Introduction
Enamel decalcification or white opaque
lesions around orthodontic attachments are a common problem during and following
fixed orthodontic treatment. Decalcification often follows plaque accumulation
promoted by appliance components and bonding materials.1-3 Subsequent
acid production by the bacterial plaque result in an alteration in the appearance
of the enamel surface.3 Early lesions appear clinically as opaque,
white spots caused by mineral loss in the surface and subsurface of the enamel.4
If mineral loss continues, then a frank cavity is formed.5,6 Clinically,
formation of white spots around orthodontic
attachments can occur as early as 4 weeks into treatment7 and their
prevalence among orthodontic patients ranges from 2-96%.8-10 The
labio-gingival area of the lateral incisors is the most common site for white
spot formation and the maxillary posterior segments are the least common site.7
The incidence of white spot formation is usually more among male patients
and has been attributed in part to their poorer oral hygiene standards than
that of females.8,11 The presence of white lesions at the end of
orthodontic treatment is a major esthetic problem. This problem has been recognized
and many attempts at prevention have been offered, but it continues to be
a problem.
Thus, the
main purpose of this article is to provide up-to-date knowledge on the various
factors causing white lesion formation during orthodontic treatment and contemporary
measures to consider for their prevention.
Etiology
The appearance
of white opaque lesions on the enamel surface during fixed orthodontic treatment
is due to a multiplicity of factors. Co-existence of the four factors namely,
bacterial plaque, fermentable carbohydrates, a susceptible tooth surface and
a sufficient period of time are necessary for white opaque lesions to develop.
Microbial
factors
It has been documented that the initiation
and progression of the smooth surface caries are associated with Streptococcus mutans and their prevalence
is significantly associated with caries prevalence and its increment.12,13
It is seen that Streptococcus mutans
prefer to colonize over the retentive areas of solid surfaces and thus their
presence at high level on these surfaces is an indicator of increased caries
risks.14 After initiation of the caries lesion, its progression
is caused by Lactobacillus.15
The presence of large number of lactobacillus indicates that the necessary
conditions for producing dental caries do exist.15 Increased proliferation
of the Streptococcus mutans and
Lactobacillus, and new sites of
plaque appearance on the enamel surrounding the orthodontic attachments is
common in patients undergoing fixed appliance therapy.16-18 This
may be influenced by the duration of the orthodontic treatment and the number
of orthodontic attachments.18
Salivary factors
Saliva plays
an important role that influences the dynamics of mineral loss and deposit
at the enamel-plaque interface. The amount of enamel demineralization, the
rate of demineralization and the likelihood of enamel remineralization is
influenced by salivary factors such as pH, rate of flow and buffer capacity.19
Exposure of the tooth surface to the carbohydrate, pH of the plaque and microbial
composition of the plaque are regulated by the saliva. Saliva also acts as
a vehicle for the delivery of fluoride ions to the enamel and plaque.
Tooth surfaces
that are more exposed to dietary carbohydrate with less exposure to saliva
are common sites for demineralization to occur. Because of this reason the
site with highest incidence of demineralization, that occurs during fixed
orthodontics, is the maxillary anterior teeth.9 (Figure-1 and 2)
The lingual surface of the lower incisors where salivary flow is adequate
is often the site of calculus formation, indicating mineralization.10
This suggests that sufficient amounts of saliva acts as a major factor in
preventing enamel demineralization.
Evidence shows
that salivary flow rate can influence both caries risk and caries activity.
20 Adequate flows of the saliva helps in physical cleansing of
carbohydrates from tooth surfaces, maintains its buffering capacity and anti-microbial
activities. Therefore, adequate flow of the saliva is considered as an important
factor for prevention and management of enamel demineralization.21
Enamel demineralization
is caused by the low pH of the plaque and this acidic pH is usually countered
by the alkaline pH and buffering capacity of the saliva. The pH and buffering
capacity of the saliva is, however, maintained by the rate of salivary secretion.22
An intraoral environment with low pH favors colonization of the cariogenic
bacteria, particularly Streptococcus mutans, whereas a high salivary pH maintains a higher
buffering capacity. There is also a significant negative correlation between
the salivary buffering capacity and the frequency of caries.23
Oral hygiene
The presence of orthodontic attachments
makes tooth cleaning more difficult and predisposes to plaque accumulation
on the tooth surface. Fixed orthodontic appliances also restrict the self-cleansing
action of the tongue, lips and cheek to remove food debris from the tooth
surface. Therefore, accumulated food debris, particularly fermentable carbohydrates,
encourage growth of the cariogenic bacteria such as Streptococcus mutans and Lactobacillus. Most growth sites are usually
found on the gingival margin and on the edges of orthodontic bands.24
A study showed a five fold increase in lactobacillus count in patients undergoing
active orthodontic treatment. 24
Diet
During fixed orthodontic treatment,
frequency of carbohydrate ingestion has a significant influence on enamel
demineralization. Normally following
ingestion of the fermentable carbohydrate, acids are produced inside the plaque
and plaque pH falls, and it recovers as salivary buffering occurs. However,
as the frequency of carbohydrate intake increases, the enamel surface may
be exposed to overlapping episodes of acid without intervening repair, resulting
in a net loss of minerals over time.
