Enamel the basic!

ENAMEL-
THE BASIC
D R S H R E Y A S I N G H
1 S T Y E A R P G T
D E P A R T M E N T O F P E D I A T R I C A N D P R E V E N T I V E D E N T I S T R Y

CONTENTS
• INTRODUCTION
• ORIGIN
• PHYSICAL CHARACTERISTICS
• CHEMICAL CHARACTERISTICS
• AGE CHANGES
• CLINICAL CONSIDERATIONS
• DEFECTS IN ENAMEL
• ENAMEL REGENERATION
• NEWER ADVANCES
• TAKE HOME MESSAGE
• REFERENCES

H A R D E S T
B I O L O G I C A L T I S S U E
I N T H E B O D Y !
The anatomic crown of a tooth is covered by
acellular , avascular , highly mineralized material
known as ENAMEL.

DIFFERENCES BETWEEN PRIMARY
AND PERMANENT TEETH ENAMEL.

E N A M E L I S D E R I V E D
F R O M A G E R M A N
W O R D
“ S M E L Z A N ” M E A N I N G
D I F F I C U LT T O M E LT.
ORIGIN
• Hipprocates (460–370)
• Blake (1801) called enamel the ‘cortex
striatus’ because it was composed of
innumerable fibres.
• Classified teeth as bones but realised
that teeth differed from bone by being
harder.
Reference: Trenouth M; the origin of terms of enamel
FACULTY OF DENTAL JOURNAL 2014:5(1)

PRIMARY
EPITHELIAL
BAND
DEVELOPMENT OF ENAMEL
At about 6th week of development,
certain areas of basal cells of oral
ectoderm proliferate at a more
rapid rate than adjacent areas.
There is condensation of the
mesenchymal tissue and of
capillary network beneath the
proliferating epithelium.
The thickened oral epithelium
invaginates into the mesenchyme to
for PRIMARY EPITHELIAL BAND.
REFERNCE:
Physical characteristics Textbook of oral histology&embryology:Orban Blaint:13th Edition.

by 7th week of IUL the primary
epithelial bend divides into two
processes by invagination of
underlying ectomesenchyme
bucally located is the vestibular
lamina and lingually located is
the dental lamina
the vestibular lamina contributes
to development of teeth and
dental lamina to the development
of teeth.
REFERNCE:
Physical characteristics Textbook of oral histology&embryology:Orban Blaint:13th
Edition.
in the late bell stage by 18th week of
IUL dental hard tissues start to form

Matrix
formation
Mineral-
isation
Enamel
formation

DEVELOPMENT OF ENAMEL
• Ameloblasts are differentiated from inner enamel epithelium.
• Under the inductive influence of ameloblasts, the adjacent cells of dental
papilla are differentiated to odontoblasts which lay down a layer of
dentin along membrana performativa.
• The dentin then induces the ameloblasts to intitate their secretory
activities.
Reciprocal dependence

DENTINOGENESIS
PRECEDES
AMELOGENESIS

LIFE CYCLE OF AMELOBLASTS
Morphogenic
stage
Organising
stage
Formative
stage
Maturative
stage
Protective
stage
desmolytic
stage

MORPHOGENIC STAGE
• 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.
REFERENCE : TENCATE’S ORAL HISTOLOGY 9TH EDITION

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.

ORGANIZING STAGE
• 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
• Ameloblasts enter their formative stage after the first
layer of dentin has been formed.
• 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
• Occurs after most of the thickness of the enamel matrix has
been formed in the occlusal or incisal area.
• The ameloblasts are slightly reduced in length and are
closely attached to enamel matrix.
• Stratum intermedium lose their cuboidal shape and
regular arrangement and assume a spindle shape.
• Ameloblasts display microvilli and cytoplasmic
vacuoles containing material resembling enamel matrix are
present.
• These structures indicate an absorptive function of these
cells.

PROTECTIVE STAGE
• Formation of the reduced enamel
epithelium.
• Its function is of protecting the mature
enamel by separating it from the connective
tissue until the tooth erupts.
REE = IEE +OEE +
SI

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.

LETS
RECAPITULAT
E!

