Enamel

ENAMEL
Made By:
Dr. Akshat Sachdeva
MDS Ist Year
Dept. of Conservative Dentistry and Endodontics
Sudha Rustagi College of Dental Sciences & Research

INTRODUCTION
 Hardest calcified tissue in the human body that covers the anatomic
crown of the tooth.
 Only ectodermal derivative of the tooth.
 Varies in thickness in different areas.
 Thicker at incisal and occlusal areas and becomes progressively
thinner until it terminates at CEJ.

Enamel
Dentin
Pulp Chamber
Pulp Canal
Periodontal Fibers
Cementum
Fig. 1: Showing supporting structures of tooth
Source: Sturdevant’s Art and Science of Operative Dentistry

DEVELOPMENT OF ENAMEL
 The enamel organ consists of 4 distinct layers:
 Inner and outer enamel epithelium are separated by a large mass of
cells differentiated into two distinct layers.
 Layer that is close to the inner enamel epithelium consists of two or
three rows of flat polyhedral cells called stratum intermedium.
 The other layer, which is more loosely arranged, constitutes stellate
reticulum.

OUTER ENAMEL EPITHELIUM
 Consists of a single layer of cuboid cells, separated from the
surrounding connective tissue by a delicate basement membrane.
 Cells of the outer enamel epithelium become irregular in shape at the
highest convexity of the enamel organ.
 During enamel formation, cells of the outer enamel epithelium
develop villi and cytoplasmic vesicles and large numbers of
mitochondria.

STELLATE RETICULUM
 Cells in this layer are star shaped with long processes reaching in all
directions from a central body.
 Connected with each other and with the cells of the outer enamel
epithelium and the stratum intermedium by desmosomes.
 Stellate reticulum is noticeably reduced in thickness when the first
layers of dentin are laid down.

STRATUM INTERMEDIUM
 Cells are flat to cuboidal in shape and are arranged in one to three
layers.
 Connected with each other and with the neighboring cells of stellate
reticulum and inner enamel epithelium by desmosomes.
 Tonofibrils are found in the cytoplasm.
 Cells in this layer show mitotic division even after the cells of inner
enamel epithelium cease to divide.

INNER ENAMEL EPITHELIUM
 Cells of inner enamel epithelium are derived from the basal cell layer
of oral epithelium.
 These cells assume a columnar form and differentiate into ameloblasts
that produce the enamel matrix.
 Cell differentiation occurs earlier in the region of incisal edge or cusps
than in the area of cervical loop.

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 the
cervical loop.
 When the crown has been formed, the cells of this portion give rise to
Hertwig’s epithelial root sheath.

LIFE CYCLE OFAMELOBLAST
 According to function, the life span of cells can be divided into six
stages:
 Morphogenic.
 Organizing.
 Formative.
 Maturative.
 Protective.
 Desmolytic.

MORPHOGENIC STAGE
 The cells are short and columnar, with large oval nuclei that almost
fill the cell body.
 The ameloblasts before differentiation interact with mesenchymal
cells and determine shape of the DEJ and the crown.
 Golgi apparatus and the centrioles are located in the proximal end of
the cell, whereas the mitochondria are evenly dispersed throughout
the cytoplasm.

ORGANIZING STAGE
 Inner enamel epithelium interacts with the adjacent connective tissue
cells, which differentiate into odontoblasts.
 Cells of inner enamel epithelium become longer, and nucleus-free
zones at distal ends of the cells become almost as long as the proximal
parts containing nuclei.
 Staining methods reveal presence of acidophil granules in proximal
part of the cell.

 Epithelial cells come into close contact with connective tissue cells of
the pulp, which differentiate into odontoblasts.
 Formation of dentin by odontoblasts begins during terminal phase of
the organizing stage.
 When dentin forms, it cuts off ameloblasts from their original source
of nourishment, and from then on they are supplied by capillaries that
surround the outer enamel epithelium.

Source: Essentials of Oral Biology by Maji Jose

FORMATIVE STAGE
 Ameloblasts enter this stage after the first layer of dentin has been
formed.
 Presence of dentin is necessary for the beginning of enamel matrix
formation.
 During formation of enamel matrix, ameloblasts retain approximately
the same length and arrangement.
 Earliest apparent change to appear is the development of blunt cell
processes on ameloblast surfaces, which penetrate the basal lamina
and enter predentin.

MATURATIVE STAGE
 Enamel maturation i.e. full mineralization 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.
 Ameloblasts display microvilli at their distal extremities, and
cytoplasmic vacuoles containing material resembling enamel matrix
are present.

