIOGRAPHIC FEATURES:
Enamel appears totally absent or sometimes when present may appear as a
very thin layer- tips of cusps & interproximal surfaces.

severe cases- same radio-opacity of that of dentine making it difficult to

distinguish between the two.

Thin layer enamel on

premolars

Fig 3- radiographic picture of amelogenesis imperfecta 63

comparison of surface appearance of common and enamel defects.
64
HISTOLOGIC FEATURES:

Hypoplastic type:

Disturbance in differentiation or viability of ameloblasts- leading to defects in

matrix formation & sometimes total absence of matrix.

showing hypoplastic type of amelogenesis imperfecta.

65
Hypocalcification type:

Defects in matrix structure & of mineral deposition.

showing enamel which s soft and easily chips away and is caries prone

66
X-LINKED AMELOGENESIS IMPERFECTA.( hypoplastic , hypomaturation and smooth)
67
 Hypomaturation: Alteration in enamel rod and rod sheath structures.

showing hypomaturation pitted tooth.

showing less severe form of hypomaturation type

TREATMENT:
No treatment except for improvement of cosmetic appearance ( prosthetic
rehabilitation) 68
ENAMEL HYPOPLASIA:

Incomplete or defective formation of organic enamel matrix of teeth.

TYPES:
HEREDITARY TYPE: As previously discussed under amelogenesis imperfecta.

ENVIRONMENTAL ENAMEL HYPOLPLASIA: Due to environmental factors.

They are:
•Nutritional deficiency (vit A , C& A)
•Exanthematous disease ( measels, chicken pox)
•Congenital syphilis.
•Hypocalcemia
•Birth injury, prematurity, rh hemolytic disease.
•Local infection or trauma.
•Ingestion of chemicals ( fluoride)
•Idiopathic.
69
Deep grooves arranged horizontally across the tooth surface.

70
Localized enamel hypoplasia of the mandibular central incisors.

71
CLINICAL FEATURES:

Mild cases- a few small grooves, pits or fissures on enamel surface.

Severe cases-enamel may exhibit rows of deep pits arranged

horizontally across the surface of tooth.

Most severe cases: a considerable portion of enamel may be absent

suggesting a prolonged disturbance in function of ameloblasts.

HYPOPLASIA DUE TO NUTRITIONAL DEFICIENCY & EXANTHEMATOUS

FEVERS:
Nutritional deficiency like vit A,C,D & disease conditions such as measles,
chicken pox is usually associated with pitting variety.

Since the pits tend to stain, clinical appearance of the teeth may be unsightly.

Clinical studies indicate that most cases of enamel hypoplasia involve those
teeth that form within first year after birth.

Most frequently involved sites: central & lateral incisors,cuspids &

first molars. 72
ENAMEL HYPOPLASIA DUE TO CONGENITAL SYPHILIS:

Clinical features: Characteristic, almost pathognomic appearance.

Teeth involved- maxillary & mandibular permanent incisors & first molars.

Anterior teeth affected are Hutchinson's teeth.

Upper central incisor is screw driver shaped, mesial & distal surfaces of crown
tapering & converging towards the incisal edge of tooth, in addition the incisal edge is
notched.

Fig - showing notched incisors 73

Fig - screw driver shaped incisors with notched incisors

74
Mulberry molars/moon’s molars/ Fournier's molars:

Crowns of first molars are irregular & enamel of the occlusal surface & occlusal
third of tooth appears to be arranged in agglomerate mass of globules rather than
in well formed cusps.

The crown is narrower on the occlusal surface than at cervical margin.

MULBERY MOLARS

Fig - showing mulbery molars

Note: Not all patients with congenital syphilis will exhibit these dental findings
also, occasionally patients will appear to have Hutchinson's teeth without a
history of congenital syphilis.
75
ENAMEL HYPOPLASIA DUE TO HYPOCALCEMIA:

In tetany, the calcium serum level may fall as low as 6-8 mg/100 ml & vit D
deficiency, parathyroid deficiency may result in hypoplasia of teeth which is
of pitting variety.

HYPOPLASIA DUE TO BIRTH INJURIES:

Neonatal line or ring in deciduous teeth & first permanent molars may be
thought as a type of hypoplasia because there is a disturbance produced in
the enamel & dentine, which is indicative of trauma or change of environment
at time of birth.

Fig - Showing hypoplasia of teeth affected by birth injuries. 76

ENAMEL HYPOPLASIA DUE TO LOCAL
INFECTION OR TRAUMA:

Only a single tooth is involved.

Common tooth- permanent maxillary
incisors/ maxillary or mandibular premolar.
Clinical features: any degree of
hypoplasia, ranging from a mild, brownish
discoloration of enamel to severe pitting &
irregularity of tooth crown. These single
tooth is referred to as turner’s teeth & the
condition is called as turner’s hypoplasia

Fig - showing turners teeth( mandibular premolar) 77

ETIOLOGY OF HYPOPLASIA:

If a deciduous tooth becomes carious during the period when

crown of succeeding permanent tooth is being formed, a bacterial
infection involving periapical tissues of this deciduous tooth may
disturb the ameloblastic layer of permanent tooth & result in
hypoplastic crown.

severity of hypoplasia depends on:

severity of infection.
stage of permanent tooth formation during which the infection has
occurred.
Degree of tissue involvement.