DID YOU KNOW?
• During protective phase, the composition of enamel can still be modified.
• Fluoride can be incorporated into the enamel of an unerupted
tooth!
• In children younger than 6 years fluoride is incorporated into the enamel of permanent
teeth, making the teeth more resistant to the action of bacterial and acids in food.
REFERENCE ;Tapias MA, De Miguel G, Jimenez-Garcia R, Gonzalez A, Dominguez V. Incidence of caries in an
population in Mostoles, Madrid. Evaluation of a preventive program after 7.5 years of follow-up. Int J
Pediatr. 2001;11(6):440–446. [PubMed] [Google Scholar]
THIS MAYBE THE BEST WAY TO PREVENT CAVITIES!!!

PHYSICAL CHARACTERISTICS
THICKNESS DENSITY COLOR HARDNESS
SPECIFIC
GRAVITY
PERMEABILI
TY
SOLUBILITY
REFRACTIVE
INDEX

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 edge at the neck of the the
tooth.
Refernce:The hardness of enamel and dentine. E. Newbrunt and W.Pigman. AustralTrenouthian Dental Journal, August, 1960

HARDNESS
• Hardness of enamel varies from 5-8 moh
• 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.
Refernce:The hardness of enamel and dentine. E. Newbrunt and W.Pigman. AustralTrenouthian Dental Journal,

DENSITY
• It varies from 3 to 2.84gm/ml
• Density decreases from surface to DEJ.
• Permanent teeth are denser than deciduos teeth

COLOUR
• The color of the enamel ranges from yellowish white to greyish white to bluish white.
• It is determined by differences in the translucency of enamel.
• Why is teeth yellow? 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.
Ref: Translucency of Human Dental Enamel R.H.W. Brodbelt et al J DENT RES 1981 60: 1749
Primary teeth are lighter in color, generally bluish white.

WHAT IS OPAQUE ENAMEL
• That means opacity is actually a
hypomineralisation or
hypocalcification defect that
ultimately causes alteration in
translucency of enamel.

REFRACTIVE INDEX
1.62
crystalline
birefringent

BIREFRINGENCE
Double refraction
This is an optical property of a
material.
The refractive index of these
materials depend upon
propagation and polarization of
light passing through it.

DISSOLUTION BY ACIDS IS FASTER IN
DEEPER LEVELS OF ENAMEL
• 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 increases from
dentine towards surface.
Mg
F

PERMEABILITY
• Enamel is selectively permeable.
• It has been found with radioactive tracers that it acts as a semi permeable membrane,
permitting complete or partial passage of certain molecules: like14C-labeled urea.
Ref ;Textbook of oral histology&embryology:Orban Blaint:13th Edition.
SOLUBILITY
•Enamel dissolves in acidic medium.
•The surface enamel is more resistant to dissolution in acidic meidia
than deeper surfaces.
CRITICAL PH 5.5

MODULUS OF ELASTICITY
• Modulus of elasticity is 83 GPa
• High modulus of elasticity and low tensile strength.
• On comparing the mechanical properties of the occlusal surface to the DEJ ,MOE at the
surface is higher than that at the DEJ.
RIGID BRITTLE

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.

CHEMICAL COMPOSITION
Hydroxyapatite
crystals
Ca10(oh)2(po4)
6

ORGANIC COMPOSITION
Enamelins
Amelogenins Proline
Non
amelogeninms
Cross beta
proteins

AMELOGENINS VS NON AMELOGENINS

STRUCTURE OF ENAMEL
ENAMEL RODS
ROD SHEATHS
INTERROD SUBSTANCE

ENAMEL RODS UNDER LIGHT
MICROSCOPE

DEXTROFLEXION AND
SINISTROFLEXION
Groups of rods after leaving DEJ
curve gently to right(dextroflexion)
After following a straight course for
some distance again curve gently
to left (sinistroflexion)
DEJ

•Each enamel rod is tightly packed with
crystallites.
•The mature crystals are ribbon like or
hexagonal with avg size of 1,600A(L)
*300A(B)*900A(W)
•The crystals are arranged parallel to the long
axis of rod head and deviate at about 65
degree in the tail region.
CRYSTALLINE STRUCTURE OF
ENAMEL RODS
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.

