Bleaching materials and techniques, complications

Bleaching materials and techniques, complications

2. •Introduction
•Classification – Neville’s
- Cohen’s
- Ingle’s
•Bleaching – definition
- MA
- indications & contra indication
- historical back ground
- classification

3. •Vital bleaching & its techniques
•Non vital bleaching & its techniques
•Methods
•Adverse effects

4. Classification -Neville
Extrinsic staining :
a) Tobacco - Black or brown
b) Coffee, tea, cola - Brown or Black
c) Chromogenic bacteria - Brown, Black,
Green or Orange

5. Intrinsic discolorations
•Aging - Yellow –Brown, Less translucency
•Death of the pulp - Gray-black
•Fluorosis -White, Yellow-Brown, Brown,
mottled
•TC -Yellow-brown
•Internal resorption – Pink tooth of mummery

6. •Calcific metamorphosis – yellow
•Dentinogenesis imperfecta – Blue-gray
•Amelogenesis imperfecta – yellow-brown

7. CLASSIFICATION OF
DISCOLORATION
I – EXTRINSIC STAINS
II – INTRINSIC STAINS
A)PRE-ERUPTIVE
B) POST-ERUPTIVE

8. I – EXTRINSIC STAINS
1.Metallic stains:
Cu – Green
K.Permangnate – Violet-black
AgNo
3
– Grey
SnF
2 - Golden brown
Fe – Black

9. •Non metallic stains :
- Dietary compounds
- Beverages
- Tobacco
- Mouth rinses - Chlorhexidine
- Chromogenic bacteria in children
- Medicaments

10. •Mechanism of staining with CHX:
1. earlier- break down of CHX into
Parachloraniline
- 2.CHX may reduce bacterial activity such
that partly metabolized sugars were
broken down & degraded over time to
produce brown compound.

11. •Recent –
1.Non-enzymatic browning reaction
2. Formation of pigmented sulfides of iron
& tin
3. precipitation of dietary chromogens by
CHX.

12. II – INTRINSIC STAINS
A)Pre-eruptive
B)Post-eruptive

13. Pre eruptive:
1.Alkaptonuria
– incomplete metabolism of tyrosine &
phenylalanine-build up of homogentisic acid –
- brown .

14. 2. Congenital erythropoietic porphyria
- error in porphyrin metabolism leads
to accumulation of porphyrins.
- red-brown

15. 3.Congenital hyperbilirubinaemia
-break down products of hemolysis
-large hemosiderin pigment realeased &
discolours dentin
-yellow-green
4.High fever-banding type
5.Thalassemia & Sickle cell anaemia -
Blue, Brown, green

16. 4.Amelogenesis imperfecta
• hereditary, enamel formation is disturbed with
regard to mineralization or matrix formation.
•14 sub types.
•Majority of them inherited as autosomal
dominant / x-linked
• mild hypo mature snow capped enamel to the
severe yellow to yellow-brown

17. 5.Systemic syndromes: defects in enamel
formation
- vitamin D dependent rickets,
- Epidermolysis bullosa
- Hypo parathyroidism
- Ehlers-Danlos syndrome
- Epidermolysis bullosa-pitting of
enamel due to vesiculation of
ameloblast layer.

18. 6.Dentinogenesis imperfecta
( hereditary opalescent dentine)
•Genetical /environmental.
•Bluish / brown –opalescence on
transillumination.

19. Fluorosis / Mottled enamel
• Drinking water with > 2 ppm
• Severity depends on intensity &
length of exposure.
• Hypo mineralized porous
enamel surface.
Rx: bleaching preceding
bonding.
3
rd
month of gestation –
8 years of age.

20. •7.dentin dysplasia – amber translucency-
brown discoloration.
•8.Tetracycline staining: tooth shade depends
on
- type ,
- Pt’s age at the time of administration
- Duration of uptake
•Bilateral
•Continuous or laid down in strips
•Incorporates both in enamel & dentin (mainly
dentin)

21. •MA: binds with HA of enamel & dentin
forms tetracycline orthophosphates
•it should be avoided from 4 months inutero to
7 years of age.
•Yellowish / brown-grey appearance worsens
on eruption & diminishes with time.
•Yellow tetracycline staining slowly darkens to
brown or gray-brown when exposed to
sunlight.

22. TYPE OF TETRACYCLINE

Chlortetracycline- grey-brown .
Dimethylchlortetracycline – yellow stain.
Doxycycline– does not cause staining.
Oxytetracycline – yellow stain.
Tetracycline –– yellow stain.

23. According to severity (Jordan & Boksman)
a) First degree discoloration:
Light yellow, light browns, light gray and
occur uniformly throughout the crown,
without banding.
b) Second Degree Discoloration:
More intense but without banding.

