Seminar presentation on

ENAMEL
BY- DEVANSHI SHARMA
P.G.1ST YEAR
DEPT. OF CONS. DENTISTRY & ENDO.
 WHAT IS ENAMEL???
 The anatomic crown of a tooth is covered by an avascular,
highly mineralized material known as ENAMEL.
 Origin- Enamel has an ectodermal origin
 Physical properties of enamel:
 Forms a protective covering of variable thickness- on the cusps- 2-2.5 mm
maximum thickness, knife edge thickness at the neck of the tooth.
 Comparatively thicker at the lingual surface of maxillary molars and
buccal surface of mandibular molars.
 Hardest calcified tissue in human body-forms a resistant covering-
suitable for mastication.
 Brittle in nature but the underlying dentin provide some resilience.
 Less elastic than dentin.
 Specific gravity is 2.8.
 Acts as a semi permeable membrane.
 Colour- yellowish white to greyish white.
 Chemical properties of ENAMEL:
 Organic substances and water: 4% by weight
 Inorganic material- (apatite crystals)- 96% by weight
 In volume the organic matter and water are nearly equal to the inorganic contents.
 Organic substances:
 2 main proteins:
1 Amelogenins : low molecular weight protein, 90% of enamel matrix protein, hydrophobic, rich
in Proline, Histidine, Glutamine, and Leucine.
2 non amelogenins: high molecular weight proteins, 10% of enamel matrix proteins, rich in
glycine, aspartic acid, and serine,. Examples are- Enamelin, Ameloblastin, tuftlin.

o Inorganic material:
o Hydroxyapatite – Ca10(PO4)6(OH4)2
o Crystals are hexagonal in cross section.
o The shape of a single crystal was observed to be a rod with an equilateral hexagonal base.
o The crystals are arranged to form enamel rods or enamel prisms.
o Water is present as apart of crystal, between crystals and surrounding the rods.
 DEVELOPMENT
 At the stage preceding the formation of hard
structure( dentin and enamel) the enamel organ ,
originating from the stratified epithelium of the
primitive oral cavity, , consists of 4 distinct layers;
OEE, stellate reticulam, Stellate intermedium and
IEE.
 The borderline between the IEE and the connective
tissue of dental papilla is the subseqent DEJ.
 Thus its outline determines the pattern of the
occlusal or incisal part of the crown.
 Outer enamel epithelium:
 In the early stage, the OEE consists of single layer of
cuboidal cells, separated form surrounding connective tissue
of the dental sac by a delicate basement membrane.
 Prior to the formation of hard structures, this regular
arrangement of the OEE is maintained only in the cervical
part of the enamel organ. At the highest convexity of the
organ, the cells of OEE is irregular in shape.
 The capillaries of the connective tissue surrounding the
epithelial enamel organ proliferate and protrude toward it.
 During enamel formation , cells of the OEE develop villi and
cytoplasmic vesicles and large number of mitochondria, all
indicating cell specialization for the active transport of
material.
 Stellate reticulum
 In the stellate reticulum , the cells are star shaped, with long
processes reaching in all direction from a central body..
 The structure of the stellate reticulum render it resistance
and elastic. Therefore it seems probable that it acts as a
buffer against physical forces that might distort the
conformation of the developing DEJ, giving rise to gross
morphological changes.
 It seems to permit only a limited flow of nutritional
elements from the outlying blood vessels to the formative
cells.
 The SR is reduced in thickness when the first layer of dentin
are laid down, and the inner enamel epithelium is thereby
cut off from the dental papilla.
 Stratum intermedium
 The cells of stratum intermedium is situated
between the SR and the IEE.
 They are flat to cuboidal in shape and are
arranged in 1-3 layers.
 The functions of SI in not understood but it is
believed to play a role in production of the
enamel itself , either through control of fluid
diffusion into and out of the ameloblasts or by the
actual contribution of necessary formative
elements or enzymes.
