seminar on varous developmental disturbances of teeth,useful for under and post graduates

1. 1

2. DEVELOPMENTAL
DISTURBANCES OF TEETH
2

3. CONTENTS:
• INTRODUCTION
• CLASSIFICATION
• DEVELOPMENTAL DISTURBANCES IN
SIZE
• DEVELOPMENTAL DISTURBANCES IN
NUMBER
• DEVELOPMENTAL DISTURBANCES IN
SHAPE
• DEVELOPMENTAL DISTURBANCES IN
STRUCTURE
• DEVELOPMENTAL DISTURBANCES IN
ERUPTION.
• REVIEW LITERATURE 3

4. • CONCLUSION
• REFERENCES
4

5. INTRODUCTION
• DEVELOPMENT
• The orderly and sequential changes that occur
with the passage of time as an organism moves
from conception to death.
• Also referred to as gradual growth which
indicates changes in character.
5

6. INTRODUCTION
• Development of teeth and face is regulated
by genes
• Dental developmental anomalies appear as
a result of disruption in the odontogenesis
process by the action of certain disruptive
factors
• The disruptive factors can be genetic
factors or environmental factors or even
combinations of these factors.
6

7. INTRODUCTION
• But the genetic programme is very sensitive to
disturbances in the environment such as exposure
to infection or toxic chemicals, including drugs
7
DISTURBANCES OF TEETH
􀂄 Environmental
􀂄 Developmental

8. 8

9. INTRODUCTION
• Developmental disturbances means
an abnormality where the pathology
starts in the embryonic stage of
human life , before the formation of
the dentition.
9

10. • SIZE OF TEETH
• SHAPE OF TEETH
• NUMBER OF TEETH
• STRUCTURE OF TEETH
• GROWTH (ERUPTION) OF TEETH
10

11. CLASSIFICATION
Developmental disturbances in the
size of the teeth
Microdontia
Macrodontia
Developmental disturbances in the
shape of the teeth
Gemination
Fusion
Concresence
Dilaceration
Talon’s cusp
Dens-in-dente
Dens evaginatus
Taurodontism
Supernumerary root
11

12. Developmental disturbances in the number of the teeth
Anodontia
Hypodontia
Supernumerary teeth
Predeciduous dentition
Post permanent dentition
Developmental disturbances in the structure of the teeth
Amelogenesis imperfecta
Dentinogenesis imperfecta
Regional odontodysplasia
Dentin dysplasia
Developmental disturbances in the growth/eruption of
the teeth
Premature eruption
Delayed eruption
Ankylosed teeth
Submerged teeth/ impacted teeth
12

13. Anomalies at different stages of tooth
development
13
Dental lamina formation stage
Anodontia
Initiation and proliferation
Oligodontia
Supernumerary teeth
Geminated / fused teeth
Histodifferentiation -defects in multiple dental tissues
Regional odontodysplasia

14. 14
Morphodifferentiation ( defects in size & shape
Macrodontia / Microdontia
Dens invaginatus / Dens evaginatus
Hutchinson s incisors, mulberry molars‟
Talon cusp
Taurodontism
Apposition ( defects in structure of enamel &
dentin )
Amelogenesis imperfecta
Enamel Hypoplasia
Dentinogenesis imperfecta
Dentin dysplasia

15. Microdontia: it is described as teeth
are smaller than usual.
1. True Generalized Microdontia
2. Relative Generalized Microdontia
3. Focal or Localized Microdontia
DEVELOPMENTAL DISTURBANCES OF SIE
OF TEETH
15
MICRODONTA MACRODONTIA

16.  all teeth are smaller than
normal
teeth are well formed
 occur in some cases of
down syndrome.
pituitary dwarfism
 exceedingly rare
(1) True Generalized
Microdontia
16

17.  normal or slightly smaller than
normal teeth.
 are present in jaws that are
somewhat larger than normal
 Inheritance of jaw size from one
parent and tooth size from other
parent can lead to this variations.
(2) Relative Generalized
Microdontia
17

18.  common condition
 affects most often maxillary
lateral incisior + 3rd
molar
 these 2 teeth are most often
congenitally missing
(3) Focal/Localized
Microdontia
18

19.  common forms of localized
microdontia is that which
affects maxillary lateral
incisior
 peg lateral
 instead of parallel
diverging mesial + distal
surfaces
19

20.  sides converge or taper
together incisally
 forms cone-shaped crown
 root is frequently shorter
than usual
TREATMENT
• Composite / Porcelain Veneers
20

21. MACRODONTIA
Also called as megalodontia or megadontia.
It refers to teeth that are larger than usual.
21
(1) True Generalized Macrodontia
 (2) Relative Generalize Macrodontia
 (3) Focal or Localized Macrodontia

22.  all teeth are larger than
normal
 associated with
pituitary gigantism,pineal
hyperplasia with hyperinsulinism.
 exceedingly rare
(1) True Generalized
Macrodontia
MACRODONTIA
22

23.  normal or slightly larger than
normal teeth in small jaws
 results in crowding of teeth
 insufficient arch space
(2) Relative Generalized
Macrodontia
23

24.  uncommon condition
 unknown etiology
True marodontia often confused
with fused teeth.
 usually seen with
mandibular 3rd
molars
(3) Focal/Localized
Macrodontia
24

25. TREATMENT
25
􀂄 Stripping to reduce tooth size.
􀂄 Can be combined with build – up of
antimere if only one tooth is affected.
􀂄 Extraction & replacement by prosthesis.

