The document provides an in-depth overview of enamel, detailing its physical and chemical properties, structural components, and development stages. It emphasizes the significance of enamel's hardness and unique composition, describing the processes involved in its formation and maturation, as well as clinical implications such as susceptibility to decay. Additionally, it addresses various structural features like enamel rods, lamellae, and tufts, and highlights their roles in dental health and disease.

1. ENAMEL
DR. SARGAM R. PARATE , 1ST YEAR PG
DEPARTMENT OF CONSERVATIVE DENTISTRY AND ENDODONTICS.
BHABHA COLLEGE OF DENTAL SCIENCES , BHOPAL.

2.  INTRODUCTION
 PHYSICAL PROPERTIES
 CHEMICAL PROPERTIES
 STRUCTURE OF ENAMEL
 DEVELOPMENT OF ENAMEL
 AGE CHANGES IN ENAMEL
 CLINICAL IMPLICATIONS
 DEFECTS IN ENAMEL
• EPITHETIAL ENAMEL ORGAN
• AMELOGENESIS
• LIFE CYCLE OF AMELOBLASTS
CONTENTS

3. INTRODUCTION
 Enamel is the hardest substance in the
human body .
 Highly mineralized structure present as
the outer most covering of the crown.
 Epithelial derived hard tissue ,formed by
ameloblasts which cannot reform itself.
 Origin - Ectodermal
 Non-vital , acellular , avascular.

4.  Modulus of elasticity – Higher
 Hardness – 296 KHN
 Specific gravity -2.8
 Density – 2.8-3.0 gm/sq.cm
 Non –electrical conductive material
(Insulator at RTM)
 Brittle
 Translucent tissue
 Colour : Yellowish white – grayish white
 Thickness varies
 Semi-permeable membrane
PHYSICAL
PROPERTIES

5. Enamel
Inorganic
96%
Hydroxyapetite
Crystalline calcium
phosphate
Ca10 (Po4 )6 (OH4)2
Hexagonal crystals
Enamel matrix protein
Proline
Histidine
Glutamine
Leucine
Organic
+ Water
4%
Amelogenins
90%
Hydrophobhic
Non-amelogenins
10%
Enamel matrix protein
Glycine
Aspartic acid
Serine
Eg : Enamelin,Ameloblastin,
Tuftelin
CHEMICAL PROPERTIES

6. FIG : Structure of Hydroxyapatite crystal

7. STRUCTURE OF ENAMEL
 Enamel lamellae
 Enamel tufts
 Dentinoenamel Junction
 Enamel spindles.
 Enamel rods
 Incremental lines
 Hunter –Schreger bands
 Gnarled enamel
 Surface structures
 Enamel cuticle

8. ENAMEL RODS
 Enamel consists of enamel rods, prisms or
interprismatic sheaths.
 No.of rods :
5 million – Mand lateral incisor
12 million – Max first molar
 Torturous course from DEJ to outer surface
 Length is greater than thickness – oblique direction
 Dimensions :
Diameter – 4 um
Breadth – 5 um
Length – 9 um
Fig : Enamel rod

9. SUBMICROSCOPIC STRUCTURE
Cross
-section
Fish -scales
Light microscope – hexagonal / round /
Confocal laser scanning microscope– Keyhole
/paddle shaped
Fig : KEYHOLE SHAPED STRUCTURE

10. ULTRASTRUCTURE
Fig : CRYSTAL ORIENTATION SHOWING ENAMEL
BODY AND TAIL
Fig : ULTRASTRICTURE OF ENAMEL ROD

11. DIRECTION OF ENAMEL RODS
 Directions of rods :
• Right angle to the dentin surface.
• Horizontal – cervical part of deciduous
teeth.
• Oblique –middle third of the crown
• Vertical – cusp tips
Fig : Direction of enamel rods

12. CLINICAL SIGNIFICANCE
 Unsupported enamel rods should not be left
at cavity margins – soon break and produce
leakage.
 Bacteria lodge in spaces -initiation of
secondary dental caries.
 Uneven dissolution of enamel rods to get
pitted and irregular surface increases
mechanical bonding with enamel in
composites and pit-fissure sealants.
 Beveling- increase surface area – more no. of
enamel rods exposed – more retention. Fig: Unsupported and supported enamel

