MECHANISM OF TOOTH STAINING

Color pigments (Chromophores) ---- attached organic tissues

( interprismatic sites and fissures ) ---- chemical binding of their hydroxyl
and amino groups.

In addition - these pigmented substances and calcium ions forms new

molecules - varying in size and optical effect.

Eg: Tea- quercetin ( 5 hydroxyl groups)

Endogenous route - pigmented groups (eg hydroquinone) – complex with

ca ions & collagen - attached to dentin.

Metal oxides- Exo or Endo route attached to dental tissues.

Natural tooth staining can be classified in several ways:

•According to stain origin ( external or internal)

•According to color

•According to pathological or non pathological nature.

 IATROGENIC

- Dentist or physician therapy

- Dietary, environmental, habitual or age related factors.

Discoloration can be associated with Enamel, Dentin, Pulp or a combination.

DISCOLORATION ASSOCIATED WITH PULPAL INVOLVEMENT.

Intrapulpal Hemorrhage

Reddish tinge – grey brown

 ENAMEL AND DENTIN DISCOLORATION

Developmental defects in Enamel Formation.

ENAMEL HYPOPLASIA
Incomplete or defective formation of the organic enamel matrix of teeth.

2 Basic types

Hereditary type Environmental factors

AMELOGENESIS IMPERFECTA
 AMELOGENESIS IMPERFECTA
(Hereditary Enamel dysplasia; Hereditary Brown Enamel; Hereditary Brown
Opalescent Teeth)

Complicated group of conditions – developmental alterations structure of enamel-

absence of systemic disorder.

HYPOPLASTIC

3 BASIC TYPES
HYPOCALCIFIED

HYPOMATURATION
HYPOPLASTIC
 HYPOCALCIFIED

White & opaque or brownish orange

HYPOMATURATION
 Environmental Hypoplasia

3. Nutritional deficiency (vitamins A,C and D)

4. Childhood illness ( Jaundice, Porphyria etc)
5. Congenital syphilis
6. Hypocalcemia
7. Birth injury, prematurity, Rh hemolytic disease
8. Local infection or trauma
9. Ingestion of chemicals ( eg flouride)
10. Idiopathic causes

Types of Env Hypoplasia- Mild, Moderate & severe

Mild Environmental Hypoplasia

Small grooves, pits or fissures

 Moderate Environmental Hypoplasia

Rows deep pits arranged horizontally – single or multiple

 Severe Environmental Hypoplasia

Hypoplasia – injury during the formative stage of enamel.

FLUROSIS
1ppm - < Caries
>1ppm – Mottled enamel
>3ppm – Severe enamel hypoplasia

Deans Classification:
MO – Questionable changes
M1 – Very mild changes- occ white
spots or flecks
M2 – Mild changes – white spots or
flecks – whole tooth surface
M3A – Moderate changes – white
spots or flecks with corroded
appearance
M3B – Severe changes – Brown
staining
 DEFECTS IN DENTIN FORMATION

DENTINOGENESIS IMPERFECTA
(Hereditary Opalescent Dentin, Odontogenesis imperfecta)
Only Mesodermal portion affected

Shields classification
Type I - DI in families with OI (AD)
Type II - DI never with OI (AD)
Type III - Brandywine Type (AD)

Gray – brownish Violet or yellowish brown – characteristic translucent or opalescent hue.

Enamel lost early – absence of interlocking with dentin – rapid attrition

Type III – ‘Shell teeth’

 SYSTEMIC MEDICATIONS
TERACYCLINE FAMILY

1948 – Rx respiratory illness, ear infections and Acne Vulgaris

Still used – cystic fibrosis & Rocky Mountain Spotted fever

Mechanism 2 Theories

• Joining tertracycline molecule with calcium thru chelation – incorporation

into hydroxylapatite crystal during mineralization stage
• Binding tretracycline to tooth structure by metalorganic matrix
combination of tetracycline complex.
Primarily deposited in dentin.
Yellow tooth changes - brown or gray –brown
Postulated: tetracycline hydroxylapatite on photoxidation – red quinone
product (4-α,12α anhydro-4-oxo-4dedimethylaminotetracycline) (AODTC)
Continued photoxidation – bleaching of red quinione.
 First degree stains:
Light yellow, brown or gray – uniform clinical
crown; No banding

Second degree stains:

More intense , No banding

Third degree stains:

Stains intense, Horizontal color banding.