Fixed orthodontic
appliances
Insertion
of the fixed orthodontic appliance into the oral cavity creates new stagnation
areas. The irregular surfaces of the orthodontic attachments restrict the
self-cleansing action of the tongue, lips and cheek. In the presence of carbohydrate,
the reduced access by saliva also encourages lowering of the plaque pH.
These changes favor colonization of Streptococcus
mutans and Lactobacilli. 16-18,24-28
It has been found that plaque deposition is greater on resin bonded material
than on enamel29 and also more on the gingival side of bonded brackets.30
Thus, the introduction of fixed appliances into the oral cavity appears
to alter the normal microbial ecology and introduces another variable into
the system.
The contribution
of arch wire ligation materials to plaque accumulation, bacterial colonization
and enamel decalcification has also been evaluated.28,31,32 Teeth
ligated with elastomeric rings exhibited a greater number of cariogenic microorganisms
than teeth ligated with stainless steel ligature wires.28,31 However,
recent studies failed to find an alteration in the number of Streptococcus mutans around the orthodontic
brackets ligated with either ligature wire or elastomeric rings.33,34
Studies have
shown that the resting salivary flow increases during fixed orthodontic treatment.35
Since the salivary pH and buffering capacity increases with the increase rate
of salivary flow, it counteracts the demineralization tendency that arise
during fixed orthodontic treatment.22 This could be the reason
why in some patients there are little white spots around orthodontic appliances
despite moderate plaque accumulation.
Thus, at the
beginning of fixed orthodontic treatment, an assessment of patient susceptibility
to enamel demineralization seems logical. Many authors recommended a range
of factors to be examined in order to identify patients at risk of developing
demineralization.16,19,21 These factors include; assessment of
salivary flow rate, history of past enamel caries, caries incidence over the
past year, plaque scores, caries activity tests, dietary pattern and residence
of fluoridated or non-fluoridated communities.
Pathogenesis
Appearance of the white opaque lesions
on the enamel surface is basically due to subsurface demineralization resulting
in porosity and changes in the optical properties of the enamel. The demineralized,
porous enamel may appear as chalky or may associate with erosion of the surface.
The lesions appear after a series of repeated episodes of mineral loss, with
mineral from the surface being lost into the plaque fluid and saliva, and
the mineral from the subsurface reconstituting the surface. This process is
an interrupted process with episodes of repair and destruction depending on
the oral environment. Fluctuations in plaque pH directly influence the diffusion
of calcium and phosphate ions out of the enamel.
When the surface of the porous lesion
remains intact, there is the possibility of arrest or even reversal of the
lesion. This remineralization may occur spontaneously through the combined
action of the salivary minerals and fluoride from the dentifrices or through
therapeutic intervention. When the pH of the plaque remain low for long period
of time, it become conducive to long periods of mineral loss with short periods
of remineralization. As a result, a stage arises where the surface cannot
repair by reprecipitation from minerals from the subsurface and this results
in cavity formation.
Prevention
and Management
The risk of enamel demineralization
during fixed orthodontic treatment can be prevented by either eliminating
the plaque deposition on the enamel surface by improving patient oral hygiene2
or by enhancing the enamel resistance to the microbial acid by using topical
fluoride.36,37 However, maintenance of optimum oral hygiene is
frequently inadequate. Therefore fluoride is used as a principal ingredient
for the prevention of enamel demineralization during fixed orthodontic treatment.
It is found that fluoride not only inhibits the development of white spots3,38,
it also reduces the size of the white spots39 during fixed orthodontic
treatment. Fluoride also enhances enamel remineralization following orthodontic
treatment. 3,38 The cariostatic effect of topical fluoride is primarily
due to calcium fluoride formation.38 It has been documented that
a high fluoride concentration in the enamel is less important than a moderate
increase in fluoride concentration in oral fluid.40 For maximum
caries inhibition, continuous presence of fluoride, even at low concentrations,
in saliva and plaque fluid is necessary.41 Proper oral hygiene
maintenance, combined with daily use of topical fluoride, is found to significantly
reduce enamel decalcification.9 Home use of topical fluoride agents
needs patient compliance. 6,42,43 As a result, different non-compliant
topical fluoride delivery measures have been implemented to prevent enamel
demineralization around orthodontic brackets.