 Inner enamel epithelium
 The cells of IEE is derived from the basal layer
of the oral epithelium.
 Before enamel formation begins, these cells
assumes a columnar form and differentiate into
ameloblasts that produce the enamel matrix.
 Cervical loop
 At the free border of the enamel organ the outer
and inner enamel epithelial layers are continuous
and reflected into one another as cervical loop.
 When the crown has been formed , the cells of
this portion gives rise to Hertwig’s root sheath.
 Life cycle of ameloblats
 According to their function, can be divided into 6
stages:
1. Morphogenic stage.
2. Organizing stage.
3. Formative stage.
4. Maturative stage.
5. Protective stage.
6. Desmolytic stage.
 Morphogenic stage:
 Before the ameloblasts are fully differentiated and produce
enamel, they interact with the adjacent mesenchymal sells,
determining the shape of DEJ and the crown.
 During this stage the cells are short and columnar, with
large oval nuclei that almost fill the cell body.
 The golgi apparatus and the centrioles are located in the
proximal end of the cell , whereas the mitochondria are
evenly dispersed throughout the cytoplasm.
 The IEE is separated from the CT of dental papilla by a
delicate basal lamina.
 The adjacent pulpal layer is a cell-free, narrow, light zone.
 Organizing stage:
 In this stage of development the IEE interacts with the adjacent CT cells, which
differentiate into odontoblasts.
 IEE become longer, and the nucleus free zone at the distal of the cells become
almost as long as the proximal parts containing the nuclei.
 A reversal of functional polarity of the cells take place by the migration of the
centrioles and golgi region from the proximal ends of the cells to the distal
ends.
 At the same time the cell free zone between the IEE and the and the dental
papilla disappears, probably because o elongation of epithelial cells towards
the papilla.
 Thus the epithelial cells comes in the close contact with the CT of the cells of
the pulp, which differentiate into odontoblasts.
 During the terminal phase of this stage, the formation of the dentin by
odontoblasts begins.
 When dentin forms , it cuts off the ameloblasts from their original source of
nourishment, and from then on they are supplied by he capillaries that surround
and may even penetrate the OEE.
 Formative stage:
 The ameloblasts enter the formative stage after the
first layer of the dentin has been formed.
 During formation of enamel matrix the ameloblasts
retain approximately the same length and arrangement.
 Changes in the organization and number of
cytoplasmic organelles and inclusions are related to
the to the initiation of secretion of enamel matrix.
 The earliest apparent change is the development of
blunt processes on the ameloblasts surfaces which
penetrate the basal lamina and enter the pre dentin.
 Maturative stage:
 Enamel maturation occurs after most of the thickness of the
enamel matrix has been formed in the occlusal or incisal area.
 In the cervical parts of the crown, enamel matrix formation is
still progressing at this time .
 During maturation the ameloblasts are slightly reduced in in
length and are closely attached to enamel matrix.
 The cells of SI lose their cuboidal shape and regular
arrangement and assume a spindle shape.
 During maturation ameloblasts display microvilli at their distal
extremities, and cytoplasmic vacuoles containing material
resembling enamel matrix is present.
 These structures indicate an absorptive function of these cells.
 Protective stage
 After enamel has fully developed and fully calcified,
the ameloblasts cease to be arranged in a well
defined layers and can no longer be differentiated
from the cells of SI and OEE.
 These cell layers then form a stratified epithelial
covering of the enamel, the so called Reduced
enamel epithelium.
 The main function of REE is that of protecting the
mature enamel by separating it from CT until the
tooth erupts.
 Desmolytic stage
 The REE proliferates and seems to induce
atrophy of CT separating it from the oral
epithelium, so that the fusion of two epithelia can
occur.
 It is probable that the epithelial cells elaborate
enzymes that are able to destroy CT fibres by
desmolysis.
 Pre mature degeneration of the REE may prevent
the eruption of teeth.