13. INCREMENTAL LINES OF RETZIUS
 Ground section : Brownish bands
 Represents incremental deposition of
enamel i.e. successive apposition during
formation of enamel layers.
 Longitudinal section – surrounds tip of the
dentin
 Transverse section – concentric circles.
 Directions :
Cervically – Run obliquely
DEJ-Surface – deviate occlusally Fig : Incremental lines of Retzius

14. Fig : Longitudinal Fig : Transverse section
Fig: Longitudinal and
Transverse section

15. CLINICAL SIGNIFICANCE
 Lines become prominent during carious attack.
 Reflect variations in structure and mineralization
during growth.
 Helps in chronological mapping of dental
development.

16. STRIATIONS
 Dark transverse lines seen crossing the
enamel giving striated appearance to
enamel rods.
 Represents daily increments of growth
during enamel formation.
 Rate of enamel formation : 4 um
Fig: Cross-striations of Enamel rod

17. HUNTER-SCHREGER BANDS
 Alternating dark and light bands seen in
longitudinal section under oblique reflected
light.
 Optical phenomenon caused due to change in
direction of enamel rods.
 Found in inner 2/3rd of enamel starting from DEJ.
 Prisms when cut :
Longitudinally – Dark bands – Diazones
Transversely - light bands - Parazones
 Angle b/w parazones and diazones – 40 degrees.
Fig : Hunter-schreger bands

18. GNARLED ENAMEL
 Optical appearance near the dentin ,in the
region of cusps / incisal edge , bundles of rods
seem to interwine more irregularly when seen in
cut section .
FIG: Gnarled enamel

19. SURFACE STRUCTURES
 PRISMLESS ENAMEL
 PERIKYMATA
 ENAMEL ROD ENDS
 PITS
 CAPS
 ENAMEL BROCHS
 CRACKS
 NEO-NATAL LINE
Fig : Different surface structures of enamel

20. PRISMLESS ENAMEL
 Structure less layer of enamel .
 30 um thick
 Seen in 70% permanent and all deciduous
teeth.
 Commonly seen – cervical areas
least seen - cusp tips
Fig : A. Prism less enamel , B. Prismatic enamel

21. PERIKYMATA
 Transverse wave like grooves.
 External manifestation of Striae of Retzius.
 Parallel to each other and to CEJ.
 CEJ- 30 perikymata /mm
occlusal /incisal edge – 10 perikymata /mm
 Absent - occlusal part of primary teeth
present – postnatal cervical areas.
Fig: Perikymata

22. ENAMEL ROD ENDS
 Circular depressions
 Shallowest – cervical region
Deepest – incisal / occlusal edges
CLINICAL SIGNIFICANCE :
Contribute to adherence of plaque which
result to caries attack
Fig : Enamel rod ends

23. PITS
 Small depressions on enamel
surface.
 Diameter – 1-1.5 um
 Represent ends of ameloblasts
ENAMEL CAPS
 Small elevations on enamel
surface.
 Diameter – 10-15 um
 Caused due to enamel deposition
on non-mineralizable debris.
ENAMEL BROCHS
 Large enamel elevations .
 Diameter - > 10-15 um

24. CRACKS
 Narrow fissure-like structures seen on all
surfaces.
 Outer edges of enamel lamellae .
 Disappear on decalcification.
 Right angle to DEJ.
Fig: Cracks on enamel surface

25. NEONATAL LINE OR RING
 Accentuated incremental line of Retzius.
 Boundary b/w pre-natal and post-natal
enamel.
 Result of abrupt change in the nutrition of
newborn infant.
 Usually seen in deciduous teeth and
permanent first molars.
Fig: Neo-natal line

26. ENAMEL CUTICLE
 Nasmyth’s membrane / primary enamel cuticle ,
delicate membrane covers entire crown of newly
erupted tooth , soon removed by mastication.
 Secreted after epithelial enamel organ retracts from
cervical region during tooth formation.
 Function: protects the enamel surface from
resorptive activity of adjacent vascular tissue.
Fig : Enamel cuticle

