(10) dental erosion

Case (1) Dental Erosion Literature Review
Feda Zawaideh 1
INTROUDUCTION
Tooth wear or tooth surface loss is a general term used to describe the non-carious
loss of tooth structure.1
Tooth wear can be considered either physiologic or
pathologic. It is considered pathologic when the teeth become so worn that they can
not function efficiently, the aesthetics are affected and the longevity of the teeth
involved is compromised.2
Based on the aetiological factor and clinical
manifestations, tooth wear is subdivided into attrition, abrasion, abfraction and
erosion. (Table 1)
Table 1: Definitions of attrition, abrasion, abfraction and corrosion
Attrition The physiological wearing of teeth resulting from tooth to
tooth contact with or without the presence of an abrasive
substance between the teeth1
Abrasion The physical wear of tooth surface through a mechanical
process caused by factors other than tooth to tooth contact1
Abfraction Wedge-shaped defect at the cementoenamel junction of a
tooth caused by eccentrically applied occlusal forces leading
to tooth flexure3
Erosion The progressive loss of hard dental tissues by a chemical
process not involving bacterial action1
Dental erosion is becoming an increasing problem due to the increased exposure to
the elements that cause dental erosion. Dentists and dental specialist need to be more
aware of the potential for dental erosion to occur, the possible aetiological factors, the
presentation and management of the condition.
DENTAL EROSION
Dental erosion or as currently termed corrosion may be defined as tooth tissue loss
from chemical dissolution of teeth by acids other than those produced by bacteria.4
Ten Cate and Imfeld (1996) defined this clinical term as “the physical results of a
pathologic, chronic, localized loss of dental hard tissue that is chemically etched away
from the tooth surface by acid and/or chelation without bacterial involvement.5

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CLINICAL PRESENTATION
The surfaces of teeth most commonly affected with erosion are the palatal and
occlusal surfaces of maxillary teeth, as well as the buccal and occlusal surfaces of
posterior mandibular teeth. Initially erosion may be evident as dullness or matt
appearance of the enamel seen when the tooth surface is clean and dry. The lesion
progresses to a concave loss of tooth structure with wide, smooth and shiny margins
that usually lacks developmental ridges and stains and is often plaque free. As erosion
continues the underlying yellow dentine begins to show through. Due to differential
wear, cupping lesions on the cusp tips of the occlusal surfaces of posterior teeth may
occur as the dentine is lost more quickly than the surrounding enamel.6,7,8
Amalgam
and composite restorations are not affected by erosion and therefore appear “proud”
of the surrounding dental tissues. Erosive lesions occur commonly on the palatal
surfaces of maxillary anterior teeth. The lesions present as a central area of exposed
dentine surrounded by sound enamel at the gingival margin.8
This is attributed to the
buffering capacity of the gingival crevicular fluid that constantly bathes that area. The
teeth are often sensitive to touch and to temperature changes and the loss of tooth
surface is disproportionate to the age of the patient.6
Advanced erosion can lead to
pulpal, functional and aesthetic problems.6
Tooth substance loss is often multifactorial in aetiology resulting from a combination
of attrition, abrasion and erosion. Dental erosion is rarely the sole operating factor but
it can be considered a predominant factor. Erosion is believed to cause enamel surface
demineralization that makes the tooth surface softer and more susceptible to
mechanical wear by attrition and abrasion.9
For example, the surfaces affected by
erosion are frequently subjected to shear forces either from the surrounding oral soft
tissues as the keratinized dorsum of the tongue during speech and swallowing (palatal
surfaces) or through food mastication (occlusal surfaces) or from external sources
such as tooth brush and toothpaste abrasives.10
The association of dental erosion and
attrition was shown in a study involving the assessment of wear in 104 patients in
South East Queensland. Khan et al (1998) found that even if a patient is suspected to
having bruxism, erosion may be the more likely cause of hard tissue loss than attrition
alone in most cases.11

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PREVALENCE OF DENTAL EROSION
The exact prevalence of dental erosion is unknown although there is general
agreement that it is significantly high and increasing continuously, especially in the
young. It is believed that the prevalence in children and adolescents range from 5-
57%. The difficulty in determining the prevalence arises from the diversity of indices
used in the measurement of tooth wear, the inability to isolate erosion cases since the
majority of cases have a multifactorial aetiology.
Measurement of tooth wear by erosion is made difficult by the absence of stable
reference points on the tooth surfaces. A review of the techniques available to
measure tooth wear and erosion showed that none of them is ideal.12
Clinical methods
of measurement rely on visible changes on study casts or the comparison of
photographs over time. The techniques are inaccurate but are sufficient to determine
the need for treatment.12
Tooth wear indices have been suggested to evaluate the prevalence of erosion or tooth
wear in a population for epidemiological studies. The most commonly used is the
modified Smith and Knight Tooth wear index. Unfortunately, the index is still
subjective and insufficiently sensitive to detect small amounts of tooth wear.13
Table 2: Smith and Knight tooth wear index14