24. c) Third Degree Discoloration:
Very intense with clinical crown
exhibiting horizontal color banding. Most
seen at the cervical regions.
d) Fourth degree - too dark

25. •repeated exposure to sunlight-reddish
purple oxidation by product
•Natural photo oxidation.

26. •Treatment
1.Bleaching the external enamel surface
2.Intracoronal bleaching following
intentional R.C.T
•Minocycline discoloration:
- Grey color
- chelates with iron.
- drug laid in 2ry dentin & re-
secreted in saliva.

27. Erythroblastosis faetalis
•Rh incompatibility
•Green-brown discoloration

28. B) POST-ERUPTIVE
•Trauma
•Primary & Secondary caries
•Dental restorative material
•Ageing
•Smoking
•Chemicals
•Some food stuffs (long term use causes
deeper intrinsic staining)

29. Pulpal
hemorrhage
Pink spot
Enamel hypoplasia

30. Treatment planning
Bleaching
• In-office
• At Home
• Combination
Non VitalVital
• In-office
• Walking bleach
• Combination
Non Bleaching
• Microabrasion
• Macroabrasion
• Bonding partial coverage
• Full labial coverage
• Full coverage crowns

32. Causes of discoloration
•

33. WHY WHITEN TEETH ?
•Youthful appearance;
•Changing jobs;
•Getting married;
•Improving self-esteem

34. Lightening of the color of the tooth
through the application of a chemical
agent to oxidize the organic
pigmentation in the tooth.
- Sturdevent

35. Mechanism of action
•Unclear.
•Bleaching agents usually oxidizers,
usually act on the organic structure of
the hard tissues, slowly degrading them
into chemical by products such as co
2
which is lighter in color.
•Redox reaction. Unstable peroxides
convert into unstable free radicals.

36. •A) 2 H
2O
2 ---- 2H
2O + 0
2
•Using heat & light (Photo dissociation)
•0
2------ 0
.
(weak free radical)
•B) with highpH & accelerator
• (anionic dissociation)
•H
2O
2 ---- H0
2 + 0

37. Historical background
•Oxalic acids –Chappel,1987
•H
2O
2 - Harlan, 1884
•Chlorine – Taft & Atkinson, 1989
•Heated H
2O
2 –Pearson,1950
•Walking bleach –Mac Spadder- 1961
•ModificationWalking bleach - Nutting &
Poe
•Night guard bleach – Haywood & Hayman,
1989 H
2O
2

38. •Whitening tooth paste & enzyme based
dentrifrices – Rembrandt, 1992
•ADA – 1994
•Light activated bleaching- 1994
•Argon, CO
2 laser & plasma arc light
activation - 1994-97
•Diode laser - 1999

39. Universal bleaching guidelines
( Ronald A. Feinman)
•Comprehensive clinical examination
•Full mouth radiograph
•Photograph
•Evaluation of existing restorations &
pathology
•Prophylaxis with pumice
•Use of rubber dam, eye wear & glove
•No anaesthesia
•Constant patient monitoring

40. •free radicals are involved in various
physiological & pathological
consequences in proteins, lipids &
nucleic acids.
•Leads to degenerative disorders
•Cytotoxicity directly related t peroxide
concentration.
•Daily exposure to CP should not exceed
10mg /kg in a 70 kg human
- Dahl & Beeher

41. Indications
•Generalized staining;
•Ageing;
•Smoking and dietary stains such as those
of tea and coffee;
•Fluorosis;
•Tetracycline staining;
•Traumatic pulpal changes.

42. Contra-indications
•Patient’s high expectations’
•Decay and peri-apical lesions;
•Pregnancy;
•Sensitivity, cracks and exposed dentine;
•Existing crowns or large restorations in the
smile zone;
•Elderly patients with visible recession and
yellow roots.

43. Techniques
•Vital bleaching – 3 types
a) In office bleaching
b) Home bleaching
c) Combination
•Non vital bleaching – 3 types
a) In-office
b) Walking bleach
c) Combination

44. •In office bleaching : 4 methods
i) Bleaching alone (chemical)
ii) Light activated
iii) Thermo catalytic
iv) Laser activated - Argon
- CO
2 laser
- Diode

45. Bleaching materials
• Superoxol (30-35% H
2O
2 )
•Sodium perborate
•Carbamide peroxide (urea peroxide)

46. Superoxol
•30-35% H
2O
2
•Clear,colourless fluid
•pH-9.5 - 10.8
•Free radicals & perhydroxyl anions
•Indicated –in office vital & non vital
bleaching