DIRECTION OF RODS
Enamel rods in cuspal
eminence

CLINICAL THOUGHT
• 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)

STRIATIONS
Each enamel rod is built up of segments separated
by dark lines that give it a striated appearance . •
The rods are segmented because:
 the enamel matrix is formed in a rhythmic manner
and have an uniform length of about 4 μm.
 These are areas of disturbed calcifications
 Optical effect due to crystalline orientation
 Tertiary curve with periodicity at about 4 μm.

GNARLED ENAMEL Seen in section of enamel in oblique
plane

INTERROD SUBSTANCE
• Rods are semented together by interrod substance.
• Is an extension or the tail of adjacent rod.
• Hypocalcified more of organic substance.

INCREMENTAL LINES OF RETZIUS
• Irregularly shaped.
• Concentric brown lines.
• Runs obliquely across enamel rods.
• Complete an arc in cuspal region but almost
parallel in cervical and middle third region.

PERIKYMATA
• Some incremental lines of Retzius fail to reach the
enamel surface.
• As a result a wave like groove is created on the
external surface.
• These are external manifestations of the line of
retzius.
• 30 in number near CEJ and 10 at incisal edge.

NEONATAL LINES
• Found in all deciduos teeth
and cusp of permanent 1st
molar.
• These are accentuated lines
of Retzius
• Formed due to some
disturbance of birth like
abrupt change in environment
before and after birth.

HUNTER SCHREGER BANDS
• SERIES OF ALTERNATING
LIGHT AND DARK BANDS
• START AT DEJ AND RUN
PERPENDICULAR TO STRIAE OF
RETZIUS
LONGITUDINAL GROUND SECTION IN OBLIQUE REFLECTED LIGHT OPTICAL
PHENOMENON
DIAZONES
PARAZONE
S

ENAMEL TUFTS
•Tasseled or unbraided
projections.
•Extends from DEJ into enamel
upto 1/3rd of its thickness.
•Follow direction of enamel
rods
•Origin controversial

ENAMEL LAMELLAE
• thin, leaf-like structures that extend from the
enamel surface toward the DEJ.
• They consist of organic material
HYPOMINERALISED.
• Lamellae may develop in planes of tension.
• Where rods cross such a plane, a short segment
of the rod may not fully calcify.

TYPES OF ENAMEL LAMELLA
TYPE A
TYPE B
TYPE C
ENAMEL
DENTIN

CLINICAL CONSIDERATION
• 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
resistant to decay.

ENAMEL SPINDLES
• odontoblastic processes of dentine
• cross DEJ and project in enamel
• thickened at end
• formed during formative stage of
amelogenesis
• hypersensitive to pain

SPINDLE
TUFT
LAMELLA
outer surface of enamel
DEJ
DEJ TO OUTER
SURFACE
OUTER
SURFACE TO
DEJ
DEJ TO OUTER
SURFACE

ENAMEL CUTICLE
PRIMARY
ENAMEL
CUTICLE
NASMYTHS
MEMBRANE
=
PEC + REE

PRISMLESS ENAMEL
• Structure less layer of enamel.
• • 20-70 Microns
• newly erupted
• permanent teeth Least – Cusp tips Most – Cervical
area
• crystallites are arranged uni-directionally, parallel to one
another with a relatively higher density.
• Prismless enamel in primary teeth
• In a primary same tooth at different areas it varies in
thickness (5–60micro m) , is the most commonly found
feature in the primary enamel.