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The largest epidemiological study of dental erosion in the United Kingdom was the
National Children’s Dental Health Survey of 1993.15
In the study the maxillary incisor
teeth of a representative random sample 5-15 year olds were scored using the
modified Smith and Knight index. The study found that 52% of 5 year olds had
erosion on the palatal surfaces of their primary incisors, and nearly a quarter of these
cases had progressed to the pulp. Of the 12 year old children, 27% had evidence of
erosion on their incisors with about 2% of these cases had progressed to the pulp. The
2000 National Diet and Nutrition Survey (NDNS) of young people aged 4-18 years
showed that 58% of 4-6 year olds were affected with dental erosion. Table 3
summarizes the prevalence studies of tooth erosion in children in the UK.15
Table 3: Prevalence studies of tooth erosion/wear in children resident in the United
Kingdom14
A recent study that investigated the prevalence of tooth erosion in 2000 children 12
year old found that 59.7% of the children were affected with 2.7% exhibiting dentine
exposure. Significantly more boys were affected than girls and more Caucasians than

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Asian children.15
There is some evidence that socio-economic status has an influence
on the prevalence of erosion, although this is not conclusive (refer to table 4).
Table 4: Socio-economic status and prevalence of erosion14
It appears that those with low socioeconomic status have more erosion than those with
high socioeconomic status. It is suggested that this may have some relationship to oral
hygiene practices and diet as children of higher socioeconomic status could have
better oral hygiene practices than those of low socioeconomic status and a more acidic
diet.15
Deery et al (2000) conducted a study in the United States (129 subjects) and in the
United Kingdom (125 subjects) using the same examiners and based on the same
criteria. The prevalence was found to be 41% and 37% in 11-13 year old respectively.
The results indicated that there was no difference in the prevalence of dental erosion
between the two countries and that the disease is quite significant.16
The possibility of erosion and dental caries occurring simultaneously can not be
excluded. In fact this trend is being noticed more frequently as the use of acidic and
sugar-containing drinks along with poor oral hygiene. The differences between the
two conditions include the pathogenesis, the rate at which the disease progresses and
occurrence in plaque-covered and plaque-free areas.17

Feda Zawaideh 6
AETIOLOGY OF DENTAL EROSION
Dental erosion is a multifactorial condition. Shaw &
Smith (1998) constructed a VENN diagram similar to
that of dental caries to explain its aetiology (Figure
1).4,18
The contributing factors have been suggested as
having susceptible teeth, time as well as sources of
extrinsic and intrinsic acids. The overlapping between
the factors produces dental erosion. Identifying the
aetiology of dental erosion is important as it increases the possibility of successful
treatment and prevention of further wear.
The pH of the oral cavity affects the solubility of the dental tissues. The solubility of
teeth is believed to increase by 7-8 folds with each decrease of Ph when the pH falls
below 6.5. It is believed that it is the actual H+
concentration of the acidic substance
available to interact with the tooth that is more important than the pH. The type of
acid, its chemical and physical properties determine its salivary clearance from the
oral cavity.19
Erosion from intrinsic sources
Intrinsic causes for erosion are gastric acids regurgitated into the esophagus and
mouth. The pH content of the stomach acids is below 1.0, which is potentially
damaging to the teeth. It has been estimated that this damage does not occur unless
gastric acids have been acting on the dental tissues for once per week or more over a
period of at least one to two years.20
Conditions in which there is chronic vomiting
include disorders of the upper gastrointestinal tract, specific metabolic and endocrine
disorders, central emetic side effects of medications (chemotherapeutic agents,
histamine and tetracycline), alcoholism, drug abuse and certain psychomotor disorders
such as stress-induced vomiting, anorexia and bulimia nervosa.4
Gastro-esophageal reflux disease (GERD) is an important cause of dental erosion.
GER is defined as the passage of gastric contents into the esophagus while GERD is
the symptoms or complications of GER.21
It is a common condition with a prevalence
ranging from 6-10% although up to 59% of the population reports heartburn monthly,
up to 20% report weekly symptoms and 18% use prescription drugs to manage their

Feda Zawaideh 7
symptoms.21,22
The principal causes of gastro-esophageal reflux include sphincter
incompetence as in cases of hiatus hernia, drugs as diazepam, neuromuscular causes
as in cases of cerebral palsy and oesophagitis caused by alcohol. Increases gastric
pressure as in the cases of obesity can be a cause of the reflux, in addition to increased
gastric volume after a heavy meal, as result of obstruction and a spasm outcome.4
Symptoms of reflux in children and adults are listed in table 5. However, GERD can
also be silent.22
Table 5: Signs and symptoms of Gastro-esophageal Reflux Disease22
Common Symptoms in Adults Common Symptoms in Children
 Acid taste in the mouth  Difficulty sleeping
 Persistent coughing  Failure to gain weight
 Vomiting  Feeding problems
 Sense of lump in the throat  General irritability
 Stomach ache  Asthma
 Sore throat  Recurrent pneumonia
 Hoarseness of voice  Anemia
 Choking spells  Bronchitis
 Voice change  Laryngitis
 Excess salivation
 Gastric pain on awakening
 Halitosis
 Belching
 Heartburn
In children, physiological regurgitation of infancy resolves by 1 year of age unless the
child has an underlying medical condition, such as failure to thrive, feeding problems
or pneumonia. Erosion of primary and permanent teeth in children has been reported
though not to the same extent of that in adult patients with GERD. This might be
because children with GER tend to avoid acidic and carbonated foods as they
aggravate their symptoms. These children may also be refluxing into the esophagus
and not into their mouths and the success of medical treatment may contribute to the
prevention of the reflux.22
A high incidence of GERD has been reported in children
with cerebral palsy. It was even found that it is more important in the aetiology of
tooth wear than parafunctional habits.23
On the other hand, O’Sullivan et al (1998)
and Jensdottir et al (2004) concluded that dental erosion might not be as great a
problem in children with GER as it is believed to be.24,25

