Enamelautosaved 180529103526

ENAMEL
-The Basic
Dr.Vedangi Mohite
I MDS
Dept of Paediatric and preventive
dentistry
Sharad Pawar Dental college and
hospital,Maharashtra
DID YOU KNOW??
• Tooth enamel the hardest substance produced
by vertebrates isn't just found on teeth.
Good
• Lots of vertebrates have enamel-covered scales.
• Sharks are famous for having dermal denticles -
Morning!
- skin teeth – which decrease drag to help them
swim more efficiently.
DID YOU KNOW??
• Tooth enamel the hardest substance produced

by vertebrates isn't just found on teeth.
• Lots of vertebrates have enamel-covered teeth,
but some of them also have enamel-covered
scales.
• Sharks are famous for having so-called dermal
denticles -- skin teeth -- which decrease drag to
help them swim more efficiently.
Contents
• Origin & Introduction

• Physical characteristics
• Chemical characteristics
• Age Changes
• Clinical Considerations
• Clinical Implications
Authors of classical antiquity
• Hipprocates (460–370)
• Aristotle (384–322 BC)
• Galen (129–200 AD)
• classified teeth as bones but realised that teeth
differed from bone by being harder.
Aristotle- Galen-
Father of early medicine. The Philosopher. .Greek physician
Cortex striatum, substantia vitrea &
adamantine substance
• Enamel is derived from a German word
“smelzan” later becoming “esmail” in Old
French.
• The French émail or amel gave rise to the term
ameloblast, according to Le Gross and Magitot.
• Blake (1801) called enamel the ‘cortex striatus’
because it was composed of innumerable fibres.
• Currently it is used as “smalto” in Italian,
“email” in French & German and “enamel” in
English.
Dated back in time.
In analysing the tooth, its substance is not found to be
• Charles
uniform everywhere,Allen wrote the
but manifestly first bookinto
distinguishable on dentistry
in 1685
two different sortswith theone
of make: title Thebeing
of them Operator
harder,for the Teeth.
whiter and of finer texture; and the other softer, more
• He
obscure and quoted that
of a coarser the teeth are composed of two
composition.
tissues and used the term ‘enamel’ apparently
To wit, for the cover
its stony first the
time.
first is as it were a hard periosteum, that
invests the head of the tooth on all sides, lying on it the same
• Gabriel-Philippe
manner that Enamel does upon(1719)
Gold, orreported a description
any other thing.
of human enamel and the first to observe the
This natural Enamel which I call the gloss of the tooth is of a far
harder, Hunter schreger
whiter, more bands.
dense than the inward substance lying under
it.
-Charles Allen.
Trenouth M: The origin of the terms enamel, dentine and cementum:

FACULTY DENTAL JOURNAL 2014 :5 (1)
Physical characteristics
Textbook of oral histology&embryology:Orban Blaint:13th Edition.

Thickness
• On the cusps of human molars and premolars

the enamel attains a maximum thickness of
2 to 2.5 mm, thinning down to almost a
knife knife edge at the neck of
the the tooth.
• The enamel was found to be thicker in the

lingual surfaces of maxillary molars and in the
buccal surfaces of mandibular molars.
Age changes
• With age enamel becomes progressively worn

in regions of masticatory attrition.
• Wear facets increasingly are pronounced in
older persons and substantial portions of the
crown become eroded.
Ten Cate’s Oral Histology:8th edition (2013)

Attrision
The physiological wearing of tooth as a result of

tooth to tooth contact
ETIOLOGY a) Abnormal occlusion
b) Habits c) Structural defects

Erosion
• Irreversible loss of tooth substance by chemical
process that does not involve known bacterial
action.
TYPES:
i. Intrinsic
ii. Extrinsic
 Board concavities
with smooth
surface enamel.
 Cupping of occlusal surface with dentinal exposure
In deciduous teeth –Loss of enamel surface
characteristics and pulp exposure.
Shafer’s Textbook of oral pathology : 7th Edition (2012)
Extrinsic Stains
1. Carbonated & sports drink
2. Poor oral hygiene
3. Food colors
4. Existing restorations
5. Remnants of Nasmyth’s membrane
6. Chromogenic bacteria
Intrinsic Stains
1. Caries.
2. Fluorosis.
3. Tetracycline and other drugs.
4. Porphyria
5. Non vital teeth
6. Blood Dyscrasias.
Abrasion
Pathological wearing away of tooth substance

through abnormal mechanical process.
ETIOLOGY:
1. Improper brushing technique.
2. Habits
3. Occupational
 Saucer shaped defects.
 Exposed root surface.
 Associated with
Gingival recession.
Caranza Textbook of Periodontology:10th Edition

Abfraction
• Acc to Grippo(1991) the pathologic loss of both
enamel and dentin caused by biomechanical
loading forces.
• caused by clenching or grinding
• "v-shaped" notches
• Gingival 3rd of the tooth.
Caranza Textbook of Periodontology:10th Edition

Brittleness
• The structure and hardness of the enamel

render it brittle, which is particularly apparent
when the enamel loses its foundation of sound
dentin.
• Its is compensated by the cushioning effect of

underlying resilient dentin as it is viscoelastic
and subject to slight deformation.
• Thus Enamel is stiffer and more brittle than

dentin.

Colour
• The color of the enamel ranges from yellowish
white to greyish white.
• It is determined by differences in the
translucency of enamel.
• Yellowish teeth have a thin, translucent enamel
through which the yellow colour of the dentin
is visible and greyish teeth have more opaque
enamel.
• The translucency may be attributable to
variations in the degree of calcification and
homogeneity of the enamel.
Primary teeth are lighter in color, bluish white.

• Grayish teeth show a slight yellowish color at
the cervical areas.
It is used in physics and electrical engineering when a

•waveIncisal areas may
propagation in a have
mediuma bluish tinge where the
containing
discontinuities is considered.
thin edge consists only of a double layer of
enamel.
Transmission coefficient describes the amplitude,
•intensity,
The translucency of enamel
or total power increased
of a transmitted with
wave relative
to increasing
an incident wavelengths.
wave.
• The transmission coefficient at 525 nm was
0.481 mm– 1.

• Dehydration decreases the translucency but it
was reversed on rehydration.
• The translucency of wet human enamel and
enamel after dehydration was also measured by
total transmittance.
• The transmission coefficient at 525 nm
decreased from 0.482 to 0.313 mm-1 after
dehydration and was reversed on rehydration.
• The decrease in translucency occurred as a
result of the replacement of water around the
enamel prisms by air during dehydration.
Translucency of Human Dental Enamel R.H.W. Brodbelt et al J

DENT RES 1981 60: 1749
Age changes
• Teeth Darkening
• caused by
1. the addition of organic material to enamel
from the environment
2. by a deepening of dentin colour seen through
the progressively thinning layer of translucent
enamel

Hardness
• Mohs scale of mineral hardness is named
after Friedrich Mohs in 1822 ,who invented
a scale of hardness based on the ability of
one mineral to scratch another.
“Hardness may be defined to be the resistance of solid minerals to the

displacement of their particles.”
Mohs considered one body as harder than another if, as a flat surface, it was
not scratched by the other body in the shape of a point.
He devised a scale for the degrees of hardness based upon ten common
minerals.
Mohs hardness
The hardness ofscale-A
enamelphysical interpretation.D
and dentine. E. NewbruntTabor 1954 Proc.
and W.
Phys. Soc.Australian
Pigman. B 67 249D Dental Journal, August, 1960
Hardness of enamel
• Enamel is the hardest calcified tissue in the
human body i.e. 296 KHN .
• Its function is to form a resistant covering of the
teeth, rendering them suitable for mastication.
• Atkinson et al stated that deciduous teeth were

hardest of all and that permanent teeth soften
with age.
• Caldwell et al found no pronounced difference
between deciduous, permanent and unerupted
teeth.
The hardness of enamel and dentine. E. Newbrunt and W.Pigman.

