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Review Article
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Noncarious cervical lesions – A clinical concept based

on the literature review. Part 1: Prevention
RALUCA PECIE, DR, IVO KREJCI, PROF DR MED DENT, FRANKLIN GARCIA-GODOY, DDS, MS & TISSIANA BORTOLOTTO, DR, PHD

ABSTRACT: Purpose: Due to an increased prevalence of non-carious cervical lesions (NCCL), a clinical strategy for
this lesion type should be considered. Previous reviews focused mainly on etiology and prevalence. In Part 1 of this
paper, an evidence-based support for a preventive strategy of NCCL was elaborated. Methods: Literature over the last
10 years available in the MEDLINE database was reviewed in order to find clinical evidence for a preventive approach
to NCCL. Recommendations were based primarily on systematic reviews, clinical evaluations and a monograph.
Results: The etiology of NCCL is currently considered to be rather multifactorial, as clinical investigations found
multiple factors associated with this type of lesions and due to the lack of evidence to support exclusively one or
another factor. Based on the hypothesis of multifactorial origin, a preventive protocol has been established. No clinical
research exists with respect to the prevention of NCCL and long-term clinical evaluations of the proposed preventive
measures are needed. (Am J Dent 2011;24:49-56).

CLINICAL SIGNIFICANCE: The slow progression, the high capacity of self-defense by producing sclerotic dentin, and
the lack of evidence for tooth weakening in the absence of a restoration are evidence-based findings supporting a “wait
and see” philosophy. Restoration could be postponed in the absence of esthetic demands, sensitivity or threat to the
integrity of the tooth. Restoration should not always be the first treatment of choice, although there still remains to be
established to what extent prevention could replace restoration.

: Dr. Raluca Pecie, Division of Cariology and Endodontology, University of Geneva, Rue Barthélemy-Menn 19, CH-
1205 Geneva, Switzerland. E- : [email protected]

Introduction Answers to the following questions were searched: Are

there factors associated with NCCL and could these lesions be
There is an open debate as to which degree tooth wear be- prevented by an early detection of these factors? Are there any
comes a pathological condition, and when treatment should be available preventive measures capable of preventing progres-
initiated, knowing that tooth substance loss is to some degree a sion of NCCL? An update on etiology and prevalence of NCCL
physiological process, being a compensatory mechanism built was also included.
into our biological system.1 But, in today’s context of increased
life expectancy and of an increasing number of people retaining DEFINITION AND CLINICAL APPEARANCE
their teeth longer, the consequences of ignoring early signs of NCCL are defined as a loss of hard dental tissue close to the
such lesions may be severe. Considering that the objective of cemento-enamel-junction (CEJ) with the distinctive characte-
any preventive or restorative procedure is to maintain tooth ristic of hard-mineralized tissue presence, in contrast to
function throughout life and to prevent premature destruction, a caries.2,3 Commonly, their shape is like a wedge with the apex
change of approach concerning noncarious tooth substance loss pointing inwards, but they can appear in various shapes.3 His-
is needed. Knowing the relatively limited durability of restora- torically, NCCL were classified according to their appearance:
tive procedures, the approach should not only include a restora- wedge-shaped, disc-shaped, flattened, irregular, and figured
tive treatment of the already advanced lesion, but also areas. Generally, NCCL vary from shallow grooves to large
preventive therapy as well. Previous reviews of non-carious wedge-shaped defects with sharp line angles.2 A link between
cervical lesions (NCCL) focused mainly on restorative options the morphological characteristics of the lesions and the main
and etiology,2-12 but no clear guidelines for a preventive etiological factor has been suspected.10,11,13,14,18 Thus, a U-
approach could be found. Therefore, in Part 1 of this paper an shaped or disk-shaped broad and shallow lesion, with poorly
evidence-based support for a preventive strategy of NCCL was defined margins and adjacent smooth enamel points out an
searched and a preventive concept was established. extrinsic erosive cause such as ingestion of acidic foods, beve-
rages, and medication.11,15 It is important to notice that shallow
Materials and Methods
defects on smooth surfaces coronal to the CEJ are considered to
The pertinent literature over the last 10 years available in be the best predictive criteria for the diagnosis of erosion, and a
MEDLINE database was reviewed. A search for the following pathognomonic sign of erosive tooth wear.16,17 Lesions caused
keywords was performed: abfraction, cervical non-carious by abrasive forces, such as improper toothbrushing techniques,
lesions, cervical erosion, etiology cervical lesions, cervical ab- generally exhibit sharp defined margins and a hard surface with
rasion, cervical tooth wear and prevalence of non-carious le- traces of scratching. Lesions caused by abfraction mechanism
sions. Recommendations were based primarily on systematic due to abnormal occlusal loading would typically be wedge-
reviews, clinical evaluations and a monograph, in order to shaped or saucer-shaped lesions, with sharp internal angles and
detect the prevalence, tooth groups affected, associated risk an apical extent relative to the CEJ.11 However, the shape
factors and etiology of NCCL. In vitro evaluations of products cannot be considered predictive for the etiology.12
were considered when clinical trials could not be found. Clinical studies and observations2,10,28,19 have shown that
 American Journal of Dentistry, Vol. 24, No. 1, February, 2011
50 Pecie et al

Table 1. Etiological mechanisms of NCCL.

