Tooth development and its abnormalities

DEVELOPMENT OF
TOOTH AND ITS
ABNORMALITIES
Dr. V. Usha Kiran
1

Contents
• Introduction
• Tooth development and growth
- Stages of tooth development
- Histophysiology
- Molecular insights
• Developmental abnormalities of tooth
- Number
- Size
- Shape
- Structure
2

Oral Cavity
• Oral cavity has
Hard tissues – Jaw bones
Teeth
Soft tissues – Mucosal lining
Salivary glands
3

Nomenclature
• Humans have 2 sets of teeth – Primary OR Deciduous dentition.
Permanent OR Succedaneous dentition.
• Types of teeth – Incisors
Cuspids
Bicuspids
Molars
• Number of teeth – 20 primary teeth (10 in each jaw)
32 permanent teeth (16 in each jaw)
4

Human Tooth
• Diphyodont human’s teeth comprise of:
Crown – Clinical, anatomical.
Root
Periodontium
Supporting alveolar bone.
• Each tooth consists of – enamel
dentin
pulp
cementum
5

Human Tooth
Vertical Cone Beam CT Slice of
mandibular molars and premolar
6

Tooth numbering
• Palmer notation:
• FDI
7

Dental Formula
• Deciduous dentition
• Permanent dentition
8

TOOTH DEVELOPMENT AND GROWTH
• Introduction
• Dental lamina and vestibular lamina
• Stages of tooth development
Bud Stage
Cap Stage
Bell Stage
• Histophysiology
• Molecular insights
9

TOOTH DEVELOPMENT – AN OVERVIEW1
• Tooth is formed from – Ectoderm and Ectomesenchyme
• Enamel: Derived from the enamel organ which is differentiated from the
primitive oral epithelium lining the stomodeum.
• Epithelial mesenchymal interactions take place to determine
tooth shape
differentiation of the formative cells
timing of their secretions
10

Tooth Development – an overview2
• “Blast Cells” or the formative cells:
Ameloblasts – Enamel
Odontoblasts – Dentin
Cementoblasts – Cementum
Fibroblasts – Periodontal ligament
Osteoblasts – Bone
• “Clast Cells” or resorbtive cells
11

• Ectomesenchymal cells of the enamel organ
The ones close to inner margin differentiate into dental papilla.
The ones close to outer margin differentiate into dental follicle.
Dentin derived from the
Pulp dental papilla.
PDL
Cementum derived from the
Alveolar bone dental follicle.
12

• Dentin is the first hard tissue of tooth to form.
• Enamel formation starts after dentin is laid down.
• Cementum formation occurs after the root form is outlined by HERS.
• Incremental formation of tooth tissues is shown by incremental lines.
13

DENTAL LAMINA1
• Stomodeum is lined by stratified squamous epithelium called
oral ectoderm OR
primitive oral epithelium
• This epithelium contacts the endoderm of the foregut to from buccopharyngeal
membrane.
• On 27th day of gestation, this membrane ruptures and stomodeum establishes a
connection with the foregut.
• The neural crest cells underlying the oral ectoderm instruct the overlying
ectoderm to start development.
14

Dental lamina2
• This process starts in anterior portion of the future maxilla and mandible,
proceeds posteriorly.
• In 6 weeks old embryo, buccopharyngeal membrane ruptures and some basal
cells proliferate more rapidly than others, Primary epithelial band is formed.
• At about 7th week, this band divides into:
an inner (lingual) process – dental lamina.
an outer (buccal) process – vestibular lamina.
15

Dental lamina3
• Dental lamina serves as primordium for ectodermal portion of deciduous teeth
and later permanent molars arise directly from a distal extension of dental
lamina.
• Successors of deciduous teeth develop from a lingual extension of the free end
of dental lamina opposite the enamel organ of deciduous teeth which is the
Successional Lamina.
16

Dental lamina4
• Successional lamina develops from the 5th month in utero.
Permanent molar – 4th month in utero
Permanent central – 5th month in utero
Second premolar – 10th month in utero
Second molar – 1st year after birth
Third molar – 4 to 5 years after birth
18

Dental lamina5
• As teeth develop, they loose connection with dental lamina and remnants
persist in jaws and gingiva as epithelial pearl called ‘Rest of Serres’.
• Vestibular Lamina:
Independent epithelial thickening labial and buccal to the dental
lamina in each arch is vestibular lamina. This lip furrow hollows to form the oral
vestibule between alveolar portion of jaws and lips-cheeks.
19

Dental and Vestibular lamina
20

DEVELOPMENT OF TOOTH1
• Ectodermal cells proliferate rapidly in the dental lamina at sites corresponding
to the 10 maxillary and 10 mandibular teeth to form little knobs.
• These are the beginnings of enamel organs of the deciduous teeth tooth buds
• Cell Proliferation continues and enamel organ increases in size to form a cap
with – outer convex surface facing the oral cavity
inner concavity.
22

Enamel organs of
deciduous teeth and
primordia of permanent
teeth
23

Development of tooth2
• Cells in the depression of enamel organ proliferate and form dental papilla.
• Surrounding the combined enamel organ and dental papilla, the dental sac or
follicle forms and this is the third part of the tooth bud.
• Dental sac has
ectomesenchymal cells that surround the dental papilla
fibers and the enamel organ.
24

Development of tooth3
• At this stage, tooth germ has 2 components:
Ectodermal component – enamel organ.
Ectomesenchymal component – dental papilla
dental follicle.
• Tooth germ continues growing and form
into a bell shape.
• Now the tooth bud looses its connection with
epithelium of the oral cavity.
25

DEVELOPMENTAL STAGES1
• Shape of the enamel organ dictates name of the developmental stages:
Bud stage
Cap stage
Bell stage
Advanced Bell stage
Hertwig’s epithelial root sheath
26

Developmental Stages2
Bud Stage
• Enamel organ has
- peripheral low columnar cells
- central polygonal cells.
• Cells undergo mitosis and condense by:
- increased mitotic activity
- neural crest cells migration into the area.
27

