3. CAUSES OF TOOTH
DISCOLOURATION:
The coronal portion of the tooth consists of enamel, dentine and pulp. Any
change to these structures is likely to cause an alteration in the outward
appearance of the tooth caused by its light transmitting and reflecting
properties. The appearance of tooth colour is dependent on the quality of the
reflected light and is also as a consequence dependent on the incident light.
Tooth discolouration has been classified according to the location of the stain,
which may be either intrinsic, extrinsic or internalised
4. Intrinsic discolouration
Intrinsic discolouration occurs following a change to the structural composition
or thickness of the dental hard tissues.
The normal colour of teeth is determined by the blue, green and pink tints of
the enamel and is reinforced by the yellow to brown shades of dentin beneath.
Conditions causing intrinsic discoloration:
1. Alkaptonuria
2. Congenital erythropoietic porphyria
3. Congenital hyperbilirubinaemia
4. Amelogenesis imperfecta
5. Dentinogenesis imperfecta
6. Tetracycline staining
7. Fluorosis
8. Enamel hypoplasia
9. Pulpal haemorrhagic products
10. Root resorption
11. Ageing
5. Extrinsic discolouration
Extrinsic discolouration is outside the tooth substance and lies on the tooth
surface or in the acquired pellicle. The origin of the stain may be:
1. Metallic
2. Non-metallic
6. Extrinsic causes of tooth
discolouration
Non-metallic stains
Diet. Tea, coffee and other food- Brown to black
Oral hygiene, Dental plaque calculus and food particle-Yellow/brown
Chromogenic bacteria - brown/black/green/orange
Habits. Tobacco smoking/ chewing .Pan chewing. Dark brown/black ,Red-
black
Medication. Cationic antiseptics e.g.: chlorhexidine-Yellow brown
Essential oils/phenolic mouthrinse-Yellow
Systemic antibiotics e.g.- Minocycline- Green
7. Metallic stains
Medications. Iron containing oral solution- Black
Copper salt in mouthrinse- Green
Potassium permanganate in mouth rinse- Violet to black
Stannous fluoride- Golden brown
Silver nitrate-Gray
Occupation and environment. Exposure to Iron, Manganese-Silver, Black
Exposure to mercury and lead dust-Blue green
Copper and nickel-Green
Chromic acid fumes-Deep orange
8. Internalised discolouration
Internalised discolouration is the incorporation of extrinsic stain within the tooth substance
following dental development. It occurs in enamel defects and in the porous surface of exposed
dentin. The routes by which pigments may become internalised are:
1. Developmental defects
2. Acquired defects
a) Tooth wear and gingival recession
b) Dental caries
c) Restorative material
10. Dentist-Related Causes
Endodontically related
Pulp tissue remanants
Intracanal medicaments
Obturating material
Restoration related-
Amalgam
Pins and Posts
composites
11. Pre-eruptive causes of Intrinsic
discolouration
Metabolic. Hyberbilirubinemia- Yellow-green
Prophyria- Reddish brown
alkaptonuria- brown
Disturbance of tooth germ. Localized-Turner tooth- White to Yellow
Generalized-Infection (maternal or childhood)- White to yellow
Nutritional deficiency- White to Yellow
Molar incisor hypomioneralization- Yellow to Brownish
Genetic disorder. Amelogenesis imperfecta - Yellow brown
dentinogenesis imperfect- Blue brown
Dentin dysplasia- Yellow
Systemic syndrome e.g.- Epidermolysis bullosa- yellow
Medication . Tetracycline- Yellow, brown, blue or greyish
Minocycline- Blue-green
ciprofloxacin- Greenish
Fluoride supplement- Chalky white to brown/ black
Environmental. Endemic fluorosis- Chalky white to brown/black
12. Post-eruptive causes of Intrinsic
discolouration
Dental conditions.Dental caries-Incipient-Chalky white
Active -Yellowish brown
Arrested- Dark brown to black
Tooth wear-Yellowish
ageing-Yellowish
Pulpal causes.Pulpal trauma with hemorrhage-Gray-brown
Calcific metamorphosis-Yellowish to yellowish brown
Internal resorption-Pinkish
Dental materials.Amalgam-Blue-gray
Composite/GIC-Yellowish brown
Intracanal medicaments e.g.- iodoform, ledermix-Brownish gray
Obturating materials and sealers-grayish
13. THE MECHANISMS OF TOOTH
DISCOLOURATION:
Intrinsic tooth discolouration:
The formation of intrinsically discoloured teeth occurs during tooth
development and results in an alteration of the light transmitting properties of
the tooth structure.
There are a number of metabolic disorders which affect the dentition during its
formation, unlike the inherited disorders in which only the hard tissue forming
at the time may be involved.
14. 1. Alkaptonuria: This inborn error of metabolism results in incomplete metabolism of
tyrosine and phenylalanine, which promotes the build up of homogentisic acid. This
affects the permanent dentition by causing a brown discolouration.
2. Congenital erythropoietic porphyria: This is a rare, recessive, autosomal, metabolic
disorder in which there is an error in porphyrin metabolism leading to the accumulation
of porphyrins in bone marrow, red blood cells, urine, faeces and teeth. A red-brown
discolouration of the teeth is the result and the affected teeth show a red fluorescence
under ultra-violet light.
3. Congenital hyperbilirubinaemia: The breakdown products of haemolysis will cause a
yellow-green discolouration. Mild neonatal jaundice is relatively common, but in rhesus
incompatibility massive haemolysis will lead to deposition of bile pigments in the
calcifying dental hard tissues, particularly at the neonatal line.
15. 4. Amelogenesis imperfecta: In this hereditary condition, enamel formation is disturbed
with regard to mineralization or matrix formation and is classified accordingly. There
are 14 different subtypes. The appearance depends upon the type of amelogenesis
imperfecta, varying from the relatively mild hypomature ‘snow-capped’ enamel to the
more severe hereditary hypoplasia with thin, hard enamel which has a yellow to
yellow-brown appearance.
5. Systemic syndromes: Defects in enamel formation may also occur in a number of
systemically involved clinical syndromes such as Vitamin D dependent rickets,
epidermolysis bullosa and pseudohypoparathyroidism. Barabas has reported areas of
hypoplastic enamel, irregularities in the region of the amelo-dentinal and the cemento-
dentinal junctions in Ehlers-Danlos Syndrome. In epidermolysis bullosa there is pitting
of the enamel possibly caused by vesiculation of the ameloblast layer.the effect of
these conditions depends on disease activity during the development of the dentition
and is usually a minor element.
16. 6. Dentinogenesis imperfecta: Dentin defects may occur genetically or through
environmental influences. The genetically determined dentine defects may be in isolation
or associated with a systemic disorder. The main condition related to the dentin alone is
Dentinogenesis imperfecta II (hereditary opalescent dentine). Both dentitions are affected,
the primary dentition usually more severely so. The teeth are usually bluish or brown in
colour, and demonstrate opalescence on transillumination. The pulp chambers often
become obliterated and the dentin undergoes rapid wear, once the enamel has chipped
away, to expose the amelo-dentinal junction.
