Iatrogenic damages of orthodontic treatment

IATROGENIC DAMAGES OF
ORTHODONTIC TREATMENT
AND ITS MANAGEMENT
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 IATROGENICS OF ACID ETCHING
 Alternatives to acid etching
 DEMINERALIZATION AND ITS MANAGEMENT
 Topical fluoride, varnishes, ligatures, adhesives
 Sealants
 Glass ionomer cements
 Antimicrobial agents
 Low fermentable sweeteners
 Argon laser irradiation
 EXTERNAL APICAL ROOT RESORPTION AND MANAGEMENT
 ENAMEL WEAR, ABRASION AND FRACTURES - MANAGAMENT
 PERIODONTAL PROBLEMS
 Interdental recession
 RME and gingival recession
 RME – its effect on pulp and root resorption
 Alveolar bone height after treatment
 LATEX ALLERGIES AND MANAGEMENT
 NICKEL ALLERGY AND MANAGEMENT
 CYTOTOXICITY OF ADHESIVE RESINS
 INJURIES FROM ORTHODONTIC APPLIANCES AND MANAGEMENT
 ORTHODONTICS AND TMJ

IATROGENICS OF ACID ETCHING
Lehman AJO 1981
The conditioning of the enamel surface with phosphoric acid
causes loss of enamel surface contour.
Etched enamel is predisposed to the development of initial
caries, resulting in discolorations such as white spots.
Even after removal of the brackets, the histologically changed
tooth structure may be more susceptible to decalcification
processes. Gwinnett found that 50 percent phosphoric acid
produced a bulk enamel loss in excess of 5 microns but always
less than 25 microns.
Silverstone investigated the effect of etching durations of
different types of etching solutions at various concentrations. His
results showed less loss of tissue with increasing acid
concentrations, whereas the first minute's etching caused the
greatest effect.

A possible explanation of the differences in enamel
solubility may be the biologic variation in structure and
composition of the various enamel samples
investigated.
Moreover, the fluoride concentration of the enamel at
the surface plays an important role in the reduction of
enamel solubility and, consequently, in the loss of bulk
enamel due to etching.
Since the slope of the fluoride concentration gradient
within the first microns from the enamel surface seems
to be very steep, it is important to take into account the
fluoride concentration of the enamel surface to be
treated with a conditioning agent.

It was shown that topically
fluoridated tooth enamel has a
highly acid-resistant layer of 2 to 4
microns.
At least 2 minutes of etching with
phosphoric acid (50 wt. percent) is
necessary to remove such a layer
and to expose a surface with the
same solubility and etch pattern as
nonfluoridated enamel.
High fluoride concentrations
(>50 ppm) slow down the
dissolution of bulk enamel in
phosphoric acid.

A mean fluoride concentration of about 25 ppm, as present in
subsurface enamel, causes a mean loss of 6.7 microns of
bulk enamel after etching for 60 seconds with 50 percent
phosphoric acid solution.
Conventional etching with phosphoric acid is known to
produce dissolution of the outermost enamel layer and
provide mechanical attachment for bonded orthodontic
brackets when suitable acrylic or diacrylate resins are used.
Care must be taken not to induce iatrogenic effects, including
cracks, scratches, and removal of pieces of enamel. All
adhesive remnants should be removed at the time of
debonding, as abrasive wear of most orthodontic adhesives
apparently is minimal.

The following iatrogenic factors involved in acid etching
led to the development crystal growth principle.
Loss of enamel caused by etching
Retention of resin tags that can lead to possible enamel
discoloration
Leakage at bracket interface leading to bracket corrosion
and staining
Enamel loss caused by fracturing of enamel at time of
debonding.
A rougher surface with enamel cracks if debonding is
carried out improperly, resulting in increased plaque
retention.
A softer enamel surface with lower fluoride content - more
predisposed to decalcification.

Zafer et al in Angle 2000 evaluated the effects of two new
acid-etching solutions, non-rinse conditioner (NRC) and 17%
EDTA on enamel surface morphology and compared the new
solutions with traditional 37% phosphoric acid.
They found that NRC treatment produces a smooth yet
adequately rough enamel surface for bonding without a need
for prolonged etching time.
Etching with 17% EDTA was not recommended for
orthodontic purposes. Regardless of treatment time, etching
with 37% phosphoric acid resulted in irreversible damage of
the enamel surface.
They concluded that 15 secs etching time with 37%
phosphoric acid was suitable for producing acceptable bond
strength while minimizing enamel loss.

Alternatives to acid etching:
Polyacrylic acid solutions, which
contain residual sulfate ion, produce, in
addition to slight etching, a crystalline
deposit that bonds firmly to the enamel
surface and resist mechanical removal.
The crystals were shown to be calcium
sulfate dihydrate (gypsum). The crystal
formation depends mainly on the
sulfate ion concentration in the
polyacrylic acid solution and is
independent of the molecular weight or
concentration of the solution.
The potential value of this crystalline interface as mechanical
interlocking for orthodontic bracket bonding was tested in vitro
by Maijer and Smith.

Crystal growth on the enamel surface leads to the formation of a
dense growth of small, needle shaped crystals.
Sulfated polyacrylic acid is placed on the tooth for 30 to 45
sec.
This promotes reaction of the calcium in the enamel with
the sulfate component in the liquid.
This results in crystals on the enamel
There are no pores created in the enamel as in acid etch.
The micro mechanical interlocking is created at the enamel surface
(crystal growth)
The crystals are CaSo4.2H2O (Gypsum)
These calcium sulfate dihydrate crystals are 20µm in
length and 2 to 5µm in thickness.
A chemical bond occurs between enamel and gypsum
crystals.

Årtun and Bergland in AJO 1984 tested the applicability of
two crystal bonding agents in routine clinical orthodontic
practice, using two test solutions containing sulfuric acid.
The purpose of the study was to find out if debracketing and
subsequent adhesive cleanup were easier and quicker with
this method than after etching with phosphoric acid and to
determine clinically whether the two enamel-conditioning
methods result in similar or different failure rates in terms of
the number of loose brackets.
They found failure rates that were clinically unacceptable
and the mode of loosening was mainly between the enamel
surface and adhesive on the crystal-growth-conditioned
teeth.

ENAMEL DEMINERALIZATION
Enamel decalcification remains a common
negative sequelae of orthodontic treatment in
the absence of proper oral hygiene. The
presence of white spot lesions after removal
of orthodontic appliances is a discouraging
finding to a specialty whose goal is to
improve facial and dental esthetics.

Orthodontic treatment with
multibanded appliance imposes a
significant risk for development of
WSL.
The most common type is a diffuse
opacity. The opacities covered an
average of less than 1/3rd of the
labial surface of the tooth.
Studies on decalcification have
found that an approximately 7% of
patients are affected with the WSL.
Decalcification has been found to
regress following appliance removal.
There is a significant decrease in the
extent of WSL and the mean extent
of opacities 1 year after appliance
removal.

Patients undergoing orthodontic treatment have changes in
the oral ecologic, such as low–pH environment, increased
retentive sites for streptococcus mutans, and increased
retention of food particles, which may lead to post-orthodontic
treatment decalcification in certain cases.
Placement of fixed orthodontic appliances is normally followed
by an increase in oral colonization by mutans streptococci,
concomitant with an increased risk for development of carious
lesions.
Decalcification occurs when the pH of the oral environment
favors diffusion of calcium and phosphate ions out of enamel.