Feda Zawaideh 8
There is yet no single test that can consistently detect GERD, although depending on
the clinical situation, reflux can be demonstrated with several diagnostic tests such as
barium esophagography, endoscope examination, esophageal acid perfusion,
measurement of lower esophageal sphincter pressure, mucosal biopsy and standard
acid reflux test.21
The most useful diagnostic tool currently available to diagnose
GERD is 24-hour monitoring of esophageal pH by means of a catheter passed through
the nares to a point 5cm above the lower esophageal sphincter. If the PH in the distal
esophagus remains below 4.0 for more than 4% of the time, the condition is
considered pathologic.21
Treatment of GER includes a medical and non-medical
approaches outlined in table 6 and 7.21
Table 6: Non-medical treatment for GERD
21
Table 7: Medical therapy for GERD21
The term eating disorder includes anorexia nervosa and bulimia. Each illness involves
preoccupation with control over body weight, eating and food. They have a marked
prevalence in females relative to males (F: M ratio of 10:1).26
Anorexia may be

Feda Zawaideh 9
defined as “aversion to food resulting from a complex interaction between biological,
social, individual and family factors leading to severe weight loss”.27
The average age
of presentation for this condition is 16 years and a continuously increasing prevalence
of 0.2%. The prevalence is under-estimated because relatively few women seek
treatment. The condition involves conscious dietary restriction with consequent loss
of weight and it may involve stages of binge eating and vomiting. Bulimia, on the
other hand, is more common than anorexia with a prevalence of about 1% and a 25
year age of presentation. The condition involves continuous binge eating and
subsequent induced vomiting in a way to lose weight.27
The median duration of these
illnesses is up to 6 years with significant mortality (4-20%) from medical
complications and suicide in anorexia.27
Callus formation on the back of the hand and
fingers from putting the hand in the mouth to induce vomiting can be present and is
called Russell’s sign.27
Oro-dental manifestations of eating disorders vary in severity according to the length
of time the person had the eating disorder. In general dental erosion, caries, salivary
gland hypertrophy and xerostomia along with moderate periodontal destruction and
damage of the oral mucosa have been described.26
Erosion in patients with eating
disorders is mainly due to the induced vomiting and to the high dietary intake of low
pH beverages and fresh fruits. The characteristic distribution of erosion may lead to
the diagnosis of the condition. It is characterized by increased erosion on the palatal
surfaces of upper anterior teeth then extending to the occlusal and facial surfaces of
upper and lower teeth. They usually exhibit increased level of lower posterior wear on
the buccal and occlusal surfaces than other patients. The frequency, duration and total
number of vomiting episodes are not linearly associated with erosion.28
Patients with
eating disorders brush their teeth more frequently especially after vomiting episodes
thus exacerbating the wear by abrasion.29
A study by Milosevic and Dawson (1996)
analyzing the salivary factors in bulimics with or without pathological tooth wear,
found that those with tooth wear had more viscous saliva and less bicarbonate in their
saliva. In addition the salivary flow rates were less than normal which predisposes the
patients to more dental erosion.29

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Erosion from extrinsic sources
The extrinsic factors that cause dental erosion can be grouped under environmental,
medications, diet and lifestyle headings.
Environmental
This type of erosion involves the exposure to acids in the workplace or during leisure
activity, as in employees in factories manufacturing dynamite, batteries, galvanized
products and fertilizers. Swimming in gas-chlorinated pools, professional wine tasters
and printers may also be subject to erosion.19
Athletes involved in sporting activities
causing dehydration followed by consumption of acidic sports drinks also place
themselves at risk of dental caries.30
Medications
In general, any medication that has a low pH and comes in frequent and/or sustained
contact with teeth has the potential to cause dental erosion. Medications that have
been implicated in causing erosion are those with low pH (range 1.5-8.6) like iron
tonics, chewable vitamin C tablets, acid replacements or acid used for dissolving renal
stones.31
Drugs inhaled to combat asthma may have a pH low enough to cause enamel
dissolution and expose patients to dental erosion.32
Asthmatic individuals have been
proven to have an increased prevalence and increased risk of dental erosion. A non-
blind case control study of 4-10 and 11-16 year old British school children concluded
that asthmatic children had more tooth erosion than their healthy peers. In the first age
group, 61.5% with asthma had tooth erosion of the primary teeth compared to 44.3%
prevalence in children without asthma. The labial surfaces were significantly more
affected than the palatal surfaces.33
The authors attributed the greater tooth substance
loss to the reduction of salivary flow (due to the beta 2 agonist medications) and the
frequent consumption of acidic drinks on a regular basis as these children were
thirstier than their siblings as reported by their parents.33
In a case control study
conducted in south east Queensland, higher incidence of erosion was found in
asthmatic children but the study did not exclude intrinsic causes as another source of
the erosion.34
However, a study undertaken in Leicestershire and Rutland failed to
demonstrate this relationship and failed to demonstrate any significant differences in
erosion prevalence between asthmatic and non-asthmatic children.32