PROTECTIVE STAGE
 When the enamel has completely developed and has fully calcified,
the ameloblasts cease to be arranged in a well-defined layer.
 Cell layers then form a stratified epithelial covering of the enamel, the
so-called reduced enamel epithelium, which functions to protect the
mature enamel by separating it from connective tissue until the tooth
erupts.
 Anomalies may develop if connective tissue comes in contact with the
enamel.

DESMOLYTIC STAGE
 Reduced enamel epithelium proliferates and seems to induce atrophy
of the connective tissue.
 It has been suggested that epithelial cells elaborate enzymes that are
able to destroy connective tissue fibers by desmolysis.
 Premature degeneration of the reduced enamel epithelium may
prevent the eruption of a tooth.

AMELOGENESIS
 Two processes are involved in the development of enamel:
 Organic matrix formation.
 Mineralization.

ENAMEL MATRIX FORMATION
 Ameloblasts begin their secretory activity when a small amount of
dentin has been laid down.
 Ameloblasts lose their projections separating them from predentin.
 Islands of enamel matrix are deposited along the predentin.
 A thin, continuous layer of enamel is formed along the dentin.

 Amelogenin is the major component of enamel matrix proteins.
 Amelogenins have been shown to form minute nanospheres between
which enamel crystals form.
 Absence of amelogenin has been found to result in the formation of
hypoplastic teeth.
 Ameloblastin and enamelin are the other important proteins of the
enamel matrix.
 A new protein, amelotin is suggested to help in enamel formation.

DEVELOPMENT OF TOMES’ PROCESS
 Projections of ameloblasts into the enamel matrix have been named
Tomes’ process.
 They contain typical secretion granules as well as rough endoplasmic
reticulum and mitochondria.
 Tomes’ process is partially separated from cell body by an incomplete
septa formed by microfilaments and tonofilaments.

 Ameloblasts over maturing enamel are considerably shorter than the
ameloblasts over incompletely formed enamel.
 Changes occurring in the ameloblasts prior to the onset of maturation
process are called transition stage.
 During this stage:
 Ameloblasts reduce in height
 Enamel secretion stops completely and
 Process of amelogenin removal starts.
 Ameloblasts attach to the basal lamina by hemidesmosomes.

MINERALIZATION OF ENAMEL MATRIX
 Mineralization of the enamel matrix takes place in two stages.
 In the first stage, an immediate partial mineralization occurs in the
matrix segments.
 First mineral is in the form of crystalline apatite.
 Studies have shown that the initial mineral is octacalcium phosphate,
which may act as a template for hydroxyapatite.

 Second stage or maturation, is characterized by the gradual
completion of mineralization.
 Maturation process starts from height of the crown and progresses
cervically.
 The rate of formation of enamel is 4 μm/day.
 Organic matrix gradually becomes thinned and more widely spaced to
make room for the growing crystals.
 Ameloblasts undergo apoptosis after formation of enamel, hence
enamel formation does not occur later on while formation of other
hard tissues continues throughout life.

PHYSICAL CHARACTERISTICS
 Enamel forms a protective covering of variable thickness over the
entire surface of the crown.
 Color of enamel – covered crown ranges from yellowish white to
grayish white.
 Color is determined by differences in the translucency of enamel.
 Yellowish teeth have a thin, translucent enamel through which the
yellow color of the dentin is visible and grayish teeth have a more
opaque enamel.

Thickest over the cusps and incisal edges and thinnest at the cervical
margins.
Attains a maximum thickness of about 2 to 2.5 mm on the cusps of
molars and premolars.
Specific gravity of enamel is 2.8.
It has been found that enamel can act like a semipermeable membrane,
permitting complete or partial passage of certain molecules.

CHEMICAL CHARACTERISTICS
ENAMEL
Inorganic Content (96%) Organic content + water (4%)
Proteins
Amelogenins Nonamelogenins
(90%) (10%)
Amelogenins are low molecular weight proteins and are rich in
proline, histidine, glutamine and leucine.
Nonamelogenins are high molecular weight proteins and are rich in
glycine, aspartic acid and serine.

 Inorganic material of enamel is hydroxyapatite.
 Crystals of hydroxyapatite are hexagonal in cross-section.
 Average concentrations(%) of three major constituents namely
oxygen, calcium and phosphorus, are 43.4, 36.6, and 17.7
respectively.
 Minor constituents together account for 2.3%, of which sodium
carbon and magnesium are the principal constituents.