Decalcification follows plaque accumulation with subsequent
acid production leading to alteration in enamel surface.
Early lesions appear by mineral loss in the surface or
subsurface of enamel and are followed by cavitations.
Following appliance removal, WSL may regress or disappear
primarily as a result of surface abrasion but they still may
pose an esthetic problem.
Enamel Demineralization Scale
0 - No enamel opacity or surface disruption
1 - An opacity without surface disruption, or mild
demineralization
2 - An opacity having a roughened surface, or moderate
demineralization
3 - An opacity requiring a restoration, or severe
demineralization

INCIDENCE OF WHITE SPOT LESIONS:
According to Gorelick et al in AJO 1982, white spots caused by
the decalcification (non developmental) process can usually be
differentiated from abnormal enamel calcification of developmental
origin on the basis of location, shape, and dimensional stability with
time.
WSL is an optical phenomenon owing to subsurface tissue loss
and is exaggerated by thorough drying. The zones in the lesion
can be expressed in terms of spaces present or, conversely, tissue
loss.
The first zone of histologic change is called the translucent zone.
Here there is an absence of structural rod outlines and a tenfold
increase in the amount of space compared to normal, unaffected
enamel.

Progressing into the lesion, the next zone is the dark or
positive zone.
The latter is named for its appearance in polarized light
microscopy.
This zone exhibits a further increase in the volume of
spaces.
It has been suggested that the translucent zone results
from preferential dissolution of structure at the rod
periphery, which then proceeds to the cross striations
producing the dark zone. It has been shown, however, that
remineralization occurs in the dark zone.
Finally, the core of the rods is involved producing a zone of
maximum tissue destruction termed the body of the lesion.

The authors found that
mandibular posterior (15 per cent) and
Maxillary anterior (14 per cent) teeth had the highest
incidence of white spot formation.
The maxillary lateral incisors had the highest incidence of
decalcification (21 per cent), which was almost three times as
frequent as that found for the central incisors.
Study by right and left sides of the dentition and maxillary and
mandibular arches showed no consistent associations in the
distribution of white spots.
The maxillary and mandibular canines and premolars had a
high incidence.

Decalcification of the buccal surfaces of teeth during orthodontic
therapy is a problem of clinical importance, as shown by the
finding that 3.6 per cent of the teeth had white spots in the control
group and 10 per cent after treatment and that 50 per cent of the
patients experienced an increase in white spots.
O’reilly and Featherstone in AJO 1987 demonstrated that
measurable demineralization occurred around orthodontic
appliances after only 1 month and that it can be completely
inhibited and/or reversed by the use of commercially available
fluoride products. The authors suggested that a caries preventive
regimen for the orthodontic patient should be in the form of daily
home use of (1) a fluoride dentifrice coupled with (2) a low-
concentration (0.05% sodium fluoride) commercially available
fluoride mouth rinse.

Quantification of demineralization:
vitro methodologies for the study of enamel
demineralization typically employ artificial
lesions that are subsequently analysed
using
polarized light microscopy,
transverse microradiography (TMR),
clinical visualization,
Stereomicroscopy and
Electron microscopy.

Quantitative light-induced fluorescence
(QLF) is an optical, visual light-based
detection and quantification system for
assessing early demineralization of
human enamel.
The basis of the technique is that, under
defined conditions, human enamel will
auto-fluoresce.
Demineralized enamel will result in a
reduction of this fluorescence with
respect to surrounding sound enamel.
This difference in fluorescent intensities enables the degree of
demineralization to be quantified and, with several images of the
tooth taken over time, longitudinally monitored to assess lesion
activity.

QLF is an indirect method of demineralization, relying upon
the relationship between enamel fluorescence intensity and
mineralization status.
study by Pretty et al in EJO 2003 demonstrated that not only
did QLF detect demineralization, but it was also able to
monitor its development longitudinally with increased
exposure to the acidic challenge.
QLF was also able to detect demineralization before this was
visible to the trained examiner.
An aim of early caries detection is that remineralizing
therapies can be instituted and thus the risk of aesthetic
damage or restorative intervention is avoided.

MANAGEMENT OF
DEMINERALIZATION
Topical fluorides
Fluoride is known to inhibit lesion development and to
enhance its remineralization after treatment.
Daily use of fluoride along with good oral hygiene leads to
a significant reduction in demineralized areas.
Topical fluoride has been used extensively in the
prevention of demineralization around orthodontic
brackets.

Geiger et al reported a 25% reduction in the number of
patients exhibiting white spot lesions using a home
fluoride rinse program.
Although topical fluorides have been shown to be
effective, the main disadvantage of fluoride rinses is that
they require patient compliance.
Geiger et al found that poor compliance with a
preventive fluoride rinse program occurred in 50% of
patients.
They also found a clear association in which an increase
in white spot incidence occurred with decreasing dose
and decreasing compliance.

Alexander et al in Angle 2000 found that the daily use of
a 5000- ppm fluoride gel along with conventional
toothbrushing with an over-the-counter fluoride toothpaste
or the twice daily use of a 5000 ppm gel dentifrice is
significantly more effective in preventing demineralization
than the use of toothpaste and mouth rinsing with a 0.05%
fluoride solution.
A single daily exposure of a high-potency fluoride
dentifrice or a twice-daily exposure to a high-potency gel
appears to give equal protection in patients who exhibit
white-spot pathology.

Fluoride varnishes
Todd el al in AJO 1999 found that professionally applied
fluoride varnishes adjacent to orthodontic appliances may
provide protection against demineralization and still allow for
the use of proven composite resins for bonding agents.
Duraflor (duraphat) is a fluoride varnish that contains 2.26%
fluoride ion by weight in a natural colophony base.
Advantages of the fluoride varnish over other topical fluoride
regimens include providing fluoride protection of enamel
despite patient noncompliance and delivering the fluoride in
a sustained manner over a longer period of time.

The longer contact time with enamel enables fluoride
varnishes to incorporate significantly more fluoride in
enamel when compared with acidulated phosphate flouride
(APF)-gel and amine fluoride applications.
Brudevold et al observed that the efficiency of topical
fluoride applications was directly related to the exposure
period to enamel.
A longer exposure period permanently increased the
amount of fluoride retained in the enamel, enhanced the
formation of fluoridated hydroxyapatite, and reduced the
acid solubility of enamel.
The highest concentrations of fluoride is found in the
outermost layer.

Retief et al (JDR) compared Duraflor with APF- gel and
amine fluoride applications.
They found Duraflor incorporated a significantly greater
amount of fluoride that was retained in enamel by over 8
times after 1 day and over 5 times after 1 week when
compared to the other topical applications.
Arends et al found that fluoride uptake by enamel is also
greater with fluoride varnishes when compared to sodium
flouride (NaF) and monofluoraphosphate (MFP) containing
dentifrices.
Fluoride varnishes can be applied before, or at the time of
initial bracket placement in order to protect all patients from
demineralization.