Feda Zawaideh 11
Beta 2 adrenoreceptors are actually believed to promote fluid consumption, reduce
salivary protection of enamel, reduce salivary flow and buffering capacity and may
relax the esophageal sphincter predisposing patients to dental erosion.
Diet
The consumption of acidic food and beverages has been proved to be closely
associated with dental erosion.35
Acidic drinks, either as fruit juices or as carbonated
soft drinks with added organic and phosphoric acids are the most frequently cited
reason for dental erosion in children.6
Citric acid can chelate calcium in
hydroxyapatite, forming soluble citrates. Alcohol drinks as beer and wine have a low
pH and would predispose to dental erosion. The intake of pickled food which
normally has very high titratable acidity would also result in erosion.6
The method of intake of the erosive drink can influence the erosive potential. Edwards
et al (1998) conducted a clinical study in a dental school in the United Kingdom using
videofluoroscopic equipment to compare the potential influence of straw or cup
drinking on dental erosion.36
The study demonstrated that drinking through a narrow
bore straw placed more posterior behind the maxillary anterior teeth reduced the
contact of the erosive drink with the teeth.36
Based on these results, Edwards et al
(1998) recommended the following dietary advice:36
1. All fizzy drinks, fruit juices, diluting juices and flavored mineral waters are
acidic and cause dental erosion. Safe drinks are water and milk. (The authors
recommend tea and coffee but there is a possibility that caffeine causes dental
erosion).
2. It is important to cut down on acidic drinks especially the number of times
every day that these drinks are taken. If you have to have these drinks the best
time is at mealtimes.
3. It is better to swallow the drink quickly to reduce the time it spends in your
mouth. Avoid rinsing with the drink before swallowing. Drinking through a
narrow straw placed behind the front teeth prevents contact of the drink with
the teeth.
4. Brushing your teeth immediately after having an acidic drink can cause the
teeth to wear more quickly. Avoid brushing for at least an hour after having
soft drinks and try to brush with a less abrasive type of toothpaste preferably a

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gel-type and use a fluoride mouthwash. (The use of fluoride applied on the
enamel even in acidic preparations reduces enamel erosion; however, the
actual clinical benefit appears low but still recommended).37
The potential dental erosiveness of the beverages depends on different chemical
characteristics. It is the titratable acidity of the beverage not the pH that gives a better
guide to that potential. Baseline pH values give only a measure of the initial hydrogen
ion concentration and provide therefore no indication as to the presence of
undissociated acid.38
Titratable acidity, on the other hand, is the amount of alkali that
is required to add to an acid to bring it up to a neutral pH. It represents the amount of
available acid and is an indication of strength and erosive potential. The following
table represents the pH, titratable acidity and erosion potential of the most commonly
consumed acidic drink.4
Table 8: The pH, titratable acidity and erosion potential of drinks
pH Titratable acidity Erosion potential
Cola drinks 2.5 0.7 Medium
Carbonated orange 2.9 2.0 Medium
Grapefruit juice 3.2 9.3 High
Apple juice 3.3 4.5 High
White wine 3.7 2.2 Medium
Orange juice 3.8 4.5 High
Beer 3.9 0.6 Low
Lager 4.4 0.5 Low
Sparkling water 5.3 0.1 low
Cairns et al (2002) investigated the effect of dilution on the erosive potential of acidic
drinks. The results indicated that dilution had very little effect on the measured pH
values but the titratable acidity fell considerably reducing the erosive potential of the
drink.38
Unfortunately, the dilution ratios for the commonly available drinks were
immense that they were not applicable to the range of concentrations consumed.
Another factor that affects the erosion potential of the drink is the type of acid in the
drink. It is believed drinks containing citric acid are more erosive than ascorbic acid
or carbonic acid because of the high calcium chelating ability of the acid. This
increases the erosion potential not only by chelating of calcium from the

Feda Zawaideh 13
hydroxyapetite but by binding to the calcium ions in saliva thus reducing the degree
of calcium available for remineralization and favor demineralization.39
Other factors that are believed to influence the erosive potential of acidic beverages
are the buffering capacity of the drink and the ions present in the drink: the calcium
and phosphate concentrations, fluoride concentration and the addition of xylitol to the
drink.40,41
More recently, Ramalingam (2001) found that the erosiveness of sports
drinks can be reduced by the addition of low concentrations of CPP-ACP (0.09%,
0.125% and 0.25%).42
Lifestyle
There have been recent changes in the lifestyles and behavioral factors of the western
population that are considered important in the aetiology of dental erosion. Recently,
there is an increased emphasis on healthy dieting, increased consumption of raw fruits
and acidic sports drinks along with increased consumption of acidic drinks by
children.43
In addition to healthier diet, whiter teeth are sought through frequent oral
hygiene practices even after the consumption of acidic drinks which predisposes to
tooth wear. The use of anti-calculus acidic agents is believed to causes dental erosion
but this has not been proved yet. Pretty et al (2003) conducted an in vitro study to
establish the erosive risk of a number of mouth rinses currently on the market.44
It is
the fluoride content and the buffering capacity of the mouth rinses that determine their
erosive potential. In the study all but Listerine (pH 3.87, F−
0.021ppm) had no
buffering capacity and were readily neutralized. A small degree of erosion was noted
after the use of Listerine mouthwash.44
However, it was noted following 14 hours of
application which is not likely to happen in vivo but this shows the need to
recommend only short term use of mouthwashes post brushing and not before.
Conversely there are unhealthy lifestyles that may be implicated in dental erosion as
the use of the drug ‘ecstasy’ (3,4 methylenedioxy-methamphetamine) which is known
to reduce the salivary flow and expose the individuals to dental erosion.4