• Bud Stage (cont’d)
At this stage:
dental papilla is the area immediately adjacent to enamel organ.
dental sac is the condensed ectomesenchyme that surrounds tooth
bud and dental papilla.
Both dental papilla and the dental sac become well-defined and grow
into cap and bell stages.
28

• Cap Stage:
Unequal growth in different parts of the bud leads to this stage.
a. Outer and Inner enamel epithelium:
Peripheral cells of cap stage are cuboid, cover concavity of the
cap and are called outer enamel epithelium.
Cells in concavity of the cap become tall columnar and represent
inner enamel epithelium.
30

Early Cap stage
showing ectomesenchymal
condensation associated
with the epithelial cap.
31

• Cap Stage (cont’d):
b. Stellate Reticulum:
Star-shaped cells form a cellular network. The cells in the centre of the
enamel organ are densely packed and form the enamel knot.
The enamel septum divides the stellate reticulum into 2. Enamel navel is
the point of meeting of the enamel septum on the outer enamel epithelium.
Enamel knot and cord - ? Functions:
Reservoir of dividing cells for the growing enamel organ.
Enamel knot – signalling centre determining the tooth shape.
32

Enamel knot,
cord and septum
33

• Cap Stage (cont’d):
c. Dental Papilla:
Shows active budding of capillaries and mitotic figures. The
peripheral cells of dental papilla adjacent to inner enamel epithelium enlarge and
later differentiate into odontoblasts.
d. Dental Sac OR Dental Follicle:
Marginal condensation in the ectomesenchyme surrounding the
enamel organ and the dental papilla leads to development of a fibrous layer
called the primitive dental sac.
34

• Bell Stage:
As the invagination of the epithelium deepens and margins continue to
grow, the enamel organ assumes a bell shape where the crown shape is
determined.
Differential rates of mitosis and difference in cell differentiation time
determines the crown shape.
Tooth morphogenesis in controlled by
genes and their signaling molecules
growth factors
36

• Bell Stage (cont’d)
Enamel organ cells differentiate to form cusp tips and cuspal slopes. Cell
differentiation proceeds cervically and those at the cervix differentiate last.
Epithelial cells at Bell Stage of the Enamel Organ:
1. Cells from inner enamel epithelium
2. Cells from stratum intermedium
3. Cells from stellate reticulum
4. Cells from outer enamel epithelium.
Cervical loop
37

a. Inner enamel epithelium:
Single layer of cells which differentiate into tall columnar ameloblasts
prior to amelogenesis.
Cells have desmosomal attachments.
They exert an organising influence on the underlying mesenchymal
cells in the dental papilla which later differentiate into odontoblasts.
38

b. Stratum intermedium:
A few layers of squamous cells form the stratum intermedium
between the inner enamel epithelium and the stellate reticulum.
Cells are closely attached by desmosomes and gap junctions.
Work with the cells of inner enamel epithelium as a single
functional unit and form enamel.
This layer is absent in the part of the tooth germ that outlines the
root portion of the tooth which does not form enamel.
39

c. Stellate reticulum:
Expands further and cells anastomose. Desmosomal junctions are
seen between cells of stellate reticulum-stratum intermedium-outer enamel
epithelium.
This layer collapses before enamel formation begins. Cells cannot
be differentiated from the stratum intermedium and this change begins at the
height of the cusp and progresses cervically.
40

d. Outer enamel epithelium:
Cells flatten to a low cuboidal form and smooth surface of the
outer enamel epithelium is laid in folds during enamel formation at the end of
bell stage.
Between the folds, adjacent to the mesenchyme of the dental sac
forms papillae that contain capillary loops to provide nutrition for the intense
metabolic activity avascular enamel organ.
42

e. Dental Lamina:
This extends lingually as the successional dental lamina and gives
rise to enamel organs of the permanent successors of the deciduous teeth.
f. Dental papilla:
Enclosed in the invaginated portion of the enamel organ. Under
the organising influence of the epithelium, the mesenchymal cells of the dental
papilla differentiate into odontoblasts.
This ultimately gives rise to dental pulp.
43

f. Dental papilla (cont’d):
The basement membrane that separates the enamel organ and the dental
papilla just prior to dentin formation is called the membrane preformativa.
g. Dental sac:
Prior to formation of dental tissues, it shows circular arrangements of its
fibers and resembles a capsule. With root development, these fibers differentiate
into periodontal fibers that become embedded into the developing cementum-
alveolar bone.
45

• Advanced Bell Stage:
Root formation and mineralisation commence.
The boundary between inner enamel epithelium and odontoblasts
outlines the future DEJ.
Dentin formation occurs first along the future DEJ in the region of future
cusps – proceeds pulpally and apically.
Ameloblasts lay down enamel over dentin.
Cervical portion of the enamel organ gives rise to HERS.
46

• Hertwig’s epithelial root sheath and root formation:
Root development begins after enamel and dentin formation has reached
the future CEJ.
Enamel organ forms the HERS which molds the shape of the roots and
initiates radicular dentin formation.
Components of HERS:
1. Outer enamel epithelium.
2. Inner enamel epithelium.
47

• HERS (cont’d):
Cells of inner layer remain short and do not produce enamel. Remnants
persist as clumps near the external root surface and found in the periodontal
ligament of erupted teeth – “ Rests of Malassez”
Single rooted v/s multi-rooted tooth:
Prior to starting root formation, the HERS forms the epithelium
diaphragm. Differential growth of this epithelial diaphragm in multi-rooted teeth
causes the division of the root trunk into – 2 roots
3 roots.
48

• HERS (cont’d)
Multi-rooted teeth:
During general growth of enamel organ,
expansion of its cervical opening occurs such that long
tongue like extensions of this horizontal
diaphragm develop.
2 such extensions are formed in that tooth germs of mandibular
molars and 3 in maxillary molars.
49