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Erosive mechanism (Corrosion) Chemical wear as a result of extrinsic or intrinsic acids or chelators acting on plaque free tooth surfaces. Factors: acidic
beverages and foods, acidic medication, gastro esophageal disease with reflux, factors predisposing to gastric reflux (hiatus
hernia, sport activities) anorexia, bulimia nervosa, professional exposure to acids (wine tasters).1,2,10,50,63
Abrasion mechanism Physical wear as a result of a mechanical process involving foreign objects. Factors: abrasive toothpaste, improper tooth
(Exogenous friction) brushing with a horizontal technique and excessive force, particular dietary habits.1,2,10,23,50
Abfraction mechanism (Stress) Physical wear as a result of tensile or shear stress in the cement enamel junction area provoking microfractures in enamel
and dentin (fatigue wear). Factors: parafunctions, bruxism, excessive functional load, off axis load.9,10,31,34,42
Piezoelectric effect Acquisition of a surface electrical charge under load causing demineralization.10,52
Stress corrosion Tooth substance loss due to acid in combination with stress. Acid in areas of stress concentration results in either static stress
corrosion or cyclic (fatigue) stress corrosion.8,10,32,52
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NCCL are almost exclusively situated on the facial surfaces of chanical forces. Abfraction represents the mechanical flexure
teeth, seldom on lingual surfaces and rarely on proximal sur- theory, according to which tooth bending phenomena due to
faces. parallel or oblique occlusal force components, occurring during
The development of NCCL tends to be a slow process that parafunctions as well as during normal function, create flexural
occurs over an extended period of time, among the conse- stress in the cervical area with chipping away of the hard tis-
quences being sclerosis and lack of sensitivity.20 Secondary sues.3,11,31,32 Tensile stress resulting from oblique occlusal
dentin, occlusion of open dentin tubules, pulpal retreat and forces was found to be the principal factor responsible for the
other natural tooth protective measures have slowly adapted to disruption of the bonds between the hydroxyapatite crystals and
the noxious stimuli, thereby minimizing symptoms and main- the separation of the enamel from the dentin, even if repeated
taining pulpal integrity.20 compressive forces acting together with tensile stresses are also
THE PREVALENCE AND AFFECTED TEETH considered to cause microfracture, fatigue, flexure, and defor-
mation of the tooth structure.5,6,9,10,33-35 This hypothesis was
The prevalence of cervical wear has been reported to vary supported and reinforced also later by engineering studies.36-42
between 5-85%.10 Only a few studies described the prevalence Despite the hypothesis of abfraction having a fundamental role
of cervical wear alone and as investigation methods and popu- in the initiation of the process,8,10 clinical studies13,43 suggested
lation clusters vary, it is very difficult to compare the results that occlusal loading may not always be the primary factor in
obtained from different authors. Recent studies found a preva- the formation of noncarious cervical lesions. A review of more
lence ranging from 11.4% to 62.2%.13,19,21-25 recent literature reveals an important number of clinical inves-
Controversy exists regarding the distribution of NCCL tigations showing a strong correlation between bruxism, para-
within dentition. A recent study reported mandibular premolars functions and NCCL.20,23,24,29,44-48 Furthermore, although engi-
to have the highest odds ratio for developing wedge shaped neering studies were also questioned regarding their accurate
defects, followed by maxillary premolars. On the other hand, reproduction of tooth environment,4,49 more recent tests, like
compared to maxillary canines, mandibular canines proved to dynamic finite element analysis38,40 also provided evidence in
have a much lower odds ratio of incurring abfractions.26 favor of the abfraction theory. In summary, the literature sup-
Another epidemiological evaluation reinforced these findings, ports a constant implication of occlusal stress, although rather
reporting that the most commonly affected teeth were mandi- in association with other factors like erosion/abrasion, than
bular premolars, having also the highest percentage of high alone. Therefore, the etiology of these lesions is still controver-
severity lesions, and among them, first premolars were most sial, with older studies pointing out either one or the other me-
frequently affected (34.2%), followed by second premolars.22 chanism, while more recent studies recognize the multifactorial
Telles et al19 also found a higher prevalence of the lesions etiology. Therefore, there is an absence of conclusive evidence
among mandibular teeth. Other studies20,25 however reported to support exclusively one etiology.2-7,10,12,15 An important
maxillary teeth to be more frequently affected. finding regarding the etiological mechanism of tooth wear in
One more common finding is the fact that prevalence and general is the enhanced effect of causal factors as a
severity of NCCL appears to increase with age, a hypotheses consequence of their interaction. Thus, abrasion resulting from
supported by the majority of studies evaluating a large number toothbrushing or dietary habits is greater if there is a previous
of subjects.19,20,24-29 and recent exposure of the teeth to acidic challenge such as
ETIOLOGY dietary or gastric acid.2,32,50,51 The theory of stress corrosion
A number of theories regarding the etiological mechanism considers also a combined action of occlusal stress and acid
have developed over time. In the 19th century, the etiology of environment to be more harmful than either factor acting alone,
tooth wear in the absence of caries, including NCCL, was un- in the development of cervical tooth loss.8,9,32
explainable, and the lesions were not categorized.11 In 1907, Controversy exists also regarding the terminology for the
Miller30 proposed three specific categories of tooth wear – mechanisms involved in the etiology of tooth surface loss.
erosion, abrasion, attrition – suggesting also their possible etiol- While the majority of the literature refers to tooth wear etiology
ogy, which represents the current scientific classification for as erosion/abrasion/attrition or abfraction, the correct definition
tooth wear. NCCL were first classified according to their sup- of the physical and chemical processes occurring on tooth surface
posed origin: erosion or abrasion. is a source of confusion. In 2004, Grippo et al32 suggested a
Grippo31 introduced later the term “abfraction”, to refer to modification of terminology by replacing the term “erosion” with
the pathological loss of dental hard tissue caused by biome- “corrosion” and by defining abrasion and attrition as “friction”.
American Journal of Dentistry, Vol. 24, No. 1, February, 2011
Noncarious cervical lesions: Part 1 51

Table 2. Risk factors of NCCL.