26. DEVELOPMENTAL DISTURBANCES IN SHAPE AND FORM
26
 Crown
 Fusion
 Gemination
 Taurodontism
 Talon’s Cusp
 Leong’s Cusp
 Dens Invaginatus
 Peg-shaped Lateral
 Hutchinson Incisor
 Mulberry Molar

27.  Root
 Concresence
 Enamel Pearl
 Dilaceration
 Ankylosis
Shape and Form
27

28. DOUBLE TEETH
28
􀂄joined by crown,root or both
 Gemination and fusion
􀂄 May have very similar clinical appearance
􀂄 Higher frequency in anterior and maxillary
regions
􀂄 Rate is about 0.1% in permanent dentition
and 0.5% in deciduous
􀂄 Bilateral cases more infrequent.
􀂄 Etiology unknown but trauma has been
Suggested.
Clinical importance
􀂄 Crowding / spacing
􀂄 Periodontal problem
􀂄 Caries
􀂄 Eruption disturbance
􀂄 Aesthetics

29. GEMINATION
29
 an attempt of single tooth bud to divide with resultant
formation of tooth with bifid crown.
 partial cleavage
 appearance of 2 crowns
that share same root canal
 trauma has been suggested
as possible cause.

30. 30
TWINNING:
• Designate the production of equivalent
structures by division resulting in one normal
and one supernumerary tooth :

31. FUSION
31
Fusion of adjacent tooth buds with resultant formation of
joined tooth with confluence of dentin.
 Fusion may be complete or incomplete based on
the stage of tooth development at the time of fusion.
 Union of two separate tooth buds.
When counted ,tooth count reveals
missing tooth when anamalous tooth is counted as one.
Fusion of (a) molar tooth with
supernumerary, (b) maxillary
premolar with fused roots, (c) premolars

32. 32
FUSION
 Contact occurs before calcification – two teeth may
be completely united to form a single large tooth.
Contact after calcification of the crowns, the roots
may be united
Tooth may have fused or seperated root cnals

33. Differentiating factors
Check for number of teeth.
Check for root canal
33

34. Treatment of Gemination
and fusion
34
Deciduous dentition:
can results in Crowding, abnormal
spacing, delayed eruption of permanent
teeth.
 Extraction.
Otherwise:
Surgical division & endodontic treatment
is done

35. TAURODONTISM-(tauro bull, don’t_ teeth)
35
Taurodontism’ was originated by Sir Arthur
Keith in 1913.
It is an enlargement of the body and pulp
chamber of a tooth with apical displacement of the
pulpal floor .
Shaw’ classified taurodont teeth according to
degree of apical displacement of pulpal floor.
Hypotaurodont:
mild
Mesotaurodont:
moderate
Hypertaurodont:
severe

36. 36
Hereditary
Mutation resulting from odontoblastic deficiency during
dentinogensis of roots
A primitive pattern.
Failure of Hertwig's epithelial root sheath to invaginate at proper
horizontal level
Clinical Features :
The deciduous or permanent dentition (more common).
Molars.(3rd
,2nd
,1st
)
May be unilateral or bilateral.
Increased frequency in patients with cleft lip/palate,
also associated with syndromes like downs syndrome,
klinefelter syndrome,trichodento-oseous syndrome.
Oculo‐dental‐digital dysplasia.Orofacial digital synd.ectodermal
displasia
•Sex chromosomal aberrations.Amelogenesis imperfecta IE,IV
CAUSES

37. Radiographic features
37
Rectangular in
shape
Pulp chamber is large
Bifurcation or
trifircation few
millimeter
Lack of
constriction

38. TREATMENT
38
Requires no specific therapy
Pulp therapy in taurodonts :
Challenging task
bleeding during access
Canal locating , instrumenting , obturating
difficult

39. 39

40. ACCESSORY CUSPS
40
Cuspal morphology of the teeth exhibit
minor variations:
 CUSP OF CARABELLI
 TALONS CUSP
 DENS EVAGINATUS

41.  An accessory cusp located onAn accessory cusp located on
the palatal surface of thethe palatal surface of the
mesiolingual cusp of a maxillary molar.mesiolingual cusp of a maxillary molar.
May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth
& varies from cusp to small indented pit or fissure& varies from cusp to small indented pit or fissure..
41
CUSP OF CARABELLI
90% in whites and rare in Asians90% in whites and rare in Asians
Requires no therapy unless deep groove is present.Requires no therapy unless deep groove is present.

42. PROTOSTYLID
•Occasionally on the mesiobuccal cusp of
mandibular permanent or deciduous molar
42

43. TALON CUSP
43
Eagle’s talon.
•A well delineated additional cusp that is located on the surface
of an anterior tooth & extends at least half the distance from the
CEJ to the incisal edge.(lingual side)
•Composed of normal enamel and dentin and contains a horn of
pulp tissue.
•Prevalence ranges from 1%-8%
• Chawla et al-7.7% prevalence- north
Indian children.

44. •In primary dentition maxillary central incisor most
common site.
PATTERNS OF TALON CUSPS: three types based
on morphology
• Trace talon
•Semi-talon
•Talon
Forms : T –form ; Y -shaped
•Seen in patients with rubinstein teybi
syndrome,struge weber syndrome,mohr syndrome.
•Radiographically,the cusp is seen overlying the
central portion of crown & includes enamel and
dentin
•Clinical problems include esthetics, caries control
and occlusal accombidation.
44

45. TREATMENT
45
•Occlusal interference.
• Prophylactically restoring the groove to
prevent caries. Or
•Fissure sealants to prevent caries
around the margins

46. DENS EVAGINATUS
Also called Leong’s premolar, Evaginated odontome
46
•It is a developmental condition that appears
clinically as an accessory cusp or a globule of
enamel on the occlusal surface between the
buccal and lingual cusps of premolars,
•unilaterally or bilaterally.
•Rare in whites 15% in asians.
•Occurs in persons of mongoloid ancestry–chinese,
japanese, filipinos, eskimos and american indians.‐
•Evolves by proliferation and evaginationof an area of the
inner enamel epithelium and subjacent odontogenic
mesenchyme into the dental organ during early tooth
development

