Enamel clinical aspect sagar hiwale

1. PRESENTATION BY:SAGAR HIWALE
MDS 1
ST
YEAR
DEPARTMENT OF CONSERVATIVE AND ENDODONTICS
JAIPUR DENTAL COLLEGE AND HOSPITAL
PRESENTED ON :4oct 2013

2.  STRUCTURE OF ENAMEL- CLINICAL IMPORTANCE
 CLINICAL CONSIDERATIONS
 ENAMEL DEFECTS
 Carious defects
1. Incipient caries
2. Arrested caries
 Non carious defects
1.Developmental defects:
2. Systemic conditions affecting enamel
3. Regressive defects:
Discolorations
Age changes and clinical consideration
CLINICAL IMPLICATIONS
Fluoridation
Acid etching
Enamel microabrasion
Enamel macroabrasion
CONCLUSION
REFRENCES

3. MINERAL CONTENT
Enamel is the hardest tissue in the human
body. Its mineral portion is approximately 96%
of its weight,the rest is organic components
and water.
The mineral elements include hydroxyapatite
crystals, approximately 0.03μm to 0.2 μm,
surrounded by a thin film of firmly bound
water.
CLINICAL SIGNIFICANCE:-
Poorly mineralized enamel –more white
More mineralized –more translucent.

4. DIRECTION OF RODS
•The rods are oriented at right angles to the dentin
surface.
•In the cervical & central parts of the crown of a
permanent teeth, they are approximately horizontal.
•Near the incisal edge or tip of cusps they change
gradually to an increasingly oblique direction until they
are almost vertical in the region of the edge or tip of the
cusps.
•CLINICAL SIGNIFICANCE:-
•Follow the direction of enamel RODS during cavity
preparation so that enamel margins are supported.
4

5. DIRECTION OF RODS

6. •If the discs are cut in an oblique plane, the bundles of
rods seem to interwine more irregularly.

•Its optical appearance of enamel is called gnarled
enamel.
•CLINICAL SIGNIFICANCE:-
•This enamel is not subject to cleavage as regular
enamel.
•This enamel does not yield readily to pressure of hand
cutting instruments.

8. HUNTER-SHREGAR BANDS
Site: Anterior tooth- Incisal surface
Posterior tooth- Cervical region
Importance: Distribute and dissipate impact forces.

9. ENAMEL TUFTS
These projections arise in Dentine and extend into
enamel in the direction of long axis of crown,
hence may play a role in spread of caries.

10. ENAMEL LAMELLAE
Contains mostly organic material which is WEAK
AREA, therefore predisposes tooth to entry of
bacteria ,hence dental caries..

11. Perikymata :-
 Transverse wave like grooves appear to be the Transverse wave like grooves appear to be the
external manifestations of external manifestations of striae of retziusstriae of retzius..
Continuous around the tooth and parallel to each Continuous around the tooth and parallel to each
other and to the CEJ.other and to the CEJ.
Seen in freshly erupted teeth or in tooth which is Seen in freshly erupted teeth or in tooth which is
not subjected to abrasive forces.not subjected to abrasive forces.
Average of Average of 30 perikymata/mm30 perikymata/mm in cervical region in cervical region
and and 10/mm10/mm in occlusal region. in occlusal region.
These may contribute to adherance of
plaque material which results in caries.

12. Perikymata

13. NASMYTH’S MEMBRANE
Covers newly erupted tooth.
Membrane replaced by pellicle.
Microbes invade pellicle to form
plaque.
ENAMEL PEARLS
Occasionally found on root surface
towards cervical margin.
Importance: Predisposed to plaque
accumulation following gingival
recession.

14. They – act as
bacterial/ food traps

thickness of enamel

predispose tooth to
caries.
Fissure

15. CLINICAL
CONSIDERATION

16. Dental caries
Definition:
dental caries is defined as a multifactorial ,
transmissible ,infectious oral disease caused
primarily by the complex interaction of cariogenic
oral flora with fermentable dietary carbohydrates
on the tooth surface over time.
Sturdevant 6
th
edition

17. Demineralization occurs as follows

18. Definition
White opaque chalky spots observed when the
tooth surface is desiccated are termed as
incipient caries Sturdevant 4
th
edition
Radiographically seen as faint radiolucency
Chalky white spot

19. Definition:
Caries which becomes static or stationary and doesn't
show any tendency for further progression
Clinically intact ,discolored ( black or brown spots )
ARRESTED CARIES

20. Translucent zone
Dark zone
Body of the lesion
Surface zone

21. For an ideal enamel wall , following are
the Noy’s structural requirements-
1) The enamel wall must rest on sound dentine
and all carious dentine must be removed

22. 2)Enamel which forms cavosurface angle must have
their inner ends resting on sound dentin

23. 3) The rods which form cavosurface angle must be
supported on sound dentine and their outer ends
must be covered by restorative material (possibly by
giving a bevel)

24. 4) Cavosurface angle must be beveled so that the
margins will not be exposed to injury in condensing
restorative material against it.