27. ENAMEL LAMALLAE
 Thin leaf-like hypocalcified structures.
 Extend from enamel surface – DEJ
 Develops in planes of tension during enamel
maturation .
 Best visualized – Transverse section
 CLINICAL SIGNIFICANCE –
Can act as pathways for caries producing
bacteria.
Fig: B. Enamel lamellae

28. TYPES OF LAMALLAE Based on contents
of lamellae
TYPE A
Only enamel
Poorly calcified rod
segments
TYPE B
May reach dentin
Degenerated cells
TYPE C
May reach dentin
Organic matter
from saliva
More common

29. ENAMEL TUFTS
 Arise at DEJ – enamel to about 1/5th -1/3rd
of its thickness.
 Consists of hypocalcified enamel rods and
interprismatic substances.
 Consists of highest enamel protein
concentration.
 According to TENCATES , Develop due to
abrupt change in the direction of group of
rods that arise from DEJ.
 Best visualized – Transverse section
Fig : Enamel tufts

30. DENTINOENAMEL JUNCTION
 DEJ is scalloped with convexity directed
towards dentin.
 Also k/as Amelo-dentinal junction.
Fig : Dentinoenamel junction

31. CLINICAL SIGNIFICANCE
 Scalloping increases the surface area of enamel.
 Lateral spread of dental caries.
 Stress distribution and resist enamel crack propagation.
 In some pathological condition DEJ becomes flat and enamel get chipped off
easily.
1. Dentinogenesis imperfecta
2. Ehler-Danlos Syndrome
Fig : Dentinoenamel junction

32. ENAMEL SPINDLES
 Thickened odontoblastic processes passing
across DEJ to enamel.
 Appears dark in transmitted light when seen in
ground section.
 Commonly seen – cusp region (crowding of
odontoblast occur)
 Best visualized – longitudinal section
 CLINICAL SIGNIFICANCE :
Sudden sensitivity occurs during cavity
preparation as bur reaches DEJ
Fig : Enamel Spindles

33. DEVELOPMENT
OF ENAMEL
EPITHETIAL ENAMEL ORGAN
LIFE CYCLE OF
AMELOGENESIS

34. EPITHELIAL ENAMEL ORGAN
 Enamel organ, also known as the dental organ, is a
cellular aggregation seen in a developing tooth.
 Function :
 Formation of enamel
 Initiation of dentin formation,
 Establishment of the shape of a tooth's crown
 Establishment of the DEJ.
 Originate from stratified epithelium of primitive oral
cavity.
Fig : Enamel organ

35. EPITHELIAL ENAMEL ORGAN
CONSISTS OF FOUR LAYERS :
 Outer enamel epithelium
 Stellate reticulum
 Stratum intermedium
 Inner enamel epithelium
Fig : Epithelial Enamel Organ

36.  In Early stages of development of enamel
organ ,OEE has single layer of cuboidal
cells , separated from dental sac by delicate
basement membrane.
 Prior to formation of hard tissue , regular
arrangement of OEE is maintained only at
cervical parts of enamel organ.
 At highest convexity of organ , OEE cells are
irregular in shape
 During enamel formation ,OEE cells develop
villi, cytoplasmic vesicles and mitochondria
for active transport of materials.
 Forms the middle part of enamel organ.
 Star shaped, with long processes
reaching all directions from central
body.
 Connected to each other and to stratum
intermedium by desmosomes.
 Function : act as buffer against physical
forces that might distort developing
DEJ.
 Reduced in thickness after first layer of
dentin is laid.
OUTER ENAMEL EPITHETIUM (OEE) STELLATE RETICULUM