47. Extra cusp can lead to:
•Incomplete eruption
•Displacement of teeth
•Pulp exposure following occlusal wear or
fracture.
Radiographic features
•Occlusal surface exhibits a
tuberculated apearance, and often
pulpal extension is seen in the cusp
Treatment
Extraction is indicated if tooth is nonvital
Grinding of the tubercle & indirect pulp
capping with calcium hydroxide.
47

48. SHOVEL SHAPED INCISOR
48
•Associated with dens evaginatus
•Affected incisors demonstrate prominent
lateral margins creating a hallowed lingual
surface that resembles the scoop of shovel.
•Maxillary central incisors most affected
•Predominantly in asians, native
americans and alaskans

49. DENS INVAGINATUS
49
• Also called as Dens In Dente, Dilated
composite odontome
• It is a deep surface invagination of the crown
or root by enamel before calcification occurs..
• Causes :
– Increased localized external
pressure
– Focal growth retardation
– Focal growth stimulation.
• Maxi. Permanent Lateral incisor most
commonly involved while central rare.
• Condition is frequently bilateral.
• Prevalence 0.04%-10%

50. Oehlers (1957) divided this condition into 2
forms:
Coronal: Type 1,2,3.
Radicuar
Coronal dens invaginatus has been classified
into three major types:
50
Type I:
An invagination that is confined to the
crown.
Clinical significance
 Predisposition to caries
 Pulpal pathology
 Periapical pathology (Type III)
 Early diagnosis – mandatory

51. Type II
Extends below the CEJ & ends in the blind sac that
may or may not communicate with adjacent dental
pulp.
51

52. Type III:
Extends through the root & perforates in the
apical or lateral radicular area without any
immediate communication with pulp.
Enamel line often replaced by cementum
close to the radicular perforation.
Perforation provides communication from
oral cavity to the intraosseous periradicular
tissue, &often produce inflammatory lesions
52

53. RADICULAR TYPE:
53
•Radicular invagination results from infolding
of hertwig’s sheath and origin is within the
root after development is complete

54. Radiograph:
•Affected tooth demonstrate an enlargement of the
root.
•Dilated invagination lined by enamel
• Radiographs reveal a pear shaped invagination of
enamel and dentin with a narrow constriction at the
opening on the surface of the tooth and closely
approximating the pulp in its depth.
•  Severe form – an invagination that extends nearly
to the apex of the root
TYPE II CORONAL DENS INVAGINATUS
TYPE III CORONAL DENS
INVAGINATUS
54

55. Treatment:
Small type I opening of the invagination is
restored to prevent carious involvement.
Large type:
Contents of the lumen & any carious dentin
must be removed & calcium hydroxide base
is placed.
Pulpal pathosis or pulpal communication
then endodontic therapy is recommended
55

56. MULBERRY MOLARS (MOONS MOLAR)
56
•Molars have multiple poorly developed cusps.
•Seen in congenital syphilis.
•Mulerry molar shows numerous disorganized globular
projection that resembles like mulberry.
•Condition occurs due to spirochete infection of enamel
organ of teeth during amelogenesis.

57. HUTCHINSON INCISOR
57

characteristic of congenital
syphilis
lateral incisors are peg-shaped
or screwdriver-shaped
 widely spaced
 notched on their biting end
 with a crescent-shaped defect
named after Sir Jonathan
Hutchinson
 English surgeon +
pathologist who 1st
described it

58. SHAPE AND FORM
58
ROOT
Concrescence
 Union of two adjacent teeth by
cementum alone.
 May occur before or after eruption
 Seen most commonly posterior and
maxillary regions
 Etiology believed to be trauma or
Overcrowding.
Usually involves two teeth. But involving
three teeth has also been reported.

59. FACTORS ASSOCIATED:
59
LOCAL FACTORS
•Abnormal occlusal trauma
•Adjacent inflammation
•Unopposd tooth;impacted , ,without antagonist
SYSTEMIC FACTORS
Acromegaly and pituitary gigantism
–Arthritis
–Calcinosis
–Paget’s disease of bone
–Rheumatic fever
–Thyroid goiter
–Vitamin A deficiency

60. 60
•Diagnosed by radiographic
examination
Histopathology
•Deposition of excessive cementum over the original layer of
primary cementum.
•May be hypocellularor exhibit areas of cellular cementum
resembling bone called osteocementum
.
•Polarized light to differentiate dentin and cementum.

61. TREATMENT
61
often requires no therapy
unless union interferes with
eruption; then surgical
removal may be warranted
since with fused teeth,
extraction of one may result in
extraction of the other

62. DILACERATION
62
Abnormal angulation or bend in root or less frequently crown of tooth.
Majority due to trauma to tooth germ calcified portion.
Permanent maxillary incisors are frequently involved, followed by
mandibular incisors.
Dilaceration in a permanent tooth often follows traumatic injury (avulsion or
intrusion) to the deciduous predecessor in which the tooth is driven apically into
the jaw.
Can also develop secondary to adjacent cyst, tumor or odontogenic
hamartoma.
kinked tooth ” or “ sickle – tooth

63. TREATMENT
63
Vary according to severity
 Extraction: if it is non vital then surgical removal is
suggested.
 Can be problematic during extraction sometimes.
Deciduous teeth – Extraction
Permanent teeth
Minor – no treatment

64. ECTOPIC ENAMEL
64
Thought to arise from localized bulging in
the odontoblastic layer with prolonged
contact between HERS and dentin leading
to enamel formation.
Enamel in unusual location
Enamel pearlEnamel pearl
Common-roots of max. molars followed by mand.
Molar.
Deciduous molar is not rare.
1.1-9.7% - highest in Asians

65. ENAMEL PEARLS
65

66. CERVICAL ENAMEL PROJECTION
66
Represent dipping of enamel from the CEJ
toward the bifurcation of molar teeth.
Mandibular molars affected more frequent.
 prevalence is greater in Asians (8.6%-32.4%)
Extensions is correlated with localized loss of
periodontal attachment with furcation
involvement

67. TREATMENT
67
Oral hygiene should be maintained.
Flattening or removal of enamel
pearl or furcation plasty can be done.