17. Dentinogenesis imperfecta I (associated with osteogenesis imperfecta, a mixed connective
tissue disorder of type I collagen) may show bone fragility and deformity with blue sclera, lax
joints and opalescent dentin. The inheritance may be dominant or recessive, the recessive
being more severe and often fatal in early life. Opalescent teeth are more common in the
dominant inheritance pattern, the primary teeth bear a strong resemblance to the teeth in
Dentinogenesis imperfecta type I whereas the appearance of the secondary dentition is much
more variable. The enamel is much less prone to fracture, the pulp chamber is seldom
occluded by dentin (this may help to radiographically differentiate between types I and II), and
the overall prognosis for the dentition is improved.
A third type of Dentinogenesis imperfecta (type III, brandywine isolate hereditary opalescent
dentine) was described by Wiktop. In this condition, the teeth may be outwardly similar to
both types I and II of Dentinogenesis imperfecta; however, multiple pulpal exposures occur in
the primary dentition. Radiographically, the teeth may take on the appearance of ‘shell teeth’
as dentin production ceases after the mantle layer has formed. This type of Dentinogenesis
imperfecta is thought to be related more closely to type II.
18. 7. Dentinal dysplasia: Shields reclassified the inherited dentine defects in a review of the
literature in 1973 and introduced the term dentinal dysplasia. This reclassification allows
separation of the inherited types of dentine defect from Dentinogenesis imperfecta, with which
they are often confused. In type I dentin dysplasia the primary and secondary dentition are of
normal shape and form but may have an amber translucency. Radiographically the teeth have
short roots with conical apical constrictions. The pulp is commonly obliterated in the primary
dentition, leaving only a crescentic pulpal remnant in the adult dentition parallel to the
cemento-enamel junction. There are characteristic periapical radiolucencies in many,
otherwise healthy, teeth. The condition is inherited as an autosomal dominant trait.
Type II dentine dysplasia is described through a small number of case reports in Shields
review, the main characteristic is that of a thistle-shaped pulp chamber with numerous pulp
stones. A brown discolouration is seen.
19. 8. Tetracycline staining: Systemic administration of tetracyclines during development is
associated with deposition of tetracycline within bone and the dental hard tissues.
Urist and Ibsen suggested that tetracycline and its homologues have the ability to form
complexes with calcium ions on the surface of hydroxyl apatite crystals within bone and
dental tissues. Dentin has been shown to be more heavily stained than enamel.
Tetracycline is able to cross the placental barrier and should be avoided from 29 weeks in
utero until full term to prevent incorporation into the dental tissues. Since the permanent
teeth continue to develop in the infant and young child until 12 years of age, tetracycline
administration should be avoided in children below this age and in breast-feeding and
expectant mothers.
The most critical time to avoid the administration of tetracycline for the deciduous
dentition is 4 months in utero to 5 months post-partum, with regard to the incisor and
canine teeth. In the permanent dentition, for the incisor and canine teeth, this period is from
4 months post-partum to approximately 7 years of age.
20. The colour changes involved depend upon the precise medication used, the dosage and
the period of time over which the medication was given. Teeth affected by tetracycline
have a yellowish or brown-grey appearance which is worse on eruption and diminishes
with time.
The various analogues of tetracycline produce different colour changes, for instance
chlortetracycline produces a slate grey colour and oxytetracycline causes a creamy
discolouration. Since tetracycline fluoresces under ultraviolet light so do affected teeth,
giving off a bright yellow colour.
There have been recent reports of adults experiencing change in tooth colour with the
use of long term tetracycline therapy. Minocycline, a synthetic compound of
tetracycline antibiotics, is also implicated in causing discolouration in an adult patient,
following its long term use for treatment of acne.
21. 9. Fluorosis: The association between fluoride intake and its effect on enamel was noted by
Dean as long ago as 1932.
This may arise endemically from naturally occurring water supplies or from fluoride
delivered in mouthrinses, tablets or toothpastes as a supplement. The severity is related to
age and dose, with the primary and secondary dentitions both being affected in endemic
fluorosis.
The enamel is often affected and may vary from areas of flecking to diffuse opacious
mottling, whilst the colour of the enamel ranges from chalky white to a dark brown/black
appearance. The brown/black discolouration is post-eruptive and probably caused by the
internalisation of extrinsic stain into the porous enamel. These features are often described as
being pathognomonic of fluorosis, but care should be taken not to confuse the condition with
the hypomaturation type of Ameolgenesis imperfecta. Fluoride only causes fluorosis in
concentrations of greater than 1 ppm in drinking water and is not distinguishable, clinically
or histologically, from any other type of hypoplastic or hypomineralized enamel.
22. 10. Enamel hypoplasia: This condition may be localised or generalised. The most common
localised cause of enamel hypoplasia is likely to occur following trauma or infection in the
primary dentition. Such localised damage to the tooth-germ will often produce a hypoplastic
enamel defect, which can be related chronologically to the injury. Disturbance of the
developing tooth germ may occur in a large number of foetal or maternal conditions e.g.
maternal vitamin D deficiency, rubella infection, drug intake during pregnancy and in
paediatric hypocalcaemic conditions. Such defects will be chronologically laid down in the
teeth depending on the state of development at the time of interference; the effect is directly
related to the degree of systemic upset. There may be pitting or grooving which predisposes
to extrinsic staining of the enamel in the region of tooth disturbed, often then becoming
internalised.
23. 11. Pulpal haemorrhagic products: The discolouration of teeth following severe
trauma was considered to be caused by pulpal haemorrhage. Haemolysis of the red
blood cells would follow and release the haem group to combine with the putrefying
pulpal tissue to form black iron sulphide. In vitro studies have recently shown that the
major cause of discolouration of non-infected traumatised teeth is the accumulation of
the haemoglobin molecule or other haematin molecules. In the absence of infection, the
release of iron from the protoporphyrin ring is unlikely. Incidentally, it has been shown
that the pinkish hue seen initially after trauma may disappear in 2 to 3 months if the
tooth becomes revascularised.
24. 12. Root resorption: Root resorption is often clinically asymptomatic, however,
occasionally the initial presenting feature is a pink appearance at the amelo-cemental
junction. Root resorption always begins at the root surface, either from the pulpal or
periodontal aspect, as internal or external root resorption respectively. It can be difficult
to locate a resorptive cavity on radiograph until it reaches a certain size.
13. Ageing: The natural laying down of secondary dentine affects the light-transmitting
properties of teeth resulting in a gradual darkening of teeth with age.
25. Extrinsic discolouration:
Extrinsic stain can be classified as either metallic or non-metallic.
Nathoo(1997) has proposed a classification based on the chemistry of
discoloration.
N1 type dental stain (direct dental stain): The chromogen binds to tooth
surface to cause tooth discolouration. The colour of chromogen is similar to
that of dental stain. These materials generate colour due to the presence of
conjugate double bond and are thought to interact with tooth surface with an
ion exchange mechanism. These stains can be prevented by good oral hygiene
and can be removed with prophylaxis paste or tooth paste.
26. N2 type stain (direct dental stain): The chromogen change colour after binding to the
teeth. N1 type of dental stains are known to darken to N2 type stain. These stain are
more difficult to remove and may require professional cleaning.
N3 type dental stain (indirect dental stain): The prechromogen binds to the teeth and
undergoes a chemical reaction to cause stain. These are the most difficult to remove and
would probably require oxygenating agents.
