Discoloration

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.

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

IATROGENIC

- Dentist or physician therapy

- Dietary, environmental, habitual or age related factors.

DISCOLORATION ASSOCIATED WITH PULPAL INVOLVEMENT.

Intrapulpal Hemorrhage

Reddish tinge – grey brown

ENAMEL AND DENTIN DISCOLORATION

Developmental defects in Enamel Formation.

ENAMEL HYPOPLASIAIncomplete or defective formation of the organic enamel matrix of teeth.

AMELOGENESIS IMPERFECTA

2 Basic types

Environmental factorsHereditary type

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.

3 BASIC TYPES

HYPOPLASTIC

HYPOCALCIFIED

HYPOMATURATION

HYPOPLASTIC

HYPOCALCIFIED

White & opaque or brownish orange

HYPOMATURATION

Environmental Hypoplasia

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

2. Childhood illness ( Jaundice, Porphyria etc)

3. Congenital syphilis

4. Hypocalcemia

5. Birth injury, prematurity, Rh hemolytic disease

6. Local infection or trauma

7. Ingestion of chemicals ( eg flouride)

8. 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.

Type III – ‘Shell teeth’

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

SYSTEMIC MEDICATIONS

TERACYCLINE FAMILY

1948 – Rx respiratory illness, ear infections and Acne Vulgaris

Still used – cystic fibrosis & Rocky Mountain Spotted fever

Mechanism 2 Theories

1. Joining tertracycline molecule with calcium thru chelation – incorporation

into hydroxylapatite crystal during mineralization stage

2. 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

1. Age at the time of administration

2. Duration of administration

3. Dosage

4. Type of tetracycline

A. Chlortetracycline: Gray-brown

B. Dimethylchlortetracycline,

Oxytetracycline, tetracycline: Yellow

Variety of factors

1. Bacterial stains

2. Diet related stains

3. Gingival Hemorrhage

4. Tobacco

5. Chlorhexidine

6. Poor oral hygiene

7. Metallic stains

EXTRINSIC DISCOLORATION

Iron stain

AGE RELATED DISCOLORATION

DENTAL CARIES RESTORATIVE MATERIALS

Greenish grey - amalgam

Erythropoietic porphyria

SYSTEMIC DISORDERS

Hyperbilirubinemia

TREATMENT MODALITIES

1. Bleaching

2. Microabrasion

3. Macroabrasion

4. Veneers

5. Jacket crown.

In office : Power Bleach

Home : Night Guard Bleach

Walking Bleach

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

1. Teeth with opaque white spots

2. Dentin hypersensitivitysevere attrition, erosion, abrasion or abfraction – exposure of DEJ – office bleaching with isolation possible

3. Generalized dental caries or leaking restorations.

4. Heavily restored teeth

5. Teeth slated for bonded restorations or orthodontic bracketing.

6. Suspected or confirmed cases of Bulimia.

7. Patient selectionemotional or psychological problems or unrealistic goals

8. Case selectionwill 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

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

At acidic pH At basic pH

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

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

1. Surface debridement thorough scaling & polishing must performed

2. Hydrogen peroxide concentration.higher the conc- greater the oxidation; highest being 35%

3. Temperatureincrease of 10% doubles the rate of reaction

4. pHacidic pH to extend shelf life, optimum pH 9.5 to 10.8

5. Timeeffect of bleach directly related to time of exposure

6. Sealed environmentsealed env increases bleaching efficiency.

BLEACHING OF VITAL TOOTH1. In-office bleaching

2. 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

1. 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

CONTRAINDICATIONSSame as others

DELIVERY METYHODS

1. Custom trays with reservoirs

2. Foam lined tray

thin guard material lined on one side with foam – advocated with materials without carbapol

3. Boil and form guards

4. All foam stock trays

5. Bleaching tooth pastes

6. Bleaching varnishes (brush on)

7. Bleaching strips

Two basic regimen for application

1. 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’

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),

EFFICACY AND ESTHETIC RESULTS

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

•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.

Alteration of enamel surface

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).


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 change10% 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


•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

1. H202 + releasing agents – sign decrease in enamel calcium & phosphate content & morphological alterations superficial enamel crystallites

2. Acid etching of bleached enamel – loss of prismatic form – enamel surface appeared over etched.

3. Enamel & dentin organic matrix altered oxidizing effect H2O2 – not allow strong bond

4. 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.

5. Acid etching (30% H2O2) did not remove smear layer on dentin.


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

3 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.

“Bobsled tunnel”

Facial outline proximal

“Ski slope”

Ideal barrier

CASE SELECTION

Successful bleaching depends on 3 imp criteria:

1. Root canal obturation must be complete (Baratieri et al., 1995).

2. Healthy periodontal tissues

3. 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

1. Record shade

2. Record barrier probings

3. Isolate the tooth

4. Prepare the access cavity

5. Transfer barrier probings

6. Place barrier material

7. Introduce the bleaching agent

8. 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.

11. Insert temporary seal

composite or compomer (waite 1998)

12. Determine duration of walking bleach

changed every 2-4 days – pt notices appropriate tooth color

13. 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.

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.

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).

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).

Efficacy and Esthetic results

•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).

GENOTOXICITY AND CARCINOGENICITY OF BLEACHING AGENTS

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

Rinsed periodically , progress assessed

Opal cup internal bristle brush design

Rotary application of slurry

Prema or opalusture slurry applied

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:

1. Partial veneers

2. Full veneers

Accomplished by

1. Direct

2. 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

•Most cases composite veneering

•Preserves functional incisal & lingual surfaces

•Significant occlusal forces

•gingival margin to facioincisal line angle

•Tooth needs lengthening or incisal defect warrants 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 Gingival tint Gray incisal tint

Application of composite

CROWNS

INDICATIONS

1. Discoloration cannot be completely eliminated

2. Congenital discolorations

3. Congenitally malformed teeth

4. Weakening of tooth structure

5. Heavily restored teeth

6. 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

Documents

Discoloration