Feda Zawaideh 14
MODIFYING FACTORS OF DENTAL EROSION
Individual’s susceptibility to dental erosion varies considerably depending on the
presence of other predisposing and modifying factors. Among these factors are the
morphology of teeth, the presence of any soft tissue defects and saliva properties.19
The surfaces in contact with the tongue, particularly the palatal surfaces of the
maxillary teeth are much more affected by erosion than any other surface.
The manner in which the erosive fluid is taken into the mouth, as in the habit of
swishing the erosive drink around, may affect the extent and distribution of the
erosive lesions depending on the surfaces it comes into contact with and the duration
of contact.19
Salivary factors; the salivary flow rate, the buffering capacity and neutralization of
dietary acids, oral clearance as well as the presence of the acquired salivary pellicle,
are known to be intrinsic modifying factors of dental erosion.45
Sanchez and De
Preliasco (2003) conducted a case control study using standard salivary tests to assess
saliva characteristics, salivary pH, flow rate and buffering capacity in 30 children
with erosive lesions before and after soft drinks intake and compared these to
equivalent values for healthy caries-free individuals.45
Low salivary flow rate, low
carbonate production and low buffering capacity and low pH after acidic drink
consumption were significantly less in the control group. The results clearly indicate
the greater potential for erosive damage when the normal protective roles of the saliva
are reduced.45
This relationship has been clearly demonstrated and described by
Gudmnundson et al (1995) and by O’Sullivan and Curzon (2000) in previous
studies.46,47
The salivary pellicle on the enamel surfaces of teeth is also thought to act as a
permeability-selective membrane providing protection against demineralization from
erosive challenges.48
In vitro studies showed that the lubricating properties of the
viscous mucin glycoprotein and the salivary pellicle derived from the
submandibular/sublingual saliva provides enamel with the greatest and most
prolonged protection from acid dissolution.48
In addition, enamel specimens coated
with pellicle in in vivo studies revealed less extensive erosion of the enamel surface
compared to uncovered specimens.48
The rate of formation of the acquired pellicle

Feda Zawaideh 15
and its thickness that can be reduced with tooth brushing are also important
contributing factors in the protection against erosive challenges.
DIAGNOSIS OF EROSION
Given the current state of knowledge of the causes of erosion and keeping in mind the
possibility of associated attrition and abrasion, Gandara and Truelove (1999) proposed
the following protocol for patient assessment and diagnosis of dental erosion.22
Table 9: Patient assessment and diagnosis of dental erosion
I. Obtain historical data. Check for following items:
Medical History
 Excessive vomiting, rumination
 Eating disorder
 Gastroesophageal reflux disease
 Symptoms of reflux (Table 5)
 Frequent use of antacids
 Alcoholism
 Autoimmune disease (Sjogren's)
 Radiation tx of head and neck
 Oral dryness, eye dryness
 Medications that cause salivary
hypofunction
 Medications that are acidic
Dental History
 History of bruxism (grinding or
clenching)
-Grinding bruxism sounds during sleep
noted by bed partner?
-Morning masticatory muscle fatigue or
pain?
 Use of occlusal guard
Dietary History
 Acidic food and beverage
frequency
 Method of ingestion (swish,
swallow?)
Oral Hygiene Methods
 Toothbrushing method and frequency
 Type of dentifrice (abrasive?)
 Use of mouthrinses
 Use of topical fluorides
Occupational/Recreational History
 Regular swimmer?
 Wine-tasting?
 Environmental work hazards?
II. Perform physical assessment. Observe for following features:
Head and Neck Examination
 Tender muscles (bruxism?)
 Masseteric muscle hypertrophy
(bruxism?)
 Enlarged parotid glands
(autoimmune disease, anorexia,
alcoholism)
Intra-oral Examination
 Signs of salivary hypofunction:
-Mucosal inflammation
-Mucosal dryness
-Unable to express saliva from gland
ducts
 Shiny facets or wear on restorations

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 Facial signs of alcoholism:
-Flushing, puffiness on face
-Spider angiomas on skin
(bruxism?)
 Location and degree of tooth wear
(document with photos, models,
radiographs
General Survey
 Underweight (anorexia)
Salivary function assessment
 Flow rate
 pH, buffer capacity ( use of ‘Saliva
Check Buffer’ GC corporation)
Once diagnosed, it is important to record the location and severity of tooth erosion.
Complete record with study models and intra oral photos need to be taken to monitor
the progression of the condition (recommend localized silicone impressions and
accurate study models in high density die-stone).4
MANAGEMENT OF EROSION
Tooth wear could result in an aesthetic problem, loss of tooth structure, sensitivity and
pain, pulpal exposure and loss of vertical dimension which is thought to lead to
temporomandibular joint problems. The first step in the management of dental erosion
is to determine the cause of the dental erosion and to identify the associated risk
factors and where possible eliminated. The management of dental erosion involves a
preventive and a restorative part and in this seminar it will be discussed in three
phases; immediate, provisional and long term.49
Immediate management
The cause of the dental erosion should be investigated thoroughly as previously
mentioned, and eliminated whenever possible. Recording the clinical situation is an
important step to allow further monitoring of the condition. Impressions, study models
and photographs should be obtained before commencement of treatment. Prevention
of ongoing erosion comes next and this can be undertaken by reducing the exposure to
acid and enhance the ability of the oral cavity to overcome and resist the effect of the
acidic environment.49