AustralTrenouthian Dental Journal, August, 1960
Permeability
• Enamel is selectively permeable.
• It has been found with radioactive tracers that it
acts as a semipermeable membrane, permitting
complete or partial passage of certain molecules:
14C-labeled urea, I.
• The same phenomenon has also been
demonstrated by means of dyes.

Age changes
• Enamel becomes less permeable with age.

• The semipermeable membrane permits the
slow passage of water and substances of small
molecular size through pores between the
crystals.
• With age the pores diminish as the crystals
acquire more ions and as the surface increases
in size.

Modulus of elasticity Density
• 83 GPa
• The density decreases
• On comparing the from the surface to
mechanical the deeper regions
properties of the and from cuspal to
occlusal surface, to incisal region.
the DEJ.
• MOE at the surface
is higher than that at
the DEJ.

Other properties:-
• The specific gravity of deciduous teeth is 2.95

and permanent teeth is 2.8-3.1
• Enamel is a non electrical conductive material.
• Temperature resistance of enamel measured by
AC impedance spectroscopy, is in the
frequency range from 5 to 13 Hz.
• Electrical resistance ranges from 1015 to 105
ohms.

• Historically, the prophy pastes with fluoride
components have been avoided.
• On the other hand, precipitates on the enamel
surfaces which are cleaned with fluoridated
prophy paste should be taken into careful
consideration,because it is possible to influence
the longevity of the bond
Other methods of Enamel cleaning
• Pumice slurry .
• Air-polishing.
• Well-performed resin tags and higher bond
strength have been achieved on air-polishing as
compared with pumice.
• fine-grain diamond or sandblast discs
• Fuks et al found irregular etch pattern with
scattered smooth areas after grinding with
finegrain silicon carbide
• .
Primary Enamel Cleaning
• Two different procedures have been

introduced;
1. the first consists of removing only the deposits
by cleaning/polishing of the enamel
2. and the second of slight grinding leading to
superficial enamel removal.
• polishing with a rotating brush alone, only
organic films remain on the surface .
• Prophy pastes with fine particles result in an
efficient debris and organics removal while
keeping the enamel intact.
Enamel proteins do not contribute to structuring of enamel.
This is in contrast to collagen, which is the principal protein of
dentin
Ca 10(P04)6(0H4)2
Chemical formula of hydroxyapatite crystal
• They are hexagonal in cross-section.
• The shape of a single crystal was observed by
high resolution SEM to be a rod with an
equilateral hexagon base.
• The crystals are arranged to form enamel rods
or enamel prisms.
•During
The hydroxyapatite
the formation, crystal has a can
magnesium central core or
replace
calcium
C axis and carbonate
of hydroxyl ioncan replace
around hydroxyl
which calciumion.
Both
andthese substitutions
phosphorus destabilize
ions are arrangedthe lattice
in the form
due to poorer fit of these ions in the lattice
of triangles.
structure.

• The core of the crystals are richer in Mg and
carbonate and this accounts for their greater
solubility in acids than the peripheral portions.
Conc. Of
fluoride
decreases
from
surface
towards
dentin

Constituent Avg Concentration
Oxygen 43.4%
Calcium 36.6%
Phosphorus 17.7%
Sodium 0.67%
Carbon 0.64%
Magnesium 0.35%
Water is present as a part of the crystal between

crystals and rods and surrounding the rods.
Pores are present between the crystals, especially

at the boundaries of the rods and these are filled
with water.

Age Changes
• During aging, the composition of the surface
layer changes as ionic exchange with the oral
environment occurs.
• Localized increases of nitrogen and fluoride
have been found in the superficial enamel
layers of older teeth.
• If the fluoride ion is incorporated into the
crystal, it becomes more resistant to acid
dissolution.

Calcium Fluoride Phosphate
enhances chemical
reactions that lead
to precipitation of
calcium phosphate
• when a localized region of enamel is lost

mineral (e.g., a white spot lesion), the enamel
may be remineralized if the destructive agent
(dental plaque) is removed.
• The remineralization reaction is enhanced
greatly by fluoride.

Enamel Rods
• Enamel is composed of rods or
or prisms, rod sheaths, and in
some regions a cementing
interprismatic substance.
• They are cylindrical, in
longitudinal section, therefore
the term rods is more apt.
• The number of enamel rods
has been estimated from 5
million in the lower lateral
incisors to 12 million in the
upper first molars.

• The length from the DEJ
the rods run somewhat
tortuous courses outwards
to the surface of the tooth .
• The rods located in the cusps are longer than those
at the cervical areas of the teeth.
• The increase in the area of enamel at the surface
compared to their area at the DEJ is due to the
increased prism diameter and the oblique
orientation of prisms.

Enamel rods diameter
• The diameter of the rods averages 4 μm.

• However this measurement varies, since the
outer surface of the enamel is greater than the
dentinal surface where the rods originate.
• It is claimed that the diameter of the rods
increases from the DEJ toward the surface of
the enamel at a ratio of about 1:2.

Appearance
• The enamel rods have a clear crystalline
appearance, permitting light to pass through
them.
• In cross-sections of enamel, many rods
resemble fish scales appearance.
• The rods do not maintain their same outline
throughout, arcade outlines were seen near DE
junction and keyhole shaped outlines were seen
at the enamel surface.

Ultrastructure
The enamel contain rods
surrounded by rod
sheaths and separated
by interrod substance ,this
pattern is a
keyhole- or paddle shaped.
When cut longitudinally

sections pass through the
“heads” or “bodies” of
one row of rods and the “tails”
of an adjacent row.
They are 5 μm in breadth and 9

μm in length.
The “bodies” of the rods are

nearer occlusal and incisal
surfaces, whereas the “tails”
point cervically.
Keyhole pattern Staggered arches
Stacked arches Irregular rods near DEJ
Swancar VR, Scott DB, and Njemirovskij Z: J Dent Res 49:1025, 1970
• They are approximately parallel to the long
axes of the rods in their “bodies” or “heads”
and deviate about 65 degrees from this axes as
they fan out into the “tails” of the prisms.
• The length is estimated to vary between 0.05

and 1 μm.
• Fusion of the lateral branches of the crystals

were observed so that the crystals assumed
pyramidal shape with their bases towards DEJ.