HYPOPLASIA DUE TO IDIOPATHIC FACTORS:

Since ameloblasts are sensitive type of cells & easily damaged, it is

likely that causative agent have been some illness or systemic
disturbance, so mild that it made no impression on patient & was not
remembered. 78
 ENAMEL HYPOPLASIA DUE TO FLUORIDE:
(mottled enamel)

Discovered by G.V Black & Frederick s McKay in 1916.

Etiology:
Ingestion of fluoride containing drinking water during the time of tooth
formation.

Little mottling of any clinical significance at a level below 0.9-1.0 part per
million of fluoride in water & above which it becomes progressively evident.
Pathogenesis:

Due to disturbance in formative stage of tooth development, there

is histologic evidence of cell damage, it is likely that cell product-
enamel matrix is defective or deficient.

Higher level of fluoride interferes with calcification process of the

matrix.
79
clinical features:

Questionable: occasional white flecking or spotting of enamel.

Mild- white opaque areas involving most of the tooth surface areas.

Mild fluorosis

Fig - shows teeth with mild fluorosis 80

 MODERATE FLUOROSIS
Moderate & severe: shows pitting & brownish staining of surface.

Fig -shows teeth with moderate fluorosis. 81

 SEVERE FLUOROSIS

shows teeth with severe fluorosis 82

 Severe fluorosis
Even severe- corroded appearance of teeth.

Fig - shows teeth affected by severe fluorosis.

Treatment:
•Bleaching for mild cases

•Moderate cases laminate veneers

83
•Severe cases- crown & bridge.
DENTINOGENESIS IMPERFECTA:

An autosomal dominant condition affecting deciduous & permanent teeth.

Clinical features:
Affected teeth are gray to yellowish brown & have broad crowns with
constriction of cervical area. (”tulip shape”).

Teeth with gray to yellowish brown tooth with broad crowns

Radiographic features:
Tooth appears solid, lacking pulp chambers & root canals.
Classification:
DI type I : dentinogenesis imperfecta without osteogenesis
imperfecta.(opalescent dentine)

DI type 2: Brandywine type dentinogenesis imperfecta

84
Incidence:
DI type 1 common than type 2.

Dentinogenesis imperfecta type 1:

(opalescent dentine ,capdepont teeth)

Fig - showing teeth affected with DI type1

Etiology :Mutation in DSPP gene( gene map locus 4q21.3) encoding

dentine phosphorylation and dentine sialoprotien.
Clinical features:
Not associated with osteogenesis imperfecta with opalescent
dentine, affects only teeth.
Frequency – 1 in 6000-8000 children.
Teeth are blue grey or amber brown & opalescent.
Enamel may split readily from tooth when subjected to occlusal
85
stress.
Radiographic features:

Teeth have bulbous crowns, roots are narrower than normal and pulp
chambers, root canals are smaller than normal or completely obliterated.

Fig -showing teeth radiographic feature of DI with bulbous crown 86

 Dentinogenesis imperfecta type2:
(Brandy wine type dentinogenesis imperfecta).

Dentinogenesis imperfecta type 11

Clinical features:
Crowns of deciduous & permanent teeth wear rapidly after
eruption & multiple pulp exposures may appear.

87
Fig - showing dentinogenesis imperfecta with osteogenesis imperfecta with blue
sclera.

88
Radiographic features:

Deciduous dentition: shows very large pulp chambers & root canals
atleast during first few years, although it becomes reduced in size with
age.

Permanent teeth: have pulpal spaces that are either smaller than
normal or completely obliterated.

Histopathological features:

In Dentinogenesis imperfecta type1, enamel appears normal while

dentine is composed of irregular tubules, often with large areas of
uncalcified matrix.

Tubules tend to be larger in diameter & less numerous than normal in a

given volume of dentine.

Odontoblasts have only limited ability to form well organized dentinal

matrix & they appear to degenerate readily & become entrapped in this
matrix. 89
Fig - shows dentine depicting the thin zone of normal mantle dentine on the
right , with dysplastic irregular dentine replacing all but a small remnant of
coronal pulp.

90
Fig -showing large sized and widely placed dentinal tubules and the
lack of normal density of intertubular collagen deposits.

91
 Large pulp
chambers

Histopathological picture of DI with large pulp chambers.

Treatment:

Cast metal crowns on posterior teeth.

Jacket crowns on anterior teeth. 92

DENTINE DYSPLASIA: ( ROOTLESS TEETH)
It is a rare disturbance of dentine formation characterized by normal enamel but
atypical dentine formation with abnormal pulpal morphology.

Teeth affected with dentine dysplasia.

Classification:
Type 1 : Radicular dentine dysplasia.
type 11: Coronal dentine dysplasia.