• HERS (cont’d):
Before root trunk division, free ends of horizontal epithelium flaps grow
towards each other and fuse. The single cervical opening of the coronal enamel
organ is then divided into 2 or 3 openings.
If HERS cells remain adherent to
dentinal surface, they may differentiate into
fully functional ameloblasts and produce
enamel – enamel pearls.
50

HERS – Multi-rooted Tooth
51

• HERS (Cont’d):
When the continuity of HERS ruptures OR the continuity
is not established before dentin formation,
A defect in dentinal wall of pulp occurs. Such defects are found in pulpal
floor corresponding to furcation or any point of root. This accounts for
development of accessory root canal openings in the periodontal ligament
surface of the root.
52

HISTOPATHOLOGY1
• Initiation:
Mesenchyme of the dental papilla can induce or instruct the tooth
epithelium and even that non-tooth epithelium to form enamel.
Different teeth are initiated at different times.
• Proliferation:
Enhanced proliferative activity ensues at the point of initiation and
results in the successive bud, cap and bell stages.
Proliferative growth causes regular changes in the size and proportions
of the growing tooth germ.
54

INITIATION OF TOOTH DEVELOPMENT
55

Histopathology2
• Histodifferentiation:
Formative cells of the tooth germs developing during proliferation
undergo definite morphological-functional changes and acquire their functional
assignment.
Cells become restricted to their functions. They differentiate and give up
their capacity to multiply.
This phase reaches its highest development in the bell stage of the
enamel organ, just before the beginning of formation and apposition of dentin
and enamel.
56

Layers of epithelial enamel organ
57

Histopathology3
• Histodifferentiation (cont’d):
Inner enamel epithelium has organising influence on the mesenchyme
and this is evident in bell stage.
Cells adjacent to the dental papilla are differentiated into odontoblasts.
When dentin forms, inner enamel epithelium differentiates into
ameloblasts and enamel matrix is formed opposite the dentin.
Dentin formation precedes and IS essential for enamel formation.
58

Histopathology4
• Morphodifferentiation:
Basic form of the future tooth is established by differential
Relative size growth during morphodifferentiation.
Advanced bell stage marks - active histodifferentiation
outlining the future DEJ.
DEJ and CEJ act as blue print patterns, are different for each tooth type.
Enamel, dentin and cementum deposition gives each tooth its
characteristic shape and form.
59

Histopathology5
• Apposition:
Deposition of matrix of the hard dental structures is in a layer manner of
the extracellular matrix and is regular and rhythmic.
Periods of activity and rest alternate at definite intervals.
60

Molecular Insights – Tooth Morphogenesis
• Tooth development requires systemic cascading interactions between epithelial
component (brachial arch ectoderm) and ectomesenchyme (mesenchymal
component).
• Fgf-8, Pitx-2 and Bmp-4 in oral epithelium position of the tooth germ
• Pax-9 in tooth mesenchyme. is established.
• Shh expression is seen in dental ectoderm.
• Msx gene and Dlx gene.
61

Summary of Tooth Development
62

Time line of tooth development
63

Sagittal section
at 18 weeks
64

TOOTH DEVELOPMENT - ABNORMALITIES1
• Number
Anodontia
Hypodontia
Hyperdontia
• Size
Microdontia
Macrodontia
66

Tooth development - abnormalities2
• Shape
Gemination Taurodontism
Fusion Accessory roots
Concrescence
Accessory cusps
Dens invaginatus
Ectopic enamel
67

Tooth development - abnormalities3
• Structure
Enamel Hypoplasia - Developmental
- Environmental
Inherited Dentin Defects - Dentinogenesis imperfecta
- Dentinal dysplasia
Regional odontodysplasia
• Intrinsic Staining
68

NUMBER GAMES
• Terminology
Anodontia
Hypodontia
Oligodontia
Hyperdontia
Predeciduous dentition
Post-permanent dentition
Natal and Neonatal Teeth
69

Anodontia1
• Lack of tooth development.
• True anodontia:
Congenital absence of teeth.
Both dentitions may be involved.
- Total
- Partial
Eg: Hereditary ectodermal dysplasia
• False anodontia – resultant of tooth extractions.
• Pseudo-anodontia – resultant of non-eruption of teeth.
70

Anodontia2
• Clinical Features:
True anodontia is rare.
When agenesis occurs as an isolated trait, the primary dentition is
not affected and the inheritance is autosomal recessive.
• Management:
Overlay dentures can be constructed.
71

Hypodotia1
• Pathogenesis: Absence of dental lamina
Autosomal dominant.
Uncommon in deciduous dentition
Permanent dentition – mandibular second premolars
maxillary lateral incisors
maxillary second premolars.
Adult dentition – If the maxillary central incisor + maxillary first molar
are missing evaluate for Ectodermal dysplasia.
72

Hypodotia2
• Positive association with microdontia, reduced alveolar development,
increased freeway space, retained deciduous teeth.
• Clinical Significance:
Tooth spacing
Delayed tooth formation
Delayed deciduous tooth exfoliation and late permanent tooth eruption
• Management:
Resin bonded bridges
Osseo integrated implants with prosthetic crowns
73

Hyyperdontia2
• Prevalence:
Single tooth - 86%
2 teeth - 12% to 23%
3 or more teeth - less than 1%
• Presentation:
Unilateral
Bilateral
• Site of presence
74

Hyyperdontia3
• Most common site:
Maxillary incisors
Maxillary fourth molar
Mandibular fourth molar
Premolars
Canines
Laterals
75

Hyyperdontia4
• Terminology:
Mesiodens
Distodens OR Distomolar
Paramolar
Dental transpositioning
Natal teeth
Neonatal teeth
Predeciduous dentition
Post-permanent dentition
76

Hyyperdontia5
• Most common site:
Non-syndromic supernumerary teeth are more frequently seen in the
mandibular arch – Premolars, Molars, Anteriors
• Other sites: (Sites other than the oral cavity)
Sinus Maxillary tuberosity
Gingiva Spheno-maxillary fissure
Soft palate Between the orbit and the brain
Nasal cavity
77