Feda Zawaideh 17
Dietary counseling should be given after a thorough analysis of the diet. It must be
personalized to the individual bearing in mind the constraints that are operating on
them. It needs to be given in a positive, individualized way to maximize compliance.4
The patient needs to educated about the types of food and drinks that have the greatest
erosive potential, encourage the consumption of positive alternatives as water, milk,
tea, coffee without sugar because they are safer. Limitations should be placed on the
time of consumption of the drinks, preferably during mealtimes. Drinks should be
swallowed quickly without holding the drink in the mouth and preferably avoiding the
use of sipping, pop tops and spout sups.
In response to the increasing concern about dental erosion, product modifications
have been attempted to minimize the effect of dental erosion. Mahoney and Kilpatrick
(2004) reported three approaches mentioned in the literature.49
The first involves
raising the pH, reducing the titrateable acidity and adding calcium to the soft drinks
followed with the addition of hydrocolloid food gum. An example of this product is
Ribena ToothKind drink (Ribena, Glaxo Smithkline, UK). The second approach is
to add large amounts of calcium fluoride to soft drinks with the aim to supersaturate
the environment around the tooth. Unfortunately this technique is less effective than
the first one. Finally, minimal amounts of caseine phosphopeptide-amorphous calcium
phosphate (CPP-ACP) added to sports drinks (Powerade) have been shown in vitro
to reduce the erosive effect of the drink.42
Improving the resistance of the oral cavity to the effects of erosion can be achieved by
increasing the resistance of the tooth tissue to dissolution or by improving the saliva
function. The use of topical fluoride has been advocated to enhance the tooth
resistance to dissolution. The suggested method of action of fluoride in erosion
prevention involves the deposition of fluoride in the porous structure of dentine acting
as a diffusion barrier preventing further dissolution.50
Bardsley et al (2004)
demonstrated that children in non-fluoridated districts are 1.5 times more likely to
have smooth surface wear compared with children in fluoridated districts.51
In
addition, the use of fluoride twice a day in the form of toothpaste provided added
protection from dental erosion.Another option involves the use of CPP-ACP in the
form of a sugar free gum (Recaldent) or as a topical cream (Tooth Mousse).

Feda Zawaideh 18
To neutralize the acidic attack after vomiting or reflux sucking sugar free antiacid
tablets can be recommended. Rinsing with sodium carbonate or baking powder is
mentioned in the literature but with no specific scientific reason. The use of custom
trays as a method of application is also suggested.52
However, using the trays at night
in patients with reflux may result in trapping acid within and causing more erosion.
Immediate management of dental erosion also involves the management of any
sensitivity and pain experienced by the patient. The use of glass ionomer cement as a
sealant will actually resolve the sensitivity and will prevent further damage.53
Anecdotally, dentists have been using Tooth Mousse applied on a cotton bud or Gel
Kam to reduce the sensitivity.
Interim treatment
Any restorative treatment should be ideally delayed until the effect of the preventive
measures on the rate of tooth wear is assessed. In cases where function or aesthetic is
compromised active treatment is recommended. Treatment should be aimed at
restoring the missing tooth structure with minimal intervention, preventing further
tooth tissue loss and maintaining a balanced occlusion. The table below memorizes
the techniques currently available to restore teeth affected by dental erosion.
Table 10: Treatment options for the management of dental erosion49
Material Advantages Disadvantages Durability
Cast Metal
(nickel
chrome or
gold)
Fabricated in thin sections-
require only 0.5mm space
Very accurate fit possible
Does not abrade the
opposing dentition
Protective of residual tooth
structure
May be cosmetically
unacceptable due to the
shine through of metallic
grey
Can not be simply repaired
or added to intraorally
Suitable for posterior
restorations in
parafunction??
Multiple appointments
required
Success rate of 89% for
palatal veneers over 4.5
years (n=210)
Composite- Least expensive Technically difficult for Success rate of 86% for

Feda Zawaideh 19
direct
May be used as a
diagnostic tool
Can be added to and
repaired relatively simply
intraorally
Aesthetically superior to
cast metal
Single appointment
palatal veneers
Limited control over
occlusal and interproximal
contour
Requires minimum of 1mm
space
Possible inadequate wear
resistance for posterior use
labial veneers over 3 years
(n=289)
Composite-
indirect
Can be added to and
repaired intraorally
Aesthetically superior to
cast metal
Control over occlusal
contour and vertical
dimension
Inferior marginal fit
May be bulky
Possible inadequate wear
resistance for posterior use
Requires at least two
appointments
Expensive
Success rate of 96% for
palatal veneers over 2
years (n=75)
porcelain Best aesthetics
Good abrasion resistance
Well tolerated by gingival
tissues
Potentially abrasive to
opposing teeth
Brittle should be used in
bulk
Hard to repair
expensive
Multiple studies suggest a
success rate in excess of
90% over 5 years+
Many of the restorations placed may actually increase the vertical dimension.
Controversy exists over the risks associated with doing that. However, recently it
appears that increases in the vertical dimension can be tolerated especially in young
patients and a balanced occlusion is soon achieved by differential eruption of
teeth.54,55,56,57,58
Long term review
Regular review for patients suffering from dental erosion is recommended in order to
monitor further tooth loss, maintain the exciting restorations and to provide support
for the patient.