Fluoride mouthrinse
Sodium fluoride
mouth-rinse has been extensively studied and can almost totally eliminate
white spots if used throughout therapy and should be recommended to all orthodontic
patients.3,43,44 Daily mouthrinse with sodium fluoride (.05% or
0.2%) and/or weekly with acidulated phosphate fluoride (1.2%) rinse have been
found to reduce the incidence of enamel demineralization during active fixed
orthodontic treatment.3,38 After a systematic review, it is recommended
that the best method to prevent enamel demineralization during fixed orthodontic
treatment is daily use of 0.05% sodium fluoride mouth rinse.45
However, Hirschfield advocated the use of an APF mouthrinse to make enamel
more resistant to orthodontic induced decalcification.46 Geiger
et. Al. reported 25% reduction in the number of white spot lesions using fluoride
rinse.47 It was also found that following two weeks use of sodium
fluoride mouthrinse, with one rinse per day, fluoride concentration in the
saliva increased significantly.48
Fluoride gel
Many investigators
have tried Stannous fluoride gels (0.4%) during orthodontic treatment and
reported decreased enamel decalcification.49,50 Currently, Boyd
compared the use of a 1100ppm fluoride toothpaste alone or together with either
a daily 0.05% sodium fluoride rinse or a 0.4% stannous fluoride gel applied
twice daily by toothbrush.51 He found that both the gel and rinse
provided additional protection against decalcification when compared to toothpaste
alone, but neither was superior. In a previous study Hastreiter was also found
the same result.52
Fluoride toothpaste
Regular use
of fluoride toothpaste is a very common recommendation by the orthodontist,
but it is shown to be inefficient in inhibiting white spot development around
the orthodontic brackets.53-55 However, Stookey recommended that
toothpastes containing sodium fluoride are most effective against white spot
development.56
Fluoride varnish
Use of Fluor
Protector a polyurethane varnish containing 0.7% diflurosilane was found to
decrease white spot lesion formation under molar bands.57 Many
more studies have also found that fluoride varnishes are effective in preventing
enamel demineralization.58-60 Thus the use of fluoride varnishes
under orthodontic bands can be an effective way to prevent white spot formation
during orthodontic treatment. Recently, chlorohexidine varnish was also suggested
for reducing plaque accumulation and enamel decalcification.61
Pit and fissure
sealant
Frazier et.
Al. put light cured pit and fissure sealants on the labial enamel surface
adjacent to the bonded orthodontic brackets and found it effective in preventing
enamel demineralization without patient compliance.62 However,
the main problem of placing sealants in a patient’s mouth is that it is very
technique sensitive, and mechanical and chemical breaks in the sealant layer
may lead to enamel decalcification under the sealant.
Fluoride in
luting cement
Kaswiner advocated
the application of cements containing fluoride for banding.63 It
is also found that the use of glass ionomer cement can reduce enamel demineralization.64
Glass ionomer cements have been shown to decrease enamel decalcification
when compared with zinc phosphate and zinc polyacrylate cements.65 Another
study also showed that fluoride releasing cements like zinc polycarboxylate
and resin modified glass ionomer cement demonstrated less enamel demineralization
than the zinc phosphate cement.66 Millett et. Al. also found less
severe enamel decalcification around orthodontic brackets with glass ionomer
cement when compared with composite, but the difference was not statistically
significant.67
Fluoride in bonding agents
Bonding agents containing fluoride
have the potential for decreasing enamel decalcification.68-71
It was also found that fewer white spot lesions were found with the fluoride
containing composite as compared to conventional bonding agents.72,73
The use of glass ionomer cement for bonding brackets significantly reduced
enamel demineralization around orthodontic brackets.74 Recently,
it was suggested that resin-modified glass ionomer cement efficiently reduced
enamel demineralization around the bonded brackets.75 It was concluded
that the fluoride release is greater with resin modified glass ionomer cements
and also over prolonged period, as compared to the fluoride containing composites.76
However, Corry et. al. concluded
that resin-modified glass ionomer cement alone and composite with added fluoride
had equal cariostatic effects, and the inhibition of white spot formation
could best be achieved by the use of resin-modified glass ionomer cement supplemented
with topical fluorides.77 Thus, evidence
showed that glass ionomer cement, when used as a bonding agent, is more effective
at preventing enamel demineralization and post orthodontic white spot lesions
than a conventional composite resin.