27. The causes of extrinsic staining can be divided into two categories:
Those compounds which are incorporated into the pellicle and produce a stain as a
result of their basic colour, and those which lead to staining caused by chemical
interaction at the tooth surface.
Direct staining has a multi-factorial aetiology with chromogens derived from dietary
sources or habitually placed in the mouth. These organic chromogens are taken up by
the pellicle and the colour imparted is determined by the natural colour of the
chromogen. Tobacco smoking and chewing are known to cause staining, as are
particular beverages such as tea and coffee.
28. Non-metallic stains: The non-metallic extrinsic stains are adsorbed onto tooth surface
deposits such as plaque or the acquired pellicle. The possible aetiological agents include
dietary components, beverages, tobacco, mouthrinses and other medicaments.
Chromogenic bacteria have been cited in children. Particular colours of staining are said
to be associated with certain mouths, for instance, green and orange in children with
poor oral hygiene and black/brown stains in children with good oral hygiene and low
caries experience. Conclusive evidence for the chromogenic bacterial mechanism has
not been forthcoming. The most convincing evidence for the extrinsic method of tooth
staining comes from the differing amount of stain found in a comparison of smokers
and non-smokers. The staining effect of prolonged rinsing with chlorhexidine
mouthrinses and quarternary ammonium compounds used in mouthrinses is of
considerable interest to the dental profession.
29. Metallic stains: Extrinsic staining of teeth may be associated with occupational exposure to
metallic salts and with a number of medicines containing metal salts.
The characteristic black staining of teeth in people using iron supplements and iron
foundry workers is well documented. Copper causes a green stain in mouthrinses
containing copper salts and in workers in contact with the metal in industrial
circumstances.
A number of other metals have associated colours such as potassium permangenate
producing a violet to black colour when used in mouthrinses; silver nitrate salt used in
dentistry causes a grey colour, and stannous fluoride causes a golden brown discolouration.
30. Internalised discolouration:
The stains taken up into the body of enamel or dentin are the same as those
causing extrinsic tooth discolourations, including in particular dietary
chromogens and the by-products of tobacco smoking. Dental defects permitting
the entry of chromogenic material can be classified under the headings of
‘developmental and acquired’.
31. 1. Developmental defects: The most important defects are considered under the
‘intrinsic tooth discolouration’ section of this review. As described these developmental
defects create their own colour change in the tooth caused by influences on light
transmission through the dentin and enamel. Post-eruptively, however, either caused by
increased enamel porosity, or the presence of enamel defects , extrinsic stains can
penetrate into the enamel. Such examples would include fluorosis and other enamel
conditions resulting in enamel hypoplasia or hypocalcification. Alternatively,
developmental defects may expose dentin either directly or later caused by early loss of
enamel as in dentinogenesis imperfecta. Chromogens are then able to enter the dentine
directly or facilitated almost certainly by the tubule system.
32. 2. Acquired defects: Wear and tear, and disease of the teeth and supporting tissues occur
throughout life, all of which can lead directly or indirectly to tooth discolouration.
Additionally, repairs on restorations of teeth can influence the colour of teeth.
a) Tooth wear and gingival recession: Both conditions appear to have multifactorial
aetiologies but to date are poorly understood, there being limited scientific research on the
topics. Tooth wear is usually considered to be a progressive loss of enamel and dentine due
to erosion, abrasion and attrition. As enamel thins the teeth become darker as the colour of
dentin becomes more apparent. Once dentin is exposed the potential of chromogens to enter
the body of the tooth is increased. Physical trauma can also result in bulk loss of enamel or
enamel cracks, both of which facilitate internalisation of extrinsic stains. Although tooth
wear occurs at the cervical area of teeth, where enamel is most thin, exposure of dentin is
more likely caused by gingival recession. Again, the net result is dentin exposure and the
increased potential for the uptake of chromogens into the tooth.
33. b) Dental caries: The various stages of the carious process can be recognised by changes in
colour as the disease progresses. For instance, the initial lesion is characterised by an
opaque, white spot. The white spot lesion differs in colour from the adjacent enamel by
virtue of its increased porosity and the effect this has on the refractive index. The hard,
arrested lesion is black having picked up stain from exogenous sources.
c) Restorative materials including amalgam: Some of the materials used in restorative
dental treatment may have an effect on the colour of teeth. Eugenol and phenolic
compounds used during root canal therapy contain pigments which may stain dentin. Some
of the polyantibiotic pastes used as root canal medicaments may cause a darkening of the
root dentine. Clinicians are familiar with the dark grey to black colour of dentine following
the removal of a longstanding amalgam restoration. It was previously thought that mercury
was penetrating the dentinal tubules and reacting with sulphide ions. Electronmicroscopic
studies have shown that this discolouration is caused by the migration of tin into the
tubules.
34. BLEACHING:
The lightening of the colour of a tooth through the application of a chemical
agent to oxidize the organic pigmentation in the root is referred to as bleaching.
35. Tooth Bleaching or Tooth Whitening
The researchers and dental trade are trying to promote tooth whitening.
The main reason seems to be a keen desire to distance the profession from a
series of European Directives that have left tooth-whitening materials classified
as a cosmetic device. Directive 93/42/EEC on medical devices defines "medical
devices" as articles which are intended to be used for a medical purpose, but
then goes on to state “products intended to have a toiletry or cosmetic purpose
are not medical devices even though they may be used for prevention of a
disease. Examples for products for which a medical purpose can normally not
be established: tooth brushes, dental sticks, dental floss; bleaching products for
teeth.
35
36. Historical perspective:
1799- Mcintosh used Chloride of lime, called bleaching agent.
1848- Dwinelle used chloride of lime for non-vital teeth.
1860- Truman used Chloride of lime and acetic acid (Labarraque’s solution) for
Non-vital tooth.
1861- Woodnut advised placing bleaching medicament and changing it at
regular interval.
1868- Latimer used oxalic acid for vital teeth.
1877- Chapple used hydrochloric acid and oxalic acid for all discolourations.
1878- Taft used oxalic acid and calcium hypochlorite.
1895- Garretson applied Chlorine to tooth surface.
1910- Prins used 30% hydrogen peroxide on to teeth.
1916- Kaine used 18% hydrochloric acid (muriatic acid) and heat on fluorosed
teeth.
1918- Abbot discovered a high intensity light that produces a rapid temperature
rise in the hydrogen peroxide to accelerate chemical tooth bleaching.
37. 1924- Prinz used a solution of perborate in hydrogen peroxide activated by a light source.
1942- Younger used 5 parts of 30% hydrogen peroxide.
1958- Pearson used 35% hydrogen peroxide inside tooth and also suggested 25% hydrogen
peroxide and 75% ether which was activated by a lamp producing light and heat to
release solvent qualities of ether.
1961- Spasser introduced Walking bleach technique- sodium perborate and
water was sealed into the pulp chamber.
1965- Stewart introduced Thermocatalytic technique- pellet saturated with superoxyl was
inserted into pulp chamber and heated with a hot instrument.
1967-Nutting and Poe used Combination Walking bleach technique-
Superoxyl in pulp chamber ( 30% hydrogen peroxide)
1972- Klusmier used the same technique with proxigel as it was thicker and
stayed in the tray longer.
38. 1979- Harrington and Natkin reported on external resorption associated with
Bleaching pulpless teeth
1982- Abou-Rass recommended intentional endodontic treatment with internal
bleaching for tetracycline stains.