Feda Zawaideh 20
CONCLUSION
Early recognition of erosion is important to successfully manage and prevent disease
progression. A brief review of etiologic factors has been presented and
recommendations made for evaluation and management of the patient with erosion.
These include a complete problem and medical history aimed at identifying possible
risk factors, including those for other forms of tooth wear. This is important to
determine the aetiology and help direct treatment. Specialized testing such as GERD
assessment may be appropriate and necessitate referral. The management of eating
disorders requires a multidisciplinary approach. Whether or not aetiology can be
determined, a prevention protocol for prevention of progression of erosion should be
initiated. Restorative treatment is undertaken where indicated. The patient should be
monitored at regular intervals by photographs or impressions of the dentition to
determine compliance and success of treatment.

Feda Zawaideh 21
REFERENCES
1
Kelleher M, Bishop K (1999): Tooth surface loss: an overview. British Dental Journal
186:61-66.
2
Barlett D, Phillips K, Smith B (1999): A difference in perspective, the North American and
European interpretations of tooth wear. International Journal of Prosthodontics 12:401-408.
3
Imfeld T (1996): Dental erosion. Definition, classification and links. European Journal of
Oral Sciences 104:151-155.
4
Shaw L, Smith A (1998): Dental erosion-the problem and some practical solutions. British
Dental Journal 186:115-118.
5
Ten Cate J, Imfeld T (1996): Dental erosion, summary. European Journal of Oral Sciences
104:241-244.
6
Yip K, Smales R, Kaidonis J (2002): Management of tooth tissue loss from erosion.
Quintessence International 33:516-520.
7
Welbury R (2001): Paediatric Dentistry. Second edition. Oxford University Press. Chapter
6:201-215.
8
Bishop K, Kelleher M, Briggs P, Joshi R (1997): Wear now? An update on the aetiology of
tooth wear. Quintessence International 28:305-301.
9
Moss S (1998): Dental erosion. International Dental Journal 48:529-539.
10
Amaech B, Higham S, Edgar W (2003): Influence of abrasion in clinical manifestation of
human dental erosion. Journal of Oral Rehabilitation 30:407-413.
11
Khan F, Young W, Daley T (1998): Dental erosion and bruxism. A toothwear analysis from
South East Queensland. Australian Dental Journal 43:117-127.
12
Azzopardi A, Barlett D, Watson T, Smith B (2000): A literature review of the techniques to
measure tooth wear and erosion. European Journal of Prosthodontics 8:93-97.
13
Nunn J, Gordon P, Morris A, Pine C, Walker A (2003): Dental erosion-changing
prevalence? A review of British national children’s surveys. International Journal of
Paediatric Dentistry 13: 98-105.
14
Barlett D (2003): Retrospective long term monitoring of tooth wear using study models.
British Dental Journal 194:211-213.
15
Dugmore C, Rock W (2004): The prevalence of tooth erosion in 12-year-old children.
British Dental Journal 196:279-282.
16
Deery C, Wagner m, Longbottom C, Simon R, Nugent Z (2000): The prevalence of dental
erosion in a United States and a United Kingdom sample of adolescents. Pediatric Dentistry
22:505-510.

Feda Zawaideh 22
17
Nunn J, Shaw L, Smith A (1996): Tooth wear: dental erosion. British Dental Journal
180:349-352.
18
Dugmore C, Rock W (2004): Amultifactorial analysis of factors associated with dental
erosion. British Dental Journal 196:283-286.
19
Linnett V, Seow W (2001): Dental erosion in children. A literature review. Paediatric
Dentistry 23:37-43.
20
Scheutzel P (1996): Aetiology of dental erosion: intrinsic factors. European Journal of
Oral Sciences 104:178-190.
21
Barron R, Carmichael R, Marcon M, Sandor G (2003): Dental erosion in gastroesophageal
reflux disease. Journal of the Canadian Dental Association 69:84-89.
22
Gandara B, Truelove E (1999): Diagnosis and management of dental erosion. The Journal
of Contemporary Dental Practice 1:1-17.
23
Shaw L, Weatherill S, Smith A (1998): Toothwear in children: an investigation of
aetiological factors in children with cerebral palsy and gastroesophageal reflux. Journal of
Dentistry for Children ASDC: 484-486.
24
O’Sullivan E, Curzon M, Roberts G, Milla P, Stringer M (1998): Gastroesophageal reflux
in children and its relationship to erosion of primary and permanent teeth. European Journal
of Oral Science 106:765-769.
25
Jensdottir T, Arnadottir I, Thorsdottir I, Bardow A, Gudmundsson k, Theodors A, Holbrook
W (2004): Relationship between dental erosion, soft drink consumption, and gastroesophageal
reflux among Icelanders. Clinical Oral Investigation 8:91-96.
26
De Moor R (2004): Eating disorder-induced dental complications: a case report. Journal of
Oral Rehabilitation 31:725-732.
27
Milosevic A (1999): Eating disorders and the dentist. British Dental Journal 186:109-113.
28
Gordon C (2002): Oral care for patients with bulimia. Journal of the American Dental
Association 133:1689-1691.
29
Milosevic A, Dawson L (1996): Salivary factors in vomiting bulimics with and without
pathological tooth wear. Caries Research 30:361-366.
30
Sirimaharaj V, Brearely Messer L, Morgan M (2002): Acidic diet and dental erosion among
athletes. Australian Dental Journal 47:228-236.
31
Moss S (1998): Dental erosion. International Dental Journal 48:529-539.
32
Dugmore C, Rock W (2003): Asthma and tooth erosion. Is there an association?
International Journal of Paediatric Dentistry 13:417-424.
33
McDerra E, Pollard M, Curzon M (1998): The dental status of asthmatic British school
children. Paediatric Dentistry 20:281-287.
34
Sivasithamparam K, Young W, Jirattanasopa V, Priest J, Khan F, Harbrow D, Daley T
(2002): Dental erosion in asthma: a case control study from south east Queensland.
Australian Dental Journal 47:298-303.