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Age Prevalence and severity of lesions increases with age.20,22,24-26,28,29,61 Progression rate of erosion is reported also to be greater
in older people.51,68
Factors that increase lateral Wear facets, inlay restorations and occlusal cavities, altered tooth position;10,13,19,20,26,44,57,60 group function in lateral
and compressive forces movements and Class I Angle occlusion20,44 or increased occlusal contact area;25 faceting, clicking joints, occlusal
splints;24 parafunctional habits, bruxism.20,23,24,29,44,45,47,48
Abrasive factors Incorrect toothbrushing habits (force and horizontal brushing technique), incorrect hygiene habits (toothbrushing
immediately after ingestion of acidic foods/beverages),15,23,25,60,61 prominent position of the tooth in the arch that leaves it
prone to excessive forces from toothbrushing, adjacent teeth with similar lesions.15
Erosive factors Dietary habits like in patients with vegetarian diets and those who reported consuming citrus fruits, soft drinks, alcohol,
yogurt and vitamin C drinks18,23,24,28 (exogen erosion) or acidic medication;23 erosive tooth substance loss on occlusal or
palatal surfaces (smooth silky glazed appearance of the E, grooving on occlusal surfaces) are indicators for existing acidic
challenge.1 Loss of salivary protection caused by work- and sports-related dehydration, drugs and medications and certain
medical conditions.105 Bulimic or alcoholic patients, gastro-esophageal disease (intrinsic erosion).32,68,105
Individual variations Oral and dental anatomy, gingival recession, number of teeth and their mobility,29 periodontal status or phenotype;7 saliva
properties (amount, flow capacity, buffering capacity),23,51,81 crevicular fluid.32
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Nevertheless, recent reviews employ the traditional terms. sive18,23,58 factors as well as biological individual variations,7,47,59
As a conclusion, the development of NCCL is supposed to which predispose to the development of such lesions (Table 2). It
be the consequence of a synergistic action of five etiological is important to notice that the majority of these studies could not
mechanisms (Table 1). In addition to the most known three totally exclude one factor or another, pointing into the direction
theories, two other original causes have been described but of a multifactorial etiology of NCCL.15,18,24,45,47,60
somehow less investigated: the “stress corrosion theory” and A frequent implication of occlusal factors has been
the “piezoelectric effect theory”.10,32,52 reported,20,44,57 even though their positive correlation with
THE PREVENTIVE APPROACH NCCL or the predictable value of occlusion could not always
be established.15,28,43 A finite element analysis study39 identified
Several anthropologic studies have been undertaken to loading direction as a major factor contributing to restoration
clarify the physiological extent of tooth wear in general. It is failure, and showed that oblique-oriented forces induce tensile
interesting to notice that the anthropologic point of view stresses on the cervical margin, exceeding the strength of the
supports the pathologic nature of NCCL in particular, which material and the adhesive forces. Several clinical trials found
have not been observed within ancient populations and generators for oblique loading such as altered tooth position26
therefore should be viewed as “modern-day” pathology.55 and group function,20,24,29,44 as well as parafunctional habits
Therefore, no level of the lesion should be considered indicated by wear facets13,19,20,23,24,44,48,60 and bruxism,19,20,29,45 to
acceptable and ignored, and preventive or restorative measures be associated with NCCL. Nevertheless, it should be kept in
should always be implemented,56 although with different mind that available tests revealed only an association of occlusal
protocols with respect to age, severity of the lesion, risk factors loading factors and noncarious cervical lesions, which may not
and etiological factors implicated. necessarily support a causal relationship. Other types of clinical
The need of changing the approach regarding NCCL is investigations, such as observational long-term studies, would be
especially important for incipient lesions, because the early necessary to confirm the occlusal etiology theory.
detection of NCCL is the best indication for preventive therapy
as an alternative to the restorative approach. Three aspects of Prevalence, severity and progression rate of NCCL were
preventive therapy should be considered: found to increase with age.20,22,24-26,28,29 This could be explained
by the extended exposure to etiological factors, the increased
1. Risk assessment of patients and prevention of develop- occurrence of gingival recession and bone loss with more root
ment of NCCL lesions by correcting habits and surface and cementum exposure raising the risk of cervical
eliminating possible causes; lesions, the diminished quantity and quality of saliva and the
2. Early detection and management of incipient lesions; compositional and microstructural changes of enamel and
3. Management of patients already presenting advanced dentin.20
NCCL lesions.
The objectives of the preventive treatment are to prevent the THE PREVENTIVE PROTOCOL
progression of incipient lesions or the development of new ones Previous research in NCCL focused mainly on etiology and
and to assure the longevity of restorations in restored lesions, as restoration options, with no clear guidelines to a preventive
early failures of these restorations have often been reported in approach. This article proposes a preventive concept based on
the literature probably due to the same factors which originally the hypothesis of a multifactorial etiology of such lesions.
caused the lesions.3,20,39 Given the confusing multitude of restorative options and the
Although there is no consensus regarding the etiology, uncertain durability of their results, a global treatment strategy
clinical evaluations of large number of subjects have revealed for NCCL is needed, taking into consideration also the etiology
some factors more frequently associated with the occurrence of and long-term management of such lesions.
NCCL. They could serve for the risk assessment of the patient, The available knowledge on NCCL today allows for the
by suggesting a higher probability of developing such lesions. elaboration of a non-restorative, more conservative manage-
Studies have reported the preponderant presence of para- ment, as an alternative to the restorative approach. The slower
functional habits and bruxism,20,24,29,44-47,57 or abrasive and ero- progression rate in young people,61 the high capacity of self-
 American Journal of Dentistry, Vol. 24, No. 1, February, 2011
52 Pecie et al