• When cut in cross-section, the crystals are
somewhat irregular in shape and have an avg
thickness 30 nm and an avg width of 90 nm.
• The surfaces of rods are

visible in an abrupt
orientation from one rod to
another.
• Hence they are not as tightly

packed and more space for
organic matrix at these
surfaces.
• This accounts for the rod

sheath visible in the light
microscope.
Frazier PD: J Ultrastruct Res 22:1, 1968
Striations
• Each enamel rod is built up of
segments separated by dark lines that
give it a striated appearance .
• These cross striations demarcate rod
segments and become more visible by
the action of mild acids.
• The rods are segmented because
the enamel matrix is formed in a
rhythmic manner and have an uniform
length of about 4 μm.
Direction of rods
• Oriented at right angles to the
dentin surface.
• Near the incisal edge or tip of

the cusps they change gradually
to an increasingly oblique
direction until they are almost
Deciduous Permanent
vertical in the tip of the cusps.
• In the cervical region the rods deviate from the

horizontal in an apical direction.
• In the cervical and central parts of the crown of a

deciduous tooth they are approximately horizontal.
• The course of the enamel
Clinical rods is of importance in
consideration cavity preparations.
• unsupported enamel rods
should not be left at the
cavity margins.
• Enamel is brittle and does
not withstand forces in thin
layers or in areas where it is
not supported by the
underlying dentin

Clinical Implication
Ideal cavity wall should have the following

features:-
 Enamel rods which form cavosurface angle

must have their inner ends on sound dentin.
 Outer ends - covered by restorative material

by giving a bevel (for cast gold, DFG)
 Enamel walls should be parallel to the length

of the rods (for amalgam).
Types of bevel:-
Gnarled enamel.
• The optical appearance of enamel.
• The most significant deviations from a straight
radial course can be described as follows:-
Enamel
Hypocalcified
rods of tuft
Dentin DEJ
Hunter–Schreger
bands
• Alternate light and dark bands.
• Seen in ground longitudinal
• section.
• Due to abrupt change in the
• direction of enamel rod.
• Originate from the DEJ.
• Seen only in inner 2/3rd of enamel.
• Dark bands-PARAZONES
• Light bands-DIAZONES
Incremental lines of retzius
 Brownish band in ground section.

 Illustrate incremental pattern of
enamel(succesive apposition of layer of enamel)
 Attributed to periodic bending of the enamel
rods, to variations in the basic organic structure
or to a physiologic calcification rhythm.
 Prominent in permanent tooth
 The mean daily rate of enamel formation of
about 3.5 microns
 Retzius lines vary in thickness from
few microns to 100 microns.
Longitudinal and transverse
sections.
Cervial area
Cusp tip
Transverse section

Prism less
•
Enamel
Structureless layer of
enamel.
• 20-70 Microns 
• newly erupted
• permanent teeth.
• Least – Cusp
In aprismatic tipsthe crystallites
enamel, Mostare– arranged
Cervical area
uni-directionally,
parallel to one another with a relatively higher density and their C-
• More mineralized
axes perpendicular than
to the enamel
enamel . beneath it.
• NO
On theprism outline
contrary, – all enamel
the prismatic apatiteexhibits
crystal parallel
change to
of orientation
within each prism.
each other – perpendicular to striae of retzius

Prismless enamel in primary teeth
• In a primary same tooth at different areas it

varys in thickness (5–60micro m) , is the most
commonly found feature in the primary
enamel,
• A laminated band is found in primary prism
less enamel, whereas a scale-like shape is
observed in permanent teeth .
Clinical Consideration
o Acid Etching
• In this procedure the enamel surface is first
etched with an acid to remove the smear layer
created during cavity preparation.
• It is 1 μm thick and made up of burnished
cutting debris.
• Acid etching removes this smear layer and
produces an uneven dissolution of the enamel
rods so it becomes pitted and irregular.
• When a composite resin is put on this irregular
surface, it can achieve mechanical bonding with
the enamel.
Types of etching patterns
• Type I- Dissolution of the prism cores leaving

the prism peripheries intact.
• Type II- Dissolution of the prism peripheries
leaving the prism core intact.
• Type III-No prism structures are evident.
• Seen predominantly in regions where the rods
are more disoriented, such as in the primary
enamel.
In primary teeth
• Type-II pattern was detected after 15-s etching,
whereas prism peripheries were demineralized
in a homogeneous pattern after 5-s etching.
• A tendency of type-III pattern to predominate
after 15-s etching has been recorded as well .
• At the same time, random distribution of all the
type of patterns were noticed.
• Negligible morphological changes on the
enamel surface were revealed when the etching
time was increased to over 30 s .
• Etching times ranged from 15 to 30 s provided
a detailed etch pattern.
• In primary teeth the coronal part is covered by
a thin enamel layer which is generally less
mineralized than permanent enamel .
• The reduced time available for enamel
maturation may account for the relatively lower
mineral levels.
• the permeability & porosity of the primary
enamel is higher, which leads to higher pore
volume
Acid etching time:-
• Conniff and Hamby reported that a 120-sec etch
was necessary on primary enamel to establish
proper etch patterns.
• Mueller and Tinanoff found that by increasing
the etch time an increase in tag formation was
seen.
• Fuks et al found that primary enamel should be
etched for no more than 180 sec.
• Nordenvall et at found that the 15-sec etch of
primary teeth gave the greatest surface
irregularity most consistently.
Deborah A.The effect of different etching times on the sealant bond

strength,etch depth and pattern in primary teeth:Pediatric
dentistry1986:8(1)
The objective of this study was to establish the
minimum etch time of primary enamel.
The results of this study indicated that a 120-sec etch on primary enamel does
not increase the bond strength compared to 15-, 30-, or 60-sec etching.
Etching for 60 or 120 sec suggests a greater bond strength variation.
Since the etch depth increases dramatically between 60 and 120 sec, and
there is no improvement in the bond strength, it seems unnecessary to subject
the enamel to the additional loss,
or the dentist and the child to the additional time needed to complete a 120-
sec etch.
The aim of this study is to compare
micromorphological changes in primary and
permanent dentin after etching with phosphoric
acid(20% and 37,5%) for 7 and 15 sec. by SEM.
• The conclusion drawn is that the 20%
phosphoric acid applied for two different
etching times did not create dentin surface
cleaned from a smear layer.
• Better cleaning effect is found in samples from
permanent teeth
• In primary teeth this smear layer is slightly
affected.
• This is probably due to the formation of a
thicker smear layer which may be associated
with the presence of a larger amount of organic
matter in the primary teeth
Gateva N.effect of etching times and acid concentration on

micromorhological changes in dentin of both dentitions.J of
IMAB201622(2).
• The presence of residues from the smear layer
and precipitates on the dentin surface probably
will lead to unsatisfactory adhesion
• Obscuring of dentin tubules with smear plugs
will not allow the entry of a bonding agent and
the formation of adhesive tags
• Overall, this can be a reason for an adhesion
failure.

IMAB201622(2).
• The 37.5% phosphoric acid used for dentin
surface etching removed the smear layer in
primary teeth much faster than in permanent
teeth
• the application of 37.5% phosphoric acid for 7
seconds on the primary teeth and for 15
seconds on the permanent leads to a complete
removal of the smear layer.

IMAB201622(2).
• Effects of etching time of primary dentin on
interface morphology and microtensile bond
strength
• Carmona et al
• dental materials 22 (2006) 1121–1129
• . To determine the influence of different etching
times (5, 15 or 30 s) on the morphology and
micro-tensile bond strength (TBS) of primary
dentin.
• Results of this study showed the minimum
adequate etching time for primary dentin was
15 s.
Enamel Bonding Agents
• Originally EBA consisted of BISGMA and

UDMA resins with a diluent like TEGDMA.
• These agents flow easily into the micro
porosities and when polymerized with light
activation form resin tags which lock them in
the enamel surface.
• Since enamel can be kept dry these
hydrophobic resins worked well when
they were confined only to enamel.
• In the last few years the bonding agents have
been replaced by the same adhesives that are
used on dentin
• This is because of the advantage of
simultaneously bonding to both enamel and
dentin.
• Bond Strength:-
• The bond strength of composite resins to etched
enamel is 15 -25 Mpa.
Perikymata
• Transverse, wave-like grooves.
• The external manifestations of
the striae of Retzius.
• Lie parallel to each other and
to the cementoenamel junction.
• The CEJ-30 perikymata per mm.

• The occlusal or incisal edge-
10 per mm.

• The terms perikymata and imbrication lines
are used without distinction to the surface
structures of ridges or grooves.
• absent -occlusal parts of the deciduous teeth,
present - postnatal cervical parts.
• The terms perikymata or imbrication lines be
suffixed by the words:-
• Ridge or crest –elevations.
• groove or furrow-depressions.