68. SUPERNUMERARY ROOTS
68
Refers to the development of an increased
number of roots on a tooth
compared with that
described in dental anatomy.
•May involve any tooth.
•Mandibular cuspids and
bicuspidsmay have two roots.
•Maxillary and mandibular molars
may exhibit additional roots.
•Significant during extraction

69. DEVELOPMENTAL DISTURBANCES IN
NUMBER OF TEETH
69
Anodontia
Hypodontia
Hyperdontia
Oligodontia
Supernumerary teeth

70. ANODONTIA
70
•Congenital absence of teeth
Etiology:
Hereditary
Autosomal dominent
Hereditary ectodermal
dysplasia
Cleidocranial dysplasia
X-ray radiations
Types:
True
Total
Partial (hypodontia)
False
Pseudo

71. 71
Clinical features:
Women
Mongoloid
Whites
True total anodontia:
All teeth missing
Can be either deciduous or
permanent
True partial anodontia:
Absence of one or more teeth
Commonly missing teeth – 3rd
molars, max. lateral incisors,
max / mand. 2nd
premolars

72. 72
False anodontia:
Due to extraction of teeth
Pseudoanodontia:
Due to multiple unerupted teeth

73. HYPODONTIA
73
lack of development of one or more
teeth.
Common dental anomaly
Etiology:
• Familial tendency – point mutations
transmitted in autosomal dominant pattern.
• Missing third molars could be an evolutionary
trend towards fewer teeth.
•It is associated with hereditary ectodermal
dysplasia
• Xray radiation of face during early age –
affecting the sensitive tooth buds
.

74. 74
 3.5%-8% (excluding third molars)
 Female predominance about 1.5:1
 Uncommon in primary dentition
(<1%)
 About 20-23% of population
missing third molars.
 After third molars, second
premolars and laterals most frequent

75. 75
Syndromes associated with
hypodontia
 Ectodermal dysplasia
 Chondroectodermal
dysplasia (Ellis-van
Creveld)
 Progeria
 Down
 Hallermann-Streiff
 Rieger
 Crouzons
 Albright hereditary
osteodystrophy

76. 76
 Prevalence of supernumerary teeth is
about 1%-3% (higher rate in Asians)
 Single tooth hyperdontia represent 75%-
85% of cases
 More common in permanent dentition
 Almost 90% in maxilla
 Maxillary incisor region most common site
then 4th molars,premolars and canines
 If multiples, usually in mandibular premolar
region
HYPERDONTIA

77. 77
Syndromes associated with
hyperdontia
 Cleidocranial dysplasia
 Oral-Facial-Digital
 Apert syndrome.
cleidocranial
dysostosis

78. 78
Classification of
supernumerary teeth
Modified Howard s classification‟
Supplemental supernumerary teeth
Accessory supernumerary teeth
• Classified according to
morphology and location, four
different types
• Conical
• Tuberculate
• Supplemental
• Odontome

79. 79
Supplemental supernumerary teeth:
These teeth duplicate the typical anatomy of
anterior and posterior teeth
Mesiodens:
•Most common Supplemental
supernumerary teeth
•Small tooth with cone shaped crown and
short root
•Located near the midline in the incisor
region of maxilla between the central
incisors
•Occurs single / multiple, erupted /
impacted
•Causes retarded eruption, displacement of
adjacent tooth, or resorption of adjacent
root and thus improper alignment of teeth

80. 80
DISTOMOLARS:
Found in molar region
Located distal to 3rd
molars
Generally these teeth are smaller
than normal 2nd
& 3rd
molars
But crown morphology is
abnormal

81. 81
PARAMOLARS:
It is an supernumerary molar
Usually small and rudimentary
Situated buccally or lingually to one of the maxillary
molars
Inter–proximally between 1st
, 2nd
, 3rd
maxillary
molars

82. TRANSPOSITION
82
Normal teeth erupting into an
inappropriate position.
•Usually involves the canine and
first premolars.
•Canine erupting between two
premolars.
•Could be confused with
supernumerary teeth

83. 83
Developmental disturbances in
the growth/eruption of the teeth
Premature eruption.
Delayed eruption.
Ankylosed teeth.
Submerged teeth/ impacted teeth

84. 84
NATAL TEETH
Premature eruption of teeth like
structures
Present at birth
They are hyper mobile because of
their limited root development
Conical or normal in size and
shape
Some teeth are so mobile that
there is danger of displacement and
possible aspiration – removal is
indicated other wise not !!

85. 85
Sharp incisal edges
may cause laceration of
lingual surface of tongue
→ RIGA–FEDE
DISEASE
Associated with Ellis-
van creveld syndrome

86. 86
Neonatal teeth
These are the teeth or teeth like structures
that erupt prematurely during neonatal
period
From birth to 30 days

87. 87
TREATMENT
Extraction of teeth (if causing
inconvenience)
Or
Rounding of the sharp angles
of the teeth
Extraction should be done
after 10 days of life
If not necessary tooth should
not be removed

88. 88
ERUPTION SEQUESTRUM
Anomaly associated with tooth eruption in children.
 Described by Starkey and Shafer
.
 It is a tiny, irregular spicule of bone overlying the crown of
an erupting permanent molar, found just prior to or
immediately following the emergence of the tip of the cusps
through the oral mucosa.
Etiology
 As the molar teeth erupt through the bone, they can
separate a small osseous fragment from the surrounding
bone similar to a cork screw.
 In most cases, the fragment undergoes complete
resorption before eruption.
 If the bony spicule is large or the eruption is rapid,
complete resorption cannot occur and hence, it is observed

89. 89
CLINICAL FEATURES
 The child may complain of slight soreness in the
area during function.
 The spicule directly overlies the central occlusal
fossa but is within the soft tissue.
 It may be seen lying in a tiny depression over the
crest of the ridge.
 As the tooth erupts, the fragment of bone
completely sequesters through the mucosa and is
lost’
Radiographic features
 It can be recognized even before the tooth
eruption.
 Seen as a tiny, irregular opacity overlying the
central occlusal fossa but separated from the tooth
itself.