Feda Zawaideh 23
35
Milosevic A, Bardsley P, Taylor S (2004): Epidemiological studies of tooth wear and dental
erosion in 14-year old children in North West England. Part 2: The association of diet and
habits. British Dental Journal 197:479-483.
36
Edwards W, Ashwood R, Littlewood S, Brocklebank L, Fung D (1998): A
videofluoroscopic comparison of straw and cup drinking: the potential influence on dental
erosion. British Dental Journal 185:244-249.
37
Hughes J, West N, Addy M (2004): The protective effect of fluoride treatments against
enamel erosion in vitro. Journal of Oral Rehabilitation 31:357-363.
38
Cairns A, Watson M, Creanor S, Foye R (2002): The pH and titratable acidity of a range of
diluting drinks and their potential effect on dental erosion. Journal of Dentistry 30:313-317.
39
Meurman J, ten Cate J (1996): Pathogenesis and modifying factors of dental erosion.
European Journal of Oral Sciences 104:199-206.
40
Weat N, Hughes J, Parker D, Weaver L, Moohan M, De’ath J, Addy M (2004):
Modification of soft drinks with xanthan gum to minimise erosion: a study in situ. British
Dental Journal 196:478-481.
41
Larsen M, Nyvad B (1999): Enamel erosion by some soft drinks and orange juices relative
to their pH, buffering capacity and contents of calcium phosphate. Caries Research 33:81-87.
42
Ramalingam L (2001): An in vitro investigation of the effects of CPP-ACP on erosion of
human dental enamel by a sports drink. Master thesis. The University of Melbourne.
43
Moazzez R, Smith B, Barlett D (2000): Oral pH and drinking habit during ingestion of a
carbonated drink in a group of adolescents with dental erosion. Journal of Dentistry 28:395-
397.
44
Pretty I, Edgar W, Higham S (2003): The erosive potential of commercially available
mouthrinses on enamel as measured by quantitative light-induced fluorescence. Journal of
Dentistry 31:313-319.
45
Sanchez G, Fernandez De Preliasco M (2003): Salivary pH changes during soft drinks
consumption in children. International Journal of Paediatric Dentistry 13:215-257.
46
Gudmnundson K, Kristleifsson G, Theodors A, Hoolbrook W (1995): Tooth erosion,
gastroesophageal reflux and salivary buffering capacity. Oral Surgery, Oral Medicine, Oral
Pathology and Oral Radiology 79:185-189.
47
O’Sullivan E, Curzon M (2000): Salivary factors affecting dental erosion in children.
Caries Research 33:81-87.
48
Hannig M, Balz M (1999): Influence of in vivo formed salivary pellicle on enamel erosion.
Caries Research 33:372-379.
49
Mahoney E, Kilpatrick N (2004): Dental erosion: part 2. The management of dental
erosion. New Zealand Dental Journal 100:42-47.
50
Ganss C, Klimek J, Schaffer U, Spall T (2001): Effectiveness of two fluoridation measure
on erosion progression in human enamel and dentine in vitro. Caries Research 35:325-330.

Feda Zawaideh 24
51
Bardsley P, Taylor S, Milosevic A (2004): Epidemiological studies of tooth wear and dental
erosion in 14-year-old children in North West England. Part 1: The relationship with water
fluoridation and social deprivation. British Dental Journal 197:413-416.
52
Chu F, Botello m, Newsome P, Chow T, Smales R (2002): Restorative management of the
worn dentition: 3. Localised posterior tooth wear. Dental Update 29:267-272.
53
Azzopardi A, Barlett D, Watson T, Sherriff M (2004): The surface effects of erosion and
abrasion on dentine with or without a protective layer. British Dental Journal 196: 351-354.
54
Redman C, Hemmings K, Good J (2003): The survival and clinical performance of resin-
based composite restorations used to treat localised anterior tooth wear. British Dental
Journal 194:566-572.
55
Dyer K, Ibbetson R, Grey N (2001): A queation of space: options for the restorative
management of worn teeth. Dental Update 28:118-123.
56
Hemmings K, Darbor U, Vaughan S (2000): Tooth wear treated with direct composite
restorations at an increased vertical dimension: results at 30 months. Journal of Prosthetic
Dentistry 83:287-293.
57
Hunter L, Stone D (1997): Supraoccluding cobalt chrome onlays in the management of
amelogenesis imperfecta in children: a 2 year report. Quintessence International 28:15-19.
58
Rivera-Morales W, Mohli N (1991): Relationship of occlusal vertical dimension to the
health of the masticatory system. Journal of Prosthetic Dentistry 65:547-553.

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