Age
Changes
Ten Cate’s Oral Histology:8th

• Deep enamel fissures predispose teeth to caries.

• Caries penetrate the floor of fissures rapidly
because the enamel in these areas is very thin
• As the destructive process reaches the dentin, it
spreads along the DEJ , undermining the
enamel.

Enameloplasty
• It is a conservative procedure in which narrow

pits and fissures in the enamel can be ground
off with a flame shaped bur to a smooth saucer
shaped surface that is easily cleaned.

Neonatal lines
The boundary between the two
portions of enamel in the deciduous
teeth is marked by an accentuated
incremental line of Retzius-
The neonatal line or neonatal ring.

• Result of the abrupt change in the environment
and nutrition of the newborn infant.
• The prenatal enamel usually is better developed
than the postnatal enamel.
• The location varies in preterm and in post term
births.
• Forensic Odontology
• the neonatal line can be used to distinguish
matters such as if a child died before or after
birth and approximately how long a child lived
after birth.
• It is possible to estimate the exact period of
survival of the infant in days by measuring the
amount of postnatal hard tissue formation, and
thus can be an evidence to the brutal act of
infanticide.

Enamel cuticle
• A delicate membrane called Nasmyth’s

membrane or primary enamel cuticle covers the
entire crown of the newly erupted tooth but is
probably soon removed by mastication.
• This membrane is a typical basal lamina found
beneath most epithelia.
The function of enamel cuticle is to protect the
• surface of enamel
This basal lamina from the resorptive
is apparently secretedactivity
by the
ofameloblasts
the adjacent vascular
when tissue
enamel prior toisthe
formation
eruption of the teeth.
completed.
• This cuticle is apparently secreted after the
epithelial enamel organ retracts from the
cervical region during tooth development.
• The erupted enamel is normally covered by a
pellicle, which is apparently a precipitate of
salivary proteins .
• Within a day or two after the pellicle has
formed, it becomes colonized by
microorganisms to form a bacterial plaque.
• The enamel rod ends are concave shallowest in
the cervical regions of surfaces and deepest
near the incisal or occlusal edges
• Pits - 1–1.5 μm in diameter
Enamel caps
• small elevations - 10–15 μm
• The surface pits are said to represent the ends
of ameloblast and the caps are due to enamel
deposition on nonmineralizable debris.
• Larger enamel elevations are termed enamel
brochs.
• Enamel cracks -the narrow,fissure-like
structures that are seen on almost all surfaces
• originate at right angles to the DEJ .

Enamel • Thin, leaf-like structures
that extend from the
lamellae enamel surface toward
the DEJ.
• They consist of organic

material but with little
mineral content.

• Careful decalcification of ground sections of
enamel makes possible the distinction between
cracks and enamel lamellae.
The former disappear, whereas the latter persist
Cracks Lamellae

• Lamellae may develop in planes of tension.
Where rods cross such a plane, a short segment
of the rod may not fully calcify.
• If the disturbance is more severe:-
is filled by
Unerupted
surrounding
tooth
cells.
Erupted By organic
tooth substances.

Types of lamellae
Type A
• lamellae composed of poorly calcified rod segments
Type B
• lamellae consisting of degenerated cells
Type C
• lamellae arising in erupted teeth where the cracks

are filled with organic matter presumably
originating from saliva.

• Dental lamellae may also be predisposing

locations for caries because they contain much
organic material
• Fluoride-containing mixtures such as
 stannous fluoride pastes
 sodium fluoride rinses
 acidulated phosphate fluoride
• are used to alter the outer surface of the enamel
in such a manner that it becomes more resistant
to decay.

Clinical consideration
surface of the cervical enamel
bacterial plaque
decalcified
gingivitis
periodontal disease

Enamel
Tufts
• Narrow, ribbon-like structure, the inner end of

which arises the DEJ and reach into the enamel to
about one fifth to one third of its thickness.
• Their development are an adaptation to the spatial

conditions in the enamel.
• the tufts are hypo mineralized structures with

major organic component being 13.17 kd protein,
rather than amelogenin.
Dentinoenamel junction
• The surface of the dentin at the DEJ is pitted
into the shallow depressions and appears as
scalloped line.
• The convexities of the scallops are directed
toward the dentin.
• more pronounced in the occlusal area, where
masticatory stresses are greater.
• about 30 μm thick and is most prominent
before mineralization is complete.

Odontoblast processes and
enamel spindles
• Odontoblast processes pass across the
dentinoenamel junction into the enamel with
thickened ends are termed enamel spindles.
• They seem to originate from processes of
odontoblasts that extended into the enamel
epithelium.
• The direction of the odontoblast processes and
spindles in the enamel corresponds to the
original direction of the ameloblasts.
• They are found mainly in the cusp tip regions.

Summary
• Enamel is considered the hardest substance in

the human body.
• It is an important structural entity of the tooth
hence its protection is utmost important as it
protects the teeth from destruction.
• Enamel plays a very important role in
protecting teeth from decay.
• Its function is to form a resistant covering of the
teeth, rendering them suitable for mastication.
Development of the epithelial
enamel organ
• The enamel organ originates from the stratified
epithelium of the primitive oral cavity.
• It consists of four distinct layers:
Outer enamel epithelium.

Stellate reticulum.
Stratum intermedium.
Inner enamel epithelium
Dental papilla
Outer Enamel Epithelium
•The
It consists
capillaries of
in the a single
connective layer
tissue of
surrounding
enamel organ proliferate and protrude toward it.
cuboid cells,
the epithelial
separated from the surrounding connective tissue

of increased
This the dental
vascularitysac bya rich
ensures a metabolism
delicate whenbasement
a
plentiful supply of substances from the bloodstream to the inner
membrane.
enamel epithelium is required.
• This regular arrangement is maintained only in

the cervical parts of the enamel organ.
• At the highest convexity of the organ the cells
become irregular in shape and cannot be
distinguished easily.
•During
The capillaries
enamelinformation,
the connective
thetissue
cells surrounding
develop
villi
the and cytoplasmic
epithelial vesicles
enamel organ and large
proliferate and protrude
numbers
toward itof mitochondria, all indicating cell
specialization for the active transport of
• Immediately before enamel formation commences,
materials.
capillaries may even indent the stellate reticulum.
Stratum
Stellate Intermedium
Reticulum
Inner Enamel Epithelium
• These cells are flat to