37. INNER ENAMEL EPITHELIUM (IEE)
STRATUM INTERMEDIUM
 Situated between stellate reticulum and
inner enamel epithelium.
 Flat to cuboid in shape , arranged in 1-3
layers.
 Connected to each other and to
neighbouring cells by desmosomes.
 Function : believed , role in production of
enamel itself through control of fluid
diffusion in and out of ameloblasts
 Show mitotic division even after cells of
IEE cease to divide.
 Derived from basal cell layer of oral
epithelium.
 Columnar shape.
 Differentiate into ameloblasts to produce
enamel matrix.
Fig : showing OEE &IEE

38. CERVICAL LOOP
 Location on an enamel organ in
a developing tooth where the outer
enamel epithelium and the inner enamel
epithelium join.
 During root formation the inner layers of
epithelium disappear and only the basal
layers are left creating Hertwig's epithelial
root sheath (HERS).
FIG : Cervical Loop

39. LIFE CYCLE OF
AMELOBLAST
According to Function :

40. Fig: Life cycle of Ameloblast

41. MORPHOGENIC STAGE
 Stage determine morphology of the crown and DEJ.
 Cells are short and columnar
 Large oval nuclei -fill the cell body.
 Golgi apparatus and centrioles -proximal end of
cells
mitochondria –dispersed in cytoplasm
 During ameloblast differentiation terminal bars
appear , migrating the mitochondria to basal region
of cell.
 IEE is separated from C.T of dental papilla by
delicate basal lamina.
Fig: Morphogenic Stage

42. ORGANIZING STAGE
 IEE interact with adjacent C.T which differentiate
into odontoblasts.
 Change in the appearance of IEE cells occur-
longer , nucleus free –zone at distal ends .
 Reversal of polarity – migration of Golgi
apparatus and centrioles from proximal ends to
distal ends.
 Clear cell free zone b/w IEE and dental papilla
disappear , due to elongation of epithelial cells
towards papilla.
 Epithelial cells come in close contact with C.T of
pulp differentiate into odontoblasts.
Fig : Organizing Stage

43.  Pre-ameloblast secrete proteins- play role
in epithelial mesenchymal interaction.
 Terminal phase – formation of dentin by
odontoblasts begins.
 When dentin forms , original source of
nourishment of ameloblast cuts off – then
supplied by capillaries .
Fig : Organizing Stage

44. FORMATIVE STAGE
 Ameloblast enter formative stage after first
layer of dentin is formed.
 Presence of dentin necessary for the beginning
of enamel matrix formation.
 During formation of enamel matrix :
Ameloblast –retain same length and
arrangement.
Cytoplasmic inclusion and organelles – change
in organization and number.
 Earliest change –development of blunt cell
processes on ameloblast , which penetrate
basal lamina and enter predentin.
Fig : Formative Stage

45. MATURATIVE STAGE
 Enamel maturation occurs after most of the
thickness of enamel matrix is formed in occlusal
/incisal area.
 At cervical area the enamel matrix formation is
still progressing.
 Stratum intermedium cells –lose cuboidal shape
and regular arrangement , converts into spindle
shape.
 Ameloblasts – reduced in length and attached
to enamel matrix. They display microvilli at
distal extremities .
 Cytoplasmic vacuoles contains materials
resembling enamel matrix.
 These structures indicate resorptive function of
these cells.
Fig : Maturative Stage

46. PROTECTIVE STAGE
 When enamel is fully developed , fully
calcified – ameloblast is present as well-
defined layer and cease to get differentiated
from startum intermedium and OEE .
 Cells form stratified epithelial covering of
enamel k/as Reduced enamel epithelium.
 Function : protecting mature enamel by
separating from C.T until tooth erupts.
 If C.T comes in contact with enamel ,
anomalies develop .Enamel may either get
resorbed or may get covered by cementum.
Fig: Reduced enamel epithelium

47. DESMOLYTIC STAGE
 REE proliferates and induce atrophy of C.T
separating it from OEE , so that fusion of
two epithelia occur.
 Epithelial cells elaborates enzymes –
capable of destroying C.T fibers by
desmolysis.
 Premature degeneration of REE may
prevent eruption of tooth.
Fig : Fusion of OEE & IEE

48. AMELOGENESIS
Amelogenesi
Organic
formation
Mineralizatio
 Enamel formation.
 Begins at Late bell stage of
tooth development.
 Formation begins as soon as
IEE &OEE differentiate.

