non-carious cervical tooth surface loss: a literature review

R

N

Ia

b

a

A

R

R

1

A

K

O

N

l

A

T

C

P

P

0d

eview

on-carious cervical tooth surface loss: A literature review

an Wood a, Zynab Jawad b, Carl Paisley b, Paul Brunton b,*

Restorative Dentistry, Manchester University, England, United Kingdom

Restorative Dentistry, Leeds Dental Institute, Leeds University, Leeds LS2 9LU, England, United Kingdom

j o u r n a l o f d e n t i s t r y 3 6 ( 2 0 0 8 ) 7 5 9 – 7 6 6

r t i c l e i n f o

rticle history:

eceived 6 March 2007

eceived in revised form

1 June 2008

ccepted 11 June 2008

eywords:

cclusal factors

on-carious cervical tooth surface

oss

bfraction

ooth wear

ervical lesion

revention

revalence

a b s t r a c t

Objectives: As the population ages and teeth are increasingly retained for life the incidence

of non-carious cervical tooth surface loss is increasing but little is understood about the

aetiology and management of these lesions. The purpose of this literature review was to

review and critically appraise the literature as it relates to the prevalence, aetiology and

treatment of non-carious cervical tooth surface loss.

Search strategy: An electronic search, using OVID electronic bibliographic databases was

performed with no restriction on the language of publication.

Conclusions: Despite the paucity of research into non-carious cervical tooth surface loss it

was concluded that the number and size of lesions increases with age, lesions are more

common on the facial aspects of teeth and the formation of lesions appears to be multi-

factorial with lesion shape not being a predictor of aetiology. It was also concluded that the

value of restoring these lesions, where indicated, is unclear and that occlusal adjustment to

increase the retention of restorations placed to restore lesions or to halt lesion progression

cannot be supported.

# 2008 Elsevier Ltd. All rights reserved.

avai lab le at www.sc iencedi rec t .com

journal homepage: www. int l .e lsev ierhea l th .com/ journa ls / jden

1. Introduction

As an ageing population retains its teeth for longer the issue of

tooth wear is becoming of increasing importance to the dental

profession.

The phrase ‘‘non-carious cervical tooth surface loss’’

(NCCTSL) has arisen in attempt to embrace all such lesions

which occur at the neck of the tooth. Unfortunately, much

confusion arises from the use of other terminologies, such as

erosions and abrasions, which have been used at different

times and in different locations to describe similar lesions.

As long ago as 1908, Black,1 in his seminal work on

Operative Dentistry discussed the problematic aetiology of

what he termed ‘‘erosions’’ and stated that ‘‘Our information

regarding erosion is far from complete and much time may

* Corresponding author. Tel.: +44 1133436182; fax: +44 1133436165.E-mail address: [email protected] (P. Brunton).

300-5712/$ – see front matter # 2008 Elsevier Ltd. All rights reserveoi:10.1016/j.jdent.2008.06.004

elapse before its investigation will give satisfactory results’’.1

He identified eight possible causes:

� Faults in the formation of teeth.

� Friction from an abrasive tooth powder.

� Action of an unknown acid.

� Secretion from a diseased salivary gland.

� Physiological resorption, as with deciduous teeth.

� Acid associated with gouty diarethis.

� Action of alkaline fluids on calcium salts.

� Action of enzymes released by micro-organisms.

After considering each hypothesis in turn, finding fault

with all, he concluded that he had no theory of his own to

offer, which did not have features that rendered it impossible.

d.

mailto:[email protected]

http://dx.doi.org/10.1016/j.jdent.2008.06.004


Other researchers in the early part of the 20th century also

considered these lesions. Miller,2 looked at ‘‘wastings’’ and

concluded that brushing with coarse tooth powder was the

likely cause.2

In 1931, Ferrier3 was unable to offer a reasonable explana-

tion, for these lesions and in 1932 Kornfeld4 made the

observation that in all cases of cervical erosion he noticed

heavy wear facets on the articulating surfaces of the teeth

involved and that the erosion tended to be at the opposite side

of the tooth to the wear facet.3,4

The confusing use of the term erosion to describe a lesion

which may actually be caused by mechanical abrasion is

further compounded by the fact that to a chemical engineer

the process described by dentists as erosion is known as

corrosion.5 This imprecise terminology has contributed both

to the difficulty of carrying out good quality research and

making accurate diagnoses, which would enable appropriate

treatments to be recommended.