Hyyperdontia6
• Pathogenesis:
Excess of dental lamina
Splitting of the tooth bud
Extra tooth bud
Mesiodens
Distodens OR distomolar
Paramolar
78

Hyyperdontia7
• Clinical Features (cont’d):
Dental transpositioning – normal tooth misplaced and often confused
with a supernumerary tooth. Eg: Canines and first premolars.
Natal teeth – teeth present at birth or shortly after birth
Neonatal teeth – teeth that erupt within the first
30 days of life. These are prematurely erupted deciduous
teeth and usually not supernumerary teeth. Mandibular
incisors – 85%, Maxillary incisors – 11%, Posterior teeth – 4%.
79

Hyyperdontia8
Predeciduous dentition – Hornified epithelium structures without roots, on
gingiva over crest of the ridge, easily removed. Arise from accessory bud of
dental lamina ahead of the deciduous bud or from a bud of accessory dental
lamina.
Post-permanent dentition OR Third dentition – A few recorded cases have
shown patients to have teeth erupted after all the permanent teeth being
extracted. Arise probably from a dental lamina bud beyond the permanent tooth
germ.
80

Hyyperdontia9
Delay (significant) in eruption of a segment of dentition – a
supernumerary tooth should be suspected.
Early diagnosis and management are crucial in minimal esthetic and
functional problems.
• Management:
Removal of the supernumerary tooth.
81

Hyyperdontia10
• Consequences of delayed treatment:
Delayed eruption of the adjacent teeth.
Resorption
Tooth displacement with associated
crowding
malocclusion
diastema. Rare molariform supernumerary teeth
82

Hyyperdontia11
• Consequences of delayed treatment (cont’d):
The area of the dentition involved is predisposed to:
subacute pericoronitis
gingivitis
periodontitis
abscess formation
cyst/tumour formation (odontogenic)
83

ToothSize
• Microdontia
Localised
Generalised – True
Relative
• Macrodontia
Localised
Relative
84

Microdontia1
Teeth which are smaller than normal and outside
usual limits of variation are said to be microdont.
Types:
Localised
Relative
85

Microdontia2
• Localised microdontia:
Involves only 1 tooth or a few teeth,
usually the maxillary lateral incisor or third molars
are affected.
86

Microdontia3
• True generalised microdontia:
All teeth are smaller in size than normal.
This condition is very rare.
Seen in few cases of pituitary dwarfism.
• Relative generalised microdontia:
Normal teeth are present in larger than normal jaws.
Macrognathia rather than microdontia.
87

Microdontia3
Usually involves a single tooth
maxillary lateral incisor (peg lateral)
third molars
supernumerary teeth.
Has a strong association with hypodontia.
88

Microdontia4
Esthetic consideration – Peg laterals.
Deciduous - maternal and intrauterine disturbances.
Permanent teeth are affected more by environmental disturbances.
• Management:
Treatment options are considered for esthetic reasons.
Peg laterals are often restored to normal size by full crowns.
89

Macrodontia1
• Teeth that are larger than the normal size
and beyond normal limits of variation
are said to be macrodont.
• Types:
Localised
Relative
90

Macrodontia2
• Localised macrodontia:
Macrodontia involving a single tooth.
Relatively uncommon, confused with fusion.
A variant of localised macrodontia is seen in hemihypertrophy of the face
where the teeth on the involved side
may be considerably larger than
those on the unaffected side.
91

Macrodontia3
• True generalised macrodontia:
All teeth are larger than normal.
Associated with pituitary gigantism.
Extremely rare.
• Relative generalised macrodontia:
Normal teeth in smaller jaws.
Micrognathia rather than macrodontia.
92

Tooth Shape
• Gemination
• Fusion
• Concrescence
• Accessory Cusps
• Accessory Roots
• Taurodontism
• Dilaceration
• Dens Invaginatus
• Ectopic Enamel
93

Gemination1
• Definition: Gemination is defined as a single enlarged tooth or joined
(double) tooth in which the tooth count is normal when the
anomalous tooth is counted as one.
• Pathogenesis:
An attempt at division of a
single tooth germ by an
invagination occurring at
proliferation stage
94

Gemination2
Both dentitions are affected.
Geminated tooth appears clinically as a bifid crown on a single root.
Crown is wider than normal with a shallow groove extending from the
incisal edge to the cervical region.
High incidence in the maxillary anterior region.
“Twinning” – two equivalent structures resultant of division lead to one
normal and one supernumerary tooth.
95

Gemination3
• Clinically – a geminated tooth and fusion
between a normal and a supernumerary tooth
cannot be differentiated easily.
96

Fusion1
• Definition: Fusion is defined as a single enlarged tooth or joined (double)
tooth in which the tooth count reveals a missing tooth when the
anomalous tooth is counted as one.
• Pathogenesis: Changes in pressure during tooth
development results in contact of
the developing teeth and their
subsequent fusion.
97

Fusion2
More common in deciduous dentition than
permanent dentition. (Graham and Granath)
Complete fusion – contact before tooth calcification begins.
Incomplete fusion – contact after a part of crown formation is done.
Roots may be fused or separate.
Dentin is always confluent in cases
of true fusion.
98

Fusion and Gemination
Presence leads to – crowding
delayed OR ectopic eruption of permanent teeth.
• Management:
Close clinical and radiological monitoring.
Extraction.
Surgical shaping and Full crowns.
Surgical division and endodontic therapy with full crowns.
99

Concrescence1
• Growing together.
• Union of 2 adjacent teeth by cementum alone without confluence of the
underlying dentin.
• Pathogenesis: It could be – developmental
post-inflammatory.
Diagnosis is upon radiographic examination.
Frequently in the posterior maxillary region involving a second molar
and an impacted third molar.
101

