!

!
Yan-Fang Ren, DDS, PhD, MPH
!!
Etiology, Diagnosis and
Preventive Management of
Dental Erosion:
An Update 

!
Introduction
Dental erosion is the loss of dental hard tissue associated with extrinsic and/or intrinsic acidic
substances that are not produced by bacteria. Though the chemical process of dental erosion is
similar to that of caries, i.e., dissolution of hydroxyapatite by acids, the clinical manifestations
and management of dental erosion are fundamentally different from caries because the erosive
process does not involve bacteria. Dental erosion does not begin as a subsurface enamel lesion
that is conducive to remineralization as in the caries process, but rather as a surface softening
lesion that is susceptible to wear and resistant to remineralization by conventional therapies.
Erosive dental lesions are often wide spread and may involve the entire dentition. Dental hard
tissue loss associated with erosion is almost always complicated with other forms of tooth wear
such as attrition and abrasion. Dental erosion results in tooth surface softening, which inevitably
accelerates tissue loss caused by tooth-to-tooth contact while chewing and grinding (attrition),
or by abrasive wear while mechanically brushing or cleaning tooth surfaces (abrasion). If dental
erosion is not managed through effective interventions, it may result in substantial loss of
enamel and subsequent exposure of the underlying dentin, which can in turn lead to dentin
sensitivity, loss of vertical height and esthetic problems. Early identification and intervention is
therefore the key to prevent extensive tooth wear subsequent to erosion.

Effective management of dental erosion is largely dependent on a thorough understanding of its

etiology and early recognition of its signs and symptoms in clinical practices. The purpose of the
present paper is to provide an updated overview on the causes and risk factors for dental
erosion and discuss topics related to its diagnosis and prevention.

Prevalence
Dental erosion is a common condition and its prevalence seems to be trending higher in recent
decades (1). It is difficult to accurately assess the prevalence of dental erosion from published
literature for there is not a universally accepted standard for clinical evaluation of this condition.
Dental erosion is almost always complicated with other form of tooth wear. Table 1 lists
prevalence of dental erosion in different age groups from different countries. The reported
prevalence of dental erosion varies greatly in the literature, which can be partially explained by
age, country and different evaluation standard. Recent studies continue to report large
variations of dental erosion in different age groups (2-4). The median prevalence of dental
erosion is 34.1 (interquartile range 29.0) in children and 35.6 (interquartile range 35.4) in adults.
In studies that reported prevalence of dental erosion in different age groups, there is a clear
trend of increasing prevalence with age in children and adults (5-9). Dental erosion has been
considered a common condition limited to developed countries (1). Recent studies showed that
the prevalence of dental erosion was also high in adolescents and adults in developing
countries such as China, Brazil and Sudan, ranging from 27.3 to 66.9% (median 40.0%)
(Table 1).

Data on the incidence of dental erosion is scarce. A recent study reported that 24.2% of the
erosion-free children developed dental erosion in 1.5 years (from 12 to 13.5 years of age),
yielding an annualized incidence rate of 16.1% (6). Other study reported a lower incidence rate,
showing 12.3% of erosion-free children developing new erosive lesion in a 2-year period (from
12 to 14 years of age)(5).


!
!
Etiology
Dental erosion is caused by sustained direct contact between tooth surfaces and acidic
substances. It has long been recognized that demineralization of dental enamel will occur once
the oral environmental pH reaches the critical threshold of 5.5 (10). Acids in the mouth originate
from three main sources: produced in situ by acidogenic bacteria, ingested extrinsic acids as
dietary components, and dislocated intrinsic acids through the backflow of gastric contents.
Acids of bacteria origin cause caries, while extrinsic and intrinsic acids cause dental erosion.
Clearance of acids from the oral cavity is to a large extent dependent on the saliva flow rate and
saliva buffering capacity. Low saliva flow rate and poor buffering capacity allow prolonged
retention of extrinsic and intrinsic acids in the mouth, which will accelerate the erosive process.

Extrinsic acids:

Acidic beverages:
Acidic soft drinks are considered the most important etiological factors of dental erosion (11-13).
Commercial productions of carbonated soft drinks have been growing steadily in the recent
decades, with the quantity of sales doubling every twenty years (14) (Figure 1). The
consumption of soft drinks has in consequence increased by 500% in the past 50 years, and
serving sizes have also increased from an average of 6.5 oz in the 1950s to 12 oz in 1960s and
20 oz in late 1990s (15-17). It is estimated that an average American consumes more than 56
gallons of soft drinks per year, averaging one and a half 12 oz cans per day(14, 18). The
widespread increase in soft drink consumption is especially alarming in adolescents, with about
80% of 14 year old children drinking an average of more than 20 oz of soft drinks daily (19).

Soft drinks, including carbonated beverages, fruit juices and sport drinks, are almost exclusively
acidic (p<4.0) in nature in order to maintain a fresh and fizzy mouth feel and to prevent rapid
growth of bacteria. Table 2 lists the pH ranges of common beverageson the consumer market.
These beverages, when in contact with the tooth, will reduce the pH on the tooth surface to a
level below the critical value of 5.5 for enamel demineralization.

The effects of these beverages on dental hard tissues have been extensively studied in recent
years. Numerous experimental and clinical investigations have shown that dental erosion in the
form of enamel and dentin tissue loss can be caused by carbonated soft drinks (20-23), fruit
juices (24-28), sport drinks (29-31), and wines (32-34). Epidemiological studies in different age
groups have also shown a close relationship between soft drink consumption and signs of
dental erosion (35-39). As shown in Figure 2, enamel erosion caused by orange juice is
characterized by color change and surface softening in the early stage, and subsequent enamel
tissue loss with the progression of erosive challenges. Softened enamel is susceptible to
abrasive wear. Brushing after erosive challenges will accelerate enamel tissue loss (40-44). The
effects of acidic beverages on dental hard tissues are especially alarming in patients with
prolonged and habitual ingestion pattern (Figure 3). Dental hard tissues may be “washed away”
with time and resulting in severely worn teeth that negatively affects function and esthetic
appearance.

!


!
!
Acidic foods and dietary ingredients:
Besides acidic drinks, many solid and semi-solid foodstuffs are also acidic in nature. Table 3
lists common foods and dietary ingredients that have low pH values. Though the potential
erosive effects of acidic foodstuffs are not well understood, it is believed that frequent ingestion
of these types of foods may also contribute to dental erosion.

Individual eating habits may be the most important factor affecting the erosive potential of acidic
foods. Frequent consumption of citrus fruits could significantly increase the risk for dental
erosion (45). Persons with a diet with more fruits and acidic berries may also have higher
frequencies of dental erosion(46, 47).

Other sources of extrinsic acids:

Acidic medications such as those containing Vitamin C (48, 49) and Aspirin (50, 51) may cause
erosion when used in a manner resulting in sustained contact between tooth surfaces and the
medications. Habitual use of mood enhancing drugs such as Ecstasy may also increase the risk
for erosive tooth wear (52, 53). Environmental and occupational factors may contribute to dental
erosion in selected populations including swimmers (54, 55), workers in an environment with
acidic industrial vapors (56-58), and professional wine tasters (59, 60).

Intrinsic acids:
The source of intrinsic acids in the oral cavity is mostly from the backflow of the gastric contents
through the esophageal tract. Gastric juice is mainly hydrochloric acid produced by the parietal
cells in the stomach. Presence of the highly acidic gastric juice (pH 1.0-3.0) in the oral cavity
may lead to dental erosion. Gastro-esophageal reflux disease (GERD), bulimia and rumination
are the main conditions associated with the backflow of gastric juice to the mouth.