Hue and severity depends on 4 factors

2. Age at the time of administration
3. Duration of administration
4. Dosage
5. Type of tetracycline
A. Chlortetracycline: Gray-brown
B. Dimethylchlortetracycline,
Oxytetracycline, tetracycline: Yellow
 EXTRINSIC DISCOLORATION

Variety of factors
3. Bacterial stains
4. Diet related stains
5. Gingival Hemorrhage
6. Tobacco
7. Chlorhexidine
8. Poor oral hygiene
9. Metallic stains

Iron stain
 AGE RELATED DISCOLORATION

DENTAL CARIES RESTORATIVE MATERIALS

Greenish grey - amalgam

SYSTEMIC DISORDERS
Hyperbilirubinemia

Erythropoietic porphyria
 TREATMENT MODALITIES

In office : Power Bleach

• Bleaching Home : Night Guard Bleach

Walking Bleach

• Microabrasion

• Macroabrasion

• Veneers

• Jacket crown.
 BLEACHING
The lightening of the color of a tooth through the application of a chemical agent to
oxidize the organic pigmentation in the tooth

HISTORY
 1ST century roman physicians – brushing teeth with particular Portuguese urine
whitened teeth
 1300’s most requested dental treatment after extraction was tooth whitening
 14th century – Guy De Chauliac – cleaned teeth with honey & burnt salt with vinegar
 Barber surgeons – after abrading teeth with coarse metal files would apply
“aquafortis”- continued to 18th century
 1848 – Dwinelle- non vital tooth bleaching with chloride of lime
 1861 - ‘Kingsbury’ – potassium cyanide for amalgam stains
 1864 - ‘Truman’ – chlorine from calcium hypochloride & acetic acid for non-vital
bleaching
 1868 – Latimer- bleaching of vital tooth
 1877 – Chapple – oxalic acid & HCL acid
1884 – Harlan – 1st use Hydrogen peroxide
1888 – Taft – calcium hypochlorite
1889 – Krick EC – Sulphorous acid ( reducing agent)
1892 – Atkinson – pyrozone/Ether Peroxide (25% sol H2O2 in ether
1893 – Sodium Peroxide
Once hydrogen peroxide became established as the most effective solution, the major
advances focussed on ways to facilitate the absorption of bleaching agent.
1895 – Garreston – chlorine to bleach Nonvital teeth
1911 – Rosental – U-V waves
1916 – Walter Kaine – fluorosed teeth using muriatic acid(18%HCL)
1918 – Abbot – introduced instrument to speed chemical reaction by raising temp
1937 – combination 5 parts H2O2 with one part ether & heat
1958 – Pearson – Superoxol sealed pulp chamber for 3 days
1967 – Nutting & Poe – “walking bleach” technique - superoxol in pulp chamber
1989 – Munro – stabilized solution of carbamyl peroxide
1994 – over the counter unsupervised home bleaching kits – 6%H2O2
BLEACHING MATERIALS

1st generation – liquid form, did not remain in tray for long, req frequent replishment
2nd generation – viscous & gel form , prevents leaching out and soft tissue irritation
3rd generation – differ vehicle & color, more patient friendly.

DIFFERENT BLEACHING AGENTS:

Hydrogen Peroxide
Superoxol
Cabarmide peroxide
Sodium perborate
McInnes solution.
 CONTRAINDICATIONS FOR BLEACHING

3. Teeth with opaque white spots

4. Dentin hypersensitivity
severe attrition, erosion, abrasion or abfraction – exposure of DEJ – office bleaching with
isolation possible
• Generalized dental caries or leaking restorations.
• Heavily restored teeth
• Teeth slated for bonded restorations or orthodontic bracketing.
• Suspected or confirmed cases of Bulimia.
• Patient selection
emotional or psychological problems or unrealistic goals
12. Case selection
will bleaching improve the esthetics?
9. Pregnancy, lactating mothers & children
 CHEMISTRY OF BLEACHING

Work by oxidation – Organic materials CO2 + H2O

“Oxidation - reduction reaction” or redox reaction
Oxidizing agent – free radicals – gives it up – becomes reduced
Reducing agent – accepts the electrons – becomes oxidized.
 CHEMISTRY OF HYDROGEN PEROXIDE

H2O2 – strong oxidizing agent through the formation of free radicals, reactive oxygen
molecules and hydrogen peroxide anions (Cotton & Wikinson 1972)

At acidic pH At basic pH

The optimum pH is 9.5 to 10.8

In the presence of decomposition catalysts and enzymes

2H2O2 2H2O + O2
These enzymes- present in mouth-body’s defense against O2 toxicity
Hence imp dry teeth and free of debris
 BLEACHING MECHANISM.