• The cuboid
cells areinstar
shapeshaped, with
It is resistant and elastic
•and
long ItThese
is noticeably
acts
cellsas
processes arereduced
aderived
reaching buffer
in all
inItthickness
•against helps inwhen
physical the
forces
production
from
first
directions
that the basal
layers of
fromenamel cell layer
dentinitself,
adistort
central are
body.
of might
the the
of the
laid oralthrough
down,
developing
either epithelium.
and thecontrol
DEJ.
• They ofare
inner connected
enamel
fluid diffusionwithinto
each
epithelium
and outis thereby
of onlythea
It
othercut seems
and to
offwith permit
fromthe thecells of the
dental the
ameloblasts
Beforeflow
•limited enamel or by
of nutritional
papilla,
actual its original
contribution of
outerelements
enamel
formation
source from
epithelium
begins,
of supply. these the
and
necessary
outlying blood formative
vessels to
cells
the assume
elements
thestratum
formative a
or columnar
enzymes.
intermedium
cells.
form and differentiate
into
• These by desmosomes.
ameloblasts
showthatmitotic
division
produce the even
enamel after the
Matrixcells of the inner
enamel epithelium
cease to divide.
• The inner enamel epithelium
is separated from the
connective tissue of the
dental papilla by a delicate
basal lamina.
• The adjacent pulpal layer

is a cell-free, narrow, light zone
containing fine argyrophil fibers
and the cytoplasmic processes
of the superficial cells
of the pulp.
Morphologic
Desmolytic Organizing
Life cycle
of the
ameloblasts
Protective
Formative
Maturative
Morphogenic stage
Interaction of ameloblast with the

the adjacent mesenchymal
cells, determines the shape of the DEJ.
• Short and columnar cells , with large oval
nuclei that almost fill the cell body.
• The Golgi apparatus and the centriole are
located in the proximal end of the cell,
• The mitochondria are evenly dispersed
throughout the cytoplasm.
Organizing Stage
• The inner enamel epithelium interacts with the

adjacent connective tissue cells odontoblasts.
• The cells become elongated in size.
• Reversal of the functional polarity of these cells

takes place by the migration of the centrioles
and Golgi regions from the proximal ends of
the cells into their distal ends.
 The clear cell-free zone between
the inner enamel epithelium and the
dental papilla disappears.
 Thus the epithelial cells come into

close contact with the connective tissue
cells of the pulp, which
differentiate into odontoblasts.
 Preameloblasts secrete proteins similar

to those of enamel matrix and they play
a role in epithelial mesenchymal
interaction.
Terminal phase of the organizing
• During this stage the formation of the dentin by

the odontoblasts begins.
• This cuts off the ameloblasts from their original

source of nourishment.
• This reversal of nutritional source is

characterized by proliferation of capillaries of
the dental sac and gradual disappearance of the
stellate reticulum.
Formative stage
• The ameloblasts enter their formative stage

after the first layer of dentin has been formed.
• The presence of dentin seems to be necessary

for the beginning of enamel matrix formation.
• This mutual interaction between one group of

cells and another is one of the fundamental
laws of organogenesis and histodifferentiation.
• During formation of the enamel matrix the
ameloblasts retain approximately the same length
and arrangement.
• The earliest apparent change is the development
of blunt cell processes on the ameloblast surfaces,
which penetrate the basal lamina and enter the
predentin.
Maturative Stage
• Enamel maturation occurs after most of the
thickness of the enamel matrix has been formed
in the occlusal or incisal area.
• During enamel maturation the ameloblasts are
slightly reduced in length and are closely
attached to enamel matrix.
• The cells of the stratum intermedium lose their

cuboidal shape and regular arrangement and
assume a spindle shape.
• The ameloblasts also play a part in the
maturation of the enamel.
• During maturation, ameloblasts display
microvilli and cytoplasmic vacuoles containing
material resembling enamel matrix are present.
• These structures indicate an absorptive function
of these cells
Protective stage
Ameloblast
cease to
Fully differentiate
calcified
Enamel
completely
developed
• These cell layers then form a stratified epithelial

covering of the enamel called the reduced
enamel epithelium.
• Its function is of protecting the mature enamel

by separating it from the connective tissue until
the tooth erupts.
• During this protective phase, the composition
of enamel can still be modified.
• Fluoride can be incorporated into the enamel of

an unerupted tooth.
• evidence indicates that the fluoride content is

greatest in those teeth that have the longest
interregnum between the completion of enamel
formation and tooth eruption
Desmolytic stage
• The reduced enamel epithelium after

proliferation induces atrophy of the connective
tissue separating it from the oral epithelium.
• The epithelial cells elaborate enzymes that are

able to destroy connective tissue fibres by
desmolysis.
• Premature degeneration of the reduced enamel

epithelium may prevent the eruption of a tooth.
Light micrographs of various stages in life
cycle of ameloblasts.
Cytologic changes seen at different stages in the
life-cycle of the ameloblast in various regions.
AMELOGENESIS
Organic
matrix
formation
.
Development
of enamel
Mineraliz
ation
Formation of enamel matrix
• The secretory activity of ameloblasts begins

when a small amount of dentin has been laid
down.
• The ameloblastic projections penetrate the basal

lamina separating them from the predentin.
• As enamel deposition proceeds, a thin,

continuous layer of enamel is formed along the
dentin.

Differentiating ameloblasts extend cytoplasmic projections (*)
through the basal lamina (BL), separating them from the forming
mantle predentin.
The ameloblasts lose the projections that had penetrated the

basal lamina separating them from the predentin and islands of
enamel matrix are deposited along the predentin.
As enamel deposition proceeds, a thin, continuous layer of

enamel is formed along the dentin.
Amelogenin

Amelogenin has a functioning role in
maintaining space between the crystals.
• Ameloblastin and enamelin help in nucleation
and growth of crystals.
• Tuftelin, is localized to DE junction and is
involved in cell signaling.
• Recently, amelotin, a new protein was reported
to be secreted by maturative ameloblast.
• During early amelogenesis, ameloblasts
transiently express dentin sialoprotein and
dentin phosphoproteins.
• These proteins are localized to DEJ.
Development of Tomes’ processes
• This
The interdigitation
surfaces of the is due to the facing
ameloblasts long axes
the of the
ameloblasts
developing are not parallel
enamel are not to the long
smooth. axesisofan
There
the rods.
interdigitation of the cells and the enamel rods
that they produce.
These projections of the ameloblasts into the

enamel matrix is called, “Tomes’ processes”.
• The junctional complexes encircle the
ameloblast at their distal and proximal ends.
• These serve to control the substances that pass
between ameloblast and enamel.
• The juctional complexes which form at the
distal end are called distal terminal bars.
• These terminal bars separate the Tomes’
processes from the cell proper.
• Secretions from areas close to junctional
complexes and from adjacent ameloblasts form
the interrod enamel.
• They occur earlier and serve to outline the pit
into which secretions from Tomes’ process
occur later.
• The distal portion of the Tomes’ process
lengthens and becomes narrower.
Relationship between enamel rods
and ameloblast
• The bulk of the “head” of each rod is formed by

one ameloblast, whereas three others contribute
components to the “tail” of each rod.
• According to this interpretation, each rod is
formed by four ameloblasts.
• each ameloblast contributes to four different
rods
Ameloblast covering the enamel
• shorter than the ameloblasts over incompletely
formed enamel.
• The changes occurring in the ameloblasts after

secretory stage and prior to the onset of
maturation process are called transition stage.
• About 50% of ameloblasts undergo apoptosis.

reduce in height,
enamel secretion stops
• The organelles involved completely &
in protein synthesis
process of amelogenin
undergo autophagocytosis.
removal starts.
• Ameloblasts deposit a basal lamina, which
adheres to the enamel surface and the
These changes are referred to as
ameloblast attaches to the basal lamina by
modulation.
hemidesmosomes.
• Ameloblasts alternate cyclically in developing
smooth and ruffled borders in the apical
cytoplasm during the maturative stage in a
cervicoincisal direction.
• Modulation between the two forms occur many

times in a day (every 5 to 7 hours).
ameloblasts ruffle ended smooth ended
Distal junctions tight Leaky
Proximal junctions Leaky tight
Lysosomes and Numerous less

Endocytic activity
Ca ions Pass actively Passively

secreted proteases by
Membrane bound proteins present in the
Ameloblasts ameloblasts
alter the basic structure of amelogenenins by
1. CD63
hydrolysis into many low molecular weight
fragments. 2. annexin A2
3. lysosomal associated glycoprotein
• interact
Metalloproteinases & Serine
with secreted proteins proteases
to initiate removal
of the organic matrix.
The organic components & water are lost in

Function as bulk digestive enzymes to clear matrix
mineralization.
proteins.
Over 90% of the