STRUCTURE
 Enamel is composed of enamel rods or prisms, rod sheath and an
interprismatic substance.
 Enamel rods normally have a clear crystalline appearance, permitting
light to pass through them.
 In cross-sections of human enamel, many rods resemble fish scales.

ULTRASTRUCTURE
 A more common pattern is a keyhole or paddle-shaped prism in
human enamel.
 Rods measure about 5 μm in breadth and 9 μm in length.
 Each enamel rod is built up of segments separated by dark lines that
give it a striated appearance.
 Striations are suggested to be due to a diurnal rhythm in the enamel
formation and that in these areas rods show variation in composition.

Source: Manual of Oral Histology and Oral Pathology by Maji Jose

HUNTER – SCHREGER BANDS
 Alternating dark and light strips of varying widths.
 Occur due to abrupt change in direction of enamel rods.
 Prisms cut longitudinally to produce dark bands are called parazones,
while those cut transversely to produce light bands are called
diazones.
 Angle between parazones and diazones is about 40 degrees.

INCREMENTAL LINES OF RETZIUS
 Appear as brownish bands in ground sections of enamel.
 Illustrate the incremental pattern of enamel, i.e. the successive
apposition of layers of enamel during formation of the crown.
 Incremental lines of Retzius appear as concentric circles.
 Reflect variations in structure and mineralization of enamel.

GNARLED ENAMEL
 Arrangement of enamel rods becomes more complicated in the region
of cusps and incisal edges.
 Enamel rods become more irregular and intertwine with each other
especially near the DEJ.
 This creates an optical appearance called as gnarled enamel.

SURFACE STRUCTURES
 Structure less layer of enamel, called prismless enamel has been
described in 70% of permanent teeth and all deciduous teeth.
 Found least often over the cusp tips and most commonly toward the
cervical areas of the enamel surface.
 In this layer, the apatite crystals are parallel to one another and
perpendicular to the striae of Retzius.

 Perikymata are transverse, wave-like grooves, believed to be the
external manifestations of the striae of Retzius.
 They are continuous around a tooth with a fairly regular course and
usually lie parallel to each other and to the CEJ.
 Pits of about 1–1.5 μm in diameter and small elevations of about 10–
15 μm called enamel caps are seen on the irregular enamel surface.
 Larger enamel elevations are termed enamel brochs.

NEONATAL LINE
 Prominent incremental line separating prenatal and postnatal enamel.
 Prenatal enamel usually is better developed than the postnatal enamel.
 Fetus develops in a well-protected environment with an adequate
supply of all the essential materials.
 Found to be more frequently absent in permanent first molars of boys
than girls.

ENAMEL CUTICLE
 Primary enamel cuticle or Nasmyth’s membrane covers the
entire crown of newly erupted tooth but is probably soon
removed by mastication.
 Erupted enamel is covered by a pellicle, a precipitate of salivary
proteins.
 Within a day or two after pellicle formation, it becomes
colonized by microorganisms to form bacterial plaque.

ENAMEL LAMELLAE
 Leaf like structures extending from outer surface of enamel towards
dentin.
 Three types of lamellae are seen:
i. Type A: Composed of poorly calcified enamel rods. Restricted to
enamel.
ii. Type B: Consists of degenerated cells and may extend into dentin.
iii. Type C: Filled with organic matter derived from saliva and maybe
extended into dentin.

ENAMEL TUFTS
 Ribbon like structures extending from DEJ into enamel.
 Resemble tufts of grass when viewed in ground sections.
 Consist of hypocalcified enamel rods and interprismatic substance.
 Extend in the direction of long axis of the crown.

ENAMEL SPINDLE
 Odontoblastic processes crossing DEJ and extending to the enamel.
 Appear as dark spindle shaped structures.
 In ground sections of dried teeth, the organic content of the spindles
disintegrates and is replaced by air, and the spaces appear dark in
transmitted light.
 Found mainly in cusp tip region.

DENTINO-ENAMEL JUNCTION
 Appears as a scalloped line with convexity directed towards dentin.
 Crystals of dentin and enamel mix with each other.
 More pronounced in the occlusal area, where masticatory stresses are
greater.

AGE CHANGES
 Most apparent age change in enamel is attrition or wear of the
occlusal surfaces and proximal contact points as a result of
mastication.
 This is evidenced by a loss of vertical dimension of the crown
and by flattening of the proximal contour.
 It has been seen that facial and lingual surfaces loose their
structure rapidly than do proximal surfaces, and anterior teeth
loose their structure more rapidly than do posterior teeth.