• Hydrogen peroxide diffuses thru organic matrix of enamel and dentin.

• Radicals have unpaired electrons – extremely electrophilic and unstable- attack
most organic molecules- achieve stability.
• Radicals react with unsaturated bonds- results in disruption of electron
conjugation and change in absorption energy of the organic mol.
• Simpler molecules – reflects less light formed- whitening action.
 CARBAMIDE PEROXIDE CHEMISTRY
( Urea Peroxide)

Composition:
•Hydrogen peroxide stabilized in glycerol sol & coupled with urea [CO(NH2)2-H2O2 ]
•10% carbamide peroxide 6.4% urea + 3.6% H2O2
•Urea further decomposed to CO2 & ammonia
•High pH ammonia facilitates bleaching procedure (Sun 2000)
( basic sol lower activation energy is required for free radical formation)
 FACTORS THAT AFFECT BLEACHING

• Surface debridement
thorough scaling & polishing must performed

5. Hydrogen peroxide concentration.

higher the conc- greater the oxidation; highest being 35%

7. Temperature
increase of 10% doubles the rate of reaction

9. pH
acidic pH to extend shelf life, optimum pH 9.5 to 10.8

11.Time
effect of bleach directly related to time of exposure

13.Sealed environment
sealed env increases bleaching efficiency.
 BLEACHING OF VITAL TOOTH
2. In-office bleaching
3. Home bleaching

FOUR DIFFERENT APPROACHES Barghi (1998):

(1) DENTIST ADMINISTERED
high conc H2O2 ( 35 to 50%) or CP ( 35 to 40%),
often supplemented with a heat source

(2) DENTIST SUPERVISED

bleaching tray - high conc CP ( 35 to 40%) –
30 min to 2 hrs while the patient is in the dental office

(3) DENTIST PROVIDED

known as "at-home" or "night-guard" bleaching
administered by the patient - 5 to 22% solution of CP with custom-made tray;

(4) OVER THE COUNTER PRODUCTS

often based on CP OR H2O2 of various conc & placed in a pre-fabricated tray,
or by the recently introduced strips (Gerlach, 2000)
HIGH CONC BLEACHING AGENTS SHOULD:
•Have a conc range of 20-50%
•Take the form of a gel, preferably prepared just before use

METHODS OF ACTIVATING PEROXIDES

• by light
• by heat
• chemically
AVAILABLE LIGHT SOURCES

1. Conventional Bleaching Light

Lamp – 12-14 inches for 20-30 mins.
Supplied energy to H2O2 by adding heat – vigorous release oxygen
Slow & Uncomfortable

2. Tungsten Halogen Curing Light

provides heat & activates light sensitive chemicals
time consuming process (40-60 sec per tooth)

3. Xenon Plasma Arc

Non laser high intensity, produces high heat – stimulates catalyst
brief 3 sec periods- great potential for thermal trauma to pulp and tissues

4. Argon Laser
stimulates catalyst , no thermal effect.
less dehydartion of enamel & rebound effect
rapid treatment time 10 sec per tooth.

5. Diode Laser Light

true laser, produces no heat, 3-5 sec to activate bleaching agent.
 IN OFFICE BLEACHING OF VITAL TEETH: STEP BY STEP GUIDELINES

3. Pretreatment photographs / shade matching - baseline data,

Teeth cleaned surface stains and plaque
2. Isolate and protect teeth and mouth.

Waxed dental floss, nonmetallic clamps, guaze saturated with cold water to protect lips
 PROCEDURE

• Place gauze saturated with bleaching agent or mini brush

• Position the bleaching light

• Keep gauze continually wet with bleaching
agent – time depends upon material – 15mins- 30
mins

• Remove gauze, flush with warm water

FINISHING

• Polish with yellow banded aluminum oxide abrasive disks and wheels( shofu cosmetic
contouring kit)
•For sensitivity – 1.1% neutral sodium fluoride gel.
•After last treatment polish with yellow & white rotary polishing wheel - high enamel
luster
•Severe sensitivity – nonsteroidal anti-inflammatory tablets.