90. DELAYED ERUPTION
90
In deciduous and permanent teeth, it is
difficult to assess unless a gross variation is
present.
•Caused by Systemicconditions like rickets,
cretinism, cleidocranial dysplasia
•Localfactors like fibromatosis gingivae.
•Treatment of the primary condition may lead
to eruption of teeth

91. 91
IMPACTED TEETH
 occurs due to obstruction
from crowding
 from some other physical
barrier
 occasionally, may be due
to an abnormal eruption
path, presumably because
of unusual orientation of
tooth germ

92. 92
Any tooth may be impacted –usually
mandibular third molars(22%),
maxillary third molars(18%) and
maxillary cuspids(0.9%), premolars
and supernumerary teeth.
Mandibular teeth are more severly
impacted.

93. ANKYLOSIS
93
fusion of a tooth to surrounding
bone
 with focal loss of periodontal
ligament, bone + cementum
become inextricably mixed
 cause fusion of tooth to
alveolar bone

94. 94
Reported prevalence of clinically
detectable ankylosis- 1.5% to 9%
 Primary molars are most commonly
involved teeth with most cases in mandible
Even with extreme root resorption, teeth
lack mobility.

95. 95
•Diagnosis is suspected clinically and confirmed
with radiographs.
•There is partial absence of the periodontal ligament
with areas of apparent blending between the root of
the tooth and alveolar bone.
complications
Development of malocclusion
•Local periodontal disturbance
•Dental caries of both the ankylosed tooth and
adjacent teeth.
TREATMENT
Depends on whether tooth are ankylosed or not
permanent successor present or not

96. 96
DEVELOPMENTAL DISTURBANCES
IN THE STRUCTURE OF THE TEETH
Amelogenesis imperfecta
Dentinogenesis imperfecta
Regional odontodysplasia
Dentin dysplasia
Enamel hypoplasia

97. AMELOGENESIS IMPERFECTA
97
 also known as:
 Hereditary Enamel Dysplasia
 Hereditary Brown Enamel
 Hereditary Brown Opalescent Teeth

98. 98
Group of conditions caused by
defects in the genes encoding
enamel matrix proteins
 genes that encode for enamel
proteins:
 amelogenin mutated in
 enamelin in patients
 others with this
condition

99. 99
A heterogeneous group of hereditary
disorders that demonstrate developmental
alterations in the structure of enamel in the
absence of a systemic disorder
 Many subtypes
 Numerous patterns of inheritance
 Wide variety of clinical
manifestations
 Frequency varies between 1:718
and
1:14,000
 Both dentitions involved

100. 100
Formation of enamel a multistep
process
Formation of enamel matrix
Mineralization of matrix
Maturation of matrix
Hereditary defects of enamel
formation usually classified as:
 Hypoplastic
 Hypocalcified
 Hypomaturative

101. 101
Amelogenesis imperfecta
Witkop classification

102. 102
Hypoplastic
Amelogenesis Imperfecta
 Inadequate formation of matrix
FEATURES
Teeth erupt with insufficient amounts
of enamel.
 Enamel present is mineralized
appropriately and contrasts well with
dentin on radiograph.
 Teeth may have abnormal shape
and open contacts.
 Open bite may be present

103. 103
•Hypoplastic generalized pitted
pattern.
•Hypoplastic localized patern.
•Hypoplastic autosomal dominant smooth
pattern
•Hypoplastic rough pattern

104. 104
HYPOPLASTIC GENERALIZED
PITTED PATTERN

Pin point to pin head sized
pits scattered.
Buccal surfaces affected
mure severly
Pits may arranged in rows
and columns.

105. 105
HYPOPLASTIC LOCALIZED
PATTERN

Horizontal rows of pits,a linear
depression.
Middle third of buccal surfaces of
teeth is aeffected.
 Both dentition orprimary only may
be aeffected

106. 106
HYPOPLASTIC AUTOSOMAL
DOMINANT SMOOTH PATTERN
Enamel of all teeth exhibit smooth
surface,thin hard glossy surface.
Absence of appropriate enamel
thickness.
Colour varies from opaque white to
translucent brown.
Radiographically, thin peripheral
radiopaque enamel.

107. SMOOTH PATTERN
107

108. HYPOPLASTIC ROUGH PATTERN
108
Enamel is thin with hard
rough surface
Teeth taper towards
incisal-occlusal surfaces.
open contact points
significant attrition and anterior
open bite

109. 109
•ENAMEL AGENESIS
•Demonstrate total lack of enamel
•Teeth are shape and colour of dentin with yellow brown hue
•Open contacts
•Crowns taper towards incisally
•Dentin is rough
•Radiograph demonstrates no peripheral enamel overlying dentin
•A lack of eruption of many teeth occurs frequently

110. HYPOMATURATION TYPE
110
Enamel matrix is laid down properly and
begins to mineralize but there is a
defect in
maturation of enamel’s crystal structure
 Affected teeth normal in shape
 Mottled appearance-white, brown or
yellow
 Enamel soft and chips away from
dentin
 Enamel has similar radiodensity to
dentin

111. 111
AUTOSOMAL DOMINANT
HYPOMATURATION TYPE
AUTOSOMAL
RECESSIVE
X LINKED RECESSIVE

112. HYPOMATURATVE-AUTOSOMAL
DOMINANT
112
Commonly in males
Both permanent and
primary
primary teeth-ground
glass opaque white.
Permanent teeth –
mottled yellow
white,darkened on
absorption of stains