defense by producing sclerotic dentin, and the lack of evidence 6. Elimination of possible causal factors by providing
for tooth weakening in the absence of a restoration62 could instructions for correct oral hygiene techniques, dietary
possibly support a “wait and see” philosophy. As suggested for counseling, treating of general disorders such as gastric
the management of erosion, restoration could be postponed in reflux, bulimia, anorexia and correcting parafunctions and
the absence of esthetic demands, sensitivity or threat to the occlusal habits. The fabrication of an occlusal guard is a
integrity of the tooth.63 Restoration should not always be the reasonable protective measure in case of high occlusal
first treatment choice; although there still remains to be stress, but there is still a controversy about the need for
established up to which extent prevention could replace occlusal equilibration on teeth with NCCL.12 Occlusal
restoration. adjustment is suggested by the frequent association of
Early diagnosis may stop the progression of such lesions, if NCCL with functional stresses, especially with oblique
etiological factors are controlled, a close recall and monitoring forces leading to tensile stress at the cervical region.10
is undertaken, and patients comply with the recommendations. Nevertheless, very few clinical investigations64 exist to
The risk assessment evaluates the risk of a patient to confirm the positive effect of occlusal therapy, and a recent
develop NCCL over time and it is a part of the general review12 reported the ineffectiveness of this measure in
examination. Practitioners should be aware of the possible prolonging the longevity of cervical restorations. The
causes of such lesions and associated risk factors (Table 2) and uncertainty of occlusion as an etiological mechanism of
search for signs of their presence in every patient to treat. This NCCL or a predictability factor28 constitutes also a
approach is especially important in young patients presenting contraindication for performing “preventive” invasive
premature signs of tooth wear not in accordance with their age occlusal therapy.43 This is substantiated by study results45
and where etiological factors are present which could lead over showing that the presence of occlusal pathology does not
time to the development of NCCL. always lead to the development of NCCL, even if a positive
association may exist. It might be concluded that the
EARLY DETECTION AND TREATMENT OF INCIPIENT NCCL
presence of NCCL alone should not constitute a
In some cases where lesions are small and just start to recommendation for indiscriminate occlusal adjustment and
develop, restoration is not the most appropriate strategy, due to further clinical investigations are needed to confirm this
the uncertain clinical longevity. In an in vivo study,20 the hypothesis. Dietary counseling should address the uptake
correlation between age and depth of lesions led to the frequency of acidic containing foods and beverages, the
conclusion that NCCL progression is a slow process. An in ingestion habits, as well as the type of foods with a
vitro study62 concluded that the presence of NCCL on extracted buffering capacity. Thus, the use of a straw for acidic
teeth does not negatively affect their fracture resistance, and beverages as well as drinking milk or eating a piece of
that restoration does not result in an increase of fracture cheese shortly afterwards should be encouraged in young
resistance, despite the belief of strengthening the remaining people for whom lifestyle changes would be particularly
tooth structure by restoring the defect.56 Thus, in small lesions, difficult to achieve.50
preventive measures together with a causal therapy and a close 7. Local chemical preventive measures (educating the patient
monitoring of the patient are the strategy of choice. The same is for correct toothbrushing and regular applications of topical
true for lesions which do not cause any esthetic or functional fluorides and professional application of fluoride products
problems, lesions without sensitivity or which do not com- and/or adhesive coatings) for enhancing resistance of tooth
promise the integrity of the tooth. As the clinical effectiveness structures to erosion and abrasion.
of Class V restorations seems to be controversial, the 8. Regular monitoring of the patient. The recall interval should
elimination of the causes, instead, might be more beneficial in vary upon age, as the progression rate of erosive/abrasive
the long-term. lesions was found to be higher in older people.51 It is known
The preventive approach in patients already presenting that the evolution of NCCL is generally a slow process, but
advanced lesions is more complex. Beside the restorative no specific progression rates for NCCL were given in the
therapy of the advanced lesions, elimination of causes should literature. Therefore, an individual monitoring protocol has
always be considered to assure stability and longevity. Local to be established, by assessing the severity of the present
preventive measures like professional application of fluorides lesions, the age and the existing etiological and risk factors.
and educating the patient is crucial for preventing the For patients particularly exposed to intrinsic or extrinsic
development of new lesions. acids or presenting a rapid progression, the measurement
procedure should be repeated at 6-month intervals, but for
The strategy in detail is as follows: most other cases, annually is acceptable.67 The progression
1. Elimination of local or general etiological factors. can be assessed clinically by measuring the width and
2. Enhancement of resistance against acid attack. length of the lesion with a graded probe, and also by
3. Brushing with desensitizing and fluoride containing comparatively examining photographs.
dentifrices, daily use of fluoride rinse, fluoride gels, soft RECOMMENDATIONS FOR PATIENTS PRESENTING NCCL
toothbrush. 1. Use a soft toothbrush and low abrasion fluoridated tooth-
4. Professional application of a fluoride varnish, desensitizer paste (around 1100 pm F) or a calcium containing
(potassium oxalate, arginine-calcium carbonate or other toothpaste.50,63,68,69 Avoid toothpaste and mouthrinse with low
tubule-occluding agents) or of an adhesive coating. pH.50 In case of softened enamel, power or sonic toothbrushes
5. Close monitoring of the patient. may lead to significantly higher loss of substance.70
American Journal of Dentistry, Vol. 24, No. 1, February, 2011
Noncarious cervical lesions: Part 1 53

2. Avoid toothbrushing immediately after an erosive challenge factors, diseases are often difficult to control. Therefore, the use
in order to preserve the salivary pellicle.68,71-73 Brushing is of professional preventive measures was suggested as part of
recommended prior to rather than after the erosive chal- the preventive strategy.88,89 Beside the known caries protective
lenge.74-76 Instead, use a fluoride containing mouthrinse or an properties, fluoride products have been proposed as a protective
iron containing mouthrinse77 after the erosive challenge.50,68 measure against erosion/abrasion. Fluoride has a dynamic
3. Gently apply concentrated topical fluoride without dis- implication in the remineralization-dissolution process around
turbing the protective pellicle of the tooth surface.68 tooth surface, suggesting thereby a possible interference with
4. Professional application of fluoride varnishes. Repeated the erosion mechanism, described as a dissolution and outflow
application is necessary, due to temporary protection.63,78 of ions towards tooth surface.59
5. Adhesive systems may protect dentin from erosion and Professional applications are also necessary as high
abrasion for a limited period of time.63,79,80 concentrations of fluorides are needed to achieve a good
6. Use of sugar-free chewing gum or non-acidic saliva protective effect.89 Concentrated gels and varnishes are the
stimulating products. Sugar free chewing gum and even options. Beside the remineralizing effect of fluoride on the
fluoride containing or carbamide containing gum are erosion lesions, the varnish is expected to provide mechanical
advised in order to increase salivary flow, knowing that protection of the tooth surface against acid diffusion and
saliva is an important protective factor through the pellicle reduction of hypersensitivity.78,87,91,92 As long as they remain
formation and the buffering capacity.50,63,68,73,76,81 Stimu- attached to the tooth surface, fluoride varnishes may be more
lating salivary flow has been shown in vitro to reduce effective than solutions and gels in prevention of erosive
abrasion/erosion82 and it might also be a treatment for defects due to their better capability to adhere to the tooth
patients with symptomatic reflux, by helping to reduce surface and create a calcium fluoride reservoir, although they
postprandial esophageal acid exposure.68 present the shortcomings of short term effectiveness and
7. In case of hypersensitivity, use a toothpaste containing therefore the need for repeated applications in multiple layers.78
fluoride and desensitizers, and professional application of However, further clinical investigation is required to understand
adhesive coating/desensitizers/fluoride varnish. the role of fluoride in protecting mineralized tissues from such
LOCAL PREVENTIVE MEASURES processes.35,50,93
The presumed erosive and abrasive nature of NCCL might ADHESIVE COATINGS
support the introduction of local preventive measures. As a In vitro79 and later in vivo80 tests found dentin sealing with
consequence of erosive challenges, tooth substance was resin based adhesives to be an effective strategy against
reported to exhibit a change in microhardness and a higher erosive/abrasive tooth wear as well. Compared to unsealed
susceptibility to substance loss by a subsequent abrasive surfaces, coated dentin exhibited less substance loss after
challenge.59 Therefore, in vitro and in situ evaluations have erosive and abrasive challenge.94 Resin-based adhesives were
measured the effect of different products applied to the altered shown to be more efficient against further substance loss in
tooth surfaces. Fluoride products, calcium containing tooth- comparison to fluoride mouthrinses in an in vitro study.94
pastes, iron containing mouthrinses and adhesive coatings were Nevertheless, they need frequent reapplication due to their low
tested in vitro and in situ for their protective effect against wear resistance. Some tested products are Seal and Protecta
79,80,94
erosive-abrasive tooth substance loss. and Optibond Solo.b,79,80 Seal and Protect, a self-
adhesive, light-curing, translucent sealing material is designed
FLUORIDES to prevent the development and progression of wedge-shaped
The most efficient long-term strategy seems to be a daily lesions by producing a hard coat increasing the resistance of
repeated application of fluoride products, this being achieved cervical areas against abrasive and erosive forces. It is
mainly with products used at home.68,83 Therefore, patient specifically designed to protect exposed dentin, similar to pit
education and compliance becomes a very important part of the and fissure sealants.
preventive strategy. Generally, toothpastes provide fluoride on
a regular basis and in vitro studies report an anti erosive/ OTHER PRODUCTS
abrasive effectiveness.74,83,84 Apart from fluoridated toothpaste Another type of topical preventive measures includes
and mouthrinse,83 patients with NCCL should regularly apply calcium and phosphate based remineralization systems like
fluoride gels, as their protective effect seems also to be casein phosphopeptide-amorphous calcium phosphate (CPP-
greater.85 In vitro and in situ studies suggest that a combination ACP) nanocomplexes. Calcium-containing sodium bicarbonate
of different fluoride products used regularly by the patient may based toothpastes, chewing gums and mouthrinses were tested
significantly reduce erosion.83 Nevertheless, there are some and reported to be even more efficient than toothpastes
discrepancies regarding the protective effectiveness against containing only fluoride.96-98 Most of the investigations found
abrasion or attrition, with some studies showing no protection these products able to harden enamel surface by delivering
against the abrasive challenge or reporting even an increase of minerals and to reduce surface roughness, recommending these
the amount of wear86,87 probably due to imperfections of products also for erosive/ abrasive tooth substance loss.96,99,100-
102
laboratory conditions or the highly acidic formula of the A recent review103 however reported the need for more
employed product. investigation on their long-term effects. Promising results were
A preventive approach aiming to reduce the contact of the obtained rather by combining this remineralizing system with
tooth tissues with the erosive agents may pose some difficulties fluoride, as the association with fluoride in the same product
due to patient compliance. In case of erosion due to intrinsic was shown to be more effective in remineralizing enamel, than
 American Journal of Dentistry, Vol. 24, No. 1, February, 2011
54 Pecie et al