The application procedure consists of
1) normal toothbrushing followed by,
2) drying of the teeth, and
3) varnish application.
Bennett and Murray reported that, in comparison with eight
other topical fluoride applications, Duraflor was the easiest
and quickest to apply, with a minimum of chair time and
much less discomfort to the patient.
Many fluoride applications require an impression tray to
deliver the material for 4 minutes.
Kimura et al in AJO 2004 found that the application of
fluoride varnish does not affect the bond strength of
orthodontic brackets to enamel with conventional or self-
etching primer systems.

Fluoride ligatures:
Fluoride containing elastomeric ligature ties released
significant amounts of fluoride; this was characterized by
an initial burst of fluoride during the first 2 days and was
followed by a logarithmic decrease over the remainder of
the 6 month test period.
The amount of fluoride released from elastomerics in vivo
may be influenced by mouth temperature fluctuations,
saliva, plaque, diet and tooth-brushing procedures.
Wiltshire et al AJO 1999 -residual, leachable fluoride was
present in fluoride impregnated and nonfluoride
elastomeric ligature ties after 1 month intraorally. Fluoride
was imbibed by elastomerics in vivo.

Sealants
Frazier et al found that light-cured pit and fissure sealants
placed on the labial surface adjacent to bonded orthodontic
brackets were 80% effective in preventing demineralization in
vitro and required no patient compliance.
Sealant placement in vivo is very technique sensitive, and
breaks in the sealant layer may result in decalcification under
the sealant.
Mechanical and chemical wear of the sealant must also be
considered in vivo.

Glass ionomer cements:
While the composite bonding system relies on acid etching to
create a mechanical bond, GIC requires no more etching
other than cleaning with pumice and moderate drying with a
cotton roll.
The absolute dryness required for composites have been
found to be unnecessary and even harmful for GIC bonding.
This eliminates the damages of acid etching.
The bond strength of GIC to enamel is approximately one-half
that of composite resin bonding after etching.
GIC acts as a reservoir of fluoride ions; They release fluoride
ions for 12 months directly into the enamel.

Patient compliance in the use of fluoride regimen can be
reduced by using GIC cements for bonding.
These cements may offer an advantage over composite
resins in preventing decalcification as enamel etching is
unnecessary for bonding with GIC.
A less cariogenic challenge, plaque accumulation and a lower
acid production in plaque are the other benefits. Greater
relevance to the cariostatic potential is the release of fluoride
from the GIC.
Stephen et al in AJO 98 compared the shear bond strength
of 3 resin-modified GIC used as bracket adhesives with a
composite resin.

They concluded that all the cements had shear bond strength
equivalent to composite resin when bracket placement was
combined with 10% polyacrylic acid etching, but showed lower
bond strengths when the enamel surface were not etched.
Millet et al in ANGLE 1999 in a randomized clinical trial
found that there was no difference in the mean number of
teeth affected by decalcification when GIC and resin materials
were used as bonding materials.
At 12 months post-debond, there was a reduction in the mean
number of teeth affected regardless of the bonding material
used.
Other fluoride preparations combined with thorough oral
hygiene practices and dietary control may have a greater
effect on the prevention of decalcification.

Fluoride releasing adhesives
Fluorapatite formation resulting from Fluoride release from
orthodontic adhesives could be more advantageous in
reducing decalcification during fixed appliance treatment
than other preventive modalities.
Fluoride- releasing composites generally have lower levels
of fluoride release than GICs but they have been shown to
provide some degree of protection from demineralization.
Combinations of GICs and composite resins have been
developed to provide greater fluoride release without
compromising bond strength.

Incorporation of inorganic fluorides into dental resins creates
problems of phase separation and loss of mechanical integrity
because of the highly polar nature of the fluoride salts and low
polarity of dental resins.
Organic fluoride incorporation has a plasticizing effect that
also yields poor properties.
Zimmermann et al in AJO 1989 introduced Ortho adhesive,
a fluoride releasing adhesive.
This fluoride releasing resin was unique in that the fluoride ion
was incorporated as a mobile ion charge, in an anion-
exchanging resin.
Fluoride release occurred when fluoride ions were
exchanged for other anions in the oral environment.

Rather than supplying fluoride to the oral environment by
material dissolution, the fluoride was given up in exchange for
other anions and the structure integrity of the resin was
maintained. It was effective in reducing 93% of
demineralization.
Oggard et al in AJO 97 found that with the fluoride releasing
adhesive orthodontic cements, the anti cariogenic effect was
due to release of fluoride in to the local environment than
elevation of fluoride level in saliva.
Chung et al in JCO 2000 compared the clinical bond strength
of fluoride releasing with non-fluoride releasing adhesive.
They concluded that fluoride releasing adhesive was clinically
strong enough for use as an orthodontic bonding adhesive

Antimicrobial agents:
Chlorhexidine is one of the most widely used broad-spectrum
antimicrobial agent in dentistry. It has proven to be very effective
in the maintenance of plaque control and gingivitis without
developing resistant organisms. Side effects of using
chlorhexidine that limit its widespread acceptance include brown
staining of the teeth, increase in calculus deposition, and the
difficulty in completely masking its taste when used as a rinse.
It has been suggested that chlorhexidine combined with thymol in
a varnish could have the following effects:
a desensitizing effect on the teeth,
lower bacterial activity in plaque while maintaining an ecologic
balance,
have excellent adsorption to the tooth surface and
are well tolerated.

The application of a chlorhexidine varnish before and during
orthodontic treatment was found to affect the salivary mutans
streptococcal levels.
Application of chlorhexidine to the enamel surface could add
increased protection around the bracket periphery but could
also influence the bond strength, depending on the method of
application.
Chemical agents such as chlorhexidine or benzydamine used
in the form of mouth rinses or sprays have been shown to be
useful adjuncts in plaque control.
Varnish forms of the other antibacterial solutions such as
benzydamine, triclosan and xylitol could be helpful in
orthodontic patients for suppressing levels of oral mutans or
other microbes for long periods after application when used
before the placement of fixed orthodontic appliances.

 Bishara et al in AJO 1998 conducted a study to determine
whether the application of chlorhexidine with or without a
sealant, to the etched enamel will affect the shear bond
strength and the bracket/adhesive failure modes of
orthodontic brackets.
 Findings of the study indicated that shear bond strength was
not significantly affected when chlorhexidine was applied over
the bracket and tooth surfaces after the bonding procedure
was completed and when used as a prophylactic paste over
the unetched enamel surface.
 On the other hand, in all the experimental groups in which the
chlorhexidine varnish was applied as a layer on the etched
enamel surface or over the sealant, shear bond strength
values and bracket failure rates were of a magnitude that
made them clinically unacceptable.

Karaman et al in angle 2004 conducted a study to determine
whether different types of antimicrobial agents when
combined with hydrophilic primer and applied to etched
enamel will affect bond strength and bracket adhesive failure
mode of metal brackets.
Two types of chlorhexidine varnishes (Cervitec and
Certichem) and a chlorhexidine mouthwash combined with
Transbond MIP in different proportions were evaluated.
The authors found that the bond strength of teeth treated with
chlorhexidine varnish was clinically acceptable.
Application of hydrophilic primer, when different antimicrobial
agents are mixed, significantly altered the site of failure during
debonding.