NUMBER OF APPOINTMENTS
•Vary from case to case, teeth stained by coffee, tea, flurosis or aging – 1 or 2 appts.
•Severe stains like tetracycline – 3 or more visits
•Yellow or yellow-brown easier to remove than gray
•Incisal portion – bleached quickly than cervical portions (thinner dentin and thicker
enamel)
 NIGHT GUARD VITAL BLEACHING
( Home bleaching, matrix bleaching, mouth guard bleaching, dentist
prescribed/home-applied bleaching)

Technique involves application of a mild bleaching agent to the teeth through

the wearing of custom made, vacuum-formed appliance.
10% carbamide peroxide is recommended.

Carbamide peroxide
1st world war – inflammatory antiseptic , 2nd world war – trench mouth & wound
debrtidement
1960’s- Klusmier – tooth lightening using Glyoxide given to assist post
traumatic tissue healing
Clinical reports of tooth lightening during gingivitis treatment stimulated its use
for tooth lightening
1st reported in literature – Haywood & Heymann 1989
CONSTITUENTS OF BLEACHING GELS

Carbamide peroxide
Hydrogen peroxide
Thickening agent: Carbopol (polyacrylic acid polymer)
enhance viscosity and delays break down on contact with saliva
Urea:
stabilizes H2O2, elevated pH of solution
Vechicle: Glycerin, dentrifice, glycol
Glycerin – enhances viscosity and ease of manipuilation
Surfactant and pigment Dispersers:
Surfactant – wetting agent – allows H2O2 diffuse tooth boundary
pigment dispersers keeps pigments in suspension
Preservatives: Phosphoric acid, citric acid or sodium stannate
provides durability and stability
Flavourings
FEATURES OF HOME BLEACHING

•Lower conc of carbamide peroxide and H2O2

•Less rapid color change
•Use of custom fabricated tray
•No rubber dam
•Fewer office visits
•Less sensitivity

ADVANTAGES

•Relative ease of application

•Lower cost
•Availabilty to all socio economic classes of pts
•High percentage of successful treatments

CONTRAINDICATIONS
Same as others
DELIVERY METYHODS

3. Custom trays with reservoirs

4. Foam lined tray
thin guard material lined on one side with foam –
advocated with materials without carbapol
6. Boil and form guards
7. All foam stock trays
8. Bleaching tooth pastes
9. Bleaching varnishes (brush on)
10. Bleaching strips

Two basic regimen for application

13. Night time application
usually takes 2-6 weeks optimal results
2. Daytime use
30 mins to 2 hrs – replenished- not exceeding 12
hrs
FABRICATION OF BLEACHING TRAYS
NIGHT GUARD WITH ‘WINDOW DESIGN’
 EFFICACY AND ESTHETIC RESULTS

It is generally advocated that most teeth are susceptible to bleaching,

provided that the treatment is carried out for a sufficiently long time (
Haywood, 1996; Goldstein, 1997; Heymann, 1997; Dunn, 1998; Leonard, 1998).

Night-guard vital bleaching - 6 wks (10% CP), 92% lightening of the treated teeth (
Haywood et al., 1994).

10% CP - 43% perceived their tooth color as stable 10 yrs after bleaching (Ritter et al., 2002)

10% CP nightly 2 wks- on an average, 8 units lighter on the Vita shade guide, (Swift et al.
, 1999). follow-up- darkened 2 units on shade guide - occurred during the first 6 months

20% CP- lighter teeth than with 7.5% H202 - evaluated immediately at termination 14-day
at-home bleaching procedure (Mokhlis et al., 2000). However, no difference was observed 10
wks later.

Bleaching strips – 30mins 2 daily – 5 unit shade change - (Gerlach et al., 2001)

Bleaching strips and 10% CP in trays, bleaching strips more efficient (Sagel et al., 2002),
 LOCAL SIDE-EFFECTS

Tooth sensitivity

Tooth sensitivity is a common side-effect of external tooth bleaching (Tam, 1999)

•10% CP - 15 to 65% of the patients reported increased tooth sensitivity (Haywood et al., 1994;
Schulte et al., 1994; Leonard et al., 1997; Tam, 1999).

• Higher incidence of tooth sensitivity (from 67 to 78%) after in-office bleaching with H202
in combination with heat (Cohen and Chase, 1979; Nathanson and Parra, 1987).
• sensitivity persists for up to 4 days after the cessation of bleaching treatment (
Cohen and Chase, 1979; Schulte et al., 1994),

•longer duration of up to 39 days has been reported (Leonard et al., 1997; Tam, 1999).
•sensitivity to cold and intermittent spontaneous pain lasting up to one day after treatment (
Cohen and Chase, 1979)
•The mechanisms that would account for the tooth sensitivity after external tooth bleaching
have not yet been fully established.