Many practitioners felt that over enthusiastic tooth-

brushing and the use of abrasive toothpastes were the

primary cause of these lesions but Lee and Eakle6 put

forward the hypothesis that tensile stresses created in the

tooth during occlusal loading may have a role in the

aetiology of cervical erosive lesions.6 They described three

types of stress placed on teeth during mastication and

parafunction:

� C
ompressive—the resistance to compression.
� T
ensile—the resistance to stretching.
� S
hearing—the resistance to twisting or sliding.
The authors stated that in a ‘‘non-ideal’’ occlusion large

lateral forces could be created which would result in

compressive stresses on the side of the tooth being loaded

and tensile stresses in the opposite side. As it was

well known that enamel is strong in compression but

weak in tension, it was suggested that those areas in tension

were prone to failure. The region of greatest stress is found

at the fulcrum of the tooth. The characteristic lesion

described was wedge-shaped with sharp line angles and

situated at or near the fulcrum of the tooth, where the

greatest stress is generated. It was suggested that the

direction of the lateral force governed the position of

the lesion and its size was related to the magnitude and

duration of the force.

Grippo put forward a new classification of hard tissue

lesions of teeth.7 He defined four categories of tooth wear.

� A
ttrition—the wearing away of tooth substance as a result of
tooth to tooth contact during normal or parafunctional

masticatory activity.

� A
brasion—the pathological wear of tooth substance through
bio-mechanical frictional processes, e.g. tooth brushing.

� E
rosion—the loss of tooth substance by acid dissolution of
either an intrinsic or extrinsic origin, e.g. gastric acid or

dietary acids.

� A
bfraction—the pathologic loss of tooth substance caused
by bio-mechanical loading forces. It was postulated that

these lesions were caused by flexure of the tooth during

loading leading to fatigue of the enamel and dentine at a

location away from the point of loading. The word

‘‘abfraction’’ was derived from the Latin ‘‘to break away’’.

Grippo then went on to further describe five categories of

abfraction:

� H
airline cracks.
� S
triations—horizontal bands of enamel breakdown.
� S
aucer-shaped—a lesion entirely within enamel.
� S
emi-lunar-shaped—a crescent-shaped lesion entirely
within enamel.

� C
usp tip invagination—a depression on the cusp tip seen in
molar and premolar teeth.

Lambert and Lindenmuth8 considered that the profession

should now consider occlusal stress as a primary factor in the

creation of cervical notch lesions and a considerable body of

theoretical work was accumulating to support the theory.8 To

date it would appear that practitioners widely accept that

abfraction is related to atypical occlusal loading despite there

being a paucity of evidence other than purely theoretical to

support this hypothesis. The purpose of this review of the

literature was to review and critically appraise the literature as

it relates to the prevalence, aetiology and treatment of non-

carious cervical tooth surface loss.

2. Prevalence

The profession has been aware of NCCTSL for many years and

studies of their prevalence in the population have revealed

conflicting results. Shulman and Robinson9 recorded preva-

lence as low as 2%, whereas Bergstrom and Eliasson10

recorded findings of 90%.9,10 This is partly explained by the

fact that different populations were included in the respective

studies. In the above examples, Shulman and Robinson9 were

examining young male freshmen, whereas Bergstrom and

Eliasson10 examined adult patients in the 31–60 age range. All

studies showed a tendency for prevalence to increase with

age, which goes some way to explain the disparity in their

findings.