25. 1)Amelogenesis Imperfecta-
Hereditary defect of enamel
Ectodermal disturbance
Genes causing Amelogenesis Imperfecta:
•AMELX (5% cases)
•ENAM (most cases)
•MMP20
•KLK

26. o Defective matrix formation.
oEnamel has not formed to full normal thickness

Hypoplastic type
Hypocalcified type
oEnamel is so soft that it can be removed by a
prophylaxis instrument.
oDefective mineralization of formed matrix
Hypomaturation type
oImmature Enamel crystals
oDefective enamel can be pierced by an explorer
point under firm pressure

27. 1) Small teeth with short root
2) Open contact
General features of Amelogenesis
Imperfecta

28. 3) Discoloration ranging from
yellow to dark brown.
4)Thin enamel
5)Enamel could look wrinkled
6)Delay in eruption
7)Occlusal surfaces and incisal edges severely
abraded
8)Sensitivity

29. 1.Enamel may be totally absent
2.Appear as thin layer, chiefly over the tips of the
cusps and the interproximal surfaces.
3. Same radiodensity as dentin , it become
difficult to differentiate between two
Radiographic features

30. Treatment
1)Full veneering
2)Selective odontotomy esthetically reshaping the
teeth.

31. II)Enamel
Hypoplasia
Incomplete or defective formation of the organic
matrix
Causes:
1.Nutritional defect
2.Exanthametous diseases
3.Congenital syphilis
4.Ingestion of fluoride

32. 1) Hutchinsons incisors
(screw driver shaped central incisors)
2) Mulberry molars
(small globular masses of enamel on occlusal surface)
Hypoplasia due to syphilis

33. Treatment
•Selective odontotomy and esthetic reshaping of the
tooth enamel
•Metallic restorations
•Bleaching

34. Tetracycline
Generalized type of intrinsic stain
 When the tetracycline is administered during
the time of enamel formation it forms a
complex chelating compound with the organic
and inorganic components of the enamel. The
created compound is very stable.
Discoloration depends upon:
Dosage
Length of time over which administration occurred
Form of tetracycline

35. According to Moffitt:
Critical period for tetracycline induced
discoloration in deciduous dentition
• 4 months in utero to 3 months postpartum
(maxillary and mandibular incisors)
• 5 months in utero to 9 months postpartum
(maxillary and mandibular canines)
In permanent dentition
•3-5 months postpartum to 7 yrs of age

36. Discoloration varies from yellow –orange to dark blue
Drugs:
Chlortetracycline –grayish stains
Minocycline –grayish discoloration
Oxytetracycline –yellow stains

37.  Treatment
Conservative methods:
I.Bleaching
I.Microabrasion
II.Macroabrasion
III.Veneering

38. Fluorosis
Generalized intrinsic stain
Chronic ingestion of flouride ions interfers with
ameloblast function during formative stage of
tooth development and disturb their activity

39. Clinical features
1)Mild changes
• White flecking or spotting of
enamel
2)Moderate to severe changes
•Brown staining of surface
•Pitting
•Tendency of enamel to fracture

40.  Treatment
Conservative methods:
I.Bleaching
I.Microabrasion
II.Macroabrasion
III.Veneering

41. Discoloration:
Can occur due to
Extrinsic factors:
1.Tobacco/tea stains
2.Poor oral hygiene
3.Food colors
4.Gingival bleeding
5.Existing restorations
6.Chromogenic bacteria
Intrinsic factors:
1.Caries.
2. Fluorosis.
3. Tetracycline and other drugs.
4. Age changes.
5. Non vital teeth
6. Internal resorption.
7. Hereditary disorders.

42. DISCOLORATION

43. EXTRINSIC DISCOLORATIONS
Avoidance of the foods and beverages that cause stains
Using proper tooth brushing and flossing techniques
Professional tooth cleaning: Some extrinsic stains may
be removed with ultrasonic cleaning , enamel
microabrasion, enamel macroabrasion
INTRINSIC DISCOLORATIONS
Bleaching
Enamel microabrasion
Enamel macroabrasion
Veneering

44. Definition:
Surface tooth structure loss resulting from
direct frictional forces between contacting teeth
. (Marzouk 1
st
edi)
Types of Attrition
1.Occluding surface attrition
2.Proximal surface attrition
Causes
1. Tooth to tooth contact
2.Parafunctional mandibular movements

45. Clinical features
1.Sensitivity
2.Flattening of incisal and occlusal surface
3.Flattening of inclined planes
4.Flattening of proximal contact areas
5.Facet formation
6.Reverse cusp
7.Loss of vertical dimension of teeth
8.Decay at occluding areas
9.Angular chelitis
10.Cheek bite
11.Temporo mandibular problems
Flattening of incisal

46. Treatment
1.Para functional activities should be controlled
with protecting occlusal splints.
2.Endodontic therapy for pulpally involved teeth
3.Occlusal equilibration, by selective grinding of
tooth surfaces
4.Restorative modalities(only metallic restoration)