1989-Haywood and Heyman introduced Nightguard vital bleaching using 10% Carbamide
peroxide in a tray.
Introduction of commercial over-the-counter bleaching product to activate bleach.
1991-Grabber and Goldstein introduced Combination bleaching ( Power and
home bleaching)
1994-American Dental Association established safety and efficacy of tooth
bleaching agent under the ADA seal of approval.
1996-Food and Drug Administration approved ion Laser technology. Argon
and CO2 laser for tooth whitening with patented chemicals.
1996- Reyto introduced Laser tooth whitening.
1997- Settembrini et al introduced Inside/Outside bleaching.
1998- Carrillo et al used 10% Carbamide peroxide in custom tray in open pulp chamber.
Present day techniques include Plasma arc and light activated bleaching
Technique, Power gels for in-office bleaching, Laser activated bleaching, Home bleaching
available in different concentrations and flavours.
40. Hydrogen peroxide:
Various concentrations of this agent are available, but 30 to 35% stabilized
aqueous solutions (Superoxol, Perhydrol Merck & Co.;West Point, Pa.) are the
most common. Silicone dioxide gel forms containing 35% hydrogen peroxide
are also available, some of them activated by a composite curing light.
Hydrogen peroxide is caustic and burns tissues on contact, releasing toxic free
radicals, perhydroxyl anions, or both. High-concentration solutions of hydrogen
peroxide must be handled with care as they are thermodynamically unstable
and may explode unless refrigerated and kept in a dark container.
41. Sodium perborate:
This oxidizing agent is available in a powdered form or as various commercial
preparations. When fresh, it contains about 95% perborate, corresponding to
9.9% of the available oxygen. Sodium perborate is stable when dry. In the
presence of acid, warm air, or water, however, it decomposes to form Sodium
metaborate, Hydrogen peroxide, and nascent oxygen. Three types of sodium
perborate preparations are available: monohydrate, trihydrate, and tetrahydrate.
They differ in oxygen content, which determines their bleaching efficacy.
Commonly used Sodium perborate preparations are alkaline, and their pH
depends on the amount of hydrogen peroxide released and the residual Sodium
metaborate.
42. Carbamide peroxide:
This agent, also known as Urea hydrogen peroxide, is available in the concentration
range of 3 to 45%.However, popular commercial preparations contain about 10%
Carbamide peroxide, with a mean pH of 5 to 6.5. Solutions of 10% Carbamide
peroxide break down into urea, ammonia, carbon dioxide, and approximately 3.5%
Hydrogen peroxide. Bleaching preparations containing Carbamide peroxide usually
also include glycerine or Propylene glycol, Sodium stannate, phosphoric or citric
acid, and flavour additives. In some preparations, carbopol, a water-soluble
polyacrylic acid polymer, is added as a thickening agent. Carbopol also prolongs the
release of active peroxide and improves shelf life. Carbamide peroxide–based
preparations have been associated with various degrees of damage to the teeth and
surrounding mucosa. They also may adversely affect the bond strength of composite
resins and their marginal seal.
43. BLEACHING MECHANISMS
The free radicals produced by H2O2 are responsible for bleaching effects.
H2O2 diffuses through the enamel and dentin, producing free radicals that react
with pigment molecules breaking their double bonds.
The change in pigment molecule configuration and/or size may result in changes in
their optical properties, and consequently, the perception of a lighter color by human
eyes.
Other possible mechanisms include cleansing of tooth surface, temporary
dehydration of enamel during the bleaching process and change of enamel surface.
43
44. Hydrogen peroxide:
Hydrogen peroxide is an oxidizing agent and has ability to produce free
radicals, which are very reactive. In pure aqueous form H2O2 is weakly acidic.
. The hydrogen peroxide breaks down to water and oxygen, and for brief period
forms free radical, perhydroxyl. The free radical is very reactive and has great
oxidative power.
It can break large macromolecular stain into smaller stain molecule that can be
expelled to the surface by diffusion.
It can attach to inorganic structure and protein matrix (Fasanaro).
It can oxidize tooth discolouration.
Under photochemically initiated reactions using light or lasers, the formation of
hydroxyl radicals from hydrogen peroxide has been shown to increase.
45. Carbamide peroxide:
In dental bleaching, Carbamide peroxide is used in concerntrations of 10% to
15%. It breaksdown into hydrogen peroxide which ionzses to give free radicals.
Chemical breakdown of Carbamide peroxide
Chemical breakdown of Carbamide peroxide
CH2 N2O H2O2
↓ ↓
NH3 + CO2 H2O2
46. Dental bleaching mechanism:
hydrogen peroxide diffuses through the organic matrix of the enamel and dentin. Because the
radicals have unpaired electrons, they are extremely electrophilic and unstable and will attack
most other organic molecule to achieve stability, generating other radicals. These radicals can
react with most unsaturated bonds, resulting in disruption of electron conjugation and a
change in absorption energy of the organic molecules in tooth enamel. Simpler molecules that
reflect less light are formed, creating a successful whitening action. This process occurs when
oxidizing agent reacts with organic material in spaces between the inorganic salts in the tooth
enamel.
Saturation point:
As bleaching proceeds a time is reached at which only hydrophilic colourless structure exist.
This is materials saturation point. Lightening then slows down dramatically, and the bleaching
process, if allowed to continue, begins to break down the carbon backbones of proteins and
other carbon containing materials. Compounds with hydroxyl group (usually colourless) are
split, breaking the material into yet smaller constituents. Loss of enamel being rapid, with the
remaining material being quickly converted into Carbon dioxide and water.
47.
48. 48
In a study done by J.F. Bortolatto et .al.(2014) The bleaching agent with the lower
concentration 15% H2O2 bleaching agent containing nanoparticles of TiO_N
promoted lower levels of tooth sensitivity and presented greater efficacy compared
to the 35% H2O2 .
49. NON-VITAL BLEACHING
TECHNIQUES:
Intracoronal bleaching of endodontically treated teeth may be successfully
carried out many years after root canal therapy and discoloration. A successful
outcome depends mainly on the etiology, correct diagnosis, and proper
selection of bleaching technique .
There are a number of nonvital bleaching techniques used today.
These include:
- Walking bleach and modified walking bleach
- Non-vital power bleaching, also known as thermo/photo bleaching and
- Inside/Outside bleaching.
50. Indication:
Discolorations of pulp chamber
Dentin discolorations
Discolorations not amenable to extracoronal bleaching
Contraindication:
Superficial enamel discolorations
Defective enamel formation
Severe dentin loss
Presence of caries
Discolored composites
51. Walking Bleach
The term walking bleach was first coined by Nutting and Poe in 1961 referring
to the bleaching action occurring between patients' visits. Since that time, the
technique evolved and underwent few modifications, mainly by. eliminating
the use of Superoxol (H2O2 30%) making it a very popular and safe technique.
The walking bleach technique should be attempted first in all cases requiring
intracoronal bleaching.
51
52. It involves the following steps:
1. Familiarize the patient with the possible causes of discoloration, the procedure
to be followed, the expected outcome, and the possibility of future
rediscoloration.
2. Radiographically assess the status of the periapical tissues and the quality of
endodontic obturation.