Low fermentable sweeteners:Low fermentable sweeteners:
Xylitol,Xylitol, a five carbon natural sugar alcohol, is a successful dentala five carbon natural sugar alcohol, is a successful dental
caries preventive natural carbohydrate sweetener. Variouscaries preventive natural carbohydrate sweetener. Various
mechanisms have been proposed for the caries preventive effect.mechanisms have been proposed for the caries preventive effect.
Xylitol is not fermented by most dental plaque bacteria but alsoXylitol is not fermented by most dental plaque bacteria but also
interferes with the in vitro growth of streptococcus mutans.interferes with the in vitro growth of streptococcus mutans.
Sengun et al in ANGLE 2004Sengun et al in ANGLE 2004 evaluated the influence of a xylitolevaluated the influence of a xylitol
lozenge on the dental plaque profile of patients with fixed orthodonticlozenge on the dental plaque profile of patients with fixed orthodontic
appliances. They found that xylitol lozenges can reduce theappliances. They found that xylitol lozenges can reduce the
acidogenicity of dental plaque. After a sucrose challenge, plaque pHacidogenicity of dental plaque. After a sucrose challenge, plaque pH
returned quickly to the resting value because of the use of xylitolreturned quickly to the resting value because of the use of xylitol
lozenges. A xylitol based caries preventive program has the followinglozenges. A xylitol based caries preventive program has the following
advantages:advantages:
no expensive equipment is requiredno expensive equipment is required
no additional procedures are requiredno additional procedures are required
there is individual control in intakethere is individual control in intake

Argon laser irradiation:
An interesting application of argon lasers in orthodontics involves
its ability to alter enamel rendering it less susceptible to
demineralization.
Argon lasers have the ability to cure composite resins quickly
and at the same time potentially confer demineralization
resistance to the enamel.
Argon laser irradiation of enamel reduces the amount of
demineralization by 30-50%.
Fox et al in JDR 1992 found that, in addition to decreasing
enamel demineralization and loss of tooth structure, laser
treatment can reduce the threshold pH at which dissolution
occurs by a factor of five.
Irradiation could considerably alter the surface morphology while
maintaining an intact enamel surface.

Several mechanisms for the enhanced caries resistance of
enamel after laser irradiation have been proposed, although
the exact mechanism is not known.
The most likely mechanism for caries resistance is through
the creation of microspaces within lased enamel.
The microspaces created act to trap the released ions and act
as sites for mineral reprecipitation within the enamel surface.
Thus lased enamel has increased affinity for calcium,
phosphorus and fluoride ions.
Noel et al in ANGLE 2003 found that the use of argon lasers
resulted in a significantly lower mean lesion depth when
compared with visible light control.
The results showed that demineralization resistance imparted
by argon laser might prevent a large percentage of WSLs
during the course of treatment.

EXTERNAL APICAL ROOT RESORPTION:
External apical root resorption is the most common and
frequent iatrogenic consequence of orthodontics.
Fortunately, truly severe resorption that threatens the
longevity of the tooth is rare.
RR has a multifactorial etiology; although it has been
recognized as a consequence of mechanically induced tooth
movement, its causes are still poorly understood.
Therefore it is not possible to predict who will develop RR or
the extent of involvement. Orthodontically induced root
resorption starts adjacent to hyalinized zones and occurs
during and after elimination of hyalinized tissues.

Incisors are most susceptible to EARR, probably because of
their root’s spindly apex and because incisors typically are
moved farther than other teeth during correction.
Intrusion is probably the most detrimental direction of tooth
movement, although simply the distance the apex is moved is
often correlated with the degree of root shortening.
The strongest single association with EARR seems to be a
person’s genotype. Familial studies show that a person’s
genotype accounts for about two thirds of the variation in the
extent of periapical resorption.
RR occurs when the pressure on the cementum exceeds its
reparative capacity and dentin is exposed, allowing
multinucleated odontoclasts to degrade the tooth substance

There is a positive association between removal of hyalinized
necrotic tissue and RR.
Because cementum normally is most resistant than bone,
forces applied to a tooth usually cause bone resorption than
loss of cementum.
However, forces are concentrated at the root apex, because
orthodontic tooth movement is never entirely translatory,
which places the narrow periapical region in harm’s way.
The principal difficulties in studying root resorption are the
infrequency of severe shortening and the many possible
factors that can be associated with the condition.
Albert Ketcham was the first to report that apical root
resorption is a common and occasionally, a severe iatrogenic
consequence of orthodontic treatment.

Classification:
Can be classified into at least 3 categories:
Surface resorption
Inflammatory resorption and
Replacement resorption
Surface resorption occurs constantly as micro defects on all roots;
these normally repair themselves without notice. It can occur
anywhere on the root but is most common periapically. It stops when
the inciting agent (pressure) is removed and there is repair of the
cementum.
Inflammatory resorption occurs when root resorption progresses
into the dentinal tubules to pulpal tissue that is infected or necrotic or
into an infected leukocyte zone.
Replacement resorption produces ankylosis of the tooth because
bone replaces the resorbed tooth substance.

The ordinal scale used to score EARR
Grade 0 – normal, intact root morphology
Grade 1 – evidence of erosion periapically
Grade 2 – scalloping and blunting of apex
Grade 3 – 1/4th
of root has been resorbed
Grade 4 – loss of atleast ½ the original root length.
Measurement methods:
Visually assessed grades of resorption
Measurement with callipers
Other methods
Computer aided devices
Electron mocroscopy
Histomorphometric methods

Factors affecting root resorption
biologic factors:
individual susceptibility
Genetics
Systemic factors – hypothyroidism, hypopituitarism, hyperpituitarism,
hyperparathyroidism, hypophosphatemia, paget’s disease.
Nutrition – deficiency of dietary calcium and Vit. D
Chronological age: RR increased in adults
Dental age: root development affected by tooth movement
Gender: no predilection
Presence of RR before orthodontics: high correlation between RR
before treatment and after treatment
Habits: nail biting, tongue thrust with open bite, tongue pressure
Tooth structure: deviating root form more susceptible
Previously traumatized teeth
Endodontically treated teeth: higher frequency for RR
Alveolar bone density: Direct contact between roots and cortical
bone can precipitate root resorption
Specific tooth vulnerability

mechanical factors:
appliances:
fixed Vs removable: FA more detrimental to roots
Begg Vs Edgewise: Begg third stage – more RR
intermaxillary elastics: jiggling forces – more RR
extraction Vs Non extraction
other appliances: RME and cervical traction- RR on molars
and anchor teeth
orthodontic movement type: intrusion most detrimental
orthodontic force: high stresses increase RR
combined biologic and mechanical:
treatment duration: longer treatment duration – increased
risk

Stephanie et al in WJO 2003 evaluated the amount of apical
root resorption of central incisors with periodontal involvement
in patients undergoing orthodontic intrusion.
The amount of radicular resorption was evaluated on
standardized intraoral radiographs. They found that at the end
of treatment, mean resorption of 3.46% of the initial root
length was found.
They suggested that by using light and continuous forces,
EARR could be kept to a minimum. This is true even for
incisors with marginal bone loss.
Scott et al in ANGLE 2000 conducted a study to examine
posterior teeth in patients following orthodontic treatment and
to determine whether an association existed between the
incidence of EARR and the type of fixed appliance used, the
length of treatment, and whether extractions were performed
as part of treatment.