ACID ETCHING IN PRIMARY
&PERMANENT TEETH
30sec
etch
30sec
wash
15sec
dry
Reference article by international academy of dental research. 2014
20sec
etch
30sec
wash
15sec
dry
P e r m a n e n t
p
r
i
m
a
r
y

NEWER RECOOMENDATIONS
• ETCHING TIME OF PRIMARY AND PERMANENT TEETH IS SAME!
20sec
etch
30sec
wash
15sec
dry

AGE CHANGES IN ENAMEL
Attrition
Abrasion
Erosion
Abfraction
Caranza Textbook of Periodontology:10th Edition

ATTRITION
• Attrition The physiological wearing of tooth as a result of tooth
to tooth contact.
etiology
Abnormal
occlusion
Habits
Structural
defectsCaranza Textbook of Periodontology:10th Edition

PRESENT ON
OCCLUSAL OR
INCISAL
SURFACES
CALLED
FACETS
SHINY ,
SMOOTH AND
CURVIPLANAR
FACETS BEST
INDICATOR
WHY SHINY?
ENAMEL RODS
GET
FRACTURED &
ARE HIGHLY
REFLECTIVE TO
LIGHT
IN YOUNG
(ABNORMAL
ACTIVITY eg
BRUXISM) VS
OLDER ADULTS
(FUNCTIONAL
WEAR).

Horizontal
facets
Forces directed
along vertical
axis of tooth
Periodontium
adapts
Angular
facets
Forces
directed
laterally
Risk of
damage to
periodontium
Angle of facets and periodontium

ABRASION
• Abrasion Pathological wearing away of tooth substance
through abnormal mechanical process. ( OTHER THAN
MASTICATORY FORCES)
ETILOGY
OCCUPATIONAL
IMPROPER
BRUSHING
TECHNIQUE
HABITS

Saucer shaped or wedge shaped indentations with
smooth and shiny surface.
Starts on exposed cementum surface instead of enamel
and spreads to dentin of root surface.
Horizontal brushing at right angles causes most severe
abrasion.
Abrasion can also take place in incisal edges due to
habits like holding objects.

EROSION: THE DENTO-ALVEOLAR ABLATIONS
• Irreversible loss of tooth substance by
chemical process that does not involve
known bacterial action
• Wedge shaped depression in cervical area
generally facial surface of teeth.
• Long axis of eroded area perpendicular to
long axis of teeth.
• Starts on enamel . Early stages confined to
enamel , cementum and dentin are involved
later
Etiology
forceful frictional
actions between
oral mucosa
and dental hard
tissues
acidic fruits ,
GERD, low ph
of saliva e.t.c.

ABFRACTION
• Acc to Grippo(1991) the pathologic loss of both enamel and dentin
caused by biomechanical loading forces.
• caused by clenching or grinding that causes tooth flexure resulting in
microfractures.
• "v-shaped" notches
• Gingival 3rd of the tooth.

IDENTIFYING THE
WASTING
DISEASES OF
TEETH
LETS CO-RELATE!

erosion
abfraction
abrasionattrition

DEFINITION
• Defined as incomplete or defective formation of organic matrix of enamel.
• Occurs in the formative stage of amelogenesis.
• 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 dentition is involved or sometimes
even a single tooth and both enamel and dentin are affected.

FACTORS ASSOCIATED WITH
ENVIRONMENTAL TYPE
Nutritional
deficiency
exanthematous
disease
Congenital
syphilis
hypocalcemia
Birth injury,
prematurity, Rh
haemolytic
disease
Local infection
or trauma
Ingestion of
chemicals
idiopathic

NUTRITIONAL DEFICIENCY
• Due to deficiency of vitamin A, B & C.
• HORIZONTAL PITTING IS OBSERVED IN TEETH i.e.
THIS IS PITTING TYPE.
• Commonly seen in central and lateral incisors and
cuspids.

EXANTHEMOUS DISEASES
• 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 and first molar.

CONGENITAL SYPHILIS
• 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
Treponema
pallidum
Non pitting type

HYPOCALCEMIA
Vitamin D
deficiency
• And
parathyroid
deficiency.
tetany
• Serum
calcium level
may fall to 6
to 8 mg/100
ml
hypocalcemia • Enamel
hypoplasia

TRAUMATIC 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

INGESTION OF CHEMICALS- FLUORIDE
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.