Human esophagus is a muscular tube connecting the oropharyngeal space with the stomach. It
has muscle sphincters at the upper and lower ends, serving as barriers to prevent the backflow
of gastric contents into the orophayngeal space and the respiratory tract. Dysfunction of these
sphincters may allow movement of gastric contents into the esophagus and mouth and result in
typical symptoms of GERD, including heartburn, chest pain, regurgitation and dysphagia.
Regurgitation describes the passing of gastric contents into the mouth, which is the underlying
mechanism for the occurrence of dental erosion in patients suffering from GERD. The
prevalence of GERD is higher in western populations, with 25% of people reporting heartburn at
least once a month, 12% at least once per week, and 5% having daily symptoms, while it is
lower in eastern Asian populations, with 11% reporting heartburn monthly, 4% weekly and only
2% having daily symptoms (61). Though dental erosion has not been identified as one of the
extrapharyngeal manifestations of GERD by gastrointestinal specialists (61, 62), there have
been numerous observational studies reported in dental journals describing an association
between GERD and dental erosion (63-66). A recent systematic review concluded that there is a
strong association between GERD and dental erosion (67). The median prevalence of dental
erosion in GERD patients was 24%, with a large range (5-47.5%), and the median prevalence of
GERD was 32.5% (range: 21-83%) in adults patients with dental erosion and 17% (range:
14-87%) in pediatric populations (67). However, the prevalence of dental erosion in GERD


!
!
reported in the review is not higher than that in the general population (1). Jaeggi and Lussi
reviewed the prevalence of dental erosion from 26 epidemiological studies involving different
age groups of children and adults and found that the median prevalence of dental erosion was
37% in general populations (1), even higher than the 24% median prevalence of erosion in
GERD. It was reported that the pH in the oropharynx almost never reach the level of <4 and
seldom (10% of time) reach the level of <5.5 even in the severe cases of GERD (68). Therefore,
the acidic challenge from GERD appears to be less severe than that from dietary factors. In
addition, some clinical studies found no correlation between GERD and dental erosion (69, 70).
Di Fede and co-workers found that the prevalence of dental erosion, measured by the Smith
and Knight Tooth Wear Index, was 9.0% in the 200 patients with GERD (diagnosed with
endoscopy and 24-hour pH-metry) and 13.0% in the 100 healthy controls (69). Though the
available evidence indicates that the association between dental erosion and GERD is weak in
population studies, it by no means diminishes the importance of intrinsic acid in the etiology of
erosion in some individual patients, especially those with reflux breaching the upper esophageal
sphincter and resulting in pH<5.5 in the oropharynx.

Voluntary reflux of gastric contents (rumination) has been reported in special populations as a
potential cause of dental erosion (71-73). Though it is rare in occurrence, rumination should be
considered as one of the potential etiological factors in patients with unknown causes of erosive
tooth wear. Patients suffering from bulimia may ruminate multiple times daily over a prolonged
period of time, which may cause typical dental hard tissue loss on the palatal aspect of the
maxillary teeth (74). The prevalence of dental erosion is higher in bulimic patients than in non-
bulimic controls (74, 75). Dental erosion in bulimic patients is most likely associated with oral
retention of regurgitated gastric contents. The dietary habits of bulimic patients may include
binging on high energy foods and foods with high erosive potential, which may further
exacerbate erosion (75).

Saliva flow and buffering capacity:

When acidic substances enter the mouth, salivary glands will reflectively increase secretion and
saliva flow will accelerate to clear the acids from the oral cavity. As human saliva contains
bicarbonates and urea, it rapidly neutralizes the acidic remnants and returns the oral pH to
normal – which is known as the buffering capacity of saliva, an important mechanism for oral pH
regulation. Many factors affect saliva flow rate and buffering capacity, including autoimmune
diseases (e.g. Sjögren syndrome), medications (e.g. antidepressants and antipsychotics), and
aging. When saliva flow rate is reduced, its clearance and buffering capacity will be negatively
impacted, resulting in abnormal acid retention in the mouth, which in turn may contribute to
dental erosion. Saliva flow rate and buffering capacity is therefore an important etiological factor
of erosion (76-78). Low saliva flow rate and poor buffering capacity were often found to be
associate with the development of dental erosion (45, 79-82). Composition of the saliva is also
considered a significant factor in the development of dental erosion (83).



!
!
Diagnosis
Accurate diagnosis of erosion and erosive tooth wear begins with an in depth assessment of
risk factors for erosion and of medical and dental histories. Visual inspection of tooth surfaces
and wear patterns provides direct evidence of dental erosion. Because dental hard tissue loss
associated with erosion is not reversible and a severely worn dentition represents a great
challenge to dentists and patients, it is imperative to recognize the risk factors early, preferably
before any sign of erosive tooth wear occurs, to facilitate early intervention

Risk factor assessment:

As described earlier, extrinsic and intrinsic acids are the predominant etiological factors for
dental erosion. Therefore, erosion risk assessment mainly involves identification of these factors
in a specific patient and evaluation of their roles in the development of dental erosion.

Risk factors for dental erosion include:

• Frequent use of acidic dietary products, especially soft drinks, fruit juices and acidic foods
(Table 3)

• GERD, rumination, regurgitation, and frequent involuntary vomiting

• Prolonged use of chewable acidic medications, especially Vitamin C and Aspirin

• Occupational hazards that include direct contact with acidic substances, e.g, wine makers
and tasters, swimmers, and battery workers

• Sustained use of recreational drugs such as Ecstasy

• Low saliva flow rate and inadequate saliva buffering capacity

Patient with any of the above factors is at risk of developing dental erosion. Though the current
paradigm is for dental practitioners to look for these risk factors after they see signs of erosion
and erosive wear, identification of these factors before the existence of any sign of erosion may
be more important. Early intervention for prevention of dental erosion is a more effective
therapeutic strategy than any attempt to restore lost dental hard tissue due to erosion. As
dietary acids are the most important etiological factors, a thorough evaluation of dietary habits
will be helpful in assessing the erosive potential of acidic foodstuffs. Patients should record all
their dietary activities in a diary over a 4-day period including weekend (84). The time of day and
quantity of all food and beverage intakes should be included in the diary. Careful review of
medical history and consultation with patient’s primary care physician may help to identify
erosion from intrinsic acids (e.g. GERD) and patients with salivary hypofunction. Review of
current medications and their ingestion methods are also helpful in finding drugs that cause low
saliva flow and that may cause erosion if ingested inappropriately. Both stimulated and non-
stimulated saliva flow rates can be assessed in dental offices by simply measuring the amount
of saliva collected in a 5 or 10 minutes period. Patients with a non-stimulated saliva flow rate of
less than 0.12ml/min may be considered as having low saliva flow (85).

!


!
!
Clinical evaluation:
Though dental erosion often coexists with attrition and abrasion, it has some distinctive
characteristics in location, appearance and morphology. The most frequently affected areas are
the palatal surface of maxillary incisors and the occlusal surface of the mandibular first molars in
adolescents (1). Lussi et al described that erosion of facial surfaces were commonly seen on
maxillary and mandibular canines and premolars, occlusal erosion were seen on maxillary and
mandibular premolars and molars, and palatal erosion on maxillary incisors and canines (8).
Early sign of erosion often appears as smooth and flat facets on facial or palatal surfaces, and
shallow and localized dimpling on occlusal surfaces (Figure 4). Without intervention, erosive
wear will progress, leading to the deep cupping lesions with exposed dentin and eventual loss of
occlusal morphology (Figure 5).

Cervical and incisal grooves are typical erosive lesions in premolars, canines and incisors
(Figure 6). Shallow defects with a broad base on facial surfaces above the cementum-enamel
junction were found to be associated with acidic dietary habits but not with abrasive diets (86).