 Tooth Darkening:
 Teeth appear to darken with age.
 Darkening may be caused by deepening of dentin color seen through
the progressively thinning layer of translucent enamel.
 Permeability:
 Enamel becomes less permeable with advancing age.
 Decrease in permeability is caused due to increase in the size of the
crystals which in turn decreases the pores between them causing a
reduction in permeability.

CLINICAL CONSIDERATIONS
 Course of the enamel rods is of importance in cavity preparations.
 During cavity preparation, it is important that unsupported enamel
rods are not left at the cavity margins because they would soon break
and produce leakage.
 Bacteria would lodge in these spaces thus inducing secondary dental
caries.

Deep enamel fissures predispose teeth to caries.
Caries penetrate the floor of fissures rapidly because the enamel in
these areas is very thin.
Eventually, an area of dentin becomes carious because the entrance to
the cavity is minute.
Careful examination is necessary to discover such cavities because
most enamel fissures are minute.

TETRACYCLINE STAINING
 Discoloration of teeth due to tetracycline may occur if therapeutic
regimens are taken either during pregnancy or following childbirth.
 Forms a complex with calcium ions in the surface of hydroxyapatite
crystals.
 Usually avoided during pregnancy or till the child completes 8 years.

ECTOPIC ENAMEL
 Also called as enamel pearl or enameloma.
 Presence of enamel in unusual locations, mainly the tooth root.
 Usually develops on roots of maxillary permanent molars.
 Most incidental findings require no therapy.
 Meticulous oral hygiene should be maintained to prevent localized
loss of periodontal support.

CLINICAL CONSIDERATIONS
 The principal expressions of pathologic amelogenesis are:
 Hypoplasia occurs when matrix formation is affected and is
manifested as pitting, furrowing, or even total absence of the enamel.
 Hypocalcification results when maturation is lacking or incomplete
and can be seen in the form of opaque or chalky areas on normally
contoured enamel surfaces.
 Causes of such defective enamel formation can be generally classified
as systemic, local, or genetic.

 If drinking water contains fluoride in excess of 1.5 parts per million,
chronic endemic fluorosis may occur as a result of continuous use
throughout the period of amelogenesis.
 It is important to urge substitution of water with levels of fluoride
(about 1 part per million) well below the threshold for fluorosis.
 Teeth most frequently affected are incisors, canines and first molars.

 A small amount of fluoride (about 1 to 1.2 parts per million) reduces
susceptibility to dental caries without causing mottling.
 If an injury occurs in the formative stage of enamel development,
hypoplasia of the enamel will result.
 An injury during the maturation stage will cause a deficiency in
calcification.

AMELOGENESIS IMPERFECTA
 Structural defect of tooth enamel.
 Also called as:
 Hereditary enamel dysplasia.
 Hereditary brown enamel.
 Hereditary brown opalescent teeth.
 Prevalence of this condition has been estimated to range from 1 in 718
to 1 in 14,000, depending on the population studied.

 Classification of amelogenesis imperfecta (AI) according to Witkop
(1989):
 Type – I: Hypoplastic.
 Type – II: Hypomaturation.
 Type – III: Hypocalcified.
 Type – IV: Hypomaturation-hypoplastic with taurodontism.
 Hypoplastic AI represents 60–73% of all cases, hypomaturation AI
represents 20–40%, and hypocalcification AI represents 7%.

 Modified Classification of AI:

Etiology of AI is related to the alteration of genes involved in the
process of formation and maturation of the enamel.
Defective gene has been found to be closely linked to the locus
DXS85 at Xp22.
This also has been identified as the general location of the human gene
for amelogenin, the principal protein in developing enamel.

 Hypoplastic AI is characterized by:
 Thin enamel possessing yellowish-brown color.
 Glossy square-shaped crown.
 Lack of contact between adjacent teeth.
 Flat occlusal surfaces of posterior teeth due to attrition.
 Radiographically, there is a presence of thin radiopaque layer of
enamel with normal radiodensity.
 Histologically, defect in the enamel matrix formation is seen.

Hypocalcified form of AI is characterized by:
 Softer enamel which wears down rapidly.
 Pigmented dark brown colored enamel.
Radiographically, thickness of enamel is normal but radiodensity of
enamel is less than that of dentin.
Histologically, defects of matrix structure and mineralization is seen.