Amelogenesis
 Structures present in enamel:
 Rods or Prisms
 interrods
 Rod sheath
 Striations
 Hunter schreger bands
 Incremental lines of retzius
 Surface structures
 Enamel cuticle
 Enamel lamellae
 Enamel tufts
 Dentino-enamel junction
 Odontoblast processes or enamel spindles.
 Hypocalcified structures of enamel
 Rod sheath
 Incremental lines of retzius
 Enamel lamellae
 Enamel tufts
 Enamel cracks
 Enamel spindles
 Neonatal lines.
 RODS OR PRISMS :
 Basic structural unit of enamel.
 Shape: like a cylinder
 INTERROD:
 Thin peripheral layer.
 Surrounds each rod.
 The direction are orientated in a direction different
from those making the rods.
 ROD SHEATH:
 The narrow space containing organic material
demarcating the rod and interrod.
 ENAMEL RODS OR PRISMS
 Number of rods: it varies in different tooth; lower central incisor – 5 million, upper
first molar- 12 million.
 Dimension of rods: breadth – 5 microns, length- 9 microns, diameter- 4 microns ,
approximately.
 It is claimed that the diameter of rods increases from DEJ towards the surface of enamel
at a ratio of 1:2.
 Length of the rod:
 From DEJ the rods runs in a wavy and tortuous course outward the surface of the tooth.
 Length of the rod> thickness of the enamel
 Length of the rod in the cusp area> length of the rod at the cervical area
 Appearance: has a clear crystalline structure.
 Cross section: occasionally appear hexagonal, sometimes round or oval. In human
enamel , they resemble fish scales.
 If we see the ultra structure, the most common pattern is a key hole or paddle shaped
prism in human enamel.
 Key hole pattern has a ‘body’ and a ‘tail’.
 Direction of rods:
 Generally, rods are oriented at right angles to the dentin surface.
 In cervical areas- the rods deviate from a horizontal to an apical
orientation.
 Near the incisal edge or cusp tips they change gradually to an increase
oblique direction until they are almost vertical in the region of edge or
cusp tip.
 In deciduous teeth they are approximately horizontal in cervical and
central part.

 GNARLED ENAMEL:
 An optical illusion when cut in an oblique plane- seen near cusps or
incisal edge- due to bundles of rods are intertwined more irregularly.

 At pits and fissure- rods converge in their outward course.

 Striations:
 Each enamel rods is built up of segments separated by
dark lines the 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 rhythmic manner. In human these segments
can be seen in to be a uniform length of about 4
microns.
 There is a diurnal rhythm in the enamel formation.
 Striated areas also show variation in composition.
 Clinical significance of enamel rods:
 It confers strength to the enamel.
 Because of interwoven network of rods, teeth can resist
masticatory forces upto 20-30 lbs per tooth.
 Their direction is important consideration in the cavity
preparation for restoration.
 Fracturing of unsupported rods in poorly designed
restorative preparation cause loss of enamel around the
margin of the restorative material resulting in marginal
leakage and makes the tooth more susceptible to caries.
 The different inclination of rods in permanent and
deciduous teeth must be accounted for during cavity
preparation.
 HUNTER- SCHREGER BANDS:
 This is an optical phenomenon seen in reflected light.
 Alternate light and dark bands are seen in ground longitudinal
section.
 Dark bands- parazones
 Light bands- diazones
 Due to-
1) Abrupt change in the direction of enamel rods. (most accepted
theory)
2) Variation in calcification of enamel.
3) Alternate zones having different permeability and organic
material.
 They originate from the DEJ and pass outward ending at some
distance from the outer enamel surface.
 INCREMENTAL LINES OF RETZIUS
 Increment lines of growth
 Eccentric growth rings.
 Brownish bands in ground section
 Reflect variation in structures and mineralization.
 Broadening of these lines in case of metabolic disturbances.
 In longitudinal section they surrounds the tip of the dentin.
In the cervical part they run obliquely from DEJ to surface
then deviate occlusally.