Variations in diagnosis and terminology outlined earlier,

along with possible local variables, such as dietary differences

and oral hygiene habits between one population and another,

also contribute to the variable picture which emerges from

considering previous studies. Levitch et al.,11 in a review of 15

studies carried out between 1941 and 1991 reported prevalence

in the range 5–85% with a strong correlation with age.11 The

older the population studied, the greater the percentage of

lesions found, the greater the number of lesions per individual

and the larger the lesions. They also noted that many studies

had shown a link between good oral hygiene and the

frequency of NCCTSL. People who brush twice daily have a

statistically significant higher prevalence of NCCTSL than

those who brush less frequently.12 Bruxism is also identified as

a source of occlusal stress and the work of Xhonga13 is

frequently quoted which reported that 87% of bruxists had

NCCTSL while only 20% of non-bruxists exhibited similar

lesions.13 This was, however, a small study with only 15

patients examined in each category hence the results should

Table 2 – Prevalence of cervical abrasions according totooth type

Tooth type Number of teethwith abrasion

cavities (%)

Maxillary first molars 30 (17.3)

Maxillary first bicuspids 25 (14.5)

Mandibular first bicuspids 25 (14.5)

Maxillary second bicuspids 23 (13.3)

Mandibular second bicuspids 21 (12.1)

Maxillary cuspids 13 (7.5)

Mandibular cuspids 9 (5.2)

Mandibular first molars 8 (4.6)

Maxillary second molars 8 (4.6)

Mandibular central incisors 5 (2.9)

Maxillary lateral incisors 3 (1.7)

Maxillary central incisors 2 (1.2)

Mandibular lateral incisors 1 (0.6)

j o u r n a l o f d e n t i s t r y 3 6 ( 2 0 0 8 ) 7 5 9 – 7 6 6 761

be interpreted with caution. Graehn et al.14 however studied

915 patients, identifying 23% as having wedge-shaped lesions.

Of these, 65% had confirmed parafunctional habits.14,15

The idea of classifying lesions according to their possible

aetiology was put forward by Levitch et al.11 They proposed

that an erosive lesion could be found on either the lingual or

facial aspect of the tooth, be shallow, U-shaped or disc-like

and would have smooth angles and a smooth surface. An

abrasion lesion would be facially located, wedge-shaped or

grooved with sharp angles and possibly a smooth or scratched

surface. A lesion associated with tooth flexure would be found

facially and would be wedge-shaped or composed of over-

lapping wedges, have sharp angles and a rough or corrugated

surface. Oddly this classification ignores the fact that a small

number of wedge-shaped lesions thought to be of flexural

origin have been identified in epidemiological studies.11

Levitch et al.11 go on to point out that the methodology of

many of the earlier studies was flawed and a significant

number of co-factors exist, which have not always been

considered. Another problem identified was the failure to

define criteria for lesions or consider a possible multifactorial

aetiology. Most studies are limited to looking at factors

associated with a single aetiological mechanism.

3. Intraoral distribution

NCCTSL lesions do not present with an equal distribution

within a given individual. Rees et al.,16 in a recent paper on the

formation of abfraction lesions in maxillary incisors, canines

and premolars reported that these lesions were more

prevalent on the labial surface of maxillary incisors.16,17

Sognnaes et al.,18 also found a preponderance of abrasion/

erosion type lesions in the incisors.18 Radentz et al.12 however,

undertook a study on 100 enlisted military personnel aged

from 17 to 45 which identified 80 of them as being suitable for

inclusion in the study. Before assessing factors which may be

associated with cervical abrasions (the term abfraction was

not yet in use) the distribution of existing lesions was

recorded. Their findings are summarised below (Tables 1

and 2) and show maxillary first molars to be the most

commonly affected teeth with maxillary incisors amongst the

least affected. This report, written before occlusal stress was

considered a possible aetiological cause, concluded that

cervical abrasion is related to factors associated with the

initial stages of tooth brushing and that the excessive use of

dentifrices, habitually placed undiluted in the same area of the

mouth, may produce abrasion.12

A study by Zipkin and McLure19 analysed the distribution of

erosive cavities in a sample largely drawn from a population

Table 1 – Prevalence of cervical abrasion according tointraoral region

Intraoral region Number of teeth with abrasion (%)

Maxillary 104 (60.1)

Mandibular 69 (39.9)

Right side 95 (54.9)

Left side 78 (45.1)

with a pre-existing diagnosis of erosion.19 They also found that

maxillary teeth were more severely affected than mandibular

teeth with no significant difference between the right and left

sides of the mouth. They, however, found the maxillary first

premolars to be the worst affected teeth, also noting that the

maxillary first molars were twice as badly affected as the

mandibular first molars.