either product alone.102 The synergistic effect of CPP-ACP and 26:767-768, 770-774, 776.
8. Lyons K. Aetiology of abfraction lesions. N Z Dent J 2001;97:93-98.
fluoride may result from the formation of CPP-stabilized 9. Rees JS. A review of the biomechanics of abfraction. Eur J Prosthodont
amorphous calcium fluoride phosphate resulting in the Restor Dent 2000;8:139-144.
increased incorporation of fluoride ions into plaque, together 10. Rees JS, Jagger DC. Abfraction lesions: Myth or reality? J Esthet Restor
with increased concentrations of bioavailable calcium and Dent 2003;15:263-271.
11. Terry DA, McGuire MK, McLaren E, Fulton R, Swift EJ Jr. Perioesthetic
phosphate ions.102 approach to the diagnosis and treatment of carious and noncarious cervical
lesions: Part I. J Esthet Restor Dent 2003;15:217-232.
Conclusions 12. Wood I, Jawad Z, Paisley C, Brunton P. Non-carious cervical tooth surface
loss: A literature review. J Dent 2008;36:759-766.
The etiology of NCCL is currently considered to be rather 13. Pegoraro LF, Scolaro JM, Conti PC, Telles D, Pegoraro TA. Noncarious
multifactorial, as clinical investigations have found multiple cervical lesions in adults: Prevalence and occlusal aspects. J Am Dent
factors associated with this type of lesions and due to the lack Assoc 2005;136:1694-700. Erratum in: J Am Dent Assoc 2006;137:447.
14. Vandewalle KS, Vigil G. Guidelines for the restoration of Class V lesions.
of evidence to support exclusively one or another factor. No Gen Dent 1997;45:254-260.
clinical research exists with respect to the prevention of NCCL 15. Piotrowski BT, Gillette WB, Hancock EB. Examining the prevalence and
and long-term clinical evaluations of the proposed preventive characteristics of abfraction like cervical lesions in a population of U.S.
measures are needed. The possible erosive or abrasive nature of veterans. J Am Dent Assoc 2001;132:1694-1701.
16. Lussi A: Dental Erosion. Monogr Oral Sci 2006;20:32-43.
the lesion and the difficult-to-control etiology may justify 17. Young A, Amaechi BT, Dugmore C, Holbrook P, Nunn J, Schiffner U,
professional applications of topical fluorides (especially Lussi A, Ganss C. Current erosion indices. Flawed or valid? Summary.
fluoride varnishes) or of adhesive systems of general use or Clin Oral Investig 2008;12 (Suppl 1):S59-63.
specially conceived products (e.g. Seal and Protect) and the 18. Khan F, Young WG, Shahabi S, Daley TJ. Dental cervical lesions associated
with occlusal erosion and attrition. Aust Dent J 1999;44:176-186.
home use of different fluoride or calcium containing products. 19. Telles D, Pegoraro LF, Pereira JC. Incidence of noncarious cervical lesions
Their protective effect against erosion/abrasion could be and their relation to the presence of wear facets. J Esthet Restor Dent
confirmed in several laboratory and in situ studies, but the 2006;18:178-183.
20. Aw TC, Lepe X, Johnson GH, Mancl L. Characteristics of noncarious
effectiveness and optimum application frequency still need to cervical lesions: A clinical investigation. J Am Dent Assoc 2002;133:725-733.
be established in clinical trials. Additionally, calcium- and 21. Lussi AR, Schaffner M, Hotz P, Suter P. Epidemiology and risk factors of
phosphate-based remineralization systems obtained promising wedge-shaped defects in a Swiss population. Schweiz Monatsschr Zahnmed
results, which however, also need further clinical confirmation. 1993;103:276-280. (In German).
22. Borcic J, Anic I, Urek MM, Ferreri S. The prevalence of non-carious
Progression rate of NCCL, generally slow, represents cervical lesions in permanent dentition. J Oral Rehabil 2004;31:117-123.
important information which has to be measured in the future 23. Faye B, Sarr M, Kane AW, Toure B, Leye F, Gaye F, Dieng MB.
on an individual level, in order to establish an optimized recall Prevalence and etiologic factors of non-carious cervical lesions. A study in
a Senegalese population. Odontostomatol Trop 2005;28:15-18.
interval for patients at risk of developing such lesions. 24. Smith WA, Marchan S, Rafeek RN. The prevalence and severity of non-
As restorative options for NCCL are still not satisfying carious cervical lesions in a group of patients attending a university hospital
regarding esthetics and longevity, prevention should take the in Trinidad. J Oral Rehabil 2008;35:128-134.
leading role within the management strategy of NCCL. Early 25. Takehara J, Takano T, Akhter R, Morita M. Correlations of noncarious
cervical lesions and occlusal factors determined by using pressure-detecting
detection and management of incipient lesions become of sheet. J Dent 2008;36:774-779.
primary importance to avoid premature non-carious destruction 26. Bernhardt O, Gesch D, Schwahn C, Mack F, Meyer G, John U, Kocher T.
of teeth. Epidemiological evaluation of the multifactorial aetiology of abfractions. J
Oral Rehabil 2006;33:17-25.
a. Dentsply, Milford, DE, USA. 27. Akgül HM, Akgül N, Karaoglanoglu S, Ozdabak N. A survey of the
b. Kerr, Orange, CA, USA correspondence between abrasions and tooth brushing habits in Erzurum,
Turkey. Int Dent J 2003;53:491-495.
Disclosure statement: The authors have no conflict of interest. 28. Chan DC, Browning WD, Pohjola R, Hackman S, Myers ML. Predictors of
non-carious loss of cervical tooth tissues. Oper Dent 2006;31:84-88.
Dr. Pecie is a post-graduate student, Dr. Krejci is Professor of the Division of
29. Tomasik M. Analysis of etiological factors involved in noncarious cervical
Cariology and Endodontology, Dr. Bortolotto is Research Section Head,
lesions. Ann Acad Med Stetin 2006;52:125-136.
Division of Cariology and Endodontology, University of Geneva, Switzerland.
Dr. Garcia-Godoy is Professor and Senior Executive Associate Dean for 30. Miller WD. Experiments and observations the wasting of tooth tissue
Research and Director, Bioscience Research Center, College of Dentistry, variously. Designated as erosion, abrasion, chemical abrasion, denudation,
University of Tennessee Health Science Center, Memphis, Tennessee, USA. etc. Dent Cosmos 1907;49:225-247.
31. Grippo JO. Abfractions: A new classification of hard tissue lesions of teeth.
J Esthet Dent 1991;3:14-19.
References 32. Grippo JO, Simring M, Schreiner S. Attrition, abrasion, corrosion and
abfraction revisited: A new perspective on tooth surface lesions. J Am Dent
1. Lussi A. Dental Erosion. Monogr Oral Sci 2006;20:9-16.
Assoc 2004;135:1109-1118.
2. Bartlett DW, Shah P. A critical review of non-carious cervical (wear)
lesions and the role of abfraction, erosion, and abrasion. J Dent Res 33. Lee HE, Lin CL, Wang CH, Cheng CH, Chang CH. Stresses at the cervical
2006;85:306-312. lesion of maxillary premolar. A finite element investigation. J Dent
3. Ceruti P, Menicucci G, Mariani GD, Pittoni D, Gassino G. Non carious 2002;30:283-290.
cervical lesions. A review. Minerva Stomatol 2006;55:43-57. 34. Rees JS. The role of cuspal flexure in the development of abfraction
4. Litonjua LA, Andreana S, Patra AK, Cohen RE. An assessment of stress lesions: A finite element study. Eur J Oral Sci 1998;106:1028-1032.
analyses in the theory of abfraction. Biomed Mater Eng 2004;14:311-321. 35. Rees JS. The biomechanics of abfraction. Proc Inst Mech Eng H
5. Litonjua LA, Andreana S, Bush PJ, Cohen RE. Tooth wear: Attrition, 2006;220:69-80.
erosion, and abrasion. Quintessence Int 2003;34:435-446. 36. Borcic J, Anic I, Smojver I, Catic A, Miletic I, Ribaric SP. 3D finite
6. Litonjua LA, Andreana S, Bush PJ, Tobias TS, Cohen RE. Noncarious element model and cervical lesion formation in normal occlusion and in
cervical lesions and abfractions: A re-evaluation. J Am Dent Assoc malocclusion. J Oral Rehabil 2005;32:504-510.
2003;134:845-850. 37. Borcić J, Antonić R, Urek MM, Petricević N, Nola-Fuchs P, Catić A,
7. Litonjua LA, Andreana S, Cohen RE. Toothbrush abrasions and noncarious Smojver I. 3-D stress analysis in first maxillary premolar. Coll Antropol
cervical lesions: Evolving concepts. Compend Contin Educ Dent 2005; 2007;31:1025-1029.
American Journal of Dentistry, Vol. 24, No. 1, February, 2011
Noncarious cervical lesions: Part 1 55