Fluorides in elastomers
Several manufactures are marketing
elastic ligatures and power chains containing fluoride. Many investigations
also suggest that fluoride-releasing elastomeric modules were effective in
reducing plaque accumulation and enamel decalcification around the brackets.78-80
However, recently Benson, Shah and Campbell concluded that fluoridated elastomers
had no effect on the quantity of disclosed plaque around orthodontic brackets.81
Joseph, Grobler and Rossouw reported that fluoride release from a fluoride
containing elastic chain was high for the first week and decreased significantly
after that.82 Thus, for optimum fluoride release it is necessary
to change the elastic chain on a weekly basis. Due to the short-term nature
of fluoride release these elastomeric ligatures had no significant anti-cariogenic
benefits in patients undergoing orthodontic treatment.83 An in
vitro study by Whiltshire showed fluoride release for up to 6 months by fluoridated
elastomers.84 It was also found that the fluoride release, in vivo,
is about 7 times more as compared to in vitro during one week period.85
In the presence
of fluoridated toothpaste and mouthrinse the fluoride release is
also significantly more.
Thus, fluoridated elastomers may imbibe fluoride from their environment.85
Argon laser
The mode of
action of the argon laser for the prevention of enamel decalcification is
by altering the crystalline structure of the enamel has been suggested.86,87
Blankenau et. al. for the first time found an average of 29.1% reduction in
the depth of enamel decalcification with argon laser irradiation.87
Many other studies are also reported significant reduction in lesion depth
after argon laser irradiation of enamel.88,89 Thus, argon laser
irradiation can be considered as an effective method in reducing enamel decalcification
during orthodontic treatment.
Mechanical
plaque control
Since plaque is the primary cause of
demineralization, thorough mechanical plaque control is also of paramount
importance. It is found that tooth brushing is the most practical and acceptable
method for plaque control.90 Proper method of tooth brushing during
fixed orthodontic treatment has also been recommended.91,92 A modification
of the standard toothbrush has also been suggested for use by patients with
fixed orthodontic appliances.91 Use of disclosing solutions or
tablets is also helpful for self monitoring of oral hygiene effectiveness.91,92
Use of a power toothbrush or daily water irrigation in combination with manual
tooth brushing may be a more effective method in reducing plaque accumulation
than manual tooth brushing alone. Bracket attachment by direct bonding exposes
the proximal surfaces to enamel demineralization because of the difficulty
in maintaining oral hygiene with archwires in place.90 Dental flossing
has proved helpful in interproximal cleaning.63 A floss threader
can be used for threading the floss under the main archwire.92
A soft rubber interdental stimulator can also be helpful in cleaning and massaging
the interproximal areas.91
Fate of Enamel Scars
Several studies
have reported that demineralization ceases following removal of fixed orthodontic
appliances.93,94 This could be due to physical removal of the overlying
acid-producing plaque and improved accessibility to saliva. The demineralized
enamel that appear as white spot may disappear either because of surface abrasion
or result from a reparative precipitation of mineral deposits.95-96
Fitzpatrick and Way demonstrated that after acid etching the return to a normal
enamel surface was because of a filling-in of material and not because of
wearing away of the etch97. Some investigations also indicated
that it was of an appatitic nature, with only minor amount of impurities96,98.
However some evidence suggests that clinical improvement in incipient lesions
is not entirely due to remineralization and it could be due to surface abrasion
of the enamel surface. It has been suggested that polishing or abrasion of
the dull and irregular enamel surface results in the exposure of the more
tightly packed enamel crystals which give a harder and glossier clinical appearance.93
It is important
that remineralization is significantly enhanced by fluoride. Therefore, routine
fluoride mouthrinse might serve a valuable purpose also in the time period
after debonding99. It has
been suggested that lesions that develop in a highly fluoridated environment,
during orthodontic treatment, may form a diffusion barrier against subsurface
uptake of minerals from saliva, as a result the subsurface area remain hypomineralized.
Such lesions do not disappear completely and may remain as white spot for
several years after treatment.93,100 However, the appearance of
white lesions that persists after orthodontic treatment can be improved by
a hydrochloric acid-pumice micro-abrasion technique.101
Conclusion
White spot lesions are one of the common
complications of fixed orthodontic treatment. It is the responsibility of
an orthodontist to minimize the risk of the patient having decalcification
as a consequence of orthodontic treatment. The necessity for excellent oral
hygiene practice, during fixed orthodontic treatment, must be explained. Patients
must be given a vigorous fluoride supplement in the form of mouthrinsing in
preventing enamel decalcification during and after fixed orthodontic treatment.