Degrades theinitially secreted
enamel proteins intoprotein is lost
small polypeptides
duringto be absorbedmaturation,
enamel by the ruffle ended
andameloblast
that which
remains forms envelopes around individual
crystals.
Mineralization & maturation of the
enamel matrix
• In the first stage
1. Partial mineralization occurs in the matrix
segments and the interprismatic substance .
2. No matrix vesicles are observed in enamel
formation and no unmineralized matrix is seen
during enamel formation.
3. Therefore, apatite crystals are not preformed
when they are released by the secretory
granules.
4. Nucleation is initiated by the apatite crystallites
of dentin on which enamel is laid.
• The first mineral is in the form of
CRYSTALLINE APATITE.
• However, studies have shown that the initial

mineral is
OCTACALCIUM PHOSPHATE.
• It is however unstable and convert into

hydroxyapatite with one unit of it forming two
units of hydroxyapatite.
The second stage(maturation)
is characterized by the gradual completion of

mineralization.
• The process of maturation starts from the
height of the crown and progresses cervically .
• Maturation begins at the dentinal end of the
Maturation
rods. begins before the matrix has reached
its full thickness.
•Thus
Thusitthere
is going
is anonintegration
in the inner, first-formed
of two processes:
matrix at the same time as initial mineralization
1.is each rod
taking matures
place in thefrom therecently
outer, depth to the surface
formed
matrix.
2. the sequence of maturing rods is from cusps or
incisal edge toward the cervical line.
• (Fig. 4.55).
Newly deposited enamel matrix
Tomes process
Intercellular matrix
process
Crystals
Mature enamel
matrix
• Tuftelin participate in the nucleation of enamel
crystals.
• Other enamel proteins regulate enamel
mineralization by binding to specific surfaces of
the crystal and inhibiting further deposition.
• The rate of formation of enamel is 4 μm/day
• The crystal sizes increase further after tooth

eruption due to ionic exchange with saliva.
• The organic matrix gradually thins and creats
space for the growing crystals.
CLINICAL
CONSIDERATIONS
Amelogenesis imperfecta
Hereditary enamel dysplasia
• A hereditary condition Hereditary
that affects theenamel
brown
Hereditary brown opalescent teeth.
 formation of the enamel matrix
OR
 the enamel mineralisation process of both the
Prevalence
primary and-secondary
1 in 718-14,000
dentition.
• AI has either autosomal dominant, autosomal
Hypoplastic
recessive, sex-linked or AI- 60-70%
sporadic inheritance
patterns.
Hypo maturation AI-20-40%
Hypocalcification AI- 7%
Witkop’s Classification(1989)
Hypoplastic AI
 Defective formation of enamel matrix.
 Enamel has not formed to full normal thickness on

newly erupted teeth.
 Histologically: Disturbance in viability of

ameloblast
Autosomal dominant
Generalized Localized pitted Diffuse smooth Diffuse rough

pitted. 1.Horizontal 1. thin hard and 1.hard with
1.Pinpoint to rows of pit. glossy. rough granular
pinhead. surface.
2. Middle 3rd of 2.Opaque white
2.Enamel is the buccal to translucent 2. White to
normal yellow- surface. brown. yellow white.
white color.
3. 1/4th to 1/8th of 3.Denser than
3.Incisal or its normal the smooth
occlusal surfaces thickness. pattern.
not affected
Autosomal recessive
Localized pitted: Enamel agenesis:

1.Type IC most severe 1.Total lack of enamel
type. formation.
2.All teeth are involved 2. yellow brown colour.
in both dentition. 2.Surface is rough, &
Anterior open bite seen
3.Teeth are widely
spaced and many are
missing in dentition.
X-linked dominant
In males: In females:
1.Diffuse thin smooth 1.Verticle Furrows of
shiny enamel in both thin enamel alternating
dentition. between bands of
2.Open contact point. normal thickness.
3.Colour varies from
brown to yellowish
brown.
Hypomaturative AI
 Defect in maturation of the enamel crystals structure.
 Enamel can pierced with a explorer point under firm

pressure.
 Histologically: alternation in enamel rods and

sheaths
Pigmented pattern
• Surface is mottled & agar brown in color.

• Anterior open bite and unerupted teeth
undergoing resorption is uncommon.
• Occasionally the softness of the surface can be
similar to hypocalcified
• Extensive calculus deposition seen.
X-Linked pattern
In Males In Females
• Permanent teeth- • Vertical bands of

opaque yellow white white opaque
• Primary teeth- enamel and normal
opaque white translucent enamel
appearance with seen.
translucent mottling. • Seen on
transillumination.
Snow capped teeth
• Site: on incisal and occlusal 1/3rd
Maxillary teeth affected more commonly .
• Color of teeth: white opaque appearance.
• Dipped in white paints appearance.
• Dentition: Both dentition are involved.

Hypocalcified AI
 Defective mineralization of formed matrix.
 Enamel is so soft that it can be removed by

prophylaxis instrument.
 Histologically: Defective matrix structure.

Autosomal dominant and
autosomal recessive:
1. Thickness of enamel: Enamel is of normal
thickness areas of hypoplasia occasionally seen on
middle 3rd on labial surface of teeth.
2. Consistency: Enamel is so soft that it lost soon after

eruption, leaving crown composed of only dentin.
It is of cheesy consistency
3. Color: Newly erupted teeth are covered with
dull lusterless opaque, white honey colored or
yellowish orange or brown .
4. Significance: Dentin may be hypersensitive.
Anterior open bite.
Patient with this condition are prone to

calculus rapidly
Hypomaturation-hypoplastic with
taurodontism:
 Hypomaturation-
hypoplastic with
taurodontism autosomal
dominant:
 Hypoplastic – hypomaturation
 appears as yellow-white to
with taurodontism autosomal
yellow-brown
dominant:
 Pits seen on the buccal surface.
 In this type enamel is thin &
• Radiographically: Enamel appears hypo mature.
similar to dentin with large pulp
chambers. 145
Etiology
• Due to the alteration of gene involved in the

process of formation and maturation of enamel.
• The autosomal form is less understood.
• The X-linked AI have shown defective gene

linked to the locus DXS85 at Xp22.
• This is also the location for amelogenin.

Treatment
Main Delayed
Problems erruption
Caries
Tooth
impaction
Anterior
open bite Gingival
Inflammation.
Treatment
highly defective enamel . Rapid attrition occurs.
Full coverage required.
If treatment delayed more loss of crown

lengths occurs
Type-
Other types- less loss of enamel
seen.
ID,IE,
IG,
IIA, Over- Esthetic consideration
dentures full crowns or facial veneers.
IIIA,IIIB
,IVB Gic with dentin adhesives
results in durable restorations
• Temporary phase — undertaken during the
primary and mixed dentition
• Transitional phase – when permanent teeth are
erupting and continue till adulthood
• Permanent phase – occurs in adulthood.
In the primary dentition,
• aims to ensure favorable conditions for the

eruption of the permanent teeth .
• In primary molars,
1. stainless steel.
2. In the anterior teeth-
• polycarbonate crowns,
• resin modified glass ionomers (RMGI),
prefabricated crowns
• direct composite resin can be used as
alternative restorations.
In mixed dentition
• Aim –
1. to preserve tooth structures
2. maintain tooth vitality
3. decrease tooth sensitivity
4. vertical dimension
5. improve esthetics
• As permanent teeth erupt, orthodontic and
prosthetic assessment is essential.
• However, rehabilitation in the mixed dentition
is complex, since teeth have different eruption
sequence
• For permanent molars-
stainless steel crowns.
casting onlays
Direct or indirect composite resin veneers
full-coverage adhesive composite resin
polycarbonate crowns
In Permanent Dentition
• the final treatment objective is-
1. diminish tooth sensitivity
2. to restore vertical dimension of occlusion,
function, as well as esthetics.
• The final treatment often starts as soon as
clinical height of the crown and the gingival
tissue have been stabilized and the pulp tissues
have receded.
• Full mouth rehabilitation combined with a
multidisciplinary approach may be
advantageous .
Intra coronal restoration
• Seow et al reported GIC and composite resins