3. Assess the quality and shade of any restoration present and replace it if
defective. Tooth discoloration is frequently the result of leaking or discolored
restorations.
4. Evaluate tooth color with a shade guide and, if possible, take clinical
photographs at the beginning of and throughout the procedure.
5. Isolate the tooth with a rubber dam. The dam must fit tightly at the cervical
margin of the tooth to prevent possible leakage of the bleaching agent onto the
gingival tissue.
52
53. 6. Remove all restorative materials from the access cavity, expose the dentin, and refine
the access. Verify that the pulp horns and other areas containing the pulp tissue are
clean.
7. Remove all materials to a level just below the labial-gingival margin. Orange
solvent, chloroform,or xylene on a cotton pellet may be used to dissolve sealer
remnants.
8. Apply a sufficiently thick layer, at least 2 mm, of a protective white cement barrier,
such as polycarboxylate cement, zinc phosphate cement, glass ionomer, intermediate
restorative material (IRM) , or Cavit to cover the endodontic obturation.
9. Prepare the walking bleach paste by mixing sodium perborate and an inert liquid,
such as water, saline, or anesthetic solution, to a thick consistency of wet sand.
sodium perborate plus 30% H2O2 mixture may bleach faster, in most cases, long-
term results are similar to those with sodium perborate and water alone and therefore
need not be used routinely. With a plastic instrument, pack the pulp chamber with
the paste. Remove excess liquid by tamping with a cotton pellet.
53
54. 10. Remove the excess bleaching paste from undercuts in the pulp horn and gingival area
and apply a thick well-sealed temporary filling (preferably IRM) directly against the paste
and into the undercuts. Carefully pack the temporary filling, at least 3 mm thick, to ensure
a good seal.
11. Remove the rubber dam and inform the patient that bleaching agents work slowly and
that significant lightening may not be evident for several days.
12. Evaluate the patient 2 weeks later and, if necessary, repeat the procedure several times.
Repeat treatments are similar to the first one.
13. As an optional procedure, if initial bleaching is not satisfactory, strengthen the walking
bleach paste by mixing sodium perborate with gradually increasing concentrations of
H2O2 (3% to 30%) instead of water.
14. In most cases, discoloration will improve after 1 to 2 treatments. If after three attempts
there is no significant improvement, reassess the case for correct diagnosis of the etiology
of discoloration and treatment plan.
54
61. Thermocatalytic
This technique involves placement of the oxidizing chemical, generally 30% to
35% H2O2 (Superoxol), into the pulp chamber followed by heat application
either by electric heating devices or specially designed lamps.Care must be
taken when using these heating devices
To avoid overheating of the teeth and the surrounding tissues. Intermittent
treatment with cooling breaks is preferred over a continuous session. In
addition, the surrounding soft tissues should be protected with Vaseline,
Qrabase, or cocoa butter during treatment to avoid heat damage.
Potential damage by the thermocatalytic approach is external cervical root
resorption caused by irritation to the cementum and the periodontal ligament.
This is possibly attributable to the oxidizing agent combined with
heating.Therefore, application of highly concentrated H2O2 and heat during
intracoronal bleaching is questionable and should not be carried out routinely.
61
63. Ultraviolet Photooxidation
This technique applies ultraviolet light to the labial surface of the tooth to be
bleached. A 30% to 35% H2O2 solution is placed in the pulp chamber on a
cotton pellet followed by a 2-minute exposure to ultraviolet light. Supposedly,
this causes oxygen release, like the thermocatalytic bleaching technique.
63
64. RESTORATION OF INTRACORONALLY
BLEACHED TEETH
64
Proper restoration is essential for long-term successful bleaching results.
Microleakage of lingual access restorations is a problem, and a leaky
restoration may again lead to tooth discoloration. There is no ideal method for
filling the chamber after intracoronal bleaching.
The pulp chamber and the access cavity should be carefully restored with a
light shade, light-cured, acid-etched composite resin. The composite material
should be placed at a depth that seals the cavity and provides some incisal
support.
Light curing from the labial surface, rather than the lingual surface, is
recommended since this results in the shrinkage of the composite resin toward
the axial walls, reducing the rate of microleakage. Placing white cement
beneath the composite access restoration is recommended.
.
65. 65
waiting for at least 7 days after bleaching, prior to restoring the tooth with
resin composites, has been recommended. Catalase treatment at the final visit
may enhance the removal of residual peroxides from the access cavity.
Packing calcium hydroxide paste in the pulp chamber for a few weeks prior to
the placement of final restoration, to counteract acidity caused by bleaching
agents and to prevent root resorption.
Filling the chamber completely with composite may cause loss of translucency
and difficulty in distinguishing between composite and tooth structure during
rebleaching.As stated previously, residual H2O2 from bleaching treatment may
adversely affect the bonding strength of composites
66. COMPLICATIONS AND ADVERSE EFFECTS
FROM INTRACORONAL BLEACHING
66
External Root Resorption
Intracoronal bleaching may induce external cervical root resorption and . This
is probably caused by the highly concentrated oxidizing agent, particularly 30
to 35% H2O2 The mechanism of bleaching-induced damage to the
periodontium or the cementum is not completely clear. Presumably, the
irritating chemical diffuses via unprotected dentinal tubules and cementum
defect and causes necrosis of the cementum, inflammation of the periodontal
ligament,and, subsequently, root resorption. The process may be enhanced if
heat is applied so or in the presence of bacteria. Previous traumatic injury and
age may act as predisposing factors.
67. 67
Chemical Burns
Superoxol (H2O2 at 30%) is highly caustic and causes chemical burns and sloughing
of the gingiva. When using such solutions, the soft tissues should always be
protected with Vaseline, Orabase, or cocoa butter
Inhibition on Resin Polymerization and Bonding Strength
Oxygen inhibits resin polymerization; consequently, residual H2O2 in tooth structure
after bleaching adversely affects the bonding strength of resin composites to enamel
and dentin . Scanning electron microscopy (SEM) examination has shown an
increase in resin porosity. This presents a clinical problem when immediate esthetic
restoration of the bleached tooth is required. It is therefore recommended that
residual H2O2 be totally eliminated prior to composite placement.
68. Intentional Endodontics and
Intracoronal Bleaching:
Intrinsic tetracycline and other similar stains are incorporated into
tooth structure during tooth formation, mostly into the dentin, and
are therefore more difficult to treat from the external enamel
surface. Intracoronal bleaching of tetracycline-discolored teeth
has been shown clinically and experimentally to lead to
significant lightening. The technique involves standard
endodontic therapy (pulpectomy, cleaning and shaping, and
obturation) followed by an intracoronal walking bleach technique.
Preferably, only intact teeth without coronal defects, caries, or
restorations should be treated. This prevents the need for any
additional restoration, thereby reducing the possibility of coronal
fractures and failures. The most discolored tooth should be
selected for trial treatment. The procedure should be carefully
explained to the patient, including the possible complications and
sequelae. Sacrificing pulp vitality should be considered in terms
of the overall psychological and social needs of the individual
patient as well as the possible complications of other treatment
options. The procedure has been shown to be predictable and
without significant clinical complications.
69. VITAL BLEACHING
TECHNIQUES
Many techniques have been advocated for
extracoronal bleaching of vital teeth. In these
techniques, oxidizers are applied to the external
enamel surface of the teeth.7
These methods uses different whitening agents,
concentrations, times of application, product
formats, application modes, and light activation
method.