Both the Zipkin and McLure19 study as well as Radentz

et al.12 note a very low occurrence of lingual lesions in either

arch. A figure of 2% has been suggested by Khan et al.20 in a

more recent study to compare the relationship between

cervical lesions and occlusal erosion and attrition. They also

found less erosion in maxillary teeth than mandibular, with

more NCCTSL on mandibular molars and premolars than on

maxillary teeth.20 They did, however, find more lesions on

mandibular premolars than mandibular canines, which is in

line with the findings of Radentz et al.12 They concluded that if

wedge-shaped lesions were caused solely by stresses arising

from occlusal forces they would only be found on teeth with

wear facets and they would tend to appear in pairs on

opposing teeth.

Pegoraro et al.21 in a study on 48 dental students aged

between 16 and 24 found that 52% of the students had NCCTSL

(Table 3).

4. Theories of NCCTSL formation

Much of the historical thinking around the formation of

NCCTSL centres on abrasive damage caused primarily by

toothbrushing, and erosion caused by acid of a non-bacterial

origin, which may be either intrinsic or extrinsic in origin.

Many of these studies have already been referred to

previously.

Miller2 created cervical lesions in vitro with abrasive tooth

powders and toothbrushing. Radentz et al.12 and Levitch

et al.11 discussed the fact that people with good oral hygiene

are more prone to NCCTSL and state that patients who brush

twice daily have a statistically significant higher incidence of

NCCTSL than those who brush less frequently. Right-handed

people have more lesions on the left side of their mouths and

Table 3 – Distribution of NNCTSL in a dental studentpopulation

Teeth affected Percentage

First mandibular molar 21.3

First maxillary molar 16

First maxillary premolar 12.8

First mandibular premolar 11.7

Second mandibular premolar 11.7

Second maxillary premolar 9.6

Second mandibular molar 3.2

Maxillary central incisors 3.2

Second maxillary molar 2.1

Mandibular central incisors 2.1

Lower second molar 2.1

Maxillary lateral incisors 1.1


conversely left-handed people have more lesions on their right

side. The first quadrant to be cleaned also has a higher

incidence of lesions but the stiffness of the brush used did not

have any impact and the low abrasivity of modern toothpastes

was thought to minimise their impact. It was suggested by

Radentz et al.12 that teeth in the middle of the brushing arc

were more severely affected. There is an acceptance that

many lesions may have a multifactorial aetiology but no

explanation has satisfactorily explained the isolated lesions in

otherwise healthy mouths, the lingual lesions which were

impossible to reach with a toothbrush or multiple lesions on

the same tooth.

As early as 1932 Kornfeld4 had made the observation that

many teeth with cervical erosions also had heavy wear facets

on their articulating surfaces, but it was not until 1984 that Lee

and Eakle6 published a paper which explored the possible role

of tensile stress in the aetiology of these ‘‘idiopathic cervical

lesions’’.4,6 Work had been published in the 1970s by Thresher

and Saito,22 Selna et al.23 and Yettram et al.,24 which showed

by finite element analysis that stresses were concentrated in

the cervical regions of the teeth and the authors suggested

that these tensile stresses were the primary aetiological factor

in creating wedge-shaped cervical lesions.6,22–24

4.1. Occlusal loading

The behaviour of a tooth under occlusal load is governed by a

number of factors:

� T
he support provided by the bony socket.
� T
he gross morphology of the tooth.
� T
he microscopic structure of the tooth.
� T
he presence and size of restorations.
� T
he direction of the force applied.
The anatomy of the periodontal ligament and the

surrounding alveolar bone is designed to absorb the forces

applied to the teeth during mastication. Picton25 reported that

alveolar bone surrounding a tooth distorted under loads of less

than 100 g.25 Horizontal loads caused initially compression of

the periodontal ligament and then dilatation of the alveolar

bone. The labial plates tended to distort more than the lingual

plates. This would imply that more force would be transmitted

to the tooth itself when horizontal forces were applied in a

lingual or palatal direction and may support the finding that

more NNCTSL are found on the facial surfaces of the teeth.