Numerous classification and index systems have been developed with the purpose to better
quantify the severity of dental erosion and differentiate erosion from attrition or abrasion. None
of these classification systems has been universally accepted, and their validities has been
challenged lately (87). Nonetheless, the erosive tooth wear index or classification system
represents a benchmark that allows direct comparison between clinical data from different
centers or from different time points and will continue to be used in clinical studies before a
golden standard is established. The index systems developed by Smith and Knight (88), Eccles
(89), and Lussi (90) are among the frequently used methods in clinical studies and practices
and are described below.

!
Eccles classification of dental erosion (89):

Class  I Early  stages  of  erosion,  absence  of  developmental  ridges,  smooth  glazed  surface  occurring  
mainly  on  labial  surfaces  of  maxillary  incisors  and  canines

Class  II Facial Den?ne  is  involved  in  less  than  one-­‐third  of  the  facial  surface  
Type  I:  ovoid  or  crescent,  concave  lesion  at  cervical  region  of  facial  surface,  which  is  
different  from  wedge-­‐shaped  lesions  
Type  II:  irregular  lesion  en?rely  in  the  crown,  which  has  a  punched-­‐out  appearance.  
Enamel  is  absent  from  the  lesion  floor.

Class  IIIa Facial More  extensive  destruc?on  of  den?n  par?cularly  of  the  anterior  teeth.  Most  lesions  affect  
a  large  part  of  the  surface,  but  some  are  localized  and  hollowed-­‐out.

Class  IIIb Palatal/   Lesions  affect  more  than  one  third  of  the  surface  area.  Incisal  edges  become  transparent  
lingual due  to  loss  of  den?n.  Den?n  appears  smooth,  and  in  some  cases  flat  or  hollowed-­‐out.  
Gingival  and  proximal  margins  have  a  white,  etched  appearance.



!
!
Class  IIIc Incisal/   Incisal  edges  or  occlusal  surfaces  are  involved  into  den?n,  flaLening  or  cupping.  
occlusal Restora?ons  are  seen  raised  above  the  surrounding  tooth  surface.  Incisal  edges  appear  
translucent  due  to  undermined  enamel.

Class  IIId All Severely  affected  teeth,  where  both  labial  and  lingual  surface  are  extensively  involved.

!
Smith and Knight Tooth Wear Index (88):

0 B/L/O/I No  loss  of  enamel  surface  characteris?cs

C No  loss  of  contour

1 B/L/O/I Loss  of  enamel  surface  characteris?cs

C Minimal  loss  of  contour

2 B/L/O Loss  of  enamel  exposing  den?n  for  less  than  one  third  of  the  surface

I Loss  of  enamel  just  exposing  den?n

C Defects  less  than  1  mm  deep

3 B/L/O Loss  of  enamel  exposing  den?n  for  more  than  one  third  of  the  surface

I   Loss  of  enamel  and  substan?al  loss  of  den?n

C Defect  1-­‐2  mm  deep

4 B/L/O Complete  loss  of  enamel,  or  exposure  of  secondary  den?n,  or  pulp  exposure

I Exposure  of  secondary  den?n  or  pulp  exposure  

C Defects  more  than  2  mm  deep,  or  exposure  of  secondary  den?n,  or  pulp  exposure

!
Lussi’s Dental Erosion Index (90):

Facial

Grade  0 No  erosive  enamel  ?ssue  loss.  Surface  with  a  smooth,  silky-­‐glazed  appearance  absence  of  
developmental  ridge  possible

Grade  1 Loss  of  surface  enamel.  Intact  enamel  found  cervical  to  the  lesion  concavity  in  enamel,  the  
width  of  which  clearly  exceeding  its  depth,  thus  dis?nguishing  it  from  tooth  brush  
abrasion,  undula?ng  borders  of  the  lesions  are  possible,  den?n  is  not  involved



!
!
Grade  2 Involvement  of  den?n  for  less  than  50%  of  the  tooth  surface

Grade  3 Involvement  of  den?n  for  more  than  50%  of  the  tooth  surface

Occlusal/  
Lingual  
!
Grade  0 No  erosive  enamel  ?ssue  loss.  Surface  with  a  smooth,  silky-­‐glazed  appearance  absence  of  
developmental  ridge  possible

Grade  1 Loss  of  surface  enamel.  Slight  erosion,  rounded  cusps,  edges  of  restora?on  rising  above  
the  level  of  adjacent  tooth  surface,  grooves  on  occlusal  aspects.  Den?n  is  not  involved

Grade  2 Severe  erosion,  more  pronounced  signs  than  Grade  1.  Den?n  is  involved

These classification and index systems are obviously subjective and their accuracies in clinical
practices are affected by many factors such as examiner bias, lighting conditions patient’s oral
hygiene condition and the presence of staining and discoloration. A recent study demonstrated
that the accuracy of visual assessment of dentin exposure was poor, with only 65% of areas
with exposed dentin being diagnosed correctly (91). Dentin exposure was found in even the
minor cupping and grooving lesions that were considered limited to enamel upon clinical
evaluation. These findings may invalidate current classification systems using dentin
involvement as the criteria differentiating initial and advanced erosive lesions.

Prevention and management

If not intervened effectively at an early stage, the eventual outcome of dental erosion is severe
loss of dental hard tissues that adversely affects function and esthetics (Figure 7). In patients
with extensive dentin exposure, transient as well as persistent pain due to dentin sensitivity and
pulp pathology may further aggravate quality of life deterioration. Severe erosive tooth wear
shown in Figure 7 require restorative therapies. Composite resins and ceramics can be used for
partial and full coverage restorations and restore the esthetics and function of the teeth.
However, if the restored teeth continue to be subjected to severe erosive challenges that
caused the original teeth wear, the restorations may fail in due course following marginal
deterioration and continued loss of surrounding dental hard tissues. Therefore, preventive
measures for dental erosion are not only essential for early intervention and primary prevention
of erosive tooth wear, it is also important for secondary prevention of erosion around the
restorations.

To better understand the effectiveness of common preventive measures for dental erosion, it is
helpful to review the chemical process associated with erosion. Dental hard tissues are largely
composed of mineral crystals of hydroxyapatite with the formula Ca10(PO4) 6(OH)2. Dental
hydroxyapatite is often described as “calcium deficient” and “carbonated” for some calcium ions
may be substituted by sodium, magnesium and potassium and some phosphates (PO4) by
carbonates (CO3), which renders the minerals more susceptible to acid dissolution (92). On the
other hand, some hydroxyl groups (OH-) can be replaced by fluoride ions (F-) to form fluoro-



!
!
hydroxyapatite, Ca10(PO4) 6(F,OH)2, which has increased crystalline stability and decreased
susceptibility to acid dissolution during acidic challenges as compared to hydroxyapatite (10).

Acid dissolution of dental hard tissues can be expressed in the following equation:

Ca10(PO4)6(OH)2 + 20 H+ = 10 Ca+2 + 6H3PO4 +2H2O

From our knowledge we know that hydroxyapatite is less likely to dissolve under the following
conditions:

• If there is no direct contact with acid (no supply of H+)

• If hydroxyapatite is replaced with fluorohydroxyapatite

• If the environment is saturated with calcium and phosphates (oversupply of Ca+2 and
PO4)

Therefore, effective strategies for prevention of dental erosion may be formulated

correspondingly as follows:

• Avoid or reduce direct contact with acids through behavioral and clinical interventions

• Increase acid resistance of dental hard tissues through fluoride therapy

• Increase resistance to hydroxyapatite dissolution through provisions of calcium and

phosphates

In addition, there is adequate evidence to conclude that toothbrushing abrasion can potentially
be a major contributing factor to erosive tooth wear (42, 93, 94). Dental hard tissue loss
associated with erosion can be viewed as a process of initial chemical softening followed by
physical removal of the softened tissue. A fourth strategy therefore includes reducing
mechanical abrasion of teeth through proper toothbrushing instructions.