The authors found that the incidence of EARR in the posterior
teeth was positively associated with tooth position; type of
appliance used and tooth extraction.
The incidence of EARR was 2.3 times higher for patients
treated with Begg appliances compared with edgewise
appliances, and it was 3.72 times higher for whom extractions
were performed, compared with those for whom no
extractions were performed.
The authors concluded that non-extraction patients with
edgewise appliance demonstrated relatively less posterior
EARR compared with patients in which extractions or a Begg
appliance was used.

Akira et al in AJO 1998 found that root approximation to the
palatal cortical plate during orthodontic treatment could
explain approximately 12% of the RR observed.
Tooth extrusion and crown lingualization also contributed to
root resorption. Root approximating to palatal cortical plate
followed by excessive incisors retraction and by extrusion of
incisor were revealed to be factors influencing amount of
apical root resorption.
Narrowing of alveolar bone width also influences apical root
resorption.
Janson et al in AJO 1999 conducted a study to compare the
amount of root resorption after orthodontic treatment between
the simplified standard edgewise technique, the edgewise
straight wire system, and the Bioefficient Therapy.

Bioefficient Therapy presented less root resorption than the
others. It was speculated that the factors responsible for the
lesser resorption in this technique were the use of heat-
activated and superelastic wires with the bracket design in
this technique as well as the use of a smaller rectangular
stainless steel wire (0.018 × 0.025 inch) in a 0.022 × 0.028
inch slot during incisor retraction and the finishing stages, as
compared to the other techniques.
The prevalence of resorption for each incisor indicated, in
decreasing order, a greater resorption for the upper centrals,
followed by the upper laterals, lower centrals, and lastly the
lower lateral incisors.
According to Sinclair et al in AJO 2001, the average amount
of resorption found for molars and premolars was very low
(less than 1 mm).

There was no difference found between right and left sides,
first premolars and second premolars or between the upper
and lower arch.
Maxillary anteriors were more frequently affected than the
mandibular anteriors. Incisors were more affected than the
canines.
Most severely resorbed teeth were maxillary lateral incisors
(1.47 mm), followed by maxillary central incisors (1.24 mm),
maxillary canines (1.14 mm), mandibular canines (0.89 mm),
mandibular lateral incisors (0.80 mm), and mandibular central
incisors (0.68 mm).
Maxillary lateral incisors – more affected due to abnormal root
shapes, abnormal crown morphology (peg shaped, barrel
shaped) developmental anomalies, slender roots.

Results revealed that Asian patients had significantly less root
resorption than white or Hispanic patients.
Abnormal root shape was a significant factor.
In general, dilacerated teeth (particularly maxillary lateral
incisors) had the most resorption, followed by bottle-shaped
and pointed teeth.
Teeth that were classified as blunted had less resorption than
normal-shaped teeth.
A positive but weak correlation was found between initial tooth
length and the amount of root resorption. In other words, a
longer root was more likely to be resorbed than a shorter root
because a longer root is displaced farther for equal torque.

Adults have significantly more resorption than children in the
mandibular anterior teeth only.
There was no difference between male and female patients
for root resorption for any teeth. Increased tooth length and
overjet were correlated with greater root resorption for the
maxillary anterior dentition.
Increased overbite was weakly correlated with more root
resorption in maxillary lateral incisors only.
Treatment variables clearly play an important role in the
occurrence of external apical root resorption as the result of
orthodontic tooth movement.
Displacement of the root apex was found to be significant, but
only in the horizontal direction.

Extraction pattern was also found to be a significant factor in
root resorption. Patients who underwent 4 first premolar
extraction therapy had greater resorption than those patients
who were treated with nonextraction.
Interestingly, patients with only upper premolar extractions did
not have more resorption than the nonextraction cases.
Longer treatment time was found to be significantly
associated with increased root resorption for maxillary central
incisors.
The mechanical treatment variables in our study were not
significantly associated with apical resorption. Slot size and
archwire type were not found to be important. Use of elastics
was also not associated with increased resorption.

Genetic predisposition
Riyad et al in AJO 2003 found that the IL-1B polymorphism
accounts for 15% of the total variation of maxillary incisor
EARR. Persons homozygous for the IL-1B had a 5.6 fold
increased risk of EARR greater than 2 mm as compared with
those who are not homozygous.
Data indicate that allele 1 at the IL-1B gene, known to decrease
the production of IL-1 cytokine in vivo, significantly increases
the risk of EARR.
These findings are consistent with an interpretation of EARR as
a complex condition influenced by many factors, with the IL-1B
gene contributing an important predisposition to this common
problem.
Defining genetic contributions to EARR is an important factor in
understanding the contribution of environmental factors, such
as habits and therapeutic biomechanics.

Management of EARR
Current clinical recommendations are to use caution in
moving abnormally shaped teeth a long distance for a long
time.
Taking progress periapicals is recommended a few months
after active tooth movement for patients at risk.
Orthodontic treatment should begin as early as possible since
there is less root resorption in developing roots and young
patients show better muscular adaptation to occlusal
changes.
Adults have poorer adaptive ability and need more rigid and
longer lasting mechanical forces. The orthodontic force should
be intermittent and light.
Habits such as nail biting or tongue thrust should be stopped,
since it was shown that root resorption is more severe in such
orthodontic patients.

If root resorption is found, the literature supports an inactive
phase of 4 to 6 months before the resumption of treatment.
In extreme cases, treatment must be halted; appliances must
be removed, and a surgical or prosthetic treatment plan must
be adopted.
If root resorption continues after appliance removal or during
retention, sequential root canal therapy with calcium
hydroxide is advisable.
Gutta-percha filling is the definitive therapy only after root
resorption ceases.
Appropriate counseling and follow-up are necessary should
severe resorption be encountered. Root resorption rarely
results in significant morbidity after orthodontic therapy, and
the resorptive process ceases with the removal of active
forces.

ENAMEL WEAR AND FRACTURES
Enamel wear has been reported to occur when ceramic
brackets are in contact with enamel surfaces even for very
short times.
Enamel fractures are the most serious problem associated with
ceramic brackets and has been reported to occur during
debonding or from accidental impact.
Ceramic brackets because of their low fracture resistance and
high bond strengths, can pose a problem when being removed,
either to reposition or at the completion of treatment.
The bracket/adhesive bond strength may exceed that of the
enamel/adhesive bond strength, such that when the bracket is
removed some enamel may be removed at the same time.

Bracket breakage while removing it
increases treatment time and has the
potential health risk of swallowing or
aspirating bracket fragments.
It seems highly advisable to use
debonding methods designed specifically
for ceramic brackets. A squeezing motion
(as opposed to a rotational motion) pulls
the bracket away from the tooth
perpendicularly, creating a tensional force
in which the enamel is structurally
weakest.

Laser light energy has been
shown in other studies to degrade
resins by thermal softening,
thermal ablation, or photoablation.
Enamel fracture upto 100µm have
been reported with ceramic
brackets.
Bond strengths more than
13.5Mpa – Enamel prone to
fracture
PLIERS – Pointed pliers
reduce contact area with
bracket and applying force at
diagonally opposite corners
recommended

ETD – Heating the bracket and applying a tensile force.
Disadvantage – Pulp damage (above 550
) / Bulky Hand
piece
Ultrasonic scalers – time consuming
LASERS – Less time / decreases debonding forces/
decreased enamel damage.
Thermal ablation and Photoablation techniques better than
thermal softening. Co2 laser better than Nd: YAG Lasers
A new ceramic bracket design was introduced in an attempt to
minimize some of the problems that are encountered by the
clinician. The new bracket had a metal-lined arch wire slot.
The metal slot helps strengthen the bracket in order to
withstand routine orthodontic torque forces. The new bracket
also incorporated a vertical slot, designed to help create a
consistent bracket failure mode during debonding.