Concrescence2
Therapeutic intervention only if interferes with eruption.
Post inflammatory concrescence may pose:
Significant extraction difficulties.
May require surgical separation.
Minimal trauma to surrounding bone is of vital.
102

Accessory Cusps1
Cuspal morphology of teeth exhibits 3 distinctive patterns:
1. Cusp of Carabelli
2. Talon’s cusp
3. Dens evaginatus
103

Accessory Cusps2
1. Cusp of Carabelli:
• Accessory cusp located on the palatal surface of mesiopalatal cusp of a
maxillary molar.
• Presentation is seen in both dentitions.
• Could be in the form of a – definitive cusp
small indented pit
small fissure
• Most pronounced on a first molar.
104

Accessory Cusps3
1.Cusp of Carabelli (cont’d):
• Protostylid: An analogus cusp on mesial half of buccal
surface of a mandibular permanent or deciduous molar.
Meticulous oral hygiene maintenance is vital.
• Management:
When it presents as a deep groove – may need sealing to prevent caries.
105

Accessory Cusps4
2. Talon’s cusp:
Dens evaginatus of an anterior tooth.
A well-delineated additional cusp that is
located on the surface of an anterior tooth and extends
at least half the distance from CEJ to incisal edge.
Clinical Features:
About 3/4th of the cases are reported in permanent dentition.
106

Accessory Cusps5
2. Talon’s cusp (cont’d):
Clinical Features (cont’d): Maxillary laterals – 55%
Maxillary centrals – 33%
Mandibular incisors – 6%
Maxillary canines – 4%
Very rare in deciduous dentition – maxillary centrals.
Often seen is association with other dental anomalies – peg laterals, impacted
teeth, supernumerary teeth, odontomas.
107

Accessory Cusps6
Nomenclature: The accessory cusp projects from
the lingual surface of the affected tooth and forms
a 3-pronged pattern that resembles an Eagle’s talon.
Gardner and Giris have reported this condition
to be more prevalent in persons with Rubinstein-Taybi
Syndrome.
Composition: Enamel, dentin, pulp.
108

Accessory Cusps7
Clinical Significance: Complications that may arise due to this cusp are
Occlusal interference
Tooth displacement
Caries
Periodontal complications
Soft tissue irritation – tongue, mucosa
109

Accessory Cusps8
Management:
Selective grinding to relieve occlusal interference.
When the cusp has pulpal components, incremental grinding with time
being allowed for – tertiary dentin deposition
pulpal recession
110

Accessory Cusps9
3. Dens Evaginatus:
• A cusp like elevation of enamel on the central groove or lingual ridge of
buccal cusp of permanent premolar or a molar tooth.
• Has enamel, dentin and pulpal components.
• Pathogenesis: Inner enamel epithelium with mesenchyme
proliferates and evaginates in dental organ.
• Clinical Features: Usually bilateral in presentation – mandibular premolar.
Mandibular arch prevalence
111

Accessory Cusps10
3. Dens Evaginatus:
Shovel-shaped incisors – Coronal variant of
dens evaginatus where the incisors have prominent lateral
Margins creating a hollowed lingual surface that resembles
The scoop of a shovel.
This is prevalent in Asians – 15%
Native Americans and Alaskans – 100%
Maxillary laterals and centrals are most affected.
112

Accessory Cusps11
3. Dens Evaginatus:
Clinical Significance: Dens evaginatus can cause occlusal interference and is
prone to fracture leading to pulpal exposure. Pulpal necrosis can lead to
cessation of root formation. (Premolar eruption time is 10-12 yrs, Second molars
10-13 yrs).
Management:
a) Apexification with Ca(OH)2 to achieve root closure.
b) Cusp elimination while maintaining tooth vitality.
c) Shovel-shaped incisors - surface defects should be sealed.
113

Accessory Roots1
• An increased number of roots are developed in a tooth compared to normal
anatomy.
• Clinical and Radiological Features:
Both dentitions are affected.
Prevalence – third molars
bicuspids
cuspids
114

Accessory Roots2
Exodontia – affected teeth extraction becomes
complicated especially when accessory
root is divergent.
Endodontics – failure to recognise the presence of an
accessory root often undermines success
of endodontic therapy.
115

Dens Invaginatus1
• A deep surface invagination of the crown or root that is lined by enamel.
• Pathogenesis:
Focal growth proliferation in certain areas of tooth
Focal growth retardation bud before calcification.
Lingual pit.
Radicular dens invaginatus – HERS proliferation with
enamel strip formation that extends along the root surface.
116

Dens Invaginatus2
• Clinical and Radiological Findings:
Presentation – coronal or radicular.
Maxillary arch predominance.
Teeth affected.
Type I, II, III, Dens in dente,
Dilated odontome,
Radicular dens invaginatus.
117

Dens Invaginatus3
The invagination of the affected tooth provides excellent environment for
bacterial growth, so early diagnosis and management is vital.
• Management:
Type I – restore and seal the surface defect.
Type II – remove lumen contents-restore with a base-apexification-
endodontic therapy.
Type III – endodontic therapy for the periradicular lesions.
118

Dilaceration1
• An angulation or a sharp bend or curve in the root
or crown of a formed tooth.
• Pathogenesis: An injury that displaces the
calcified portion of the tooth germ where
the remainder of the tooth is formed at an
abnormal angle.
• Root is affected more than the crown.
119

Dilaceration2
Frequently involved teeth – permanent maxillary incisors
mandibular anterior – neonatal laryngoscopy
endotracheal intubation
Factors determining the extent of malformation.
Age of the patient
Direction of force
Degree of force.
120

Dilaceration3
Tooth is usually impacted, non-vital with periapical lesions.
Posterior teeth have apical half malformations with unaltered eruption patterns.
Deciduous tooth – inappropriate resorption.
Orthodontic considerations.
Exodontia.
Endodontic considerations.
Prosthodontic considerations.
121