!
!
Strategy #1: Avoid or reduce direct contact with acids:

Behavioral interventions:
1. Reduce frequency of dietary intakes of acidic beverages and foods: Frequency and duration
of direct contact between teeth and acids are important factors for the development of erosive
lesions (95-97). Prolonged sipping of acidic drinks will increase the risk of erosion, while gulping
will minimize the risk.

2. Adopt drinks habits that limit contact time with teeth: Using a straw will reduce contact time
between teeth and acidic drinks. Rinsing with water or drinking milk immediately following the
drinking of acidic beverages will accelerate clearance of acids and help return oral pH to neutral.

3. Avoid misuse of acidic medications including Vitamin C: Chewing this type of medications or
using them as lozenges increase risks for dental erosion. Acidic medications should be
swallowed if possible.

4. Use proper protection to avoid occupational hazards: Masks, mouth guards, and neutralizing
agents should be used to reduce contact with acidic vapors and fluids.

Clinical interventions:
1. Apply unfilled resins or bonding agents to tooth surfaces susceptible to erosion: Though the
effect of this type of treatment may not be long-lasting due to its susceptibility to abrasive wear,
a temporary protective film will reduce direct contact between teeth surfaces and acids when it
is in place. It may be used as a transitional therapy before other more effective strategies can
be instituted.

2. Treat underlying diseases for intrinsic acids: This includes GERD, bulimia, regurgitation and
rumination. It is often necessary to establish close consultation with patient’s physicians when
an intrinsic cause of erosion is suspected.

3. Treat conditions causing salivary hypofunction: When low saliva flow rate is established as a
factor for erosion in a specific patient, measures should be taken to improve saliva flow. This
may include consultation with patient’s physicians on adjustment of medications causing dry
mouth and referrals for evaluation and treatment of autoimmune diseases such as Sjogren
Syndrome.

Clinical interventions:
It has been shown that fluoride could minimize the erosive effects of soft drinks when applied as
a vanish (98-100), a mouthwash (101), a topical gel (102, 103) or as a dentifrice (104, 105). A
dose-response effect has been observed when using fluoride dentifrices for treatment of enamel
erosion in situ(105). Enamel treated by dentifrices with higher fluoride concentrations was
significantly more resistant to erosive challenges than those with lower fluoride concentrations.
Though frequent application of high concentration fluoride has traditionally been considered the
regime of choice for prevention and treatment of dental erosions (106), some recent studies
questioned the usefulness of high concentrations of fluoride for prevention of dental erosion and


!
!
suggested that patients at risk of enamel erosion should consider preventive measures other
than fluoride therapy (107). However, the findings that high concentrations of fluoride lacked
efficacy in prevention of dental erosion are more likely related to the study design than a true
absence of therapeutic effects. In the study in situ conducted by Rios et al, the authors
evaluated bovine enamel disks subjected to erosive challenge and fluoride treatments ex vivo
for 7 days, and concluded that neither the high (5000ppm) nor the low (1100ppm) concentration
fluoride treatment was effective against erosion (107). This study had a small sample size
(n=10) and was seriously underpowered (40% power). The perils of underpowered clinical
studies are well known, the most serious of which are failing to identify the true effects of the
intervention and arriving at a misleading conclusion (108, 109). The authors did find less enamel
loss with increasing fluoride concentrations, but such a trend was not recognized as statistically
significant due to the lack of statistical power (107). In another study that found no added
benefits of higher fluoride concentrations, the authors identified the brief treatment protocol (3
minutes total) as the probable cause for the negative finding, implying that too short an
application time would not allow the formation of the protective calcium fluoride on the treated
enamel surfaces (110). Some experimental studies showed that the formulation of fluoride may
affect the efficacy of fluoride against erosion. Mouth rinses containing tin and fluoride compound
were shown to be more effective against erosion than those with fluoride alone (101, 111).
Recent studies shown that the addition of various organic polymers(112-114), protein (115), or
the amino acid arginine(116, 117), may improve the anti-erosion efficacy of fluoride-containing
toothpastes. It is believed that these organic compounds may form a protective layer and retain
fluoride on the eroded dental surfaces for a longer time, thus enhancing their protective effects.

Strategy #3: Increase resistance to acid dissolution using calcium and

phosphates:
Addition of calcium and phosphates to acidic beverages could significantly reduce their erosive
potential (118-121). It was shown that addition of 40 mmol/l calcium and 30mmol/l phosphate
could significantly diminish the erosive potential of orange juice (122). Supplementation of soft
drinks with calcium was more effective in reducing erosion than with phosphate and fluoride
(123). Addition of 0.5-1.5mmol/l calcium was found to be effective in reducing the erosive
potential of citric acid. The effect of adding calcium phosphate to toothpastes on erosion
remains unclear, as some experimental studies showed that toothpastes containing casein/
calcium phosphate were useful in protecting enamel against erosive challenges (124, 125) but
others did not find any such protective effect (126).

Strategy #4: Minimize toothbrushing abrasion of eroded enamel:

It has been shown that timing of brushing, toothbrush bristle stiffness and abrasivity of
toothpastes can all affect erosive tooth loss (41, 42, 93). For patients at risk of dental erosion,
toothpastes with low abrasivity should be used with a soft toothbrush. Toothbrushing should be
performed before an erosive challenge, and avoided after consumption of erosive drinks or an
erosive episode such as vomiting. If toothbrushing needs to be done after erosive challenges,
the waiting period should be as long as possible.

Table 3 summarizes above strategies as concise recommendations to patients at risk of dental

erosions.


!
!
The above strategies may prove to be effective in patients who have risk factors for dental
erosion but have not developed significant tooth wear. For patients who have significant tissue
loss associated with erosion, these preventive strategies may slow down the progression of the
lesions but may not halt the disease process as it is impossible to completely eliminate all
potential erosive and abrasive challenges in the oral cavity. Figure 8 shows different stages of
erosive lesions on the occlusal surfaces. If the lesion is not intervened early, it will continue to
develop in size and may eventually result in the loss of anatomic form (Figure 8, A to F).
Therefore, for patients who have already have visible erosive lesions, a minimally invasive
procedure such as composite resin restoration should be considered as early as possible.




!
!
Concluding remarks
Dental erosion is a common condition in children and adults in all regions of the world.
Prolonged contact between extrinsic or intrinsic acids with tooth surfaces will results in softening
and dissolution of surface minerals. If not recognized and treated early, erosive challenges may
cause severe loss of dental hard tissues that adversely affect esthetics and function of the
mouth. Early intervention is key to effective prevention of erosive teeth wear. Effective
prevention of dental erosion includes measures that can avoid or reduce direct contact with
acids, increase acid resistance of dental hard tissues and minimizes toothbrushing abrasion.
For teeth that already have tissue loss due to erosion, a minimally invasive restorative
procedure should be considered as early as possible to prevent further disease progression.