Bishara et al in AJO 1997 evaluated a collapsible ceramic
bracket (clarity) and found that the when debonding the
Clarity brackets with the Weingart pliers, there was a greater
tendency for most of the adhesive to remain on the enamel
surface.
Such a debonding pattern had the advantage of protecting the
enamel surface and the disadvantage of having more residual
adhesive material after debonding that needs to be removed
by the clinician.
The failure at the bracket-adhesive interface decreases the
probability of enamel injury but necessitates the removal of
more residual adhesive after debonding.
The Clarity brackets had a greater incidence of partial bracket
failure when the Weingart pliers were used because the point
of force application is at the tie wings of the brackets

Clinical reports of bracket fracture and enamel surface damage
that occur during debonding of ceramic brackets continue to be
of concern to clinicians. To reduce the clinical incidence of
irreversible enamel surface damage, three methods of
debonding ceramic brackets have been suggested:
(1) Conventional methods using pliers or wrenches,
(2) An ultrasonic method that uses special tips, and
(3) The electro thermal method involving an apparatus that
transmits heat to the adhesive through the bracket.
Reported enamel damage during mechanical debonding
Swartz (JCO 1988)
Joseph & Roussow (AJO 1990)
Ghafari (Angle 1992)
Read & Shivapuja (JCO 1991)
Storm (JCO 1990)
Cribbs (BJO 1992)

Sudden nature of bracket failure could cause enamel fracture
Risk of bracket fracture, where remaining fragments have to
removed with a diamond bur in a bur produces ceramic dust
an irritant.
This grinding may generate heat damaging the dental pulp.
Monocrystalline – more enamel loss while debonding.
Ceramic bracket with chemical retention – more enamel
damage
Bishara et al – enamel damage is even higher if the integrity
of tooth structure is compromised by developmental defects,
enamel cracks & large restorations and non-vital teeth.

Involve heating the bracket with a rechargeable heating
gun while applying a tensile force to the bracket.
The bracket separates once sufficient heat has
penetrated the bracket adhesive interface.
Bishara et al – ETD technique is quick, effective and
devoid of bracket or enamel fracture but a potential for
pulp damage was reported (Ruggerberg et al Angle
1992). Risk of dropping a hot bracket in the patients
mouth (Bishara)
Electrothermal debonding (ETD)

ULTRASONIC SCALERS
Decreased chance of enamel damage or bracket fracture.
Residual adhesive can be removed with same instrument.
Disadvantages
Time consuming
Extensive wear of expensive ultrasonic tips.
LASERS
Irradiation of labial surfaces with laser light
Significantly reduces the residual debonding force, risk of
enamel damage and incidence of failure compared with
other conventional methods.
Less traumatic and painful, less risky for enamel damage

Remedies for enamel fractures
In order to overcome the potential damage of enamel
during debonding, a ceramic bracket (cerama Flex) with
a thin polycarbonate laminate on the base has been
introduced.
The bond to the enamel is not through an adhesive to
the ceramic base, but to the thin polycarbonate laminate.
Fox (BJO) and Franklin in JCO 1993 have suggested
that these Cerama Flex brackets are easy removed and
are comparable to metallic brackets.

Paul J. Feldon et al (AJO Jan 2003) have reviewed in
laser debonding of ceramic brackets. Suggestions by them
Time spent to debond ceramic brackets is less when using
lasers
Debonding forces are significantly reduced with lasers.
Risk of enamel damage and bracket fracture is reduced
with lasers
The Co2 super – pulse laser is superior to normal pulse
Co2 laser and YAG lasers.
MMA resins are recommended over BIS-GMA resins.
Use of monocrystalline brackets is suggested over
polycrystalline brackets
Ceramic brackets should be irradiated and debonded one
by one immediately after laser exposure.
The risk of pulpal damage is significantly reduced if super –
pulse Co2 lasers for less than 4 seconds is used.

ENAMEL ABRASION AND WEAR
In addition to enamel fractures that may occur during
debonding actions, enamel damage can occur during
contacts of ceramics with occluding teeth.
Viazis et al 1990 AJO studied on enamel abrasion using
a simulated oral environment
Stainless steel induce lesser enamel abrasion than
ceramic brackets
Single crystal ceramic causes more enamel abrasion
than polycrystalline ones.

Viazis et al – 1989 AJO –
suggestions to prevent enamel
abrasion
Ceramic brackets used on
mandibular teeth should be
kept out of occlusion.
Crossbites should be corrected
before placing ceramic
brackets
Use of ceramics brackets only
on anterior maxillary teeth
While avoiding deleterious
effects of enamel wear on
occluding teeth.

PREVENTION OF ENAMEL ABRASION
Deep bite cases- correction of bite opening and use of bite
planes must be advocated to minimize interference.
Due to hardness to ceramic brackets, bonding brackets on
mandibular incisors and occlusal contacts should be avoided
to prevent wearing of enamel surfaces.
Klocke et al in AJO 2003 -plasma arc light was used for
bonding ceramic brackets, the location of bond failure was
consistently at the bracket adhesive interface, thus reducing
the risk for enamel fractures.
Birnie et al
Special elastomeric rings that cover the occlusal surface of
ceramic bracket
Techniques to eliminate occlusal interferences and control
parafunctional habits

PERIODONTAL PROBLEMS
INTERDENTAL RECESSION – open
gingival embrasures
Kokich in AJO 2001- adult patients
present a challenge because they often
have dental conditions that may
complicate treatment, such as tooth
wear, poorly contoured restorations, and
periodontal disease.
In some adults, a black triangular space
may appear between the maxillary
central incisors and the cervical gingival
margin after orthodontic treatment.
The height of the alveolar bone relative to the interproximal
contact is a significant factor in determining whether a papilla will
fill the gingival embrasure. The location and the size of the
interproximal contact and divergent root angulation have been
cited as potential causes of open gingival embrasures.

Triangular-shaped crown form also may be associated with
open gingival embrasures.
Increased distance from the crest of the alveolar bone to the
interproximal contact is significantly related to open gingival
embrasures. The average distance from alveolar bone to CEJ
in patients with normal and open gingival embrasures was
1.95 mm and 2.28 mm, respectively.
The contact position can be changed by removing
interproximal enamel, adding a restoration, or altering root
angulation.
When mesial crown form, alveolar bone–interproximal
contact, and interproximal contact–incisal edge variables are
constant, a 1° increase in root divergence increased the odds
of an open gingival embrasure by 14% to 21%.
Taylor detected 3 basic types of incisor crown forms and
listed them in decreasing frequency: square, tapered, and
ovoid. Tapered crowns are more susceptible to open gingival
embrasures.

 Lupi et al in AJO 1996 have reported that most adults
undergoing orthodontic treatment will demonstrate some
level of bone loss and root resorption.
 Adults with pre-existing recession tend to show the
greatest number of sites with new or further recession
over time. The measure of clinical crown height is an
indirect quantification of buccal attachment loss.
 It is possible for the gingival tissue to be intact while
masking the underlying dehiscence of bone.
 Nevertheless, gingival recession of a significant nature is
not obligatory following RME and only modest crown
lengthening was observed.