49. Stages of
Amelogenesis
PRESECRETORY STAGE
MORPHOGENIC PHASE
DIFFERENCIATION PHASE
SECRETORY STAGE
MATURATION STAGE
TRANSITIONAL PHASE
MATURATION PROPER
UNDER ELECTRON MICROSCOPY

50. Fig : Stages of Amelogenesis

51. PRESECRETORY STAGE
MORPHOGENIC PHASE :
 Shape of crown is determined.
 Low columnar cells with centrally located
nucleus and poorly developed Golgi
bodies, mitochondria are scattered
throughout cell.
 First junctional complex develop (
ameloblasts near St. intermedium)
DIFFERENCIATION PHASE:
 Cells of IEE become tall columnar and
nucleus shifts towards St. intermedium.
 Increase in RER and Golgi bodies shift
distally.
 Second junctional complex develop(b/w
tome’s process towards enamel)
 Development of tome’s processes occur.

52. FORMATION OF TOME’S PROCESSES
Projection of ameloblast
enamel matrix - Tome’s
processes.
Initially only proximal
is formed.
After initial layer of
deposition , distal portion
formed.
Fig : Formation of Tome’s Processes

53. SECRETORY STAGE
Formation
secretory
globules
Golgi bodies are
surrounded by
cisternae of RER
mRNA are
translated into
ribosomes of
RNA enters RER
and enamel
proteins are
secreted.
Proteins are
bounded to
membrane
bound secretory
granules.
Secretory
granules are
migrated into
Tome’s
processes.

54. ENAMEL FORMATION
Ameloblasts deposit
secretory globules via
Tome’s process
Interdigitation with
dentin. Enamel without
rods are formed.
Distal portion of Tomes
formed by elongation
of ameloblasts
Proximal part starts to
secrete enamel proteins
for interrod formation.
Distal part lays down
enamel.
Enamel and interrod
made of same material
but differ in direction
of deposition.
As ameloblasts lay
down enamel at the
end they lose their
distal part and there is
no more interrod.
Sandwiched prismatic
enamel between non
prismatic enamel
formed.

55. Fig : Enamel Formation

56. MATURATION STAGE
 Before tooth erupts in the oral
cavity, enamel hardens by the
process of maturation.
 Takes place at the expense of
enamel fluid and matrix proteins.
 During this stage ameloblats are
called pre-secretory cells (secrete
min amount of ameloblastin and
amelogenin)
TRANSITIONAL
Transformation of
ameloblast into post
secretory cells.
Decrease in cell
organelle , cell
size,apoptosis.
MATURATION
Bulk removal of water
and organic material.
Introduction of ruffled
border and smooth
ended ameloblasts for
incorporation of
inorganic content.

57. SMOOTH BORDER
• Causes balancing
of pH.
• Distal junctions
tight and leaking
proximal
• No membrane
calcium ATP ,
contains only
proteins.
• Constitute 20% of
cell life
RUFFLED BORDER
• Prepares acidic
environment for
enamel
• Calcium binding
proteins,
lysosomes,
adenosine
triphosphates
present.
• Constitute 80% of
cell life.

58. MINERALIZATION
2
STAGE
MINERALIZATIO
70%
Maturation
30%
Immediate partial

59. Immediate partial
mineralization
Occurs in matrix segments and
interprismatic enamel
Apatite crystals of dentin –
nucleation – enamel is laid.
Initial mineral – octacalcium
phosphate (unstable)
Hydroxyapatite
1 unit HA -> 2 unit HA Fig : Immediate partial mineralization

60. Maturation
(gradual completion of
mineralization)
Process starts – height
of crown – cervically
Begins before enamel
matrix has reached full
thickness.
Apatite crystals increases in
thickness
Size – 1.5-25 microns
Tuftelin –nucleation of
enamel crystals.
Other proteins – inhibit
enamel deposition.
Rate – 4 um / day
1 layer of enamel – 1mm
thickness – 240 days
Permanent teeth > deciduous
teeth
Crystal size increases
after tooth eruption –
ionic exchange with
saliva
After formation of
enamel
Ameloblast – apoptosis
Enamel formation
ceases.