In 1991, Goel et al.,26 published a paper in which they

developed a three-dimensional, linear, elastic finite element

stress model of a maxillary first premolar.26 Finite element

stress analysis is a mathematical-modelling technique which

examines the deformations of a model composed of a

meshwork of elements with given properties. They were

interested in the stresses arising at the amelodentinal junction

(ADJ) during function and had noted that the shape of the ADJ

was different under working cusps than under non-working

cusps. Functional cusps had a concave ADJ in the occlusal

third and non-functional cusps did not. Their theory was that

this difference in ADJ anatomy may contribute in some way to

the instigation of cervical lesions. The results of the study

showed that tensile stresses were elevated towards the

cervical enamel and also that although enamel and dentine

were organically bonded they had the capability to respond to

forces differently. They suggested that mechanical interlock-

ing between the enamel and the dentine is weaker in the

cervical region than in other areas of the tooth which may

make it susceptible to cracking which could eventually

contribute to cervical caries.

One of the problems associated with early finite element

models was the difficulty of allocating appropriate physical

characteristics to the different constituent parts of the tooth.

Spears27 looked at the data available for the Young’s Modulus

for enamel which varied considerably.27 He proposed a model

which functioned at two levels. At a crystalline level enamel

behaves as a simple composite, i.e. long parallel crystals in an

organic matrix with a stiffness dependant on chemical

composition and crystal orientation. At a prismatic level

enamel is considered to behave like a hierarchical composite

made up of prisms within which the crystal orientation is

heterogeneous. The actual stiffness of the enamel is then

dependant on the chemical composition and prism orienta-

tion. He concluded that values for stiffness were greater along

the direction of the prisms than across them and that

consequently enamel behaved in an anisotropic manner.

A further finite element study by Rees28 has shown that

premolar teeth with occlusal restorations present had a

greater concentration of peak tensile and shear stress in the

buccal cervical region when loaded with an eccentric force of

100 N than unrestored teeth. The recorded stresses were in

excess of the known failure stresses for enamel. Rees28 also

noted that the deeper the restoration present, the greater the

amount of cusp flexure that was found and he concluded that

the weakening effect of cavity preparation may contribute to

the development of NNCTSL.28

In 2003 Rees et al.16 published a further paper comparing

the cervical stress profiles of individual tooth types in the

maxilla using two-dimensional finite element stress analy-

sis.16 They found that the labial/buccal stress profile in the

cervical region of a maxillary incisor was always greater than

that found in a canine or premolar tooth with canines having

the lowest readings. They concluded that these findings

provide a bio-mechanical explanation for the clinical variation

seen in the prevalence of NCCTSL which ties in with their

statement that these lesions are most common in the

maxillary incisors but does not agree with the results of the


prevalence studies described earlier.12,21 This suggests that

the hypothesis as proposed is flawed.

The theory that occlusal forces can result in tensile

stresses in the cervical regions of the teeth is however,

supported by the work of Chen et al.,29 who measured cervical

strain perpendicular to the tooth using strain gauges attached

to extracted maxillary second premolars when a force was

applied to the lingual (palatal) cusp.29 They found that an

occlusal load could produce a tensile strain in the cervical

region of the tooth and that this strain increased with the

load. Tensile forces were detected on both the lingual and

buccal aspects of the tooth but were greater on the buccal

aspect. This again supports the theory that the formation of

cervical wedge-shaped lesions may be related to occlusal

forces.

This conclusion is further supported by the research of

Nohl et al.30 into the effect of load angle on strains induced in

maxillary premolars in vitro which showed that near axial

tensile strains were induced on the contra lateral side of the

tooth when loads were applied to the inner cusp inclines.30

The authors felt that this may be of significance in the

aetiology of NCCTSL.