47. Sodium perborate
•Releases 9.9% of available oxygen.
•Types- monohydrate,
trihydrate,
tetra hydrate
•Mixed with water, saline or H
2O
2
•Indicated in intracoronal bleaching

48. Carbamide peroxide
•5-15% available.
•10% cp pH 5-6.5
•Breaks down in to urea,NH
3
, H
2
O
2

•Thickening agents - carbopol (water soluble poly
acrylic acid polymer)
•glycerol ,propylene glycol, sodium stannate,
citric acid.
•Indicated – in Night guard vital bleaching

49. Vital Bleaching
Indication-
- mild-moderate discoloration.
-1
st
& 2
nd
degree of TC discoloration
Contraindications-
-tooth hypersensitivity
- opaque & white spots
- dark stains

50. - Restored tooth with laminates & ceramics
-Uncooperative patient attitude
-Allergic to bleaching agents
•Rome was
not
constructe
d in a day

51. •Carbamide peroxide,
hydrogen peroxide
gels on polyethylene
strips (White strips
[Procter and Gamble,
Cincinnati, Ohio,
USA])

52. Tc-In-office
vital bleach

53. THERMOCATALYTIC
BLEACHING
•2 METHODS:
- Electrical heating unit
- Bleaching light
•Thermobleaching:
30% H
2O
2 + heating enamel surface
with heat lamp or electrical device

54. •Photo bleaching:
- U.V rays used
- Keep light 13 inches from tooth

55. •Adverse effects:
a) post-operative pain
b) Pulpal damage
c) hard tissue damage
d) mucosal damage

56. Advantages:
• usage of caustic chemicals under
dentists control
• soft tissue protection possible
•Rapid bleaching take place
Disadvantages:
•Cost
•Unpredictable out come
•Discomfort of rubber dam
•Chair side time

57. Power bleaching
•In-office tooth whitening with a xenon
plasma arc or a laser
•Goal : to obtain controlled temperature
elevation of H
2
O
2
or dumping high
energy protons to pump H
2O
2
up to high
vibrational state

58. Review of light sources
•Conventional bleaching light
•Tungsten-Halogen curing light
•Xenon plasma arc light
•Laser: a) Argon laser
b) Diode laser ( 980 nm GaAlAs): ultra
fast. no heat
c)CO
2

59. Dentist prescribed Night Guard
Vital Bleaching (NGVB)
•Matrix bleaching
•3-7% H
2O
2
or 5-15% CP
•Available oxygen in 10% Cp-3% H
2O
2
•Vaccum formed soft mouth guard is
used

60. Indications
•Superficial enamel stains
•Mild yellow discolorations
•Brown fluorosis stains
•Age related discolorations
Disadvantages:
- tooth hypersensitivity
- opaque & white spots
- dark stains
- Bruxism

61. •Treatment time:
4-8 weeks for night time bleaching and 2-4
weeks for day time regime of multiple
application

64. Complications:
a) Transient effects:
Tooth sensitivity
Altered enamel morphology
Reduced bonding
Effect on restoration
Gingival tissue irritation
Pulpal damage
Occlusal disturbances

65. •ii) Potential major long term / systemic
damage:
as an oxidant H
2O
2
causes
carcinogenicity,
genotoxicity,
cytotoxicity,
aging,
lung injury
-Soft tissue injuries like gastric irritation, sore
throat

66. Wahls modification of NGB
•Used to bleach single endodontically
treated tooth
•Preformed plastic crown

67. Mc Innes technique
•Recommended by grossman for fluorosis
•Solution: 5 parts 30% H
2O
2, 5 parts 36%
HCl ,1 part diethyl ether.
•Modified Mc Innes technique:
HCl substituted with NaOH

68. Pulpal response to vital bleach
•Reiter et al
10% CP for 6 weeks was safe for
the pulp up to 10 years postoperatively.
- if minor inflammatory changes can be
reversible by fluoride application.
J Esthet Restor Dent 14:275, 2002

69. NON VITAL BLEACHING

70. Paint-on -dam

71. Modified power bleach technique

73. Adverse effect
•External cervical resorption
•Prevent by placing barrier: place the
barrier & contour it to follow the out line of
CEJ and about 1mm incisal to it.
•barrier should be minimum of 2mm
thickness.

74. Inside / Out side bleaching
•Settembrini
•Modified by Liebenberg

75. Adverse effects
•External cervical resorption
•Chemical repair
•Damage to the restoration
•Apical tissue irritation

76. Intentional RCT + Intra coronal
bleaching

78. y

80. Brown stain

81. White spot

86. Current bleaching solution
•Custom made trays / 1 size fits all the trays.
• H
2O
2 gels on polyethylene strips.
•Disposable trays pre filled with 9% gel.
•Non peroxide bleaching solutions-
Opelescence SP