 Etiology:
 Periodic bending of enamel rods.
 Variations in organic structure.
 Physiologic calcification rhythm.
 Surface structures:
 PRISMLESS ENAMEL
 PERIKYMATA
 ENAMEL PITS
 ENAMEL CAPS
 ENAMEL BROCHS
 PRISMLESS ENAMEL
 A relatively structureless layer of enamel,
approximately 30 microns thick, called prismless
enamel, it has been described in in 70% of the
permanent teeth and all deciduous teeth.
 The structureless enamel is found least often over
the cusp tip and most commonly towards the
cervical areas of the enamel surface.
 It is also somewhat more heavily mineralized
than the bulk of enamel beneath it.
 PERIKYMATA:
 Perikymata are transverse wave like grooves,
believed to be the external menifestations of the
striae of retzius.
 They are continuous around a tooth and usually
lie parallel to each other and to the CEJ.
 ordinarily, there are 30 perikymata per mm in the
region of CEJ and their concentration generally
decrease to about 10 per mm near the
occlusal/incisal edge.
 ENAMEL PITS, CAPS AND BROCHS:
 The surface of enamel appears very uneven . Pits
of about 1-1.5 microns in diameter and small
elevations of about 10-15 microns called enamel
caps are seen.
 The surface pits are said to represent the ends of
ameloblast and the caps are due to enamel
deposition on non- mineralizable debris.
 Larger enamel elevations are termed enamel
brochs.
 NEONATAL LINES
 It is present in all deciduous teeth and 1st permanent
molar.
 It is the most prominent incremental line in primary teeth.
 This line separates the enamel formed before birth and
enamel formed after birth.
 This line is due to sudden change of nutrition and
environment after birth.
 Prenatal enamel is less pigmented and more free of
defects than postnatal enamel.
 More frequently absent in permanent 1st molar of boys
than girls.
 ENAMEL CUTICLE:
 It is a delicate membrane called Nasmyth’s
membrane or primary enamel cuticle.
 This is typical lamina that is secreted by
ameloblasts after completion of enamel
formation.
 This thin membrane covers the newly erupted
teeth but soon after eruption it is removed by
masticatory forces.
 What is pellicle?
 A layer directly on the top of enamel 1-3 microns
thick ( could reach upto 10 microns)
 Mainly the precipitate of salivary proteins.
 The pellicle reforms within hours after an enamel
surface is mechanically cleaned.
 Within a day or two after the pellicle has formed ,
it becomes colonized by microorganisms to form
bacterial plaque.
 ENAMEL LAMELLAE:
 These are thin leaf like structure extends from enamel surface to DEJ,
sometimes may penetrate dentin.
 Lamellae are rich in protein with little mineral content.
 Lamellae may also develop in planes of tension. The rods crosses
such planes and short segments of rod remains uncalcified those later
on are filled with organic contents.
 3 types of lamella can be differentiated:
1) Type A: lamellae containing poorly calcified rod segments. These are
restricted to enamel.
2) Type B : consisting of degenerated cells. May cross the DEJ and
reach the dentin
3) Type C: lamellae in erupted teeth where cracks are filled with
salivary proteins.
 CRACKS: fissures like structures seen on the surface, they are outer
edges of lamellae. They are less than 1 mm in length.
 ENAMEL TUFTS
 It arises at the DEJ and reach into the enamel to
about 1/5th to 1/3rd of its thickness.
 They were so termed because they resemble tufts
of grass when viewed in ground sections.
 Tufts consists of hypocalcified enamel rods and
interprismatic substances.
 DENTINO-ENAMEL JUNCTION
 The surface of the dentin at the DEJ is pitted.
 Into the shallow depression of the dentin fit the
rounded projections of the enamel.
 DEJ therefore appears as a scalloped line – the
convexity of the scallops are towards the dentine.
 The pitted DEJ is pre formed even before the
development of hard tissues and is evident in the
arrangement of the ameloblasts and the basement
membrane of the dental papilla.