!
!
Table 1: Prevalence of dental erosion in different age groups

study prevalence age group n Country

Mulic  2013   38.0   18   1456   Norway  

Habib  2013   12.0    2  –  12   243   USA  
Wiegand  2006 32.0 2  -­‐  7 463 Germany

Kazoullis  2007 68.0 5.5-­‐14.6 714 Australia

Larsen  2005 14.0 15-­‐17 558 Denmark

Williams  1999 17.0 14 525 UK

Ganss  2001 70.6 8-­‐14 1000 Germany

Harding  2003 47.0 5 202 Ireland

Jaeggi  &  Lussi  2004 100.0 5-­‐9 42 Switzerland

Luo  2005 5.7 3-­‐5 1949 China

Millward  1994 50.0 4 178 UK

Milosevic  1994 30.0 14 1035 UK

Truin  2005 24.0 12 324 Netherland

McGuire 45.9 13-­‐19 USA

Wang  2010 27.3 12-­‐13 1499 China

Van  Rijkom  2002 3.0 10-­‐13 400 Netherland

30.0 15-­‐16 345

Bardsley  2004 53.0 14 2385 UK

Bardolia  2010 20.0 13-­‐14 629 UK

Deery  2000 41.0 11-­‐13 129 UK

37.0 11-­‐13 125 US

Caglar  2005 28.0 11 153 Turkey

Al-­‐Malik  2002 31.0 2-­‐5 987 Saudi  Arabia

Al-­‐Dlaigan  2001 100.0 14 418 UK



!
!
Auad  2007 34.1 13-­‐14 458 Brazil

Arnadohr  2003 21.6 15 278 Iceland

El  Aidi  2008 32.2 12 622 Netherland  

42.8 13.5 622

El  Karim  2007 66.9 12-­‐14 157 Sudan

Dugmore  &  Rock  2003 56.3 12 1753 UK  

64.1 14 1308

Isaksson  2013   75.9   20   499   Sweden  

Xhonga  and  Valdmanis  1983 25.0 14-­‐88 527 USA

Johansson  1996 28.0 21 95 Saudi  Arabia

Lussi  &  Schaffner  2000 8.0 32-­‐36 55 Switzerland

26.0 52-­‐56 55

Hou  2005 45.8 20 179 China

Jaeggi  1999 82.0 19-­‐25 417 Switzerland

Lussi  1991   35.6 26-­‐30 194 Switzerland

42.6 46-­‐50 197



!
!
Table 2: pH values of common beverages (11, 127, 128)

Carbonated drinks pH Juice drinks pH Other drinks pH

Coke 2.7 Orange  juice 3.4 Ice  tea 3.0

Pepsi 2.7 Grapefruit  juice 3.2 Fanta  orange 2.9

7-­‐Up 3.2-­‐3.5 Cranberry  juice 2.3-­‐2.5 Red  Bull 3.4

Sprite 2.6 Apple  juice 3.4 Gatorade 3.3

Mountain  Dew 3.2 Pineapple  juice 3.4 Isostar 2.4-­‐3.8

Dr.  Pepper 2.9 Kiwi  juice 3.6 Coffee 2.4-­‐3.3

Lemon  Nestea 3.0 Grape  juice   3.4 Tea  (black) 4.2

Root  bear 3.0-­‐4.0 Carrot  juice 4.2 Beers 4.0-­‐5.0

Ginger  ale 2.0-­‐4.0 Beetroot  juice 4.2 Wines 2.3-­‐3.8



!
!
Table 3: pH values of common foodstuffs (127, 128)

Fruits pH Other foodstuffs pH

Apple 2.9-­‐3.5 Cranberry  sauce 2.3

Apricots 3.2-­‐3.6 Fruit  Jams/jellies 3.0-­‐4.0

Blueberries 3.2-­‐3.5 Italian  salad  dressing 3.3

Cherries 3.2-­‐4.7 Ketchup 3.7

Grapes 3.3-­‐4.5 Mayonnaise 3.8-­‐4.0

Grapefruits 3.0-­‐3.5 Mustard 3.6

Lemons/limes 1.8-­‐2.4 Pickles 2.5-­‐3.0

Oranges 2.8-­‐4.0 Relish 3.0

Peaches 3.1-­‐4.2 Rhubarb  puree 2.8

Pears 3.4-­‐4.7 Sauerkraut 3.1-­‐3.7

Pineapples 3.3-­‐4.1 Sour  cream 4.4

Plums 2.8-­‐4.6 Tomatoes 3.7-­‐4.7

Raspberries 2.9-­‐3.7 Fermented  vegetables 3.9-­‐5.1

Strawberries 3.0-­‐4.2 Yogurt 3.8-­‐4.2



!
!
Figure Legends:

Figure 1: Soft drink production measured by number of 12-ounce cans sold per person in the
U.S. (National Soft Drink Association; Beverage World)

!
Figure 2: Progression of enamel erosion in situ. After 5 days of consuming orange juice (Minute
Maid® Premium) 4 times a day, enamel surface exposed into the oral cavity shows color
changes and softening. Enamel tissue loss (arrows) begins after 10 days, and becomes more
evident after 15 days of orange juice challenge. (Images taken with a vertical scanning
microscope at a magnification of x200)



!
!

Figure 3: A patient with severe erosive wear of teeth due to prolonged habitual ingestion of
cranberry juice. Patient had been for 6 years drinking large quantities of cranberry juice daily
throughout the day as a means to “distribute sugar intake evenly” in a 24-hour period. Cervical
lesions of the central incisors are typical of those abrasive wear of eroded tooth surfaces.

!
Figure 4: Mandibular premolar and molars with signs of early stage of erosion – smooth and flat
facets on non-occluding surface (black arrow) and small, localized dimpling on occlusal surfaces
(white arrows).




!
!

Figure 5: Mandibular molars with advanced erosive wear – rounding of cusps, deep cupping
lesions with exposed dentin, and loss of typical occlusal surface morphology.

!
Figure 6: Mandibular incisor, canine and premolar with moderate to advanced erosive wear –
grooving, cupping and broad-base cervical lesions are typical signs of erosive wear in incisal,
occlusal and cervical areas of these teeth.




!
!

Figure 7: Severe dental erosive wear affecting esthetics and function. Incisor, canine and
premolars have lost the morphological characteristics for normal functions of cutting and
grinding foods.




!
!

Figure 8: Different stages of occlusal erosive wear ( A to F) illustrate progression of the disease
process without restorative intervention. As the lesion is not a self-healing one, a minimally
invasive procedure such as resin composite restoration should be performed at the earliest
stage possible (A) to prevent rapid progression of the lesion.



!
!
References
1. Jaeggi T, Lussi A. Prevalence, incidence and distribution of erosion. Monographs in Oral Science
2006;20:44-65.

2. Mulic A, Tveit AB, Skaare AB. Prevalence and severity of dental erosive wear among a group of
Norwegian 18-year-olds. Acta Odontologica Scandinavica 2013;71(3-4):475-81.

3. Isaksson H. On dental caries and dental erosion in Swedish young adults. Swedish Dental Journal -
Supplement 2013(232):1-60.

4. Habib M, Hottel TL, Hong L. Prevalence and risk factors of dental erosion in American children.
Journal of Clinical Pediatric Dentistry 2013;38(2):143-8.

5. Dugmore CR, Rock WP. The progression of tooth erosion in a cohort of adolescents of mixed
ethnicity. International Journal of Paediatric Dentistry 2003;13(5):295-303.

6. El Aidi H, Bronkhorst EM, Truin GJ. A longitudinal study of tooth erosion in adolescents. Journal of
Dental Research 2008;87(8):731-5.

7. Lussi A, Schaffner M. Progression of and risk factors for dental erosion and wedge-shaped defects
over a 6-year period. Caries Research 2000;34(2):182-7.

8. Lussi A, Schaffner M, Hotz P, Suter P. Dental erosion in a population of Swiss adults. Community
Dentistry & Oral Epidemiology 1991;19(5):286-90.

9. van Rijkom HM, Truin GJ, Frencken JEFM, Konig KG, van 't Hof MA, Bronkhorst EM, et al.
Prevalence, distribution and background variables of smooth-bordered tooth wear in teenagers in the
hague, the Netherlands. Caries Research 2002;36(2):147-54.

10. Hicks J, Garcia-Godoy F, Flaitz C. Biological factors in dental caries enamel structure and the caries
process in the dynamic process of demineralization and remineralization (part 2). Journal of Clinical
Pediatric Dentistry 2005;29(2):119-24.

11. Jain P, Nihill P, Sobkowski J, Agustin MZ. Commercial soft drinks: pH and in vitro dissolution of
enamel. General Dentistry 2007;55(2):150-4; quiz 55.