However, three fundamental bleaching
approaches exists:15
In-office or power bleaching
At-home bleaching bleaching, and
70. Indications:
Light enamel discolorations
Mild tetracycline discolouration
Endemic fluorosis discoloration
Age-related discolorations
Contraindications:
Severe dark discolorations
Severe enamel loss
Proximity of pulp horns
Hypersensitive teeth
Presence of caries
Large/poor coronal restorations
71. In-office treatments:
In-office systems typically use a 15%, 30%, or 35% Hydrogen peroxide whitening agent, either heated or non heated, and the
recommended use of
gingival isolation, either by means of a gingival dam or a gingival paint-on barrier product. The product is applied in the office.
Advantages:
Minimal dependence on patient compliance and
Immediate visible results
Disadvantages:
are higher patient cost,
the use of chair time, and
the requirement of multiple in-office visits to get optimal results and retain them.
Examples of products include:38
Illumine (DENTSPLY Professional), containing 15% hydrogen peroxide
OfficeWhite (Life-Like Cosmetic Solutions), containing 40% hydrogen
peroxide
Perfection White (Premier Dental Products), containing 35% hydrogen
peroxide
Niveous (Shofu Dental), containing 25% hydrogen peroxide
Opalescence Xtra Boost (Ultradent Products), containing 35% hydrogen
peroxide
72. In-office bleaching:
In-office bleaching is useful in the removal of stains throughout the arch, or for lightening a
single tooth in an arch, or perhaps even treating specific area in a single tooth.
Names associated with In-office bleaching:36
Chairside bleaching
Power bleaching
Laser bleaching (the term is often used for any light source)
Dentist administered/applied bleaching (Barghi 1998)
Assisted bleaching (Miller 1999)/dentist supervised bleaching (Barghi)
Equipments needed:
The power bleaching material
Tissue protector: rubber dam or light activated liquid resin (e.g. Paint-on-dam by Den-Mat
Corporation and Opaldam, by Ultradent, USA)
Energising/activating source: this can be heat or light
There are many different lights available:
Regular halogen curing light
Plasma arc light
Argon and CO2 laser
Xenon power arc light
Heat source: some bleaches are heated in hot water first or heated over flame before
application over the tooth. The use of radiosurgery unit spoon-shaped electrode has been
advocated for accelerated bleaching procedure. (Sherman 1997). The curing light and
plasma arc lights produce only relatively small amount of heat.
Protective clothing and eyewear
73. Procedure:
Patient is assessed clinically and radiographically, and the proposed treatment plan
is discussed.
Pre-operative photograph of the teeth is taken.
The teeth are isolated with a protective mucous membrane seal and the gingival
are protected.
A rubber dam is placed and the teeth are ligated with floss to protect the material
from creeping under the dam.
The teeth are cleaned with pumice prophylaxis paste.
The bleaching material is applied to the teeth.
The light is applied close to the teeth. If plasma arc light is used, it is applied 6-
7mm away from the gel. A composite curing light can be used in addition or on its
own.
This is continued for a period of three, 3-minutes intervals or 10-15 minutes, and
the bleach is removed from the teeth via the high volume aspirator. This can also
be done with a damp gauze to avoid splutter.
The teeth are then washed, rinsed and the bleach is reapplied for a further 10
minutes. The process is repeated for 45 minutes to 1 hour.
The teeth are polished with diamond polishing paste or aluminium oxide discs of
varying degree of abrasiveness to achieve an enamel lustre.
The dam and mucosal protectant is then removed and the shade of teeth is
assessed.
Local anaesthetic are not administered during power bleaching treatment in order
that the dentist can monitor any patient discomfort and avoid tissue tingling and
74. Light-activated treatments
Light-activated treatment involves application in the office of a high concentration
hydrogen-peroxide agent, which is then ‘‘activated’’ by plasma arc, light-emitting
diodes, argon lasers, and metal halide and xenon-halogen
light sources. The theory behind the treatment is that light or heat will speed
the breakdown of the hydrogen peroxide and thus lighten the teeth more
rapidly. The assumed benefit is that the procedure is less time-consuming
while producing faster results. Current studies have produced equivocal results
with some touting the benefits while others conclude there is no benefit .
Examples of products include38
LaserSmile (Biolase Technology), containing 37% hydrogen peroxide
ArcBrite (Biotrol), containing 30% hydrogen peroxide
BriteSmile (BriteSmile), containing 15% hydrogen peroxide
Rembrandt Lightening Plus (Johnson & Johnson), containing 35%
hydrogen peroxide
Zoom (Discus Dental), containing 20% hydrogen peroxide
LumaWhite Plus (LumaLite), containing 35% hydrogen peroxide
75. Light sources for activation of
bleaching procedures:
A variety of light sources that greatly differ in their
properties are available to date to be used for light
activation of bleaching products.
If light is projected onto a bleaching product, such as
a bleaching gel, a small fraction is absorbed and its
energy is converted into heat. Most likely, this is the
main mechanism of action of all light-activated
bleaching procedures. In order to increase light
absorption and, as a result, heat conversion, some
bleaching products are mixed with specific colorants,
e.g. carotene. The orange-red colour of carotene
increases the absorption of blue light. In order to
increase the absorption of red and infrared light, small
silica particles in the nm- or lower µm scale may be
added, which gives these products a bluish
appearance
76. Light sources: Incandescence lamps like quartz–tungsten–
halogen (QTH) lamps, plasma arc lamps (used synonymously for
xenon gas discharge or xenon
short arc lamps) and laser sources (laser = light amplification by
stimulated emission of
radiation) of a variety of different wavelengths as well as light
emitting diodes (LED) have been proposed for light activation of
bleaching products. Metal halide lamps work in a similar way to
xenon discharge lamps, except that metal ions are the source of
light emission rather than ionized xenon gas.
A fundamental difference between these light sources is that lasers
emit a well-defined monochromatic light at a single wavelength only
(with some exceptions where two or three single wavelengths are
emitted at the same time). In contrast, QTH and plasma arc lamps
emit a wide wavelength range from ultraviolet, across the entire
visible spectrum deep into the infrared.
Curing lights:43
Various types of curing lights are used to activate the bleaching gel
or expedite the whitening effect. Initially, conventional curing lights
were used but these were quickly joined by lasers and plasma arc
77. Halogen Curing Lights:
Curing lights such as Demetron 501(Kerr Dental Ltd, Peterborough, UK)
can be used with a number of different systems such as Polar Office (SDI,
Victoria 3153, Australia) or Quick White Net (DMDS UK, Canterbury, UK).
Activation is via the light’s bleach mode for 30 sec per tooth and,
generally, the application involves three 10-minute passes. Some
products available, such as Opalescence Xtra (Ultradent Products, South
Jordan, Utah, USA) are based on a pre-mixed 35% hydrogen peroxide
gel that contains carotene which converts light energy
to heat and therefore increases the activation of the hydrogen peroxide by
encouraging further breakdown into active free radicals.
Plasma Arc Lam:
Systems that use these lights are usually based on three 10-minute
passes with light activation in whitening mode for 3 sec per tooth
performed twice during the pass. Alternatively, a full smile adaptor is used
to illuminate both arches together for the full 10-minute pass with the light
switching on and off in 5-sec bursts but giving out lower intensity.