61. FIG: Mineralization in molar from
occlusal to cervical region
Fig : Maturation stage of mineralization

62. AGE CHANGES
IN ENAMEL
ATTRITION
• Wear facets seen in older people
• Loss of vertical dimension of
crown and flattening of proximal
contour.
DISCOLOURATION
• Teeth darken with age.
• Addition of organic
material / deepening of
dentin colour.
PERMEABILITY
• Teeth become less
permeable.
• With age pores diminishes
as crystals acquire more
ions.
MODIFICATION OF
SURFACE
• Generalized loss of
enamel rods.
• Slower flattening of
perikymata later
disappear completely.

63. CLINICAL IMPLICATIONS
DENTAL FLOURIDATIO
ACID ETCHING
TECHNIQUE
BLEACHING

64. DENTAL CARIES
 Destruction of enamel surface with acid, lead
to the dissolution of enamel matrix, following
carious attack.
 Caries preferentially attack cores of rods and
more permeable striae of Retzius – promote
lateral spread of caries and undermining
adjacent enamel.
Fig : Dental caries

65. FLOURIDATION
 Incorporation of fluoride ions make
hydroxyapatite crystals more resistant to
carious attack.
 Decreases rate of demineralization.
 Increases rate of remineralisation.
Fig : Fluoride Application

66. ACID ETCHING TECHNIQUE
 Removes plaque , debris and thin layer of
enamel.
 By dissolving minerals in enamel, etchants
can remove outer 10 um of enamel
surface, and makes a porous layer of 5-50
um deep into enamel.
 Increases porosity through dissolution of
crystals.
 Helps in mechanical bonding of
composites to enamel surface.
Fig : Acid etching technique

67. BLEACHING
 Lightening of colour of tooth through the
application of chemical agent helps in
oxidizing the organic pigmentation of
enamel.
Fig : Bleaching of teeth

68. DEFECTS IN ENAMEL
GENETIC
 Amelogenesis Imperfecta
1. Hypoplastic (Type 1)
2. Hypomaturation (Type 2)
3. Hypocalcified (Type 3)
NON –GENETIC
 Dental caries
 Attrition
 Abrasion
 Abfraction
 Erosion
 Localised non-hereditary enamel
hypoplasia
 Localised non-hereditary enamel hypo
calcification.
 Fluorosis

69. SR.
NO
DISEASE DEFECT CLINICAL FEATURE PICTURE
1. AMELOGENESIS IMPERFECTA Defect in gene encoding enamel
matrix protein.
Type 1- Hypo plastic AI • Defect in formation of
matrix protein
• Ameloblast fail to lay down
sufficient matrix
• Enamel – pitted, grooved,
thin ,hard translucent
• Small teeth with open
contacts.
Type 2-Hypomaturation AI • Defect in maturation stage. • Enamel softer and chips off
easily.
• Mottled brown -yellow
white
Type 3-Hypocalcified AI • Defect in calcification stage. • Most common
• Enamel – normal thickness,
easily lost by attrition.
• Dull , lustrous, honey
colored , stains easily.
GENETIC DEFECT

70. SR.NO DISEASE DEFECT PICTURE
1. Dental caries Demineralization of inorganic part and
destruction of organic substance .
2. Attrition Loss of tooth structure from direct
frictional forces.
3. Abrasion Mechanical wear other than mastication
4. Abfraction Caused by forces placed on teeth during
biting, eating, chewing .
NON-GENETIC DEFECT IN ENAMEL

71. SR.NO DISEASE DEFECT PICTURE
5. Erosion Dissolution of mineralized tooth
structure by chemical process.
6. Localized non hereditary enamel hypoplasia Defect in ameloblasts during
formation stage.
7. Localized non hereditary enamel hypo
calcification
Defect in mineralization stage.
8. Fluorosis • Hypo mineralization of enamel
caused due to excessive ingestion
of fluoride during enamel
formation.