RME and gingival recession
Handelmann Angle 2000
Proclination of the mandibular incisors in class III patients,
prior to orthognatic surgery has been shown to be associated
with gingival recession.
Labial expansion of incisors in experimental animals will
cause the gingiva to recede.
Vanarsdall states that RME in adults will cause the teeth to
perforate their thin plate of buccal bone, and consequently the
gingiva will recede.
According to Handelmann, extent of the attachment loss was
not clinically significant, averaging 0.6 mm for female and 0.3
mm for the male. The average increase in crown length of 0.5
mm observed in the female RME patients above that of the
controls is best defined as buccal attachment loss rather than
gingival recession.

RME – its effect on pulp and root resorption
Nazan et al in AJO 1994 evaluated the effect of RPE (haas
type) on root resorption.
Root resorption and repair areas were observed on the buccal
surfaces of premolars. These defects were found to be
repaired with cellular cementum.
Nazan et al in AJO 2000 investigated the effects of heavy
forces of RPE on the pulpal tissues of anchor premolars.
They found that the forces applied by RPE appliances caused
an adaptive vascular tissue response as well as fibrotic
changes, in the affected upper premolars.

Alveolar bone height after treatment
 Alveolar bone response to orthodontic tooth movement
depends on force levels, type of tooth movement and the
presence of dental plaque.
 There is no evidence of a relationship between treatment time
and alveolar bone resorption or influence of extraction or non-
extraction treatment on alveolar bone resorption.
 Different fixed orthodontic techniques seem to show similar
effects on alveolar crest height after treatment.
 Bondemark et al in AJO 1999 studied the effect of
orthodontic treatment on the interdental bone level and
compared it with untreated individuals.
 Neither group had any sites with clinically significant bone
loss, i.e., a distance > 2 mm between the cementoenamel
junction and the alveolar bone crest.

Janson et al in AJO 2003 compared the heights of
alveolar crest in patients treated with bioefficient therapy
with a group of patients treated with conventional and
preadjusted systems and a control group with untreated
malocclusions.
Results showed that after a mean treatment period of 2
years, all the treated groups had a larger statistically
significant CEJ- alveolar crest differences compared to
the untreated groups, primarily at the extraction sites.
They found no difference in the different techniques that
were studied on the alveolar crest.

LATEX ALLERGIES
Reactions to latex materials have become more prevalent.
studies relate the allergic reactions to the use of latex gloves
and the development of stomatitis with acute swellings and
erythematous buccal lesions to the use of orthodontic elastics.
Most documented allergic reactions to latex products have
identified the residual rubber protein as the antigen.
Reactions to latex carry with them a wide range of risk,
including dermatologic reactions, respiratory reactions, and
systemic reactions—in the extreme, anaphylactic shock.
Mucosal or parenteral contact—as with the use of orthodontic
elastics—is more likely to induce a rapid systemic reaction
such as anaphylactic shock.

Latex allergy – Management
Russell et al in AJO 2001 suggested that as the
incidence of latex allergic reactions increases, the use of
non-latex products is increasing within the orthodontic
specialty.
The use of non-latex orthodontic elastics is required in
patients with known latex sensitivities and will likely
become more common if the incidence of latex
sensitivities continues to rise.
However, the mechanical properties of non-latex
elastics cannot be assumed to be—and indeed are not—
the same as those of latex elastics.

NICKEL ALLERGY
Nickel has been reported to be one of the most common
causes of allergic contact dermatitis, particularly in women.
Factors that have been documented to influence the
development of sensitization include mechanical irritation,
skin maceration, increased environmental temperatures,
increased intensity, and duration of exposure.
Genetic factors also have been reported to play a role.
The diagnosis of nickel allergy has usually been based on
patient history, clinical findings, and the results of patch
testing.
Patch test reactions properly interpreted are acceptable as
evidence of sensitivity to a particular allergen.

Bass et al in AJO 1993 found that the
Prevalence of nickel allergy is higher in females than
males. (28% in females, 0% in males.)
Nickel-containing orthodontic appliances had little or no
effect on the gingival and oral health of the patient.
Orthodontic treatment may induce nickel sensitivity
Wires containing nickel are routinely used in
orthodontics. If these wires are susceptible to corrosion
with subsequent release of nickel, their use may elicit a
reaction in a patient with nickel allergy or may contribute
to the development of nickel allergy.
According to Matasa et al, potential of an alloy to cause
an allergic reaction depends on the pattern and mode of
corrosion. Corrosion occurs in all base metal alloys and
it is greater in nickel containing alloys than in gold alloys.

Bishara in AJO 1993 conducted a study to determine
whether orthodontic patients accumulate measurable
concentrations of nickel in their blood during their initial
course of orthodontic therapy.
Results showed that patients with fully banded and bonded
orthodontic appliances neither had a significant nor consistent
increase in nickel blood levels during the first 4 to 5 months of
orthodontic therapy.
Orthodontic therapy using appliances made of alloys
containing nickel-titanium did not result in a significant or
consistent increase in the blood levels of nickel.
The results obtained indicated that orthodontic appliances
used, in their "as-received" condition, corrode in the oral
environment releasing both nickel and chromium, in amounts
significantly below the average dietary intake.

Kocadereli et al in ANGLE 2000 studied on the
alterations in salivary chromium and nickel in patients
during orthodontic treatment.
They found that fixed appliances do not significantly
affect the nickel and chromium concentrations of saliva
during treatment.
They concluded that minor amounts of nickel and
chromium dissolved from appliances could be important
in cases of hypersensitivity to nickel.

Tulin et al in ANGLE 2001 evaluated the concentration
of nickel and chromium ions in salivary and serum
samples from pts treated with fixed appliances.
They found that fixed orthodontic appliances release
measurable amount of nickel and Cr when placed in the
mouth, but this increase doesn’t reach toxic levels for
nickel and chromium in saliva and are similar to values
found in healthy individuals.

Nickel allergy – alternatives
Kim et al in ANGLE 1999 found that titanium wires were
the most inert and can be used intraorally in a corrosive
environment.
It contains no nickel and is an excellent alternative for
orthodontic patients with nickel allergy.
If nickel titanium wires have to be used, then epoxy
coating of the wire is recommended.
This would reduce the corrosive potential and the
subsequent release of nickel.
If the epoxy coatings can be maintained during
orthodontic procedures, corrosion of the wire and the
subsequent release of metal ions into the oral
environment are minimized.

According to Hamula et al in JCO 1996, the problems of
nickel sensitivity, corrosion, and inadequate retention of SS
brackets has been solved with the introduction of new, pure
titanium bracket (Rematitan).
Its one-piece construction requires no brazing layer, and thus
it is solder- and nickel-free.
A computer-aided laser (CAL) cutting process generates
micro- and macro-undercuts, making it possible to design an
“ideal” adhesive pattern for each tooth.
Sernetz et al in 1997 evaluated the qualities and advantages
of titanium brackets.
The biocompatibility of these brackets is maintained by
preserving the integrated base made of a single piece of pure
titanium.
Lesser stiffness of titanium compared to stainless steel allows
torque to be fully expressed without deforming the bracket
wings.