Xe-Halogen Technology:
These systems utilize a full smile illuminator placed a few centimetres in
front of both arches to activate 35% hydrogen peroxide gel with the usual
protocol being three 10-minute passes. However, some authors have
recommended the use of a combination of carbamide peroxide (22%) and
hydrogen peroxide (38%) for 20-minute passes repeated three times, but
this protocol must be questioned in terms of possible penetration into the
pulp chamber and whether there is any benefi in combining 22%
78. Diode Lasers:
Both 830 nm and 980 nm wavelength diode lasers can be used for tooth
bleaching in combination with 35–50% hydrogen peroxide gel. The gel is
produced by mixing the hydrogen peroxide liquid with a powder mainly
containing fumed silica and a blue dye. The blue dye absorbs the laser
wavelength and heats up to cause the controlled breakdown of the
hydrogen peroxide to oxidizing perhydroxyl free radicals. The system is also
based on applying 2–3 mm of gel to teeth in the smile zone and three 10-
minute passes
with activation using 1–2 W of laser energy for 30 sec per tooth. It is
essential that all present, including the dentist, patient and nurse are
correctly protected with eye protective glasses as ocular damage is a real
risk with the use
of these lasers.
Metal Halide Lamp:
The Zoom light (Discus Dental, Culver City, CA 90232, USA) is used with a
two part 25% hydrogen peroxide gel in a dual arch technique employing
three 20-minute passes followed by the application of sodium fluoride gel.
Chemical activation:43
Systems such as Opalescence Xtra-Boost (Ultradent Products, South
Jordan, Utah, USA) are based on 38% hydrogen peroxide two part gel
system.
It consists of one syringe, containing hydrogen peroxide, that is chemically
activated by mixing with the second syringe, containing a unique proprietary
79. Dual activated systems:43
Hi Lite (Shofu Dental Products, Tonbridge, Kent, UK ) is a
system that contains both ferrous and manganese sulphate
which are chemically and light activated, respectively, to
accelerate the bleaching process to 7–9 minutes. The system
is based on 35% hydrogen peroxide blue gel that is activated
using a conventional light curing unit. After about 2 minutes,
the gel changes colour to green, following oxidization, and
then to cream, before finally becoming chalky coloured on
complete inactivation. At this point it is removed and a fresh
mix is applied, with the procedure being repeated up to six
times in one session.
Ultrasonic technology:43
The latest addition to in-surgery bleaching systems is the
SoniWhite Whitening System (DMDS UK, Canterbury, UK)
which utilizes ultrasonic technology with a 6–7.5% hydrogen
peroxide gel in upper and lower trays. The procedure only
involves approximately two cycles of 5 minutes but it is
thought that the use of the ultrasonic energy indirectly
80. Thermo/Photo Bleaching:
This technique basically involves application of 30 to 35% hydrogen
peroxide and heat or a combination of heat and light or ultraviolet
rays to the enamel surface. Heat is applied either by electric heating
devices or heat lamps. The technique involves the following steps:
1. Familiarize the patient with the probable causes of discoloration,
procedure to be followed, expected outcome, and possibility of
future re-discoloration.
2. Make radiographs to detect the presence of caries, defective
restorations, and proximity to pulp horns. Well-sealed small
restorations and minimal amounts of exposed incisal dentin are not
usually a contraindication for bleaching.
3. Evaluate tooth colour with a shade guide and take clinical
photographs before and throughout the procedure.
4. Apply a protective cream to the surrounding gingival tissues and
isolate the teeth with a rubber dam and waxed dental floss ligatures.
If a heat lamp is used, avoid placing rubber dam metal clamps as
they are subjected to heating and may be painful to the patient.
5. Do not inject a local anaesthetic.
6. Position protective sunglasses over the patient’s and the
operator’s eyes.
7. Clean the enamel surface with pumice and water. Avoid
81. 8. As an optional procedure, acid etch the darkest or most severely
stained areas with buffered phosphoric acid for 10 seconds and rinse with
water for 60 seconds. A gel form of acid provides optimum control. Enamel
etching for extracoronal bleaching is controversial and should not be
carried out routinely.
9. Place a small amount of 30 to 35% hydrogen peroxide solution into a
dappen dish. Apply the hydrogen peroxide liquid on the labial surface of
the teeth using a small cotton pellet or a piece of gauze. A bleaching gel
containing hydrogen peroxide may be used instead of the aqueous
solution.
10. Apply heat with a heating device or a light source. The temperature
should be at a level the patient can comfortably tolerate, usually between
125°F and 140°F (52°C to 60°C). Re wet the enamel surface with
hydrogen peroxide as necessary. If the teeth become too sensitive,
discontinue the bleaching procedure immediately. Do not exceed 30
minutes of treatment even if the result is not satisfactory.
11. Remove the heat source and allow the teeth to cool down for at least 5
minutes. Then wash with warm water for 1 minute and remove the rubber
dam. Do not rinse with cold water since the sudden change in temperature
may damage the pulp or can be painful to the patient.
12. Dry the teeth and gently polish them with a composite resin polishing
cup. Treat all of the etched and bleached surfaces with a neutral sodium
fluoride gel for 3 to 5 minutes.
13. Inform the patient that cold sensitivity is common, especially during the
first 24 hours after treatment. Also, instruct the patient to use a fluoride
82. 14. Re-evaluate the patient approximately 2 weeks later
on the effectiveness of bleaching. Take clinical
photographs with the same shade guide used in the
preoperative photographs for comparison purposes. If
necessary, repeat the bleaching procedure.
83. Assisted bleach technique or
Waiting room bleach technique:
The bleaching technique can be used for both vial and
non-vital teeth.
This technique was invented by Den-Mat when the Quick-
Start product was introduced to be used to initiate the
bleaching procedure and for the patient to continue
bleaching at home.
The teeth are polished with prophylaxis paste. Cheek and
lip retractor are placed.
35% Carbamide peroxide is used which can be heated
gently, by holding the syringe under hot running water for
2-3minutes prior to use, but this is not mandatory. Heating
the syringe accelerates the activity of material before it is
loaded into the mouthgaurd.
Dentist applies the material into a custom made bleaching
tray, and after the excess material is removed, the patient
return to the waiting room for a period of about 30 minutes
with bleaching tray in the mouth.
After 30 minutes, the bleach is suctioned off the teeth
84. Compressive bleaching
technique:
Miara (2000) suggests that the power bleaching
technique could be made more effective by
compressing the bleaching material onto the
tooth.
He recommends using 35% hydrogen peroxide in
a bleaching tray, sealing the tray edges with light
cured resin to prevent damages to the soft tissue.
The benefit of this method is that it influences the
penetration of oxygen ions into the tooth enamel,
which improves tooth shade significantly.
85. Laser bleaching
Laser-assissted bleaching has been introduced as a bleaching technique, in an attempt to accelerate he
bleaching process56. Laser bleaching officially started
in 1996 with the approval of ion laser technology’s argon and Co2 lasers by FDA.