38. Ichim I, Li Q, Loughran J, Swain MV, Kieser J. Restoration of non-carious Separating fact from fiction. Aust Dent J 2009;54:2-8.
cervical lesions Part I. Modelling of restorative fracture. Dent Mater 67. Bartlett D, Ganss C, Lussi A. Basic Erosive Wear Examination (BEWE): A
2007;23:1553-1561. new scoring system for scientific and clinical needs. Clin Oral Investig
39. Ichim IP, Schmidlin PR, Li Q, Kieser JA, Swain MV. Restoration of non- 2008;12 (Suppl 1):S65-S68.
carious cervical lesions. Part II. Restorative material selection to minimise 68. Lussi A. Dental erosion. Monogr.Oral.Sci 2006;20:190-199.
fracture. Dent Mater 2007;23:1562-1569. 69. Lynch RJ, ten Cate JM. The anti-caries efficacy of calcium carbonate-based
40. Ichim I, Schmidlin PR, Kieser JA, Swain MV. Mechanical evaluation of fluoride toothpastes. Int Dent J 2005;55(3 Suppl 1):175-178.
cervical glass-ionomer restorations: 3D finite element study. J Dent 70. Wiegand A, Begic M, Attin T. In vitro evaluation of abrasion of eroded
2007;35:28-35. enamel by different manual, power and sonic toothbrushes. Caries Res
41. Rees JS, Hammadeh M, Jagger DC. Abfraction lesion formation in 2006;40:60-65.
maxillary incisors, canines and premolars: A finite element study. Eur J 71. Wiegand A, Meier W, Sutter E, Magalhães AC, Becker K, Roos M, Attin
Oral Sci 2003;111:149-154. T. Protective effect of different tetrafluorides on erosion of pellicle-free and
42. Rees JS, Hammadeh M. Undermining of enamel as a mechanism of pellicle-covered enamel and dentine. Caries Res 2008;42:247-254.
abfraction lesion formation: A finite element study. Eur J Oral Sci 72. Wiegand A, Bliggenstorfer S, Magalhaes AC, Sener B, Attin T. Impact of
2004;112:347-352. the in situ formed salivary pellicle on enamel and dentine erosion induced
43. Estafan A, Furnari PC, Goldstein G, Hittelman EL. In vivo correlation of by different acids. Acta Odontol Scand 2008;66:225-230.
noncarious cervical lesions and occlusal wear. J Prosthet Dent 73. Hove LH, Holme B, Young A, Tveit AB. The erosion-inhibiting effect of
2005;93:221-226. TiF4, SnF2, and NaF solutions on pellicle-covered enamel in vitro. Acta
44. Miller N, Penaud J, Ambrosini P, Bisson-Boutelliez C, Briaçon S. Analysis Odontol Scand 2007;65:259-264.
of etiologic factors and periodontal conditions involved with 309 74. Lussi A, Megert B, Eggenberger D, Jaeggi T. Impact of different
abfractions. J Clin Periodontol 2003;30: 828–832 toothpastes on the prevention of erosion. Caries Res 2008;42:62-67.
45. Ommerborn MA, Schneider C, Giraki M, Schafer R, Singh P, Franz M, 75. Wiegand A, Buchalla W, Attin T. Review on fluoride-releasing restorative
Raab WH. In vivo evaluation of noncarious cervical lesions in sleep materials. Fluoride release and uptake characteristics, antibacterial activity
bruxism subjects. J Prosthet Dent 2007;98:150-158. and influence on caries formation. Dent Mater 2007;23:343-362.
46. Pintado MR, Delong R, Ko CC, Sakaguchi RL, Douglas WH. Correlation 76. Wiegand A, Egert S, Attin T. Toothbrushing before or after an acidic
of noncarious cervical lesion size and occlusal wear in a single adult over a challenge to minimize tooth wear? An in situ/ex vivo study. Am J Dent
14-year time span. J Prosthet Dent 2000;84:436-443. 2008;21:13-16.
47. Tsiggos N, Tortopidis D, Hatzikyriakos A, Menexes G. Association between 77. Sales-Peres SH, Pessan JP, Buzalaf MA. Effect of an iron mouthrinse on
self-reported bruxism activity and occurrence of dental attrition, abfraction, enamel and dentine erosion subjected or not to abrasion: An in situ/ex vivo
and occlusal pits on natural teeth. J Prosthet Dent 2008; 100:41-46. study. Arch Oral Biol 2007;52:128-132.
48. Yang WL, Lin XF, Zou B, Li XX. Investigation on relationship between 78. Vieira A, Jager DH, Ruben JL, Huysmans MC. Inhibition of erosive wear
wedge-shaped defects and occlusal interference Hua Xi Kou Qiang Yi Xue by fluoride varnish. Caries Res 2007;41:61–67.
Za Zhi 2007;25:383-385. (In Chinese). 79. Azzopardi A, Bartlett DW, Watson TF, Sherriff M. The surface effects of
49. De Las Casas EB, Cornacchia TP, Gouvêa PH, Cimini CA Jr. Abfraction erosion and abrasion on dentine with and without a protective layer. Br
and anisotropy. Effects of prism orientation on stress distribution. Comput Dent J 2004;196:351-354.
Methods Biomech Biomed Engin 2003;6:65-73. 80. Azzopardi A, Bartlett DW, Watson TF, Sherriff M. The measurement and
50. Holbrook WP, Arnadóttir IB, Kay EJ. Prevention. Part 3: Prevention of prevention of erosion and abrasion. J Dent 2001;29:395-400.
tooth wear. Br Dent J 2003;195:75-81. 81. Wetton S, Hughes J, Newcombe RG, Addy M. The effect of saliva derived
51. Lussi A, Jaeggi T. Erosion. Diagnosis and risk factors. Review. Clin Oral from different individuals on the erosion of enamel and dentine. A study in