•In vitro -peroxide penetrated enamel and dentin and entered the pulp chamber (Thitinanthapan
et al., 1999),

•in vivo -dogs indicated that H2O2 alone or with heat caused alterations in odontoblasts and
deposition of dentin (Seale et al., 1981).

•penetration of restored teeth - higher than that of intact teeth (Gökay et al., 2000).

•amount of peroxide detected in the pulp chamber related to the concentration of hydrogen
peroxide in the preparations applied (Gökay et al., 2000),

• also varied among different brands of bleaching agents with the same declared
concentration of carbamide peroxide (Thitinanthapan et al., 1999).
•Structural pulp damage not observed in human premolars exposed to 35% hydrogen
peroxide in vivo and observed up to 30 days (Cohen and Chase, 1979; Robertson and Melfi, 1980;
Baumgartner et al., 1983).

•The longest exposure was three times for 30 min each even with heat (Cohen and Chase, 1979
), Robertson and Melfi, 1980).

•Histological evaluation of the human pulp after vital bleaching overnight with 10% CP -
mild inflammatory changes in 4 out of 12 teeth after both 4 and 14 days’ treatment, and
no inflammation after "recovery" phase of 14 days (González-Ochoa, 2002).
•Hemorrhage and inflammation - after bleaching, pulpal changes reversed 60 days after
the treatment (Seale et al., 1981).

CLINICAL SIGNIFICANCE
• Patients with a previous history of tooth sensitivity may thus have a higher risk for such
an adverse effect from external tooth bleaching, and this should be taken into account
before treatment begins
 Alteration of enamel surface

•Morphological alteration of the enamel following tooth bleaching has been addressed in
several studies.
•Enamel surface exposed to the bleaching agents underwent slight morphologic alterations.
•in vivo with 35% CP (30 min/day for 14 days) lost the aprismatic enamel layer, damage was
not repaired after 90 days (Bitter, 1998).
•By infrared spectroscopic analysis in vitro 35% CP for (30 min/day for 4 days )changed the
inorganic composition of the enamel, whereas 10% and 16% concentrations did not (Oltu and
Gürgan, 2000).
•Evaluation of casts made from impressions of teeth bleached with 10% carbamide peroxide for
8–10 hrs/day for 14 days revealed no or minimal changes in the enamel surface (Leonard et al.
, 2001),

•A high concentration of carbamide peroxide was detrimental to enamel surface integrity, but
the damage was less than that seen after phosphoric acid etch (Ernst et al., 1996).

CLINICAL IMPLICATION
•Teeth are more susceptible to extrinsic discoloration after bleaching due to increased surface
roughness.
 MUCOSAL IRRITATION

•A high concentration of H2O2 (30 to 35%) is caustic to mucous membranes and

may cause burns and bleaching of the gingiva.

•In animal experiments, exposure of the gingiva to 1% H2O2 for 6 to 48 hrs

resulted in epithelial damage and acute inflammation in the subepithelial
connective tissue (Martin et al., 1968).
•In clinical trials that used 10% carbamide peroxide in custom-made trays, from 25
to 40% of the patients reported gingival irritation during treatment (Leonard et al., 1997
; Tam, 1999a).

CLINICAL SIGNIFICANCE
Tray be designed to prevent gingival exposure by the use of a firm tray that has
contact with solely the teeth.
In this respect, the newly introduced bleaching strips may be unfavorable, since
the bleaching gel will come into contact with the gingiva.
 EFFECTS ON RESTORATIONS

COMPOSITES
SEM & profilometric studies – 10-16% CP – slight bust sig increase in surface roughness,
porosities of microfilled & hybrid composite resins ( Turker et al 2003, Cehreli et al 2003)
Salivary proteins absorbed on the surface decreased after bleaching with peroxide
containing agents – influence on bacterial adhesion of cariogenic bacteria (Steinerg et al 1999)
Surface reflectance- sig changes in microfilled & hybrid composites on application 30-
35%H2O2 ( Bowles et al 1996)
Controversy - impact of low conc 10-16% CP microhardness
In office whiteners – no sig affect on hardness & tensile strength (Yap et al 2002)