are better retained in small restorations
compared to amalgam restorations .
• When a more conservative approach is desired,
RMGI is recommended in occlusal non-stress
bearing areas.
• Rada et al reported composite resins provided
satisfactory esthetics and durability.
• However, a high failure rate associated with
insufficient bonding between the restoration
and enamel among variants of AI
• Venezie et al found that pretreatment of enamel
surfaces affected by AI with five percent
sodium hypochlorite resulted in an
improvement of bonding strength in vitro.
• Sonmez et al further investigated this in the

clinical setting and found that pre-treatment
with sodium hypochlorite had no significant
effect on the success of the adhesive restoration
in the intraoral condition.
Extra Coronal Restoration.
• Stainless steel crowns.

According to Robert et al ,in comparing stainless
 minimum preparation, preserving tooth
steel crownsas
structure and casting
much crowns in
as possible in preparation
restoring the
permanent
 Howeverfirst
theymolars
do not,no significant
have perfectly adapted
margins and
differences as such
in quality ortheir long-term
longevity of theuse on the
permanent teeth must be carefully considered.
restorations were found after up to 24 months of
• casting crowns
follow-up
are a viable alternative for posterior teeth . .
• Casting onlays
 protect the remaining tooth structure on the
posterior teeth and may be fabricated without
tooth preparation
 .These restorations can be used before the teeth

are fully erupted.
 It may be a concern that the placement of

supraoccluding restorations will result in an
increase of the vertical dimension and alter
occlusion negatively.
• Acrylic resin crowns or poly carbonate
crowns
 used to restore the anterior teeth, esthetically
acceptable and less expensive.
• When the enamel defects involve decreased

bonding , these crowns offer reasonable
aesthetics and retention due to their full
coverage
• However, their use in AI teeth has not been
systemically evaluated.
Porcelain fused to metal (PFM) crowns
 for the anterior and posterior teeth mostly
considered for anterior restorations because of
its esthetics .
 However, those types of crowns require
significant tooth reduction.
 Thus, the use of PFM and ceramic crowns in
young permanent teeth is not recommended
due to the presence of large pulp and short
clinical crowns.
Overdenture
• is supported both by soft tissues and the roots

of teeth or modified teeth.
• Renner et al. reported a case which was

successfully treated by maxillary overdenture.
• It provides a simplified solution to a complex

prosthodontic problem , that is both reversible
when growth and development demand that
the prosthesis be altered.
Orthodontic treatment
• Patients often need orthodontic treatment due

to dental and/or skeletal problems.
• methods such as using plastic brackets and

traditional banded appliances can be used to
improve appliance retention but the evidence is
weak.
• Moreover, the lack of uniformity of enamel

means that the second and third order bends
which are part of a pre-adjusted appliance
prescription are not fully expressed .
• Achieving perfect occlusion is not always the
treatment goal at the end of the orthodontic
treatment .
• the main principle is often to place the teeth in a

position that facilitates the placement of
restorations.
• Bouvier et al. reported an AI case that

underwent orthodontic treatment successfully
without any problems arising from the placing
of brackets on the performed stainless crown
and polycarboxylate crowns
Acc to the AAPD guidelines(2013)
Pathologies
• Children with associated
AI canwith AI are:-
exhibit accelerated tooth
The incidence
eruption of anterior
compared open
to the bite ispopulation or
normal
1. have
enlarged follicles,
late eruption.
2.50 %impacted
in hypoplastic
permanent
AI, teeth,
•
3.31Other
ectopic
% clinical implications
in hypomaturation
eruption, AI
4.
60
1. % con-genitally
of hypocalcified
rapid attrition,missing
AI. teeth,
5. crown and/or root resorption,
2.
6. excessive calculus deposition,
pulp calcification.
7. Agenesishyperplasia.
3. gingival of second molars
8. enamel resorption and ankylosis
General considerations and
principles of management:
• A primary goal for treatment is to address each
concern as it presents but with an overall
comprehensive plan that outlines anticipated
future treatment needs.
• Clinicians treating children and adolescents
with AI must address the clinical and emotional
demands of these disorders with sensitivity.
• A comprehensive and timely approach is
reassuring to the patient and family and may
help decrease their anxiety.
Preventive care:
• Early identification and preventive interven-

tions are in order to avoid the negative social
and functional consequences of the disorder.
• Regular periodic examinations.
• Meticulous oral hygiene
• calculus removal
• oral rinses
• Fluoride applications
• desensitizing agents may diminish tooth
sensitivity
• When the enamel is intact but discoloured-
During the primary
bleaching dentition,
-to enhance it is important to
the appearance.
restore the teeth for adequate function and to
maintain adequate arch parameters.
• If hypocalcified-composite resin or porcelain
veneers
Primary teeth may require composite or veneered
• If the enamel
anterior crowns or dentin
with cannotfull
posterior be bonded,
coveragefull
steel
or coverage
veneered restorations
crowns. will be required
Enamel Hypoplasia:
 Defined as incomplete or defective formation of

organic matrix of enamel.
 It results if injury occurs during formative stage.

Basic types of enamel hypoplasia:
1. Hereditary enamel hypoplasia-
both the deciduous and permanent dentitions are

involved and generally only the enamel is
affected.
2.Environmental enamel hypoplasia.
Both the denttiotion is involved or sometimes

even a single tooth and both enamel and dentin
are affected.
Factors associated
1)Nutritional deficiency
2)exanthematous disease
3) congenital syphilis
4) hypocalcemia
5) birth injury, prematurity, Rh hemolytic disease
6) local infection or trauma
7) ingestion of chemicals 8) idiopathic causes
• Features:
1. Mild: Few small grooves, pits or fissures on

enamel surface.
170
• Moderate: Enamel may exhibit rows of deep pits
arranged horizontally across tooth surface.
171
• Severe: A considerable portion of enamel is absent
due to prolonged disturbance in the function of
ameloblasts.
172
due to nutritional deficiency and
exanthmatous fever:
 Nutritional Deficiencies:
 Vitamin A, C and D.
 2/3 of this occurs during infancy period or early

childhood.
 Vitamin D deficiency causes rickettsial phenomenon,

resulting in lack of calcification of enamel matrix.
 Horizontal pitting is observed in involved teeth.

173
 Exanthematous disease:
 Measles, chickenpox, scarlet fever.
 Due to elevated temperature of body ameloblast are

affected.
 Involve those teeth formed in the first year after birth.
 The teeth most frequently involved are the central and

lateral incisors, cuspids, and first molar.
174
due to congenital syphillis:
 Involves the maxillary and mandibular permanent

incisors and first molar.
 Anterior teeth -‘Hutchinsons teeth’ while the

molars -‘Mulberry molars’.
 Due to the absence of the central tubercle or

calcification center
175
due to hypocalcemia:
 Tetany induced by decrease level of calcium in the
blood.
 Vitamin D deficiency and parathyroid deficiency
 In this condition, serum calcium level may fall
to 6 to 8 mg/100 ml and at this level enamel
hypoplasia frequently occurs.
Enamel hypoplasia is usually pitting type.