Investig 2008;12 Suppl 1:S5-13. vitro. Caries Res 2007;41:423-426.
52. Grippo JO, Masi JV Role of biodental engineering factors (BEF) in the 82. Rios D, Honório HM, Magalhães AC, Delbem AC, Machado MA, Silva
etiology of root caries. J Esthet Dent 1991;3:71-76. SM, Buzalaf MA. Effect of salivary stimulation on erosion of human and
53. Kaidonis JA. Tooth wear: The view of the anthropologist. Clin Oral bovine enamel subjected or not to subsequent abrasion: An in situ/ex vivo
Investig 2008;12 Suppl 1:S21-26. study. Caries Res 2006;40:218-223.
54. Aubry M, Mafart B, Donat B, Brau JJ. Brief communication: Study of 83. Ganss C, Klimek J, Brune V, Schürmann A. Effects of two fluoridation
noncarious cervical tooth lesions in samples of prehistoric, historic, and measures on erosion progression in human enamel and dentine in situ.
modern populations from the South of France. Am J Phys Anthropol Caries Res 2004;38:561-566.
2003;121:10-14. 84. Ganss C, Schlueter N, Friedrich D, Klimek J. Efficacy of waiting periods
55. Ritter AV, Grippo JO, Coleman TA, Morgan ME. Prevalence of carious and topical fluoride treatment on toothbrush abrasion of eroded enamel in
and non-carious cervical lesions in archaeological populations from North situ. Caries Res 2007;41:146-151.
America and Europe. Esthet Restor Dent 2009;21:324-334. 85. Lagerweij MD, Buchalla W, Kohnke S, Becker K, Lennon AM, Attin T.
56. Grippo JO. Noncarious cervical lesions: The decision to ignore or restore. J Prevention of erosion and abrasion by a high fluoride concentration gel
Esthet Dent 1992;4 Suppl:55-64. applied at high frequencies. Caries Res 2006;40:148-153.
57. Mayhew RB, Jessee SA, Martin RE. Association of occlusal, periodontal, 86. Li H, Watson TF, Sherriff M, Curtis R, Bartlett DW. The influence of
and dietary factors with the presence of non-carious cervical dental lesions. fluoride varnish on the attrition of dentine. Caries Res 2007;41:219-222.
Am J Dent 1998;11:29-32. 87. Magalhães AC, Stancari FH, Rios D, Buzalaf MA. Effect of an
58. Faye B, Kane AW, Sarr M. Noncarious cervical lesions among a non- experimental 4% titanium tetrafluoride varnish on dental erosion by a soft
toothbrushing population with Hansen's disease (leprosy): Initial findings. drink. J Dent 2007;35:858-861.
Quintessence Int 2006;37:613-619. 88. Imfeld T. Prevention of progression of dental erosion by professional and
59. Lussi A. Dental erosion. Monogr Oral Sci 2006;20:1-8. individual prophylactic measures. Eur J Oral Sci 1996;104:215-220.
60. Oginni AO, Olusile AO, Udoye CI. Non-carious cervical lesions in a 89. Zero DT, Lussi A. Erosion. Chemical and biological factors of importance
Nigerian population: abrasion or abfraction? Int Dent J 2003;53:275-279. to the dental practitioner. Int Dent J 2005;55 (4 Suppl 1):285-290.
61. Lussi A, Schaffner M. Progression of and risk factors for dental erosion and 90. Magalhães AC, Kato MT, Rios D, Wiegand A, Attin T, Buzalaf MA. The
wedge-shaped defects over a 6-year period. Caries Res 2000;34:182-187. effect of an experimental 4% TiF4 varnish compared to NaF varnishes and
62. Osborne-Smith KL, Burke FJ, Farlane TM, Wilson NH. Effect of restored 4% TiF4 solution on dental erosion in vitro. Caries Res 2008;42:269-274.
and unrestored non-carious cervical lesions on the fracture resistance of 91. Ritter AV, de L Dias W, Miguez P, Caplan DJ, Swift EJ Jr. Treating
previously restored maxillary premolar teeth. J Dent 1998;26:427-433. cervical dentin hypersensitivity with fluoride varnish: A randomized
63. Milosevic A, O'Sullivan E, Royal College of Surgeons of England. clinical study. J Am Dent Assoc 2006;137:1013-1020.
Diagnosis, prevention and management of dental erosion: Summary of an 92. Vieira A, Ruben JL, Huysmans MC. Effect of titanium tetrafluoride, amine
updated national guideline. Prim Dent Care 2008;15:11-12. fluoride and fluoride varnish on enamel erosion in vitro. Caries Res
64. Coleman TA, Grippo JO, Kinderknecht KE. Cervical dentin hypersen- 2005;39:371-379.
sitivity. Part III: Resolution following occlusal equilibration. Quintessence 93. Barbour ME, Rees GD. The role of erosion, abrasion and attrition in tooth
Int 2003;34:427-434. wear. J Clin Dent 2006;17:88-93.
65. Wood ID, Kassir AS, Brunton PA. Effect of lateral excursive movements 94. Sundaram G, Wilson R, Watson TF, Bartlett DW. Effect of resin coating on
on the progression of abfraction lesions. Oper Dent 2009;34:273-279. dentine compared to repeated topical applications of fluoride mouthwash
66. Michael JA, Townsend GC, Greenwood LF, Kaidonis JA. Abfraction: after an abrasion and erosion wear regime. J Dent 2007;35:814-818.
 American Journal of Dentistry, Vol. 24, No. 1, February, 2011
56 Pecie et al