10%H2O2 or HEATED 30% H2O2 – Clinically sign color change

10% CP – no sign changes
COMPOMERS, GIC, RESIN MODIFIED GIC
High conc – 30min, 1 week interval – no detrimental effect surface finish
Applied continuously – 1-5 days –surface degradation, softening , increase in
fluoride release & changes in coefficient of thermal expansion. (Jung 2002)

10-16% CP increase in surface roughness for some brands – others decreased SR –

effects of gels material dependent.
Low conc 6%H2O2-no sign dissolution or surface wear of GIC
REASONS FOR IMPACT
•Alteration of color – oxidation of surface pigments & amine compounds
•Differences in color change b/w materials –different amount of resin & diff degrees of
conversion of resin matrix to polymer
•Also surface phenomena- increase in porosities –deterious impact of oxidizing
bleaching agent on polymer –matrix of resin based materials
•Debated – oxidizing effect – lead to water uptake of restorative materials – complete or
partial debonding of fillers – loss of hardness
•NO STUDY – Inc surface roughness, reduction surface hardness – need for
replacement existing restorations

CLINICAL SIGNIFICANCE – Moret et al 1998- polishing of restorations advisable –

prevent increase adherence of certain cariogenic micro org to the outer surface.
 AMALGAM

10% CP on non-polished amalgam- caused corrosion – lower corrosion in polished

amalgam compared to non polished
Various studies- increased release of mercury and silver – 10%CP or 10%H2O2 – inc
conc CP led inc release
Haywood 2002- greening of tooth-amalgam interface on extended bleaching

REASONS
Oxidizing effect - higher rate of mercury realease

CLINICAL SIGNIFICANCE
•Polishing of amalgam rest prior to bleaching
•Pre-coating with protective varnish – reduce release of mercury into env
EFFECT OF BLEACHING AGENTS ON BOND STRENGTH TO ENAMEL &
DENTIN

Majority studies- shear & tensile bond strength sign decreased when composite
application performed immediately after bleaching irrespective of the application
time or conc of H2O2
A delay of 2-3 weeks is generally recommended

REASONS FOR IMAPCT

7. H202 + releasing agents – sign decrease in enamel calcium & phosphate content
& morphological alterations superficial enamel crystallites
8. Acid etching of bleached enamel – loss of prismatic form – enamel surface
appeared over etched.
9. Enamel & dentin organic matrix altered oxidizing effect H2O2 – not allow strong
bond
10. Residual oxygen present – interfere with resin infiltration or inhibit
polymerization of resins cure via free radical mech.- soft interface not able to
withstand debonding forces.
11. Acid etching (30% H2O2) did not remove smear layer on dentin.
CLINICAL SIGNIFICANCE
1-3 weeks delay recommended, optimum 3 weeks (Shinohara 2001, Cavalli 2001)
To dissolve peroxide, cavities cleaned with catalase or 10% sodium-ascorbate

PENETRATION OF PULP CHAMBER BY BLEACHING AGENTS IN RESTORED

TEETH

30% H2O2 or 10-35% CP – higher levels H2O2 penetrated pulp chamber teeth with
restorations( Gokay et al 2000)
Higher Conc CP- higher levels peroxide pulp chamber compared to low 10% CP

Clinical significance
Restorations and margins could be regarded as possible pathways facilitating peroxide
penetration - pulpal recations (eg hypersensitivity)
Dentists – examine restorations , renew insufficient fillings prior to belaching.
 BLEACHING OF NON VITAL TEETH

"walking bleach" technique.

Commonly used agents
Superoxol (30% H2O2 by wt & 100% by vol in pure distilled H20)
Sodium perborate + water (Spasser, 1961; Holmstrup et al., 1988)
sodium perborate + H2O2 (Nutting and Poe, 1963)
various heat sources -speed up the reaction and improve the bleaching effect (Howell, 1980).
Others
Sodium percarbonate (Kaneko, 2000)
Sodium perborate and 10% CP gel. (Aldecoa & Mayordomo, 1992)
SODIUM PERBORATE
Form of mono-, tri-, or tetrahydrate – used H2O2 releasing agent.
1907 – employed as oxidizer & bleaching agent – washing powder & other detergents.
SP tetrahydrate is obtained - addition of H2O2 to a sodium metaborate solution at a
temperature close to 20.degree. C.
On adding water - decomposition – H2O2 released
CERVICAL RESORPTION.
Cervical root resorption is an inflammatory-mediated external resorption of the root,
which can be seen after trauma and following intracoronal bleaching (Friedman et al., 1988).
Harrington & Nakin – 1st report- relationship b/w bleaching and resorption.
High concentration of hydrogen peroxide in combination with heating seemed to promote
cervical root resorption (Friedman et al., 1988; Baratieri et al., 1995),