 Hypomaturation form of AI is characterized by:
 Thickness of enamel is harder than hypocalcified type and may crack
away from the crown.
 Mottled-colored cloudy white/yellow/brown/snow capped.
 Radiographically, radiodensity of enamel is similar to that of dentin.
 Histologically, alterations in enamel rod and rod sheath structures had
been noted.

 There is no specific treatment for the condition.
 Main objectives of treatment include preserving patient's remaining
dentition, and to treat and preserve the patient's occlusal vertical
height.
 Esthetic issues should be considered since the color of tooth crown is
yellow from exposure of dentin due to enamel loss.
 Factors to be considered in deciding treatment options include
classification and severity of AI, the patient's social history, clinical
findings etc.

Full-coverage crowns can be used to compensate for the abraded
enamel in adults.
Aesthetics may be addressed via placement of composite or porcelain
veneers.
Patient's oral hygiene and diet should be controlled as they play an
important role in the success of retaining future restorations.
Teeth may have to be extracted in worst cases and implants or dentures
can be considered for replacement.

ENAMEL HYPOPLASIA
 Incomplete or defective formation of the organic enamel matrix of
teeth.
Hereditary type Environmental factors
- Usually involves both deciduous - Involves either dentition
and permanent dentition. and sometimes even a single
tooth.
- Generally affects only enamel. - Both enamel and dentin
affected to some degree.

 In mild environmental hypoplasia, there may be only a few small
grooves, pits, or fissures on the enamel surface.
 If the condition is more severe, the enamel may exhibit rows of deep
pits arranged horizontally across the surface of the tooth.

HEREDITARY ENAMEL HYPOPLASIA
 Genetic conditions exhibiting enamel defects:
 Treacher Collins Syndrome.
 Congenital erythropoietic porphyria.
 Ectodermal dysplasia.
 Epidermolysis bullosa.
 Tuberous sclerosis.
 DiGeorge syndrome
 Kenny-Caffrey syndrome.

 Hypoplasia results only if the injury occurs during the time the teeth
are developing, or more specifically, during the formative stage of
enamel development.
 Different factors may give rise to the condition which include:
 Nutritional deficiency (vitamins A, C, and D).
 Congenital syphilis (Hutchinson’s teeth/mulberry molars).
 Local infection or trauma (Turner’s hypoplasia).
 Ingestion of chemicals (chiefly fluoride called mottled enamel).
 Idiopathic causes.
 Treatment includes veneers for teeth affected by the condition.

MOTTLED ENAMEL
 Occurs due to intake of fluoride-containing drinking water causing
disturbance of ameloblasts during the formative stage.
 Wide range of severity exists in the appearance of mottled teeth:
 Questionable changes characterized by occasional white flecking
or spotting of the enamel.

 Mild changes manifested by white opaque areas involving more of the
tooth surface.
 Moderate and severe changes show pitting and brownish staining of
the tooth surface.

 Corroded appearance of the teeth.
 Teeth which are moderately or severely affected may show a tendency
for wear and even fracture of the enamel.
 Treatment:
 Bleaching of the affected teeth with an agent such as hydrogen
peroxide is frequently effective.
 Procedure must be carried out periodically as the teeth continue to
stain.

EFFECT OF ACID ETCHING
 Acid etching of the enamel surface has become an important
technique in clinical practice.
 Enamel surface is etched with an acid to remove the smear layer on
enamel that was created during cavity preparation, making the
relatively smooth enamel surface pitted and irregular.
 When a composite resin is placed on this irregular surface, it can
achieve mechanical bonding with the enamel.

 Depending on the crystal orientation to the surface, three types of
etching patterns are produced.
 The most common is type I, characterized by preferential removal of
rods.
 In type II pattern, the interrod crystals are preferentially removed.

 Occurring less frequently is type III, which is irregular and
indiscriminate.
 Phenomenon of acid etchants producing differing surface patterns is
still debatable.
 Most commonly held view is that the etching pattern depends on
crystal orientation.

ENAMEL RENAL GINGIVAL SYNDROME
 First described by MacGibbon in 1972.
 Extremely rare disorder characterized by an autosomal recessive
pattern featuring:
 Severe enamel hypoplasia.
 Intrapulpal calcification.
 Failed tooth eruption.
 Nephrocalcinosis.
 Suggestive cause: Mutation in gene FAM20A.

CONCLUSION
 Enamel is the hardest calcified tissue in the human body that covers
anatomic crown of the tooth.
 Cells responsible for enamel formation are the ameloblasts.
 Enamel is an important structural entity and its protection is of utmost
importance.
 Aspire to inspire before you expire!

Enamel

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