Two types of lasers can be employed: the Argon laser that emits a visible blue light and a Carbon-dioxide
laser that emits invisible infrared light. These lasers can be targeted to stain molecules and, with the use of
a catalyst, rapidly decompose hydrogen peroxide to oxygen and water. The catalyst/peroxide combination
may be damaging; therefore, exposed soft tissues, eyes, and clothing should be protected. Combination of
both lasers can effectively reduce
intrinsic stains in the dentin. An argon laser can be targeted at stain molecules without overheating the pulp.
It is easy to use and is best for removal of initial dark stains, such as those caused by tetracycline. However,
visible blue light becomes less effective as the tooth whitens, and there are fewer stain molecules. On the
other hand, the carbon-dioxide laser interacts directly with the catalyst/peroxide combination and removes
the stain regardless of the tooth colour. Some techniques involve high-concentration hydrogen peroxide
formulations as active ingredients (35 to 50%). It was reported that such laser bleaching techniques
lightened teeth faster. However, short term postoperative sensitivity can be profound.14
Advantage:36
Bleaching is faster due to high concentration of active ingredients
Disadvantage:36
Expensive
Procedure is time consuming
Pos operative sensitivity can be high
86. Procedure:36
Rubber dam or light-cured soft tissue protectant isolates the soft
tissue and gingival.
The laser bleaching gel is placed at a thickness of 1-2mm on the
buccal surface of teeth to be bleached (Reyto 1998).
The Argon laser light is applied for 30 seconds about 1-2cm from
buccal surface of each tooth.
Laser light of 488nm is applied slowly for 30 seconds and moved
from right to left over the tooth surface.
Afer the laser is applied, gel is left on tooth for 3 minutes.
The gel is then removed from the tooth first by wiping it off and
then rinsing off the excess.
The gel is reapplied in this manner five more times to equal about
one hour session of bleaching.
An alternative technique involves using both the argon and carbon
dioxide laser. The argon laser is used as described previously and
then Carbon dioxide laser is employed with another peroxide
based solution to promote the penetration of the bleaching agent
into the tooth to provide bleaching below the surface ( ADA Council
on Scientific Affairs 1998). Treatment time for this system ranges
from 1-3 hours.
87. In-office, one-hour whitening
The first bleaching of teeth to change colour was an
inoffice procedure. Currently, the most popular
systems for in-office bleaching use high concentration
hydrogen peroxides and are often referred to as “one-
hour bleaching.” These high concentration hydrogen
peroxides range from 25% to 35%. In-office bleaching
can be provided to patients as either a one-visit 1–
1.5 hour treatment or a multiple visit procedure . One
can use one of the light enhanced bleaching
techniques, a laser-activated bleach or merely a
paint-on bleaching gel or solution. For the in-office,
light-enhanced systems, usually the light can only be
used for bleaching (BriteSmile, Discus Dental;
LumaArch, LumiLite; Zoom 2, Discus Dental). One
light system is based on a plasma arc high-intensity
photopolymerization device (Sapphire PAC Light,
Den-Mat) that can be used for in-office whitening and
for resin photopolymerization.
89. OVER-THE-COUNTER TOOTH WHITENING CHOICES8,9
In the past ten years, there has been a significant increase
in the number of over-the-counter (OTC) tooth whitening
products available. The benefits achieved with bleaching
systems with trays associated with the consumers’ and
patients’ needs have stimulated the marketing of over-the-
counter (OTC) products for at-home tooth bleaching.
OTC products appeared in the USA in the beginning of the
2000s, as an alternative to treat tooth discoloration with
lower cost than traditional professional-prescribed/guided
products. The proliferation of these OTC products in the
USA was in a certain way stimulated by the Food and
Drug Administration (FDA). According to the FDA, these
products could reduce inequity in the access to the health
system, reducing the cost of treatments.
Currently, gels, rinses, gums, dentifrices, whitening strips
or paint-on films with low levels of carbamide or hydrogen
peroxide are widely available to consumers at pharmacies,
supermarkets and over the Internet.
90. 1.Whitening strips:
These products were created aiming to avoid the
use of trays. Adhesive strips containing bleaching
agents are bonded to the anterior teeth, and they
release the active ingredient during relatively
short time periods (5 to 60 minutes), once or
twice a day. The active ingredient is hydrogen
peroxide (HP) in low concentrations (5 to 14%)
Hydrogen Peroxide Strips- An OTC, 5.3%
hydrogen peroxide-coated polyethylene strip
(Crest Whitestrips, Procter & Gamble) was
recently introduced to the market. According to
the manufacturer’s recommendation, the patient
applies two strips per day for 30 minutes each.
91. 2.Whitening dentifrices:
Toothpastes that claim to have tooth-whitening
properties represent more than 50% of the OTC
products and rarely contain Carbamide or Hydrogen
peroxide, or any other kind of bleaching agent. Their
stain-removal ability is related to the large quantity of
abrasives in their formulation, which remove
superficial extrinsic stains. The active components of
tooth whitening dentifrices include enzymes that
break down the organic molecules of biological film.
Additionally, abrasives such as Alumina, Dicalcium
phosphate dihydrate and Silica are also present in the
formulation to promote stain-removal.
However, the toothpaste abrasiveness needs to be
moderated in order to prevent excessive wear to the
underlying enamel and dentine.
92. 3.Whitening mouthrinses:
They appeared recently in the market and
manufacturers advertised that they could prevent
stains and fight plaque build-up.
Generally, a low concentration of hydrogen peroxide
(1.5%) is present and sodium hexametaphosphate
can also be included in the formulation to protect the
teeth surface from new stains.
4.Whitening dental floss and toothbrushes:
Whitening dental floss has been introduced to
promote stain reduction around the interproximal and
sub-gingival areas. The stain-removal removal
properties are associated with the presence of silica
in the composition, which promotes a superficial
surface abrasion during application in the interdental
93. 5.Chewing gum:
Chewing gum with sodium hexametaphosphate
(4.0 - 7.5%) has been introduced as an OTC
product for home-use bleaching claiming to
prevent extrinsic tooth stain formation.
Paint-on gels:
Paint-on gels or varnishes are OTC barrier-free
whitening products that present hydrogen or
carbamide peroxide in a suspension that is
brushed by an applicator over the tooth surface
and which adheres to enamel.
94. OTC tray with gel activated by light:
A new product has become available recently in drug stores or
on the Internet, consisting of a universal tray that can be adapted
by the individual himself.
This tray then receives a gel that is activated by a compact LED
unit. The manufacturer claims that the bleaching effect is similar
to that of a supervised at-home bleaching with a tray, but it does
not clarify what is the active ingredient.
Disadvantages of OTC:
In terms of disadvantages, the major concern is the potential
consequences of misuse of these products, which include
burning of the gums and sensitivity of the teeth.
It can also be argued that whether due to technique of
application, strength of active ingredient, or some other factor,
OCT products are simply not as effective as Dentist Whitening
options.
Most over-the counter product fail to provide more than a
temporary removal of surface deposit on the teeth. 11
Editor's Notes
All the systems are manufactured as a viscous gel, and packaged in a syringe presentation. Recent changes have seen the gel being separated into a base material and activator. When squeezed through a special nozzle into a custom tray, the two components are evenly mixed and become active. This dual presentation has prolonged the shelf life from 12 – 18 months, to about 3 – 4 years.
Common oxidation processes associated with bleaching teeth. The saturation point, at which the optimal amount
of bleaching has occurred, is located in the middle of the diagram
