(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 teeth

1

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 flexure

3

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


Feda Zawaideh

2

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


Feda Zawaideh

3

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


Feda Zawaideh

4

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


Feda Zawaideh

5

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 GERD21

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


Feda Zawaideh

10

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


Feda Zawaideh

12

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


Feda Zawaideh

16

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.

Health & Medicine

(10) dental erosion