Taurodontism1
• It is an enlargement of the body and pulp chamber
of a multi-rooted tooth with apical displacement of
pulpal floor and bifurcation of roots.
• Term coined by Sir Arthur Keith in 1913.
Tauro = Bull
Dont = Tooth
122

Taurodontism2
• Clinical and Radiographic Features:
Rectangular teeth with large pulp chambers with increased apico-
occlusal height and a bifurcation close to the tooth apex.
Presentation – unilateral
bilateral.
Diagnosed upon routine radiographic examination.
Prevalent in permanent dentition than deciduous dentition.
123

Taurodontism3
• Degree of taurodontism
No therapy required.
Endodontic therapy challenge.
Periodontal advantage.
124

Ectopic Enamel1
• Presence of enamel in unusual locations on the tooth surface, especially the
root.
• Pathogenesis:
A localised bulging of odontoblastic layer
provides prolonged contact between HERS
and developing dentin, triggering enamel
induction.
125

Ectopic Enamel2
• Clinical and Radiological Features:
Enamel Pearls – Maxillary and mandibular molars at
the furcation area close to CEJ.
Well defined radiopaque nodules.
Cervical Enamel Extensions – Mandibular molars
predominance. Frequently present with loss of PDL
attachment and furcation involvement.
126

Ectopic Enamel3
Higher rate of furcation involvement.
‘Buccal furcation cysts’ – inflammatory cysts of cervical enamel extensions.
Need meticulous oral hygiene maintenance.
Selective grinding:
Any pulpal extension presence should be
taken into consideration.
127

Structural Defects1
• Enamel Hypoplasia
Developmental – Amelogenesis imperfecta
Environmental
• Inherited Dentinal Defects
Dentinogenesis imperfecta
Dentinal dysplasia
• Regional odontodysplasia
128

Amelogenesis imperfecta1
• Encompasses a complicated group of conditions that demonstrate
developmental alterations in the structure of enamel in the absence of any
systemic disorder
• Also known as – Hereditary enamel dysplasia
Hereditary brown enamel
Hereditary brown opalescent teeth
129

• Pathogenesis: Heterogeneous
Mutations in the enamelin (ENAM) gene located at 4q21 leads to autosomal
dominant amelogeneisis imperfecta with 2 clinically distinct forms
1.smooth hypoplastic
2. local hypoplastic
Also – mutations at KLK4 gene – associated with autosomal dominant
mutations at MMP-20 ( enamelysin) gene – autosomal recessive
130

Defective tooth structure is limited to enamel.
Hypoplastic type
enamel matrix is imperfectly formed
enamel is hard, defective in amount
enamel has rough, pitted surface
radiographs show a thin peripheral enamel outline
131

Hypocalcified type
matrix formation appears to be of normal thickness
calcification is deficient and enamel is soft
enamel becomes stained easily
132

Hypomaturation type
normal tooth shape
mottled opaque, white-brown or yellowish
enamel is soft, tends to chip off
enamel has same radio-density as dentin
• Management
133

Enamel Hypoplasia1
• Local or systemic factors interfere with normal matrix formation and cause
surface defects and irregularities
• Mild – pitting of enamel surface.
horizontal line across enamel.
• Severe – gross areas of irregular and imperfect enamel
• Usually seen as one component of many different syndromes.
134

Enamel Hypoplasia2
• Prenatal disturbance
very rare - accentuated neonatal ring in the deciduous teeth
in severe forms, enamel formation arrested at birth/during neonatal period.
• Postnatal hypoplasia – Both dentitions are affected.
• Enamel hypoplasia is common in prematurely born, LBW children – Seow and
colleagues. (? mineral deficiency)
135

Enamel Hypoplasia3
• Nutritional deficiencies
• Brain injury and neurological defects
• Nephrotic Syndrome
• Allergies Factors and conditions
• Plumbism resulting in enamel
• Local infection and trauma hypoplasia
• Cleft lip and palate
• X-radiation and Chemotherapy
• Rubella embryopathy
136

Enamel Hypoplasia4
• Nutritional Deficiencies:
Vit A, C, and D, calcium and phosphorous deficiencies.
Sheldon and colleagues demonstrated that about 70% of subjects showed
established positive correlation between enamel defects and nutritional
deficiencies
Purvis and colleagues demonstrated inverse relationship between mean
daily hours of bright sunshine and incidence of neonatal tetany and enamel
hypoplasia 3m later.
137

Enamel Hypoplasia5
Nutritional Deficiencies (cont’d):
• Pathogenesis:
Sensitive ameloblasts are affected by severe nutritional deficiency
Pitted enamel surface – stained
Incisors, cuspids, molars (formed within 1 yr after birth) are affected.
Premolar, 2nd and 3rd molars – formation does not begin until 3 yrs of age
or later – so are rarely affected.
138

Enamel Hypoplasia6
Brain injury and Neurological defects:
Cohen and Diner observed that enamel defects occurred with greatest
frequency in children with – low IQ and high incidence of neurologic defects.
Martinez and colleagues found 37% of MR children with no history of
dental trauma to have enamel defects
Significance: Chronologically disturbed enamel defects are a valuable
aid in neurologic diagnosis.
139

Enamel Hypoplasia7
Nephrotic Syndrome:
Oliver and Owings observed high incidence of enamel hypoplasia in
permanent teeth of children with nephrotic syndrome. Found a correlation
between the time of severe renal disease and the estimated time at which the
enamel defect occurred.
Koch and colleagues found high incidence of enamel defects in primary
teeth of children diagnosed with chronic renal failure in early infancy.
140

Enamel Hypoplasia8
Allergies:
Rattner and Myers found a correlation between enamel defects of
primary dentition and the presence of severe allergic reactions.
Enamel defects were present in > 50% of children with congenital
allergies.
Enamel lesions were localised in the occlusal third in primary cuspids
and first molars.
141