PATHOGENESIS
High fluoride
Matrix formation stage
Diminished matrix
production
Change in ion
transport
Diminished
withdrawal of
protein.
Maturative
stage
Diminished
withdrawal of water

LOCAL INFECTION OR TRAUMA
• Caused by local infection or trauma and is
called “Turner’s Hypoplasia” and the tooth
is called as Turner’s tooth.
• Site- Maxillary incisors & permanent
premolars Appearance- mild brownish
discoloration of enamel to severe pitting and
irregularity of crown.
Turners hypoplasia

pathogenesis
Local
infection
trauma

Deciduous tooth
becomes carious when
crown of successor
teeth is being formed.
Bacterial infection
goes to periapical
region of
deciduous tooth.
Disturbs the
ameloblastic layer of
permanent teeth.
Results in
hypoplastic
crown.
Trauma to deciduoud
teeth , teeth driven in
alveolus,
infection
trauma

QUESTIONABLE CHANGES
Few white flecks
white spots

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.

AMELOGENESIS IMPERFECTA
• Amelogenesis imperfecta is a group of clinically and
genetically heterogeneous disorders that affect the
development of enamel and result in abnormalities of the
amount, composition, and/or structure of enamel.
• These disorders are caused by mutations in a variety of
genes that are important for enamel formation.
Purely
ectodermal
disorder.
Dentin and
pulp are
normal.

TYPES
Matrix
formation • hypoplastic
Mineralisation • hypocalcification
Maturation • hypomaturation

HYPOPLASTIC TYPE
• INADEQUATE ENAMEL MATRIX FORMATION. ( MATRIX FORMATION EFFECTED)
• Therefore lack of enamel or very thin enamel on newly erupted teeth.
• Eg peg shaped lateral , screw driver shaped central incisors
C/F

R/F
H/F
Disturbance in viability / differentiation of
ameloblasts.
Enamel totally absent if present , is on cusp
tip or proximal surface.

HYPOCALCIFICATION TYPE
• Stage effected is mineralization.
Teeth of normal thickness but very soft can be easily removed by an explorer.
Change in shape of tooth takes place due to persistent fractgures of soft enamel.
C/F
Cheesy in
consistency
!

C/F
H/F
Calcification is altered so enamel now
has the same radiodensity as dentin
making it very difficult to distinguish
the two.
Defect In mineral deposition can be
attributed.

HYPOMATURATION TYPE
• Stage effected is maturation
Enamel is of normal thickness but can be pierced by an explorer under firm
pressure.
C/F
H/F
R/F
Alteration in enamel rod and rod sheath structure.
Same as hypocalcification that is radiodensity is
SAME AS DENTIN

HYPOMATURATION- HYPOPLASTIC
WITH TAURODONTISM
• Enlargement of crown at expense
of roots.
• Dentin and enamel have same
radiodensity.
• Very large pulp chambers.

GENETIC FACTORS
• Amelogenesis imperfecta have shown defective gene linked
to the locus DXS85 at Xp22. • This is also the location for
amelogenin.

PROBLEMS IN AI
Anterior
open bite
caries
Delayed
eruption
Tooth
impaction
Gingival
inflammation

DEMINERALISATION
AND
REMINERALISATION

NEWER ADVANCES
• MOLAR INCISOR HYPOMINERALISATION.
• Defined as “systemic hypomineralization” that affects one or more
permanent first molars with or without permanent incisor involvement.
• It is a qualitative defect of the enamel.
• Other names hypomineralized permanent first molars (PFMs) /
idiopathic enamel hypomineralization / nonfluoride hypomineralization /
dysmineralized PFMs.
MIH

PROBLEMS IN MIH
• Teeth with MIH have porous enamel that easily breaks under masticatory forces.
• Fracture of enamel exposed dentinal tubules high susceptibility towards degradation
hence CARIES
• Intense dentinal sensitivity
• The children affected with MIH are at a risk of developing behavior management
problems and dental fear because of the difficulties in achieving adequate anesthesia.

CHARACTERISTICS OF MIH
• The characteristic feature of MIH is the clear demarcation between
the affected and sound enamel. There is asymmetry of defects
present in the molars and incisors where one molar or incisor can
be severely affected while the contralateral tooth may be clinically
sound or have only minor defects. Rapid dental wear, loss of
enamel, inclination to caries, dentin hypersensitivity, poor esthetics,
anxiety, and tooth loss can occur in the long run.