 ODONTOBLAST PROCESSES AND
ENAMEL SPINDLES
 Occasionally odontoblast processes pass across
the DEJ into the enamel.
 Since many are thickened at their end, they have
been termed enamel spindles.
 They seem to originate from processes of
odontoblast that extended into the enamel
epithelium before hard substances are formed.
 These are hypomineralized or partially
mineralized structures.
 AGE CHANGES IN ENAMEL
 The most apparent age change in enamel is attrition or wear of the occlusal
surface and proximal contact points as a result of mastication.
 The surface of unerupted and recently erupted teeth are covered completely
with pronounced rod ends and perikymata. At the points of highest contour
of the surface these structures soon begin to disappear.
 Facial and lingual surfaces lose their structure much more rapidly than do
proximal surfaces, and anterior teeth lose their structure more rapidly than
do the posterior teeth.
 Localized increase in certain elements such as nitrogen and fluorine,
however, have been found in the superficial enamel layers of the older teeth.
 As a result of age changes in the organic portion of the enamel, presumably
near the surface, the teeth may become darker, and their resistance to decay
may increased.
 Age changing is greatly related to reduced permeability of older teeth to
fluids.
 CLINICAL CONSIDERATIONS:
 The course of the enamel rods is of importance in cavity
preparations. The choice of instruments depends on the location
of the cavity in the tooth.
 Generally the rods run at a right angle to the underlying dentin or
the tooth surface. close to the CEJ the rods run in a more
horizontal direction. In preparing cavities, it is important that
unsupported enamel rods are not left at the cavity margins,
because they would soon break and produce leakage.
 Enamel is brittle in nature and does not withstand forces in thin
layers or in areas where it is not supported by the underlying
dentin.
 Caries penetrate the floor of fissures rapidly because the enamel
in these areas are very thin. As the destructive process reaches
the dentin, it spreads along the DEJ undermining the enamel.
 Dental lamella may also be predisposing locations for
caries because they contain much organic material.
 Fluoride-containing mixtures such as stannous
fluoride pastes, sodium fluoride rinses, and acidulated
phosphate fluoride are also used to alter the outer
surface of enamel so that it becomes more resistance
to caries.
 The most effective means for mass control of dental
caries to date has been adjustment of fluoride level in
communal water supplies to 1 parts per million.
 The surface of the enamel in the cervical region
should be kept smooth and well polished by proper
home care and by regular cleansing by dentist.
 Composite resins are mechanically bonded
directly to the enamel surface. In this process the
enamel surface is first etched with an acid. This
produces an uneven dissolution of enamel rods
and their sheath so that a relatively smooth
enamel surface becomes pitted and irregular.
 It helps in mechanical bonding of composite to
the enamel surface.
 Prismless enamel found on the surface does not
provide enough mechanical retention so etching
should go beyond the prismless enamel to the
prismatic enamel below it.
 DEFECTS OF ENAMEL
GENETIC NON GENETIC
1)Amelogenesis 1) caries
imperfecta: 2) Attrition
A) Hypoplastic (type1) 3) abrasion
B) Hypomaturation(type2) 4)Erosion
C) Hypocalcified (type3) 5) localized non hereditary
enamel hypoplasia
6)localized non hereditory
enamel hypocalcification.
7) fluorosis.
 Amelogenesis imperfecta
 It is a group of conditions caused by defects in
the genes encoding enamel matrix proteins.
 Type 1: hypoplastic amelogenesis
imperfecta
 The main defect is in formation of the matrix (protein).
 Enamel is not formed to full thickness because ameloblasts
fail to lay down sufficient matrix.
 Enamel is randomly pitted , grooved or very thin, but hard and
translucent.
 Affected teeth appear small with open contacts.
 due to very thin or non existent of enamel causes thermal
sensitivity.
 Teeth are not susceptible to caries .
 The enamel is scanty and easily damaged.
 Commonly in men.