12. Johansson AK, Johansson A, Birkhed D, Omar R, Baghdadi S, Khan N, et al. Dental erosion
associated with soft-drink consumption in young Saudi men. Acta Odontologica Scandinavica
1997;55(6):390-7.

13. Zero DT. Etiology of dental erosion--extrinsic factors. European Journal of Oral Sciences 1996;104(2 (
Pt 2)):162-77.

14. Jacobson MF. Liquid Candy: How Soft Drinks are Harming Americans' Health. Washington DC; 2nd
Ed. 2005: CSPI; 2005.

15. American Academy of Pediatrics. Policy statement: soft drinks in schools. Pediatrics
2004;113:152-54.

16. Gleason P, Suitor C. Children’s diets in the mid-90s: dietary intake and its relationship with school
meal participation. . In: Office of Analysis NaE, Food and Nutriction Service, US Department of
Agriculture, editor. Alexandria, VA; 2001.



!
!
17. Putnam JJ, Allshouse JE. Food consumption, prices, and expenditures, 1970–97. . In: Food and
Consumers Economics Division ERS, US Department of Agriculture, editor. Washington DC; 1999.

18. Erickson PR, Alevizos DL, Rindelaub DJ. Soft drinks: hard on teeth. Northwest Dentistry 2001;80(2):
15-9.

19. The North Carolina School Nutrition Action Committee. Soft drinks and school-age children: trends,
effects, solutions.; 2002.

20. Kitchens M, Owens BM. Effect of carbonated beverages, coffee, sports and high energy drinks, and
bottled water on the in vitro erosion characteristics of dental enamel. Journal of Clinical Pediatric
Dentistry 2007;31(3):153-9.

21. Devlin H, Bassiouny MA, Boston D. Hardness of enamel exposed to Coca-Cola and artificial saliva.
Journal of Oral Rehabilitation 2006;33(1):26-30.

22. Moazzez R, Smith BG, Bartlett DW. Oral pH and drinking habit during ingestion of a carbonated drink
in a group of adolescents with dental erosion. Journal of Dentistry 2000;28(6):395-7.

23. Maupome G, Diez-de-Bonilla J, Torres-Villasenor G, Andrade-Delgado LC, Castano VM. In vitro

quantitative assessment of enamel microhardness after exposure to eroding immersion in a cola
drink. Caries Research 1998;32(2):148-53.

24. Ren Y-F, Amin A, Malmstrom H. Effects of tooth whitening and orange juice on surface properties of
dental enamel. Journal of Dentistry 2009;37(6):424-31.

25. Zandim DL, Correa FOB, Rossa Junior C, Sampaio JEC. In vitro evaluation of the effect of natural
orange juices on dentin morphology. Pesquisa Odontologica Brasileira = Brazilian Oral Research
2008;22(2):176-83.

26. Willershausen B, Callaway A, Azrak B, Duschner H. Influence of apple juice on human enamel
surfaces of the first and second dentition - an in vitro study. European Journal of Medical Research
2008;13(7):349-54.

27. West NX, Maxwell A, Hughes JA, Parker DM, Newcombe RG, Addy M. A method to measure clinical
erosion: the effect of orange juice consumption on erosion of enamel. Journal of Dentistry 1998;26(4):
329-35.

28. Lussi A, Jaeggi T, Jaeggi-Scharer S. Prediction of the erosive potential of some beverages. Caries
Research 1995;29(5):349-54.

29. Coombes JS. Sports drinks and dental erosion. American Journal of Dentistry 2005;18(2):101-4.

30. Milosevic A. Sports drinks hazard to teeth. British Journal of Sports Medicine 1997;31(1):28-30.

31. Rees J, Loyn T, McAndrew R. The acidic and erosive potential of five sports drinks. European Journal
of Prosthodontics & Restorative Dentistry 2005;13(4):186-90.

32. Chehal HK, Pate DH, Cohen DM, Bhattacharyya I. Dental erosion due to excessive wine
consumption. General Dentistry 2009;57(5):519-23.

33. Mandel L. Dental erosion due to wine consumption. Journal of the American Dental Association
2005;136(1):71-5.



!
!
34. Rees J, Hughes J, Innes C. An in vitro assessment of the erosive potential of some white wines.
European Journal of Prosthodontics & Restorative Dentistry 2002;10(1):37-42.

35. Waterhouse PJ, Auad SM, Nunn JH, Steen IN, Moynihan PJ. Diet and dental erosion in young people
in south-east Brazil. International Journal of Paediatric Dentistry 2008;18(5):353-60.

36. Smith WAJ, Marchan S, Rafeek RN. The prevalence and severity of non-carious cervical lesions in a
group of patients attending a university hospital in Trinidad. Journal of Oral Rehabilitation 2008;35(2):
128-34.

37. Harding MA, Whelton H, O'Mullane DM, Cronin M. Dental erosion in 5-year-old Irish school children
and associated factors: a pilot study. Community Dental Health 2003;20(3):165-70.

38. Al-Majed I, Maguire A, Murray JJ. Risk factors for dental erosion in 5-6 year old and 12-14 year old
boys in Saudi Arabia. Community Dentistry & Oral Epidemiology 2002;30(1):38-46.

39. Johansson AK, Johansson A, Birkhed D, Omar R, Baghdadi S, Carlsson GE. Dental erosion, soft-
drink intake, and oral health in young Saudi men, and the development of a system for assessing
erosive anterior tooth wear. Acta Odontologica Scandinavica 1996;54(6):369-78.

40. Yu H, Wegehaupt FJ, Wiegand A, Roos M, Attin T, Buchalla W. Erosion and abrasion of tooth-colored
restorative materials and human enamel. Journal of Dentistry 2009;37(12):913-22.

41. Wiegand A, Egert S, Attin T. Toothbrushing before or after an acidic challenge to minimize tooth wear?
An in situ/ex vivo study. American Journal of Dentistry 2008;21(1):13-6.

42. Ganss C, Schlueter N, Friedrich D, Klimek J. Efficacy of waiting periods and topical fluoride treatment
on toothbrush abrasion of eroded enamel in situ. Caries Research 2007;41(2):146-51.

43. Correr GM, Alonso RCB, Consani S, Puppin-Rontani RM, Ferracane JL. In vitro wear of primary and
permanent enamel. Simultaneous erosion and abrasion. American Journal of Dentistry 2007;20(6):
394-9.

44. Vieira A, Overweg E, Ruben JL, Huysmans MCDNJM. Toothbrush abrasion, simulated tongue friction
and attrition of eroded bovine enamel in vitro. Journal of Dentistry 2006;34(5):336-42.

45. Jarvinen VK, Rytomaa II, Heinonen OP. Risk factors in dental erosion. Journal of Dental Research
1991;70(6):942-7.

46. O'Sullivan EA, Curzon ME. Dental erosion associated with the use of 'alcopop'--a case report. British
Dental Journal 1998;184(12):594-6.

47. Linkosalo E, Markkanen H. Dental erosions in relation to lactovegetarian diet. Scandinavian Journal
of Dental Research 1985;93(5):436-41.

48. Giunta JL. Dental erosion resulting from chewable vitamin C tablets. Journal of the American Dental
Association 1983;107(2):253-6.

49. Hays GL, Bullock Q, Lazzari EP, Puente ES. Salivary pH while dissolving vitamin C-containing
tablets. American Journal of Dentistry 1992;5(5):269-71.

50. McCracken M, O'Neal SJ. Dental erosion and aspirin headache powders: a clinical report. Journal of
Prosthodontics 2000;9(2):95-8.



!
!
51. Grace EG, Sarlani E, Kaplan S. Tooth erosion caused by chewing aspirin. Journal of the American
Dental Association 2004;135(7):911-4.