Enamel Hypoplasia9
Plumbism:
Lawson and Stout observed (in areas of Charleston - South Carolina)
pitting hypoplasia in extremely high incidence among children living in very old
frame buildings.
Significance: Low socio-economic stratum must be considered as a part
of a child’s health evaluation.
Pearl and Roland observed significant delays in development and
eruption of primary teeth in child of a lead-poisoned mother - as lead crosses
placental barrier.
142

Enamel Hypoplasia10
Local infection and trauma:
Turner tooth – enamel hypoplasia resulting from an insult to tooth during
matrix formation and calcification.
Pathogenesis: Enamel defect in permanent teeth caused by periapical
inflammatory disease of the overlying deciduous tooth.
Clinically: white or yellow or brown discolouration of crown
extensive hypoplasia involving the entire crown
143

Enamel Hypoplasia11
Turner tooth (cont’d): Factors affecting extent of damage
1.Stage of tooth development
2.Length of infection (due to lack of treatment)
3.Virulence of infective organism
4.Host resistance to infection
144

Enamel Hypoplasia12
Turner tooth (cont’d)
Permanent maxillary incisors as deciduous
anterior teeth are more prone to trauma.
Permanent bicuspid, both upper and lower as
deciduous molars are more prone to periapical infections.
145

Enamel Hypoplasia13
Cleft lip and palate:
Mink demonstrated relation between incidence of repaired cleft lip and
palate defects and enamel hypoplasia.
66% - had 1/> affected primary maxillary anterior teeth.
92% - had 1/> affected permanent anterior teeth
Permanent teeth are in early stages of development at the time of surgical
procedures and so more prone for damage.
146

Enamel Hypoplasia14
X-radiation and Chemotherapy:
• Many dental abnormalities result due to high-dose exposure to radio and
chemo-therapy in children during their tooth formation ages.
• Kaste and colleagues studied acute lymphoblastic leukemia survivors and
found - root stunting – 24%
microdontia – 19%
hypodontia – 8%
taurodontia – 6%
over retention of primary teeth – 4%
147

Enamel Hypoplasia15
X-radiation and Chemotherapy (cont’d):
• Clinically
a line of hypoplastic enamel
dentin development is severely affected
root formation will be stunted.
occasionally, development of permanent teeth is arrested.
148

Enamel Hypoplasia16
Fluorosis:
• Excess ingestion of fluoride can affect ameloblasts during tooth formation
stage and cause mottled enamel.
• Affected tooth vary in appearance from white to
brown opaque or with a pitted appearance.
• Permanent dentition prevalence.
• Middle of first year – most important time for
fluorosis to develop in primary dentition.
149

Dentin Dysplasia OR Rootless Teeth1
• Rare disturbance with normal enamel and atypical dentin formation with
abnormal pulpal morphology.
• Classification:
Type I – Radicular dentin dysplasia
Type II – Coronal dentin dysplasia.
• Etiology:
Both the types are hereditary - autosomal dominant.
150

Dentin Dysplasia2
Clinical Features:
• Type I: Both dentitions are affected.
Teeth have normal morphology and colour.
Loss of root organisation leads to shortened roots and this causes tooth
mobility and premature exfoliation secondary to minor trauma.
• Type II: Root length is normal in both dentitions.
Deciduous dentition has the same opalescent appearance as
dentinogenesis imperfecta. Permanent dentition appear normal clinically.
151

Dentin Dysplasia3
• Radiological Features -Type I
Deciduous teeth are severely affected.
Little or no detectable pulp
Roots are markedly short or absent.
Roots in both dentitions are short, blunt, conical and malformed.
Degree of dentin disorganisation within the root dictates radiographic
appearance.
152

Dentin Dysplasia4
• Radiological Features -Type I (cont’d):
Early – no pulp detected, extremely
short or absent roots.
Later – crescent shaped pulp chambers,
short roots, no pulp canals.
Late – normal pulp chambers with large pulp stones, canals constricted apical to
the stones.
153

Dentin Dysplasia5
Radiological Features -Type II
• Deciduous teeth show – bulbous crowns, cervical constriction
thin roots, early pulp obliteration.
• Permanent teeth appear normal clinically.
‘Thistle-funnel’ or ‘Flame shaped’ appearance
due to significant enlargement and apical extension of the
pulp chamber.
154

Dentin Dysplasia6
• Histopathological Features:
Type I:
A portion of coronal dentin is normal. Apical to this, there are areas of
- calcified tubular dentin
- osteodentin obliterate the pulp
- fused denticles
155

Dentin Dysplasia7
Type I (cont’d): ‘Lava flowing around boulders’ – normal
dentinal tubules formation appear to have been blocked so
than new dentin forms around obstacles and takes this
characteristic appearance.
156

Dentin Dysplasia8
Type I (cont’d):
‘Cascades of dentin’ – electron microscopy by Sank and
his co-workers have suggested this pattern where
repetitive attempts to form dentin have been made.
157

Dentin Dysplasia9
Type II:
Deciduous teeth: Coronal dentin is normal.
Radicular dentin is – amorphous and atubular.
Permanent teeth: normal coronal dentin
pulp has multiple pulp stones or denticles.
158

Dentin Dysplasia10
• Clinical Significance and Treatment modalities:
Type I:
The teeth demonstrate reduced strength of radicular dentin predisposing
them to fracture during extractions.
Preventive care is important.
Shortened roots – early loss due to periodontitis.
Periapical inflammatory lesions may require endodontic therapy – pulp
canal paths need to be created.
159

Dentin Dysplasia11
• Clinical Significance and Treatment modalities:
Type II:
Meticulous oral hygiene needs to be maintained.
Endodontic therapy can be accomplished more easily as the pulp canals
are not generally obliterated.
160

Enamel and Dentin Aplasia1
Odontogenesis imperfecta OR Enamel and dentin Aplasia OR Regional
Odontodysplasia OR Ghost Teeth OR Odontodysplasia OR Odontogenic Dysplasia:
Etiology:
Altered vascular supply.
Probable causes:
Hyperpyrexia, malnutrition.
Medication used during pregnancy
Radiation therapy, somatic Mutation.
161