ETIOLOGY
•Lado et al (1983) – bleaching agents – denaturation of dentin in cervical region – induces
foreign body reaction
•Cvek & Lindvall(1985) - diffusion of H2O2 thru dentin – irritation periodontium –
bacterial colonization of tubules – trigger inflammation – external resorption.
•Harrington & Natkin(1979) – H2O2 diffuses into PDL – directly induces infl resorptive
process.
•Young pulpless tooth- dentinal tubules wide open ( sclerotic dentin cannot form) – H2O2
easily penetrate dentinal tubules
•Appl of heat - facilitates diffusion of molecules in dentin.

• - generation of hydroxyl radicals – degrade the connective tissue

•10% Defect b/w cementum and enamel at CEJ – dentinal tubules communicate b/w root
canal & PDL – facilitates penetration.
•Dentinal tubules oriented incisally

•Earlier- remove GP 1-3mm apical labial CEJ – agents diffuse to PDL below epithelial
attachment.
•Amount of H2O2 diffusion sig lower with mixture of sodium perborate & water
BARRIER TRANSFER
2 PDL Probings – custom “transfer periodontal probe”
Labial, mesial & distal
Internal level of barrier placed 1mm incisal to corresp external probing of epithelial attachment
Aim – block dentinal tubules from pulp chamber apical to epithelial attachment – agent within
access cavity
Palatal portion – equal or coronal to the barriers proximal height.
 Facial outline proximal

“Bobsled tunnel”
“Ski slope”

Ideal barrier
CASE SELECTION
Successful bleaching depends on 3 imp criteria:
• Root canal obturation must be complete (Baratieri et al., 1995).
• Healthy periodontal tissues
• Remaining tooth structure must be intact
If minor rest – tooth bleached first
If significant rest – restored with laminates or full crown
staining by alloys – bleaching less predictable.

TREATMENT TECHINQUE
• Record shade
• Record barrier probings
• Isolate the tooth
• Prepare the access cavity
• Transfer barrier probings
• Place barrier material
1. Introduce the bleaching agent
2. Thermocatalytically activate bleach

Analytic Techology Touch ‘n’ Heat –

heat for 2mins – change sol.
external brushes – to enhance bleaching effect

9. Rinse
10. Place walking bleach
Thick mix sodium perborate & superoxol or sodium perborate and water
damp cotton pellet to remove excess.
4. Insert temporary seal
composite or compomer (waite 1998)
12. Determine duration of walking bleach
changed every 2-4 days – pt notices appropriate tooth color
8. Restore access
clean access cavity – catalase or sodium hypochlorite, Ca(OH)2 for 3
weeks, moderate bevelling before Acid etch , light cure composite.
 MODIFIED WALKING BLEACH
(Liebenberg, 1997; Caughman et al., 1999).

•If the seal of the root-filling leaks, contamination of the periapical tissue
•Insufficient rinse- bleaching agent ingested
•Intracoronal dentin will be subject to discoloration from pigments in foods or
beverages.
 Efficacy and Esthetic results

No difference in the shade of the teeth bleached with SP+ 30% H2O2, SP+ 3%
H2O2, or SP in water. (Rotstein et al., 1991) (Rotstein et al., 1993), (Ari and Üngör, 2002).

in vitro studies was that sodium perborate in water, sodium perborate in 3 and
30% hydrogen peroxide, and 10% carbamide peroxide were efficient for internal
bleaching of non-vital teeth.

The need for re-treatment increased with the observation time, i.e., 10% after 1 to 2
years (Friedman et al., 1988), 20–25% after 3 to 5 years (Brown, 1965; Holmstrup et al., 1988), and
40% observed up to 8 years (Friedman et al., 1988).
 GENOTOXICITY AND CARCINOGENICITY OF BLEACHING AGENTS

•Direct contact with H202- induced genotoxic effects in bacteria and cultured cells.
However in the presence of catalase or other metabolizing enzymes, the effect was
reduced or abolished.

•A genotoxic action cannot be excluded, since free radicals formed from hydrogen
peroxide are capable of attacking DNA.

•H2O2 is shown to have a weak local carcinogenic-inducing potential.