176
due to birth injuries
• Neonatal line or ring is described by Schour in

1936 present in first permanent molars and
deciduous teeth.
• In traumatic births the formation of enamel
may even cease at this time
• more common in prematurely born children
than in normal term infants
• Gastrointestinal disturbance or some other
illness in the mother may be responsible
due to local infection or trauma:
 caused by local infection or trauma and is

called as “Turner’s Hypoplasia” and the tooth
is called as Turner’s tooth.
178
Site-
Maxillary incisors & permanent premolars
Appearance-
mild brownish discoloration of enamel to severe

pitting and irregularity of crown.
179
 Pathogenesis-
 Local infection-
If deciduous teeth become carious during the period

when the crown of succeeding permanent tooth is
formed,
then bacterial infection involving periapical tissues

may occur and this may disturb the ameloblastic
layer of permanent tooth bud, resulting in
hypoplastic crown.
180
 Trauma-
 When deciduous teeth have been driven into

alveolus and have disturbed the permanent bud
while the permanent tooth bud is still being
formed
 then resulting injury leads to yellowish or

brownish stains of enamel usually on labial surface
or as true hypoplastic pitting effect.
181
Enamel hypoplasia due to fluoride:
 Mottled type of enamel hypoplasia was first by GV

Black and Frederick S McKay in 1916.
182
 Etiology:
 ingestion of fluoride containing water during the

time of tooth formation may result in mottled
enamel.
 Mottling increases with increasing fluoride in

water.
 Water that contain in excess of 1PPM(part per

million) fluoride can affect the ameloblast during
formative stage.
183
Pathogenesis
 Formative stage: Disturbance of ameloblast during

the formative stage of tooth development and higher
level of fluoride interfere with calcification process
of matrix.
 Matrix formation stage: Diminished matrix

production, change of matrix composition and
change in ion transport .
 Maturation stage: Diminished withdrawal of

protein and water. 184
Pathogenesis
• Epidemiologic studies have reported that not

all children born and reared in an area of
endemic fluorosis exhibit the same degree of
mottling even though they have used same
water supply.
• May exhibit mild mottling even when exposed

to very low concentration of fluoride.
• Finding may be vary in total water

consumption and thus to total fluoride intake.
1. Questionable changes:
 white flecking or spotting of enamel.
186
2. Mild changes:
 white opaque areas involving more of the tooth

surface.
187
3. Moderate and severe changes:
 Pitting and brownish staining of the surface

and sometimes corroded appearance.
Moderate Severe
188
Treatment
• Cosmetic reasons it has become the practice to

bleach the affected teeth with an agent such as
hydrogen peroxide.
• Procedure must be carried out periodically
since the teeth continue to stain
due to Idiopathic factors
• The majority of cases are unknown origin

• In some cases the etiology cannot be
determined, the causative agent may have been
some illness or systemic disturbance so mild
that it made no impression on the patient.
• Relatively severe cases of enamel hypoplasia
arise with no pertinent past medical history to
account for their occurrence .
Summary.
Enamel Other hard tissues
• matrix is partially • the matrix is nonmineralized.

mineralized • There is no absorption of
• 90% of secreted matrix is secreted matrix
absorbed and this activity is
done by ameloblasts itself.
• collagen plays an important
• Noncollagenous proteins are role
involved in mineralization
• The secretory cell is an • secretory cells of hard tissues
epithelial cell are ectomesenchymal
• Ameloblasts undergo • In other hard tissues

apoptosis; hence enamel formation occurs throughout
formation does not occur life.
later on.
References
• Textbook of oral
histology&embryology:Orban Blaint:13th
Edition
• Tencates’s Oral histology :8th Edition(2013)
• Shafers Textbook of Oral pathology:7th
Edition(2012)
• Textbook of oralpathology –(Brad W.neville)]
References
• Textbook of oral pathology-Ghom(Second edition)

• Bouvier D, Duprez JP, Bois D: Rehabilitation of
young patients with amelogenesis imperfecta: a
report of two cases. J Dent Child 2006, 63:443-447.
• Espinosa R. et al. Enamel Deproteinization and Its
Effect on Acid Etching: An in vitro Study. J Clin
Pedi Dent, 2016;63:443-447.
• Brook AH, King NM. The role of stainless steel
crowns Part 2. Clinical applications.
Dent Update. 2102;9:84-85.
References
• Sengupta P.International journal of clinical and

pediatric dentistry 2011;4(2),171-175
• AAPD Guidelines on heritable dental
developmental anomalies 2013:37(6);15-16
• Robert et al.Braz Dent Sci 2013:16(4);36-39

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ENAMEL

• Tooth enamel the hardest substance produced

• Origin & Introduction

Trenouth M: The origin of the terms enamel, dentine and cementum:

Textbook of oral histology&embryology:Orban Blaint:13th Edition.

• On the cusps of human molars and premolars

• The enamel was found to be thicker in the

• With age enamel becomes progressively worn

Ten Cate’s Oral Histology:8th edition (2013)

The physiological wearing of tooth as a result of

b) Habits c) Structural defects

1. Carbonated & sports drink

2. Poor oral hygiene

5. Remnants of Nasmyth’s membrane

3. Tetracycline and other drugs.

5. Non vital teeth

Pathological wearing away of tooth substance

Caranza Textbook of Periodontology:10th Edition

Caranza Textbook of Periodontology:10th Edition

• The structure and hardness of the enamel

• Its is compensated by the cushioning effect of

• Thus Enamel is stiffer and more brittle than

Textbook of oral histology&embryology:Orban Blaint:13th Edition.

Primary teeth are lighter in color, bluish white.

It is used in physics and electrical engineering when a

Textbook of oral histology&embryology:Orban Blaint:13th Edition.

Translucency of Human Dental Enamel R.H.W. Brodbelt et al J

Ten Cate’s Oral Histology:8th edition (2013)

“Hardness may be defined to be the resistance of solid minerals to the

• Atkinson et al stated that deciduous teeth were

The hardness of enamel and dentine. E. Newbrunt and W.Pigman.

Textbook of oral histology&embryology:Orban Blaint:13th Edition.

• Enamel becomes less permeable with age.

Ten Cate’s Oral Histology:8th edition (2013)

Textbook of oral histology&embryology:Orban Blaint:13th Edition.

• The specific gravity of deciduous teeth is 2.95

Textbook of oral histology&embryology:Orban Blaint:13th Edition.

• Two different procedures have been

Textbook of oral histology&embryology:Orban Blaint:13th Edition.

Textbook of oral histology&embryology:Orban Blaint:13th Edition.

Water is present as a part of the crystal between

Pores are present between the crystals, especially

Textbook of oral histology&embryology:Orban Blaint:13th Edition.

Ten Cate’s Oral Histology:8th edition (2013)

• when a localized region of enamel is lost

Ten Cate’s Oral Histology:8th edition (2013)

Textbook of oral histology&embryology:Orban Blaint:13th Edition.

Textbook of oral histology&embryology:Orban Blaint:13th Edition.

• The diameter of the rods averages 4 μm.

Textbook of oral histology&embryology:Orban Blaint:13th Edition.

Textbook of oral histology&embryology:Orban Blaint:13th Edition.

When cut longitudinally

They are 5 μm in breadth and 9

The “bodies” of the rods are

Stacked arches Irregular rods near DEJ

• The length is estimated to vary between 0.05

• Fusion of the lateral branches of the crystals

Ten Cate’s Oral Histology:8th edition (2013)

• The surfaces of rods are

• Hence they are not as tightly

• This accounts for the rod

• Near the incisal edge or tip of

• In the cervical region the rods deviate from the