 Type 2 : hypomaturation amelogenesis
imperfecta
 Occurs during matrix maturation stage.
 Enamel is softer and chips from the underlying
dentin.
 Enamel has a mottled brown yellow white colour.
 Contact points present as enamel is of normal
thickness.
 Radiographically enamel approaches the
radiodensity of dentin.
 Type 3 : hypocalcified
amelogenesis imperfecta
 Occurs during the calcification stage.
 Most common type.
 Enamel is of normal thickness but soft, friable,
and easily lost by attrition.
 Enamel appears dull, lustrous, honey coloured
and stains easily.
NON GENETIC
 Caries
 It is an irreversible microbial disease of the
calcified tissue of the teeth , characterized by
demineralization of the inorganic portion and
destruction of the organic substance of the tooth,
which often leads to cavitation.
 Attrition
 Defined as physiological continuous, process
resulting in loss of tooth structure from direct
frictional forces between contacting teeth.
 It occurs both on occlusal and proximal surfaces.
 Attrition is accelerated by parafunctional
mandibular movements especially bruxism.
 Abrasion:
 It refers to the loss of tooth substance induced by
mechanical wear other than of mastication.
 Abfraction
 Abfraction is a theoretical concept explaining a
loss of tooth structure not caused by tooth decay
(non-carious cervical lesions).
 It is suggested that these lesions are caused by
forces placed on the teeth during biting, eating,
chewing and grinding, the enamel especially at
CEJ, undergoes large amount of stress , causing
micro fracture and tooth tissue fracture.
 Erosion
 It is defined as irreversible loss of dental hard
tissue by a chemical process that does not involve
bacteria.
 Dissolution of mineralized tooth structure occurs
upon contact with acids that are introduced into
the oral cavity from intrinsic (e.g.
gastroesophageal reflux, vomiting) or extrinsic
sources (e.g. acidic beverages, citrus fruits).
 Localised non hereditory enamel
hypoplasia
 Refers to the localised defect in the crown
portion of the tooth caused by the injury to
ameloblasts during the enamel matrix formation
stage.
 Localised non hereditory enamel
hypocalcification
 Refers to the localised defects in the crown of a
tooth due to injury to ameloblasts during
mineralization stage.
 In these defects, the enamel is normal in structure
but its mineralization is defective.
 The color of lesion varies from chalky to yellow
brown, dark brown or grayish.
 DENTAL FLUOROSIS
 Also termed as mottled enamel.
 It is an extremely common disorder,
characterized by hypomineralization of tooth
enamel caused by ingestion of excessive fluoride
during enamel formation.
 RECENT RESEARCHES ON
ENAMEL:
 Application of enamel matrix derivative (Endogain)
in endodontic therapy: Researchers suggest that EMD
can be applied in direct pulp capping and pulpotmy.
And EMD may have potential in treatment of
traumatized and immature teeth.
 Enamel matrix proteins in the regenarative therapy of
deep infrabony defects: A multicentre randomized
clinical trial was designed to know the role of EMP to
promote new bone cementum, pdl and regeneration.
 Enamel regeneration: According to the research there are
some bioactive nanofibres (BRGD-PA) present with
enamel proteins participate in integrin- mediated cell
binding to the matrix with delivery of intstructive signals
for enamel formation.
 Enamel Gel ( painting instead of drilling): Recently
Moradin oldak, a researcher, and her team engineered a
string of amino acids that contained only the parts needed
for enamel crystal creation. These shorter peptides could
be incorporated into gel. Such a product could be painted
on teeth eroded by early cavities or erosion causing pain
and tooth hypersensitivity, effectively replacing lost
enamel.
 References:
 Orban’s oral histology and embryology. 12th
edition
 Shafer’s textbook of oral pathology. 7th edition
 Journal of endodontic, Vol 44, issue 7
 Journal of clinical periodontology 29(4), 317-
325, 2002
 http://doi.org/10.1359/jbmr.080705
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