CYTOTOXICITY OF ADHESIVE RESINS
AJO 1999 Tang et al
In vitro studies have shown that chemical components
leach from cured orthodontic bonding resins.
Excessive bonding adhesive left around bracket bases is
under the influence of atmospheric oxygen that
compromises its polymerization.
Fully polymerized resins produce no harmful biological
effects.
However, complete polymerization of orthodontic
bonding resins in situ is unlikely. Epoxy resins have been
described as the strongest industrial skin allergen
produced in the last few decades.

Occasional mucosal reactions related to resin restorations in
teeth are also reported in patients.
Estrogenicity of Bis–GMA-based materials in breast cancer
cell lines has also been reported.
Although these reports were not conclusive from a clinical
point of view, meticulous care should be taken when resins
are being handled.
This is particularly important in orthodontics as the majority of
orthodontic patients are actively growing children who are
more vulnerable to irritants than adults.
The author reported that the presence of oxygen inhibited
layer renders bonding resins 33% more cytotoxic in vitro.
Light-cured and chemically cured 2-paste materials had their
mean cytotoxicities approximating their inert controls over 6
days. Chemical cured liquid-paste materials are more
cytotoxic than light-cured and chemically cured 2-paste
materials.

Davidson et al in AJO 1983 tested orthodontic bonding
materials for in vitro cytotoxicity.
All materials were found to show cytotoxicity immediately after
preparation.
Polymerized adhesives generally showed decreased toxicity.
Sealant materials showed statistically significant greater
toxicity than paste resins, both initially after mixing and after
30 days.
The significant finding in this study was that these materials
not only were toxic immediately after mixing but remained
toxic for extended periods of time.
Excess material should be removed from teeth by thorough
scaling and flushing with water and high-speed evacuation,
particularly in areas adjacent to the gingiva.

David et al in EJO 2004 - found that the quantity of nickel
released from wires in synthetic saliva was 700 times lower
than the concentration of metal required to produce cytotoxic
effects in human peripheral blood mononuclear cells for both
nickel sensitive and non sensitive patients.
Nickel and chromium levels in blood of patients prior to
orthodontic treatment and 2-5 months following start of
treatment revealed that corrosion for these appliances did not
increase blood levels for these 2 metals even in
circumstances where NiTi wires were used in treatment
(Bishara – 1993).
Results indicated that NiTi, Cu-NiTi and TMA wires are not
significantly neurotoxic, while S.S and Elgiloy wires are
significantly toxic. Specific metal responsible for the toxicity
could not be determined. Most common metals which were
implicated were Ni, Iron and Cr.

INJURIES FROM ORTHODONTIC
APPLIANCES
The standard facebow has been
pulled out, knocked or taken out of
buccal tubes while still attached to the
headgear or neckgear during sleep.
The elastic traction then acts like a
catapult and caused the facebow to
recoil, and hit the patient on the face,
head or neck.
Other problem is for the facebow to
be dislocated during sleep and cause
damage and injury to the soft tissues.

Three serious eye injuries from
face-bows have been reported
during use of facebows.
Trauma associated with the
eye injuries, may pose
additional problems due to the
presence of oral
microorganisms on the face-
bow at the time of injury
increases the risk of infection.

Despite appropriate antibiotic therapy, any resulting infection
can be very difficult to treat and on several occasions has
been unsuccessful, leading to the loss of the eye.
With the injury to one eye, there is always the possibility of the
loss of sight in the other eye because of contralateral
endophthalmitis.
Because the inner arms of the face-bow are the same width
as the eyes, there is a greater risk of a bilateral injury to the
eyes.
Penetrating injuries of the eye may be relatively
asymptomatic, which might delay the patient in seeking
treatment.

Management:
Extraoral traction should only be
prescribed to those patients who are
likely to comply with orthodontist’s
instructions.
For some young children, less dextrous
or poorly sighted patients, the parents
should be carefully instructed regarding
the use of HG.
A self retentive or locking facebow can
be used. The equipment should be
carefully checked at every appointment
The current safety devices available to
counter injuries are safety release or
snap-away headcaps/ neckstraps, plastic
safety neck straps, and several designs
of safety face-bows.

Instructions should include the following:
Patients should be advised not to wear their headgear while
playing.
If another person grabs their face-bow, the patient should also
take hold of it until the other person has released their hold. They
should then dismantle the headgear and face-bow to check that
nothing has been dislodged or broken.
Before removing the face-bow, the patient must always remove
the headgear first.
Where a locking face-bow has been fitted, patients should check
to make sure it is seated correctly, and then confirm the "lock" by
trying to pull it anteriorly.
The patient and parent should also be advised that if any eye
injury is suspected to have been caused by any part of the
orthodontic appliance, however minor, then an immediate
ophthalmologic examination is necessary because penetrating
injuries may be relatively asymptomatic and immediate antibiotic
therapy is required if any resultant infection is to be controlled.

Accidental ingestion of appliance parts
Iatrogenic damages during orthodontic treatment include
accidental ingestion of retainers, sectional wires, bands,
brackets, expansion appliance keys and appliances
Sfondrini et al in JCO 2003 reported of a case in which a rapid
palatal expander was accidentally ingested.
Hinkle et al in AJO 1987 reported of a case where a bonded
lingual retainer was accidentally ingested.
 Management:
Symptoms of tracheobronchial obstruction such as dyspnea,
coughing or choking may appear.
If serious consequences develop, then immediate removal is
essential.

Symptoms of oesophageal
obstruction include inability to
swallow, muscle in coordination, pain
on swallowing, vomiting and
hematemesis.
Anteroposterior and lateral
radiographs will reveal whether the
object is lodged in the trachea or the
oesophagus.
If the appliance is in the
gastrointestinal tract, the probability
is better than 90% that it will pass
uneventfully.
Impaction of large objects or those
with sharp objects can lead to
ulcerations and perforations and
therefore require immediate surgical
removal.

Orthodontics and TMJ
 It has been stated that failure to produce occlusal
harmony after orthodontic treatment, especially failure to
eliminate centric prematurities and nonworking contacts
on mandibular excursions, may subsequently contribute
to TMJ disorders.
 Sadowsky et al in AJO 1980 evaluated the status of
temporomandibular joint (TMJ) function and functional
occlusion was in a group of seventy-five subjects who
had been treated orthodontically with full fixed appliances
during adolescence. The findings were compared to
those of a control group of adults with untreated
malocclusions.

The findings indicated that in patients who underwent
orthodontic treatment many years previously the prevalence
of TMJ signs/symptoms was similar to that of a control group
of adults with untreated malocclusions.
No relationship was evident between subjects exhibiting
signs or symptoms of TMJ dysfunction and the presence of
nonfunctional occlusal contacts and mandibular shifts.
O'Reilly and Rinchuse in AJO 1993 concluded that Class II
elastics and extractions have little or no effect on general
TMD signs and symptoms.
They concluded that any dental procedure that did not
produce harmony between occlusion and musculoskeletal
system can predispose to joint problems – whether the
treatment undertaken was orthodontics, prosthodontics or
surgery.

Management:
 Objectives of treatment in such patients are
Maintain musculoskeletal deprogramming
Maintain mandibular posture
Avoid eccentric shifts of the mandible
Manage parafunctional habits
Avoid TMJ overload with elastics.

Iatrogenic damages of orthodontic treatment

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