113. HYPOMATURATIVE-AUTOSOMAL
RECESSIVE
113
Both primary and permanent
dentition
Enamel shows milky to shiny
agar brown deeply stained on
contact with exogenous agents
Chips away around teeth
restoration
Teeth may resorbs within
alveolus

114. HYPOPLASTIC X-LINKED RECESSIVE
114
Aeffects both dentitions
White opaque areas on
enamel of incisal and
occlusal third of crown –
SNOW CAPPED
PATTERN

115. HYPOCALCIFIED –AMELOGENESIS
IMPERFECTA
115
Proper amount of enamel matrix is
formed but but
it doesn’t mineralize properly.
 Teeth shaped normally upon
eruption but enamel
is soft and easily lost
 Enamel yellow-brown upon
eruption but quickly
becomes brown to black
 Accumulate calculus.

116. HYPOMATURATION HYPOPLASTIC TYPE
116
•Enamel hypomaturation is the
dominant feature.
•Enamel is yellowish white to‐
yellowish brown.‐
•Pits are seen on buccal surface.
•Enamel is similar to dentin in density.
•Large pulp chambers with varying
degrees of taurodontism.

117. HYPOPLASTIC-HYPOMATURATIVE AD
117
•Enamel hypoplasia is the dominant
feature.
•Enamel is thin
BOTH PATTERNS SEEN IN
TRICHODENTO OSSEOUS
SYNDROME

118. TRICHO-DENTO-OSSEOUS SYNDROME
118
•Autosomal dominant disorder.
•Shows hypoplastic hypomaturation‐
with severe taurodontism.
•Kinky hairat birth which may
straighten with age.
•Osteosclerosisof the base of skull
and mastoid process.

119. TREATMENT
119
Vary accoring to sub type and severity
Main problems associated are
esthetics,sensitivity,and loss of vertical
dimension.
Full coverage restoration recommended in
attrition cases
Less severe cases can be improved by
placements of full crowns and facial veneers

120. DENTINOGENESIS IMPERFECTA
120
•Called Hereditary opalescent dentin,
Capdepont’s teeth.
•Only the mesodermal portion of the
odontogenic apparatus is affected.
•Dentin is defective.
•Could be due to hereditary factors
•Can be seen in association with
osteogenesis imperfecta

121. CLINICAL FEATURES
121
Deciduous teeth are more severely affected
•Gray to brownish violet or yellowish brown
with a characteristic translucent or
opalescent hue.
•Broad crown with constriction of cervical area
constriction – TULIP SHAPE

122. 122
Enamel may be lost earlyon incisal and occlusal
surfaces due to the abnormal DEJ
.
•DEJ lacks the usual scalloping.
•Dentin is attrited rapidly.
•Occlusal surfaces of affected teeth are severely
flattened.

123. 123

124. CLASSIFICATION BY SHIELDS
124
Type I –DI that always occur with OI–
autosomal dominant.
•Type II –DI that never occurs with OI–
hereditary opalescent dentin –autosomal
dominant .
•Type III –DI –Brandy wine type–similar
autosomal dominant

125.  1 in 8000
occurs in families with
Osteogenesis Imperfecta
 primary teeth are more severely
affected than permanent teeth
125
TYPE I DENTINOGENESIS IMPERFECTA

126.  Radiographically:
 partial or total obliteration
of pulp chambers + root canals
 by continued formation
of dentin
 roots may be short + blunted
 cementum, periodontal
membrane + bone appear
normal
126
Type I DENTINOGENESIS IMPERFECTA

127.  never occurs in association
with osteogenesis imperfecta
unless by chance
 most frequently referred to as
hereditary opalascent dentin
 only have dentin abnormalities
and no bone disease
127
Type II DENTINOGENESIS IMPERFECTA

128.  Radiographically:
 partial or total obliteration
of pulp chambers + root canals
 by continued formation
of dentin
 roots may be short + blunted
 cementum, periodontal
membrane + bone appear
normal
Type II Dentinogenesis Imperfecta
128

129.  “Bradwine type”
 racial isolate in Maryland
 multiple pulp exposures in
deciduous not seen in type
I or II
 periapical radiolucencies
Type III Dentinogenesis
Imperfecta
129

130.  enamel appears normal
 large size of pulp chamber
is due not to resorption but
rather to insufficient + defective
dentin formation
Type III Dentinogenesis
Imperfecta
130
Witkop describes it as Shell teeth
Radiographic features
Roots are extremely short

131. HISTOLOGIC FEATURES
131
•Dentin has irregular tubules with large areas
of uncalcified matrix.
•Tubules are larger in diameter and lesser in
number
Cellular inclusions probably odontoblasts can be seen in
dentin.
•

132. 132
•The odontoblasts with limited ability to
form well organized dentinal matrix,‐
appear to degenerate readily and get
entrapped within the matrix.
•Pulp chamber is obliterated by
continuous dentin deposition

133.  Treatment:
DENTINOGENESIS IMPERFECTA
133
oPreservation of vertical dimension of occlusion
o Continued commitment & support to both child &
family
o Stainless steel crowns to protect against attrition
o
o Initial composite build – up for anteriors to be
replaced by veneers later Overdentures / implants
later.

134.  also known as “Rootless Teeth”
 rare disturbance of dentin
formation
atypical dentin formation
DENTIN DYSPLASIA
134
First described by Ballschmiede(1920) –spontaneous
exfoliation of multiple teeth.
•Rushton(1939) designated it as dentin dysplasia.