EAPD CRITERIA FOR MIH DIAGNOSIS.
• All the data were collected and scored using the European Academy of Pediatric
Dentistry (EAPD) criteria for MIH.(2003)
• 0 – Normal
• 1 – Demarcated opacity
• 2 – Posteruptive enamel breakdown
• 3 – Atypical restorations
• 4 – Extracted molar due to MIH
• 5 – Unerupted molar due to MIH.

TREATMENT OF MIH
• Restorative treatments for these hypomineralized teeth present with ten times more
requirement than teeth without this condition. It ranges from prophylactic strategies to
high complexity procedures.
• Restorative treatments for these teeth are challenging for both the patient and the
dentist due to the subclinical inflammation of pulpal cells and the altered porous
enamel structure that makes bonding risky leading to defective and frequent loss of
fillings and frequent retreatments which are painful because of anesthetizing
difficulties.

CHRONOLOGICAL HYPOPLASIA
• Chronological hypoplasia is differentiated from other forms of hypoplasia due to its
characteristic presentation (multiple, symmetrical, chronological pattern).
• Chronological hypoplasias are seen at the time tooth erupts into the oral cavity leading
to several problems like aesthetic problems, tooth sensitivity, caries and early pulpal
involvement.

TAKE HOME MESSAGE
• Knowledge of the magnitude of MIH is desirable as it is vulnerable for consequences such as
rapid caries development, early enamel loss, and sensitivity.
• Failure in treatment occurs due to lack of basic
knowledge.
• Proper understanding of the basics like ENAMEL can
lead to proper DIAGNOSIS hence proper
TREATMENT.

REFERENCES
1. Tencates’s Oral histology :8th Edition(2013)
2. Shafers Textbook of Oral pathology:7th Edition(2012)
3. Textbook of oralpathology –(Brad W.neville)]
4. Textbook of oral pathology-Ghom(Second edition)
5. 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.
6. 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.
7. 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
8. Textbook of oral histology&embryology:Orban Blaint:13th Edition
9. Carranza 10th edition

• 11.Shrestha R, Upadhaya S, Bajracharya M. Prevalence of molar incisor hypomineralisation
among school children in Kavre. Kathmandu Univ Med J (KUMJ) 2014;12:38–42. [PubMed]
[Google Scholar]
• 12. Kirthiga M, Poornima P, Praveen R, Gayathri P, Manju M, Priya M, et al. Prevalence and
severity of molar incisor hypomineralization in children aged 11-16 years of a city in Karnataka,
Davangere. J Indian Soc Pedod Prev Dent. 2015;33:213–7. [PubMed] [Google Scholar]
• 13. Yannam SD, Amarlal D, Rekha CV. Prevalence of molar incisor hypomineralization in school
children aged 8-12 years in Chennai. J Indian Soc Pedod Prev Dent. 2016;34:134–8. [PubMed]
[Google Scholar]
• 14. Krishnan R, Ramesh M. Molar incisor hypomineralisation: A review of its current concepts
and management. SRM J Res Dent Sci. 2014;5:248–52. [Google Scholar]
• 15. Jeremias F, Koruyucu M, Küchler EC, Bayram M, Tuna EB, Deeley K, et al. Genes expressed
in dental enamel development are associated with molar-incisor hypomineralization. Arch Oral
Biol. 2013;58:1434–42. [PMC free article] [PubMed] [Google Scholar]
• 16. William V, Messer LB, Burrow MF. Molar incisor hypomineralization: Review and
recommendations for clinical management. Pediatr Dent. 2006;28:224–32. [PubMed] [Google
Scholar]
• 17. Tadikonda AN, Acharya S, Pentapati KC. Prevalence of molar incisor hypomineralization and
its relation with dental caries in school children of Udupi district, South India. World J Dent.
2015;6:143–6. [Google Scholar]
• 18. Weerheijm KL. Molar incisor hypomineralisation (MIH) Eur J Paediatr Dent. 2003;4:114–20.
[PubMed] [Google Scholar]
• 19. Chellammal MR, Dharman S. Assessment of enamel defects in patients visiting Saveetha
dental college, Chennai: A pilot study. Res J Pharm Biol Chem Sci. 2016;7:995–1001. [Google
Scholar]

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