Etiology:
Transmitted as autosomal dominant characteristic.

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 Clinical features:
Type 1 –
Both dentitions are affected.

Clinically normal in morphologic appearance and color, occasionally with slight amber
translucency & exhibit a normal eruption pattern, although may be delayed in few cases.

They exhibit extreme mobility and exfoliate prematurely due to abnormally short
roots.

Affected deciduous
dentition

Fig 40 showing deciduous dentition affected

Type 11 –
Both dentitions affected
Deciduous teeth- yellow, brown or bluish grey opalescent appearance.
Permanent dentition appear normal. 94
Radiographic features:

Type 1: in both dentitions roots are short, blunt & conical.

Deciduous teeth: pulp chambers & root canals are usually completely obliterated.
Permanent teeth: a crescent shaped pulpal remnant may be seen in pulp chamber.
Periapical radiolucencies representing granuloma, cyst may also be seen…obliteration
occurs prematurely

Radiographic image of dentine dysplasia with short , blunt and conical teeth 95
Fig - Dentine dysplasia type 1 showing obliteration of the pulp except for the
occasional chevron radiolucency with periapical radiolucency.

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Fig –dentine dysplasia type 11 periapical radiographs indicating teeth with relatively
normal roots and pulp chambers that contain large pulp stones.

97
 Fig -showing teeth with obliterated pulp chamber and thistle tube
appearance.

Type 11: pulp chambers of deciduous teeth are obliterated & does
not occur before eruption.

Permanent teeth-abnormally large pulp chamber in coronal

portion of tooth – “thistle tube” in shape, within such areas
radiopaque foci resembling pulp stones may be found.

 Periapical radiolucencies do not occur 98

Histopathological features:

Type 1:
A portion of coronal dentine is normal, apical to this may be areas of tubular dentine ,
osteodentin & fused denticles. “Lava flowing around boulders”- normal dentinal tubule
formation appears to have been blocked ,so that new dentine forms around obstacles
results from repetitive attempts to form root structure.

Tooth with gnarled and rippling formation of dysplastic dentine and lava flowing around
boulders appearance 99
Type 11:

Deciduous teeth: exhibit amorphous & tubular dentine in radicular

portion while coronal dentine is normal.

Permanent teeth- relatively normal coronal dentine , but pulp has

multiple pulp stones.

Treatment:
Prognosis is poor & no treatment needed.
Requires extraction followed by prosthetic rehabilitation.

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REGIONAL ODONTODYSPLASIA: (Ghost teeth, Odontodysplasia)

Unusual dental anomaly in which one or several teeth in a localized area are affected
in an unusual manner.

fig - showing localized area of mandible in which abnormal teeth are present surrounded
by increased soft tissue.

Site: Maxillary teeth more common , commonly affected-maxillary central ,lateral

incisors & cuspids.

Dentition: Both dentitions affected.

Etiology: Unknown , may represent somatic mutation.

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Clinical features:
•Delay or total failure in eruption
•Shape markedly altered, irregular in appearance with evidence of defective
mineralization.
Radiographic features:
Marked reduction in radiodensity so that teeth assumes a “ghost appearance”.

Enamel & dentine appear very thin & pulp chamber is exceedingly large. Enamel
layer most often not evident.

Fig - showing radiographic feature of “ghost teeth” 102

 Histopathological features :
Marked reduction in amount of dentine , widening of predentine layer ,
presence of large areas of interglobular dentine & irregular tubular pattern of
dentine.

Characteristically, reduced enamel epithelium around non erupted teeth

shows many irregular calcified bodies.

Fig - shows low-power photo micrograph through the crown of a decalcified

tooth depicting remnant of the defective enamel matrix(thin normal mantle
dentine overlying severely dysplastic dentine with lobular areas of
amorphous dentine and greatly enlarged coronal pulp chamber. 103
Fig - shows surrounding soft tissues contains nodular arrangements of
connective tissue cells containing accumulations of spheric calcifications.

Treatment :
Extraction of tooth followed by prosthetic rehabilitation.

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DENTINE HYPOCALCIFICATION:

Calcification takes place in the form of globules in organic matrix

& increase in size by further peripheral deposition of salts until all
globules unite & form a homogenous structure

But in hypocalcification , these globules fail to unite leaving

interglobular areas of uncalcified dentine.

Clinical features:

Hypocalcified dentine is softer than well-calcified dentine.

Etiology is similar to environmental enamel hypoplasia & factors

that interfere with normal calcification such as rickets, parathyroid
deficiency.
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106
ANOMALIES AFFECTING SHAPE OF
TEETH

 Gemination
 Fusion
a)Complete
b)Incomplete
 Concrescence
a)True
b)Acquired
• Talon’s cusp
• Dilaceration 107
• Dens in dente

a)Coronal dens invaginatus

b)Radicular dens invaginatus
 Dens evaginatus
• Taurodontism
• Supernumeray roots
• Enamel pearls
• Globodontia
• Mulberry molar
• Hutchinson incisor
• Shovel shaped incisor

108