95. Sundaram G, Wilson R, Watson TF, Bartlett D. Clinical measurement of phopeptide-amorphous calcium phosphate. Aust Dent J 2003;48:240-243.
palatal tooth wear following coating by a resin sealing system. Oper Dent 100. Cross KJ, Huq NL, Reynolds EC.Casein phosphopeptides in oral health--
2007;32:539-543. chemistry and clinical applications. Curr Pharm Des 2007;13:793-800.
96. Charig A, Winston A, Flickinger M. Enamel mineralization by calcium- 101. Iijima Y, Cai F, Shen P, Walker G, Reynolds C, Reynolds EC. Acid
containing-bicarbonate toothpastes: Assessment by various techniques. resistance of enamel subsurface lesions remineralized by a sugar-free
Compend Contin Educ Dent 2004;25(9 Suppl 1):14-24. chewing gum containing casein phosphopeptide-amorphous calcium
97. Kardos S, Shi B, Sipos T. The in vitro demineralization potential of a phosphate. Caries Res 2004;38:551-556.
sodium fluoride, calcium and phosphate ion-containing dentifrice under 102. Reynolds EC, Cai F, Shen P, Walker GD. Retention in plaque and
various experimental conditions. J Clin Dent 1999;10(1 Spec No):22-25. remineralization of enamel lesions by various forms of calcium in a
98. Litkowski LJ, Quinlan KB, Ross DR, Ghassemi A, Winston A, Charig A, mouthrinse or sugar-free chewing gum. J Dent Res 2003;82:206-211.
Flickinger M, Vorwerk L. Intraoral evaluation of mineralization of 103. Azarpazhooh A, Limeback H. Clinical efficacy of casein derivatives: A
cosmetic defects by a toothpaste containing calcium, fluoride, and systematic review of the literature. J Am Dent Assoc 2008;139:915-924.
sodium bicarbonate. Compend Contin Educ Dent 2004;25 (9 Suppl 104. Reynolds EC, Cai F, Cochrane NJ, Shen P, Walker GD, Morgan MV,
1):25-31. Reynolds C. Fluoride and casein phosphopeptide-amorphous calcium
99. Cai F, Shen P, Morgan MV, Reynolds EC. Remineralization of enamel phosphate. J Dent Res 2008;87:344-348.
subsurface lesions in situ by sugar-free lozenges containing casein phos- 105. Young WG. The oral medicine of tooth wear. Aust Dent J 2001;46:236-250.