135. 135
Rare autosomal-dominant
condition that affects dentin
 Prevalence about 1:100,000
 abnormal pulpal morphology

136. CLASSIFICATION
136
Shields:
Type I –dentin dysplasia
Type II –anomalous dysplasia of dentin
•Witkops:
Type I –Radicular dentin dysplasia –More common.
Type II –Coronal dentin dysplasia

137.  Classification:
 Type I (Radicular Type)
 Type II (Coronal Type)
DENTIN DYSPLASIA
137

138.  both dentitions are of
normal color
Most common type
 prevalence 1:100000
Type I (Radicular Type)
138
(Rootless
teeth)
Wide variation in root formation because dentinal
disorganization may occur at different stages of tooth
development

139.  Radiographically:
 roots are extremely short
 pulps almost completely
obliterated
 periapical radiolucencies:
• granulomas
• cysts
• chronic abscesses
Type I (Radicular Type)
139

140.  autosomal dominant
Root length is normal.
Colour blue -amber to brown
translucency
 coronal pulps are usually large
(thistle tube appearance)
 filled with globules of abnormal
dentin
Type II (Coronal Type)
140

141.  Radiographically:
(Deciduous)
 roots are extremely short
 pulps almost completely
obliterated
(Permanent)
 abnormally large pulp
chambers in coronal portion of
tooth
Type II (Coronal Type)
141

142.  also known as:
 Odontogenic Dysplasia
 Odontogenesis Imperfecta
 Ghost Teeth
142
REGIONAL
ODONTODYSPLASIA

143.  one or several teeth in a
localized area are affected
 maxillary teeth are involved
more frequently than
mandibular area
 etiology is unknown
143

144.  teeth affected may exhibit
a delay or total failure in
eruption
 shape is altered, irregular in
appearance
144

145.  Radiographically:
 marked reduction in
radiodensity
 teeth assume a “ghost”
appearance
 both enamel + dentin appear
very thin
 pulp chamber is exceedingly
large
145

146.  Treatment:
 poor cosmetic appearance
of teeth
 extraction with restoration
by prosthetic appliance
146

147. ENAMEL HYPOPLASIA
147
An incomplete or defective formation of the
organic enamel matrix of teeth.
•It occurs only when the injury occurs during the
development or more specifically, formative
stage of enamel.
TYPES:
I.Hereditary type enamel
hypoplasia
II.Environmental type
hypoplasia

148. Hereditary type enamel hypoplasia
148
•This is an ectodermal disturbance that occurs during the
embryonic development of the enamel.
• The mesodermal components are normal. Both the
deciduous and permanent teeth are involved and only the
enamel is affected.
The three types of hereditary type of enamel hypoplasia
are the:
•Hypoplastic type, where there is a defective formation of
organic matrix.
•Hypocalcification type, in which there is a defective
mineralization of the matrix.
•Hypomaturation type, where there is a defective
maturation of the matrix

149. Environmental type enamel hypoplasia-
149
This is caused by the environmental factors that causes
damage to the enamel cells.
Either deciduous or permanent teeth are involved and
sometimes a single tooth is involved
Hypoplasia results only if the injury occurs during the
time the teeth are developing or more specifically during
the formative stage of enamel development.
The environmental factors which produce
enamel hypoplasia can include

150. 150

151. CLINICAL FEATURES
151
Mild:
Few small grooves, pits or fissures on
enamel surface
Moderate:
Enamel may exhibit rows of deep pits
arranged horizontally across tooth
surface.
Severe:
pitting and brownish staining of the
surface. Tendency of enamel to wear or
fracture

152. TREATMENT
152
Treatment of enamel hypoplasia is always
individualized and depends on the location and
severity of then condition.
The location of enamel hypoplasia also
affects treatment options :
> Anterior teeth -
For sensitive teeth with no wear,
desensitizing agent (such as potassium nitrate)
as needed can be used.
If there are esthetic concerns, composite or
porcelain veneers may be bonded to afected
tooth.

153. 153
Posterior teeth –
1. For sensitive teeth with minimal wear, desensitizing agent
(such as potassium nitrate) can be used.
2. For mildly hypoplastic molars, place pit and fissure sealant
on the occlusal surface. - at 6 month re-evaluation
3. Remove demineralized enamel and restore with composite.
- at 6 month re-evaluation, if composite is lost, either
replace using good isolation techniques or go to step 4
4. Perform minimal reduction of tooth and cement a stainless
steel crown - evaluate clinically and radiographically as
indicated

154. CASE REPORTS
154

155. 155
A CASE REPORT OF A PATIENT AFFECTED BY
AMELOGENESIS
IMPERFECTASHOWING A POSSIBLE MINIMAL
AND CONSERVATIVE ADHESIVE TREATMENT
APPROACH.
A 14 years old boy with amelogenesis imperfecta
consulted a dentist for full mouth rehabilitation
After examination ,step by step minimum
conservative approach planned.
S Ardu O Duc I Krejci
R Perroud
Clinical views at the patient’s first
appointment

156. 156
In the posterior area conservative resin composite onlays
were realized , whereas in the anterior area
freehand bonded composite restorations were
performed according to the natural layering technique
proposed.
Intraoral view of the conservative preparations for resin
composite onlays and clinical view after posterior
onlays placement

157. 157
Intraoral view of the preparations for freehand bonded composite
restorations and clinical view after teeth rehydration. Last image
shows the clinical view after the placement of a cantilever bonded bridge
23

158. 158
Clinical views at the end of the treatment, together with the final treatment status at the 3-month recall. Except
for the lithium disilicate
bridge from 21–23, all other teeth are single-unit lithium disilicate bonded crowns.

159. 159
•case report describes a possible application of a
minimally invasive approach for treating amelogenesis
imperfecta in a young adolescent.
•This conservative
adhesive treatment allows a two-stage
intervention that accompanies the patient during
his adolescence until the complete formation of hard
and soft tissues.
•This will allow acceptable esthetics
and lack of pain during eating and will allow the
patient to have a more normal social life.