Reduced surrounding bone
Uncommon finding, maxillary anterior predilection
Teeth usually fail to erupt and crowns of erupted teeth show small irregular
yellow-brown crowns.
Caries and associated periapical lesions are common.
Dentinal clefts and very long pulp horns lead to
pulpal necrosis.
162

• Radiological Features:
Ghost Teeth.
Dentin and enamel show no contrast difference.
• Clinical Presentation:
Delayed or failed eruption and early exfoliation.
Abscess formation.
Malformed teeth.
Non-inflammatory gingival enlargement.
163

• Histopathologic features:
In ground sections – varying thickness of enamel gives an irregular
surface. Prism structural is irregular.
Dentin has clefts scattered through a mixture of intergloublar dentin and
amorphous material.
Pulp tissue contains free or attached stones that may exhibit tubules or
consist of laminated calcifications.
164

Basic therapeutic aim – retain affected teeth, preserve surrounding bone.
Unerupted teeth – can be left untouched and the functional restoration is
done by fabricating a removable partial prosthesis until skeletal growth is
completed.
Erupted teeth – Restorations. Stainless steel crowns – fragile coronal
hard tissue and ease of pulpal exposure contraindicate any tooth extensive tooth
preparation.
165

Dentinogenesis Imperfecta1
• Hereditary development disturbances of dentin in the absence of any systemic
disorder.
• Also known as – Hereditary opalescent dentin
Capdeponts teeth.
• Pathogenesis:
Defective collagen formation.
DSPP gene mutation – Zhang and colleagues, Xiao and colleagues.
166

• Classification: Shields
Type I: DI always occurs in families with osteogenesis imperfecta
Autosomal dominant.
Type II: DI never occurs in association with osteogenesis imperfecta
Referred to as ‘Hereditary opalescent dentin’
Autosomal dominant.
Most common dominantly inherited disorders in humans
167

• Classification: Shields
Type III: ‘Brandywine Type’
Racial isolate in Maryland
Autosomal dominant
Characterised by multiple pulpal exposures in deciduous teeth.
168

Dentition involved:
Type I – Deciduous dentition is affected more
Type II & III – Both dentitions equally affected.
Colour of teeth affected may be
grey, brownish violet,
yellowish brown
Characteristic translucent or opalescent hue.
169

The usual scalloping of DEJ is lost/absent -leads to early fracturing of
enamel at incisal, occlusal surfaces - causes rapid dentinal attrition and flattened
occlusal surfaces.
• Radiographic features:
Type I and II: Partial or total precocious obliteration of the pulp
chambers and root canals by continuous dentin formation.
Seen in both dentitions.
170

Type I and II (cont’d):
Roots are short and blunt
Cementum
Periodontal ligament appear normal
Alveolar bone
Type III: ‘Shell Teeth’
171

Type III: Normal enamel, extremely thin dentin, large (due to defective,
insufficient dentin formation).
Shells of enamel and dentin surrounding extremely large
pulp chambers and root canals.
• Histological features:
Dentin adjacent to DEJ is normal. Rest of dentin - misshapen tubules
coursing through atypical granular dentin matrix with interglobular
calcifications.
172

• Management:
Goal – preventing enamel loss and subsequent loss of dentin via attrition
Treatment options:
Fluoride GIC with overlay dentures.
Composites + DBA
Veneers, full crowns (tooth preparation)
Non-precious metal castings with adhesive luting agents on unprepared
teeth ( severe vertical height loss)
CD and implants – by 30 years.
173

Intrinsic Tooth Discolouration1
• Pulpal conditions of the primary teeth give them an unusual pigmentation.
• Factors associated are:
Blood-borne pigment
Blood decomposition within the pulp
Drugs used in RCT procedures.
174

Hyperbilirubinemia:
Teeth developing during the periods of hyperbilirubinemia become
stained intrinsically.
• Conditions associated:
Erythroblastosis fetalis Congenital hypothyroidism
Biliary atresia Biliary hypoplasia
ABO blood type incompatibility Tyrosinemia
Neonatal respiratory distress Neonatal hepatitis
Significant internal haemorrhage
175

Porphyria:
• Porphyrias are inherited and acquired disorders.
• Abnormally elevated levels of porphyrins accumulate in the tissues.
• Affected teeth are purplish-brown due to deposition
of porphyrin in the developing structures.
• Permanent teeth show a lesser degree
of intrinsic staining.
176

Cystic Fibrosis: Inherited, chronic, multisystem, life-shortening disorder
characterized primarily by obstruction and infection of the airways and poor
digestion.
• Mutation in both copies of the CFTR – Cystic Fibrosis Transmembrane
Regulator gene.
• Discolouration may result from:
1. Disease alone
2. Secondary to therapeutic agents – especially tetracylines.
3. Combination of both these factors.
177

Tetracycline Therapy:
• Tetracycline therapy during the periods
of tooth calcification shows pigmentation
of the clinical crowns.
• Tetracyclines chelate calcium ions and
drug is incorporated into teeth.
• Discolouration ranges from yellow-brown to grey-black.
178

• Tetracycline Therapy:
Critical Period for the drug to cause discolouration
Maxillary and mandibular incisors – 4m in utero to 3m postpartum.
Maxillary and mandibular canines – 5m in utero to 9m postpartum.
Permanent incisors and cuspids – 3-5m postpartum till 7th year of life.
Permanent maxillary lateral incisors.
Minocycline.
179

Management:
• Vital bleaching with heat, light or laser radiation to aid in peroxide
incorporated compounds.
• Bonded veneer restorations
• Bleaching in combination with microabrasion.
180

References
1. Orban’s Oral Histology and Embryology – XIV Edition.
2. Ten Cate’s Oral Histology – VIII Edition.
3. Shafer’s TB of Oral Pathology – VII Edition.
4. McDonald’s Dentistry for the Child and Adolescent – IX Edition.
5. Neville’s Oral and Maxillofacial Pathology – II Edition
182

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