52. Brand HS, Dun SN, Nieuw Amerongen AV. Ecstasy (MDMA) and oral health. British Dental Journal
2008;204(2):77-81.

53. Milosevic A, Agrawal N, Redfearn P, Mair L. The occurrence of toothwear in users of Ecstasy (3,4-
methylenedioxymethamphetamine). Community Dentistry & Oral Epidemiology 1999;27(4):283-7.

54. Dawes C, Boroditsky CL. Rapid and severe tooth erosion from swimming in an improperly chlorinated
pool: case report. Journal of Canadian Dental Association 2008;74(4):359-61.

55. Geurtsen W. Rapid general dental erosion by gas-chlorinated swimming pool water. Review of the
literature and case report. American Journal of Dentistry 2000;13(6):291-3.

56. Amin WM, Al-Omoush SA, Hattab FN. Oral health status of workers exposed to acid fumes in
phosphate and battery industries in Jordan. International Dental Journal 2001;51(3):169-74.

57. Johansson A-K, Johansson A, Stan V, Ohlson C-G. Silicone sealers, acetic acid vapours and dental
erosion: a work-related risk? Swedish Dental Journal 2005;29(2):61-9.

58. Kim H-D, Hong Y-C, Koh D-H, Paik D-I. Occupational exposure to acidic chemicals and occupational
dental erosion. Journal of Public Health Dentistry 2006;66(3):205-8.

59. Chikte UME, Naidoo S, Kolze TJvW, Grobler SR. Patterns of tooth surface loss among winemakers.
SADJ 2005;60(9):370-4.

60. Piekarz C, Ranjitkar S, Hunt D, McIntyre J. An in vitro assessment of the role of Tooth Mousse in
preventing wine erosion. Australian Dental Journal 2008;53(1):22-5.

61. Moayyedi P, Talley NJ. Gastro-oesophageal reflux disease. Lancet 2006;367(9528):2086-100.

62. Napierkowski J, Wong RKH. Extraesophageal manifestations of GERD. American Journal of the
Medical Sciences 2003;326(5):285-99.

63. Ersin NK, Oncag O, Tumgor G, Aydogdu S, Hilmioglu S. Oral and dental manifestations of
gastroesophageal reflux disease in children: a preliminary study. Pediatric Dentistry 2006;28(3):
279-84.

64. Moazzez R, Bartlett D, Anggiansah A. Dental erosion, gastro-oesophageal reflux disease and saliva:
how are they related? Journal of Dentistry 2004;32(6):489-94.

65. Ali DA, Brown RS, Rodriguez LO, Moody EL, Nasr MF. Dental erosion caused by silent
gastroesophageal reflux disease. Journal of the American Dental Association 2002;133(6):734-7; quiz
68-9.

66. Gregory-Head BL, Curtis DA, Kim L, Cello J. Evaluation of dental erosion in patients with
gastroesophageal reflux disease. Journal of Prosthetic Dentistry 2000;83(6):675-80.

67. Pace F, Pallotta S, Tonini M, Vakil N, Bianchi Porro G. Systematic review: gastro-oesophageal reflux
disease and dental lesions. Alimentary Pharmacology & Therapeutics 2008;27(12):1179-86.

68. Moazzez R, Anggiansah A, Bartlett DW. The association of acidic reflux above the upper
oesophageal sphincter with palatal tooth wear. Caries Research 2005;39(6):475-8.


!
!
69. Di Fede O, Di Liberto C, Occhipinti G, Vigneri S, Lo Russo L, Fedele S, et al. Oral manifestations in
patients with gastro-oesophageal reflux disease: a single-center case-control study. Journal of Oral
Pathology & Medicine 2008;37(6):336-40.

70. Silva MA, Damante JH, Stipp AC, Tolentino MM, Carlotto PR, Fleury RN. Gastroesophageal reflux
disease: New oral findings. Oral Surgery Oral Medicine Oral Pathology Oral Radiology & Endodontics
2001;91(3):301-10.

71. Gilmour AG, Beckett HA. The voluntary reflux phenomenon. British Dental Journal 1993;175(10):
368-72.

72. Meshramkar R, Patil SB, Patil NP. A case report of patient practising yoga leading to dental erosion.
International Dental Journal 2007;57(3):184-6.

73. Scheutzel P. Etiology of dental erosion--intrinsic factors. European Journal of Oral Sciences
1996;104(2 ( Pt 2)):178-90.

74. Jones RR, Cleaton-Jones P. Depth and area of dental erosions, and dental caries, in bulimic women.
Journal of Dental Research 1989;68(8):1275-8.

75. Rytomaa I, Jarvinen V, Kanerva R, Heinonen OP. Bulimia and tooth erosion. Acta Odontologica
Scandinavica 1998;56(1):36-40.

76. Piangprach T, Hengtrakool C, Kukiattrakoon B, Kedjarune-Leggat U. The effect of salivary factors on

dental erosion in various age groups and tooth surfaces. Journal of the American Dental Association
2009;140(9):1137-43.

77. Brand HS, Tjoe Fat GM, Veerman ECI. The effects of saliva on the erosive potential of three different
wines. Australian Dental Journal 2009;54(3):228-32.

78. Buzalaf MA, Hannas AR, Kato MT. Saliva and dental erosion. Journal of Applied Oral Science
2012;20(5):493-502.

79. Bevenius J, L'Estrange P. Chairside evaluation of salivary parameters in patients with tooth surface
loss: a pilot study. Australian Dental Journal 1990;35(3):219-21.

80. Sanchez GA, Fernandez De Preliasco MV. Salivary pH changes during soft drinks consumption in
children. International Journal of Paediatric Dentistry 2003;13(4):251-7.

81. O'Sullivan EA, Curzon ME. Salivary factors affecting dental erosion in children. Caries Research
2000;34(1):82-7.

82. Zwier N, Huysmans MC, Jager DH, Ruben J, Bronkhorst EM, Truin GJ. Saliva parameters and
erosive wear in adolescents. Caries Research 2013;47(6):548-52.

83. Hellwig E, Lussi A, Goetz F. Influence of human saliva on the development of artificial erosions.
Caries Research 2013;47(6):553-8.

84. Lussi A, Hellwig E. Risk assessment and preventive measures. Monographs in Oral Science
2006;20:190-9.

85. Navazesh M, Christensen C, Brightman V. Clinical Criteria for the Diagnosis of Salivary Gland
Hypofunction. Journal of Dental Research 1992;71(7):1363-69.



!
!
86. Ganss C, Klimek J, Borkowski N. Characteristics of tooth wear in relation to different nutritional
patterns including contemporary and medieval subjects. European Journal of Oral Sciences
2002;110(1):54-60.

87. Ganss C. How valid are current diagnostic criteria for dental erosion? Clinical Oral Investigations
2008;12 Suppl 1:S41-9.

88. Smith BG, Knight JK. An index for measuring the wear of teeth. British Dental Journal 1984;156(12):
435-8.

89. Eccles JD. Dental erosion of nonindustrial origin. A clinical survey and classification. Journal of
Prosthetic Dentistry 1979;42(6):649-53.

90. Lussi A. Dental erosion clinical diagnosis and case history taking. European Journal of Oral Sciences
1996;104(2 ( Pt 2)):191-8.

91. Ganss C, Klimek J, Lussi A. Accuracy and Consistency of the Visual Diagnosis of Exposed Dentine
on Worn Occlusal/Incisal Surfaces. Caries Research 2006;40(3):208-12.

92. Featherstone JDB, Lussi A. Understanding the chemistry of dental erosion. Monographs in Oral
Science 2006;20:66-76.

93. Wiegand A, Schwerzmann M, Sener B, Magalhaes AC, Roos M, Ziebolz D, et al. Impact of toothpaste
slurry abrasivity and toothbrush filament stiffness on abrasion of eroded enamel - an in vitro study.
Acta Odontologica Scandinavica 2008;66(4):231-5.