160. 160
Dan Emil GEORGESCU, Rodica LUCA and Elisa
Mădălina CHIRCA
Conducted study to assess the frequency of development
anomalies of teeth and soft tissue in the anterior region, of a school
children from Bucharest.
cross sectional study is conducted
Material and methods: 226 children from two secondary schools,
aged between 5-8years
•Children were examined in the school dental office.
• The presence of dental development anomalies or of
other types was recorded.
• The frequency of developmental anomalies was
determined.
•4.87% of the examined school children had oral
developmental anomalies:
.
Fused teeth

161. 161
Dental size anomalies (0.44%) - one fusion and one
gemination and 9 abnormal maxillary frenum attachment
(3.98%).
Dental anomalies were found in front teeth, in both
dentition.
Diastema was found in permanent dentition, between the
two upper central incisors. The evaluated age group had a
low frequency for front teeth dental development
anomalies.
Follow up of all children is necessary until the eruption of
all permanent teeth
Gemination
Diastema between the two upper
permanent central incisors

162. 162
Endodontic treatment of developmental
anomalies in posterior teeth: Treatment of
geminated/fused teeth Nelly Steinbock
Two cases of complex endodontic treatment of fused/geminated
teeth are presented.
The first is an 11-year-old girl with an anomalous ‘double’ first
mandibular molar and premolar diagnosed as having necrotic
pulp with chronic apical abscess of endodontic origin;
.
Fused crowns of the mandibular right first molar
and second premolar

163. 163
 Two separate endodontic access cavities were prepared in the
fused crown in the molar
and the premolar area
•Five canal orifices were found – two leading to the
distal root canals
(emerging from the molar pulp chamber) and the other
three leading to the mesial roots and
emerging from the floor of the premolar pulp chamber
•The canals were instrumented manually using K-files
and irrigated with 3% sodium
hypochlorite solution.
• Working length was determined with an electronic
apex locator
Working length radiograph of
the fused mandibular right
first molar and second
premolar
•Follow-up 6 months later showed that the tooth
was restored with composite filling

164. 164
The second is a 16-year-old boy with ‘double’
second and supernumerary mandibular molars, who
was diagnosed with irreversible pulpitis.
Preoperative radiograph of the geminated second
molar tooth (fusion of molar with supernumerary).
Clinical examination revealed an anomalous
second molar that could have been a fusion of
the mandibular right second molar with a
supernumerary tooth in its mesiobuccal aspect
•Radiographic examination
•Two separate access cavities were prepared
•Five canal orifices were found on the mesial side of the
pulp
chamber floor – two leading to the supernumerary tooth
and three leading to the mesial root
of the molar.

165. 165
Working length determination radiograph
demonstrating five of the six canals.
•Irrigated with 3% sodium hypochlorite solution
•The tooth was obturated using
the lateral condensation technique with AH-26 as
a sealer
DISCUSSION
•Fusion and gemination are developmental
anomalies with inherently unusual and bizarre
anatomy.
•A prerequisite for endodontic treatment of
anomalous teeth is a careful examination
of radiographs from various angles
In both the cases, there was a communication between two
parts of the pulp chambers and root canal systems. Thus,
endodontic treatment was performed on both
parts of these teeth.

166. 166
Dental Anomalies in Chinese Children with
Cleft Lip and Palate
Hai Ming Wong1*, Moon Cheung Lai2 and Nigel Martyn
King3
• The prevalence of anomalies in children with CLP and to
ascertain if there were any differences between the
prevalence figures for CLP and non-CLP children
• The sample consisted of 231 pairs of age and gender matched CLP
and non-CLP southern Chinese aged between 12 and 16 years.
• The dental records of the subjects were examined to gather data on
anomalies of tooth number, size and shape.
: Missing permanent maxillary
lateral incisor and canines.
Number of types of dental anomalies per individual
Hypodontia (57.6%)
Microdontia (42.4%),
The cleft type associated with the highest
percentage of supernumerary teeth was CL (25.0%),

167. 167
•Approximately 10% of BCLP, UCLP and CP children
were found to have taurodontism
Taurodontism of permanent maxillary first
molars.
•This group of Chinese CLP children exhibited the
various types of dental anomalies.
• Statistically higher prevalences of hypodontia,
supernumerary teeth and microdontia were
demonstrated in the CLP children than in the non-
CLP children.
A conical shaped supernumerary tooth in
relation to permanent maxillary right canine

168. CONCLUSION
168
Anomalies on tooth have
aesthtic,functional,psychological
impact on the individual.so any
abnormalities or pathologies on
hard or soft tissues in oral cavity
must prompt clinician to think
beyond the local factors for
proper diagnosis and treatment

169. References:References:
 BooksBooks
 Neville, et al: Oral and Maxillofacial PathologyNeville, et al: Oral and Maxillofacial Pathology
33rdrd
EditionEdition
Shafer, et al: A textbook of Oral Pathology,Shafer, et al: A textbook of Oral Pathology,
33rdrd
EditionEdition
Anil govindrao ghom:textbook of oral medicine.Anil govindrao ghom:textbook of oral medicine.
44thth
editionedition
Cawson, R.A: Cawson’s Essentials of OralCawson, R.A: Cawson’s Essentials of Oral
Oral Pathology and Oral Medicine,Oral Pathology and Oral Medicine,
88thth
EditionEdition
169

170.  Burkits textbook of oral medicine.11th
edition.
 DentalAnomalies inChineseChildrenwithCleft LipandPalate
HaiMingWong1*, MoonCheungLai2andNigelMartynKing3
 Endontic treatment of developmentalanomalies inposteriorteeth:treatment
of fusionandgeminationteeth(endodontic journal2003)
170
Amelogenesis Imperfecta:
A Conservative and Progressive Adhesive Treatment Concept
S Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171. 171