•The mechanism is unclear, but Several studies of carcinogenesis in mice skin and
hamster cheek pouch indicate that hydrogen peroxide may act as a tumor-promoter
(Klein-Szanto and Slaga, 1982; Weitzman et al., 1986).

•The International Agency for Research on Cancer (IARC) concluded that there is
limited evidence in experimental animals and inadequate evidence in humans for
the carcinogeni-city of hydrogen peroxide and classified the chemical into Group 3:
Unclassifiable as to carcinogenicity to humans (IARC, 1999).
 MICROABRASION

1916 – Kane – heated HCL

1966 – McInnes sol. – 36%HCL, 30% H2O2 & ether 16 to 20 mins
1984 – Mc Closkey – 18% HCL
1986 – Croll modified tech – pumice + 18% HCL – paste applied tongue blade –
MICROABRASION
1990 – ‘Prema” – 10% HCL & pumice
1991 – Miara – Micro clean – HCL, pumice & low conc H2O2

Involves physical removal of enamel – no bleaching action

Microabrsion – average of 25um – every 5 sec application
Pumice – greater surface area exposed to action of HCL
 INDICATIONS
Surface stains from external sources
eg tea, coffee, tobacco

Incipient carious lesions

opaque or chalky white when dried

Developmental discoloration spots

opaque white or light brown – idiopathic

Surface discoloration due to fluorosis

 Prema or opalusture slurry applied
Opal cup internal bristle brush design

Rotary application of slurry Rinsed periodically , progress assessed

 MACROABRASION

•Alternative tech – removal localized superficial white spots or surface defects

•Utilizes 12 fluted composite finishing burs or fine grit finishing diamond bur
•Air water spray – coolant & maintain tooth in hydrated state
•30 fluted composite finishing bur – remove facets or striations
•Final polishing – abrasive rubber points

ADVANTAGES
Faster & easier
•Does not require rubber dam

DISADVANTAGES
•Technique sensitive
 VENEERS

Layer of tooth colored material applied to the tooth to restore localized or

generalized defects & intrinsic discolorations

INDICATIONS
2 Types of esthetic veneers:
2. Partial veneers
3. Full veneers

Accomplished by
• Direct
• Indirect method

Partial veneers
• Indicated for localized defects
• Areas of intrinsic discoloration

Full veneers
• Generalized defects
• Intrinsic staining inv majority facial surface
PARTIAL VENEERS
 FULL VENEER

WINDOW PREP INCISAL LAPPING

•Tooth needs lengthening or incisal defect warrants

•Most cases composite veneering
•Preserves functional incisal & lingual
surfaces
•Significant occlusal forces
•gingival margin to facioincisal line angle
restoration
•Freq used with porcelain veneers- accurate seating
& improved esthetics
•Incisal reduction – 0.75mm
•Subgingival margins only severe discoloration or
defects
“SHINE THROUGH” APPEARANCE
 COLOR MODIFIERS AND OPAQUERS

They help create highly esthetic and realistic restorations

1st modifier – 1982 – Estilux Color
Opaquers & tints – metal oxides (titanium oxide, iron oxide etc) suspended in low
viscosity bis-GMA resin or a mixture of bis-GMA and UDMA resins.
Opaquers block the light
More intense opaquer – thinner layer necessary to block unwanted color
Tints – alter existing shade or characterize a specific area
Coloring always placed beneath the final layer of restorative material.
Primary hue + secondary complementary hue = “cancel” both colors grey -
the most important relationship in dental color manipulation
Most commonly used color modifiers

Yellow and Yellow-brown

usually cervical 3rd, effective against blue-gray tetracycline stains
yellow + white – mask brown stains
used in proximal surfaces – illusion of narrowness

White
increases value of any color modifier
mask yellow stains
stimulate hypocalcifications & craze lines

Blue, Gray or Violet

incisal 3rd – stimulate translucency
reduce value ( brightness)

Red or Pink
mask blue stains, enhances vitality
stimulates gingival tones
Tetracycline staining Tooth preparation Application of opaque layer

Final opaque layer Gray incisal tint

Gingival tint
Application of composite
 CROWNS
INDICATIONS
3. Discoloration cannot be completely eliminated
4. Congenital discolorations
5. Congenitally malformed teeth
6. Weakening of tooth structure
7. Heavily restored teeth
8. Pts contraindicated for beaching
CONCLUSION:

The development of novel techniques to produces results that are superior to those of

traditional methods, or to produce results not possible at all by current methods,

would improve the general esthetic appearance of the patient