48. Abrasion
Definition:
Surface loss of tooth structure resulting from
direct friction forces between teeth and
external objects, or from frictional forces
between contacting teeth components in the
presence of an abrasive medium.
Causes
1.Improper use of tooth brush
2.Improper use of tooth pick and dental floss
3.Habitual opening of bobby pins with teeth.
4.Use of abrasive dentifrices
Marzouk 1
st
edition

49. Clinical features
1.Linear in outline(following path of brush bristles)
2.Angular peripheries
3.Notching of central incisors
4.Wedge shaped ditch on proximal
exposed root surface

50. Treatment
1.Diagnosing the cause
2.Removing the causative factor(habits)
3.Desensitizing exposed dentin(if tooth is
sensitive)
4. Restorative treatment

52. Definition
Loss of tooth structure resulting from chemico-
mechanical acts in the absence of specific
microorganisms Marzouk 1
st
edition
Causes
1.Ingested acid(lemon and citrus fruits)
2.Chronic vomiting
3.Frequent regurgitation
Rate of erosion is 1micron per day
Erosion

53. Clinical features
1.Shallow, broad, smooth ,highly polished,
scooped out depression on the enamel surface
adjacent to cementoenameljunction
2.Confined to gingival third of labial surface

54. Treatment
1.Complete analysis of diet, chronic vomiting,
environmental factors should be performed
2.Restorative treatment
(tooth colored material can be used with
minimal or no tooth preparation)

56. Abfraction
Definition:
Strong eccentric occlusal force resulting in
microfractures at the cervical area of tooth causing
wedge shaped defects
Sturdevant 6
th
edition
Causes
Heavy force in eccentric occlusion
Clinical feature
Wedge shape defect
Defect has smooth surface
Treatment
Restoration

58. Age changes & Clinical considerations
•Attrition is seen in aged people.
•Wear facets are common.
•Decrease in vertical dimension and flattening of
proximal contours.
•Color changes with age.
•Permeability decreases.
•Caries incidence is less in aged people.
•Surface composition: more amount of fluoride and
localized increase in nitrogen.

60. Fluoridation
It decreases the solubility of enamel
 It acts in the following way:
I.Forms fluoroapatite which is less soluble than
hydroxyapatite
II.Inhibits demineralization
III.Enhances remineralization
IV.Inhibits bacterial metabolism

61. Acid etching
ACID ETCHING TECHNIQUE- Buonocore in 1955
 Micromechanical bonding b/w enamel and resin
based restorative material.
Mode of action-
 Increases the porosity of exposed surfaces by
dissolution of crystals - creates a micro porous
layer from 5 to 50 µm deep

62. Three etching patterns predominate:-
(Preferential removal of rods)
TYPE II
TYPE III
(Junction b/w type 1 n type 2)
(Preferential dissolution of prism
core)
TYPE I

63.  Enamel etching transforms the smooth enamel
surface into an irregular surface

 Etched enamel has high surface energy
(72 dynes\cm) allow resin to wet the tooth surface
better when resin penetrates into micro porosities
and polymerized to forms resin tags

64. Resin tags interlocked with
the surface irregularities
created by etching which
form mechanical bond to
enamel.
Bond strength:16-20Mpa

65. Originally recommended 60 secs using 37% phosphoric
acid.
Currently,etching time for most etching gel is 15 sec
Aprismatic enamel requires double the etching time
required by prismatic
Etching time

66. Involves the surface dissolution of enamel by acid
along with the abrasiveness of the pumice to remove
superficial stains or defects

Commercially developed system for enamel
microabrasion.
[PREMA (Premier enamel micro abrasion)
Enamel microabrasion
In 1984 Mc Closkey reported this technique
In1986 Croll and cavanaugh modified this technique

67. PREMA contains a reduced concentration of
hydrochloric acid (approx 11%)+ silicon carbide
particles in a water soluble gel paste.
Mode of action
1.Physical removal of stained outer enamel layer by
stripping action of acid and abrasive action of
pumice
2.The etching action removes interprismatic
substance and changes light refraction
characteristics
3.There is oxidation of some pigments

68. Procedure

69. Removal of localized superficial white spots and other
surface stains or defects is called macroabrasion
Sturdevant 6
th
edition
12 fluted composite finishing bur or fine grit finishing
diamond in a high speed handpiece is used
Macro abrasion

70. Procedure

71. CONCLUSION
Enamel is an important structural entity of the tooth
hence its protection is utmost important.
Its function is to form a resistant covering of the
teeth, rendering them suitable for mastication.

72.  Marzouk : Operative Dentistry, First Edition
Orban :Oral Histology and Embryology,Tenth
Edition
Oral pathology SHAFER’S
Sturdevant :Art and Science of Operative
Dentistry, Fifth and sixth Edition
Ten Cates: Oral Histology , Seventh Edition
Enamel microabrasion,theodore p croll