94. Jaeggi T, Lussi A. Toothbrush abrasion of erosively altered enamel after intraoral exposure to saliva:
an in situ study. Caries Research 1999;33(6):455-61.

95. Al-Dlaigan YH, Shaw L, Smith A. Dental erosion in a group of British 14-year-old school children. Part
II: Influence of dietary intake. British Dental Journal 2001;190(5):258-61.

96. Eisenburger M, Addy M. Erosion and attrition of human enamel in vitro part II: influence of time and
loading. Journal of Dentistry 2002;30(7-8):349-52.

97. West NX, Hughes JA, Addy M. Erosion of dentine and enamel in vitro by dietary acids: the effect of
temperature, acid character, concentration and exposure time. Journal of Oral Rehabilitation
2000;27(10):875-80.

98. Murakami C, Bonecker M, Correa MSNP, Mendes FM, Rodrigues CRMD. Effect of fluoride varnish
and gel on dental erosion in primary and permanent teeth. Archives of Oral Biology 2009;54(11):
997-1001.

99. Sorvari R, Meurman JH, Alakuijala P, Frank RM. Effect of fluoride varnish and solution on enamel
erosion in vitro. Caries Research 1994;28(4):227-32.

100.Vieira A, Ruben JL, Huysmans MCDNJM. Effect of titanium tetrafluoride, amine fluoride and fluoride
varnish on enamel erosion in vitro. Caries Research 2005;39(5):371-9.

101.Schlueter N, Klimek J, Ganss C. In vitro efficacy of experimental tin- and fluoride-containing mouth
rinses as anti-erosive agents in enamel. Journal of Dentistry 2009;37(12):944-8.



!
!
102.Lagerweij MD, Buchalla W, Kohnke S, Becker K, Lennon AM, Attin T. Prevention of erosion and
abrasion by a high fluoride concentration gel applied at high frequencies. Caries Research
2006;40(2):148-53.

103.Jones L, Lekkas D, Hunt D, McIntyre J, Rafir W. Studies on dental erosion: An in vivo-in vitro model
of endogenous dental erosion--its application to testing protection by fluoride gel application.
Australian Dental Journal 2002;47(4):304-8.

104.Barlow AP, Sufi F, Mason SC. Evaluation of different fluoridated dentifrice formulations using an in
situ erosion remineralization model. Journal of Clinical Dentistry 2009;20(6):192-8.

105.Zero DT, Hara AT, Kelly SA, Gonzalez-Cabezas C, Eckert GJ, Barlow AP, et al. Evaluation of a
desensitizing test dentifrice using an in situ erosion remineralization model. Journal of Clinical
Dentistry 2006;17(4):112-6.

106.Wiegand A, Attin T. Influence of fluoride on the prevention of erosive lesions--a review. Oral Health &
Preventive Dentistry 2003;1(4):245-53.

107.Rios D, Magalhaes AC, Polo ROB, Wiegand A, Attin T, Buzalaf MAR. The efficacy of a highly
concentrated fluoride dentifrice on bovine enamel subjected to erosion and abrasion. Journal of the
American Dental Association 2008;139(12):1652-6.

108.Halpern SD, Karlawish JHT, Berlin JA. The Continuing Unethical Conduct of Underpowered Clinical
Trials. JAMA 2002;288(3):358-62.

109.Whitley E, Ball J. Statistics review 4: Sample size calculations. Critical Care 2002;6(4):335 - 41.

110.Wiegand A, Bichsel D, Magalhaes AC, Becker K, Attin T. Effect of sodium, amine and stannous
fluoride at the same concentration and different pH on in vitro erosion. Journal of Dentistry
2009;37(8):591-5.

111.Ganss C, Neutard L, von Hinckeldey J, Klimek J, Schlueter N. Efficacy of a Tin/Fluoride Rinse.

Journal of Dental Research 2010;89(11):1214-18.

112.Wang W, Xie Q, Xu T, Wang Q, Malmstrom HS, Ren YF. Fluoride release and anti-erosive effects of
dentifrices containing PVM/MA copolymers. Journal of Dentistry 2013;41(2):148-54.

113.Wang Q, Kang Y, Barnes V, DeVizio W, Kashi A, Ren YF. Dentin tubule occlusion and erosion
protection effects of dentifrice containing bioadhesive PVM/MA copolymers. Clinical Oral
Investigations 2013;17(3):775-83.

114.Ganss C, von Hinckeldey J, Tolle A, Schulze K, Klimek J, Schlueter N. Efficacy of the stannous ion
and a biopolymer in toothpastes on enamel erosion/abrasion. Journal of Dentistry 2012;40(12):
1036-43.

115.Jager DH, Vissink A, Timmer CJ, Bronkhorst E, Vieira AM, Huysmans MC. Reduction of erosion by
protein-containing toothpastes. Caries Research 2013;47(2):135-40.

116.Sullivan R, Rege A, Corby P, Klaczany G, Allen K, Hershkowitz D, et al. Evaluation of a dentifrice

containing 8% arginine, calcium carbonate, and sodium monofluorophosphate to prevent enamel loss
after erosive challenges using an intra-oral erosion model. Journal of Clinical Dentistry 2014;25(1
Spec No A):A7-13.



!
!
117.Yamashita JM, Torres NM, Moura-Grec PG, Marsicano JA, Sales-Peres A, Sales-Peres SH. Role of
arginine and fluoride in the prevention of eroded enamel: an in vitro model. Australian Dental Journal
2013;58(4):478-82.

118.Larsen MJ. Degrees of saturation with respect to apatites in fruit juices and acidic drinks.
Scandinavian Journal of Dental Research 1975;83(1):13-7.

119.Grenby TH. Lessening dental erosive potential by product modification. European Journal of Oral
Sciences 1996;104(2 ( Pt 2)):221-8.

120.Ramalingam L, Messer LB, Reynolds EC. Adding casein phosphopeptide-amorphous calcium

phosphate to sports drinks to eliminate in vitro erosion. Pediatric Dentistry 2005;27(1):61-7.

121.Magalhaes AC, Moraes SM, Rios D, Buzalaf MAR. Effect of ion supplementation of a commercial soft
drink on tooth enamel erosion. Food Additives & Contaminants 2009;Part A, Chemistry, Analysis,
Control, Exposure & Risk Assessment. 26(2):152-6.

122.Larsen MJ, Jensen AF, Madsen DM, Pearce EIF. Individual variations of pH, buffer capacity, and
concentrations of calcium and phosphate in unstimulated whole saliva. Archives of Oral Biology
1999;44(2):111-17.

123.Attin T, Meyer K, Hellwig E, Buchalla W, Lennon AM. Effect of mineral supplements to citric acid on
enamel erosion. Archives of Oral Biology 2003;48(11):753-9.

124.Ranjitkar S, Kaidonis JA, Richards LC, Townsend GC. The effect of CPP-ACP on enamel wear under
severe erosive conditions. Archives of Oral Biology 2009;54(6):527-32.

125.Panich M, Poolthong S. The effect of casein phosphopeptide-amorphous calcium phosphate and a

cola soft drink on in vitro enamel hardness. Journal of the American Dental Association 2009;140(4):
455-60.

126.Lennon AM, Pfeffer M, Buchalla W, Becker K, Lennon S, Attin T. Effect of a casein/calcium

phosphate-containing tooth cream and fluoride on enamel erosion in vitro. Caries Research
2006;40(2):154-7.

127.Clark DC, Woo G, Silver JG, Sweet D, Grisdale JC. The influence of frequent ingestion of acids in the
diet on treatment for dentin sensitivity. Journal of Canadian Dental Association 1990;56(12):1101-3.

128.Lussi A, Jaeggi T. Chemical factors. Monographs in Oral Science 2006;20:77-87.



!