4.2. Tooth susceptibility

The reaction of a tooth to the occlusal stresses set up under

occlusal loading may also be influenced by factors other than

the load itself. Cervical enamel is held to be of a poorer quality

than occlusal enamel with a greater pore volume, higher

protein content and lower mineral content. This is particularly

true of the subsurface enamel. Hammadeh and Rees31 carried

out a study to compare the erosive susceptibility of gingival

and occlusal enamel and to see if the subsurface layer was

more vulnerable to acid attack.31 They found that all samples

showed a linear loss of substance but although the rate varied

it was felt to be more to do with biological variation from

individual to individual than variation within the tooth

structure. It was considered possible that the porosity of the

cervical region was reduced by a process of post-eruption

maturation. The study concluded that it could only provide

limited support for the hypothesis that abfraction lesions may

be linked to acid erosion but went on to say that as dentine is

more easily eroded than enamel its loss could undermine

cervical enamel and hence contribute to increased enamel

failure under loading.

The same authors went on to publish a paper which was a

finite element study looking at the undermining of enamel as a

mechanism for abfraction lesion formation.32 They compared

maximum principal stresses along a buccal horizontal

sampling plane 1.1 mm above the cement enamel junction

in intact teeth and in teeth which had had an undermining

discontinuity introduced between the cervical enamel and

dentine. The discontinuity caused a dramatic rise in the

numerical value of the maximum principal stresses recorded

and in many instances these exceeded the known failure

stress for enamel. This study would seem to indicate that

lesions may be initiated by loss of cervical dentine following

gingival recession which then undermines the enamel

predisposing to mechanical failure and for the subsequent

tooth substance loss.

4.3. Other possible theories

A further possible source of disruption to the structure of the

tooth in the cervical region is the existence of electric

potentials which arise when some materials are put under

stress. This phenomenon, known as a piezo-electrical effect

was first recorded by Braden et al.33 They suspected that

although enamel, which is principally hydroxyapatite did not

give rise to any electrical potential, dentine did. This is thought

to arise from the presence of collagen in dentine and was of a

similar value to that recorded for bone. It is possible that the

bending forces arising during bruxism would be sufficient to

create a significant charge within the tooth structure and it is

postulated that this could attract active ions of, for example,

erosive agents such as organic acids and contribute to tooth

substance loss. However, the electrical response did not vary

linearly with stress so heavy occlusal loading would not give

rise to a proportionately greater electrical response and any

possible significance of this effect is not well understood.

The role of saliva in the possible formation of NCCTSL has

been considered previously. Black1 wondered whether a

possible cause of erosions might be secretions from diseased

salivary glands and Zipkin and McLure19 carried out experi-

ments to assess the amount of citrate present in saliva of

patients who had been diagnosed with erosions and compared

it to levels in a group without erosions.1,19 Their results were

not conclusive but indicated a trend of higher citric acid

content in individuals with erosions than in those without.

More recently the role of saliva has come to be thought of as

protective to the dental tissues. Levitch et al.11 stated that

patients with low unstimulated salivary flow rates are five

times more prone to cervical lesions than those with normal

flow rates and patients with xerostomia and reduced buffering

capacity are also more prone to developing lesions.11 They also

considered that the ability of saliva to remineralise tooth

structure could be important.

Khan et al.20 called in to question the idea that occlusal

loading should be considered the primary aetiological factor in

the formation of NCCTSL and proposed instead a theory of site

specific erosion.20 They concluded that occlusal erosion is as

common in bruxists as attrition is and postulated that patient

dehydration reduces salivary protection against erosion and

suggested that acid demineralisation is not only the primary

cause of the cupped lesions of erosion but also of attritional

wear facet development. In contrast to this the theory of

abfraction postulates that occlusal strains caused during

attrition are transmitted to the cervical sites causing direct

breakdown. Their study found that 96.2% of NCCTSL were

found on teeth that showed signs of either erosion or attrition

on their incisal or occlusal surfaces. Interestingly 5.2% of the

NCCTSL occurred on teeth with no occlusal wear. More lesions

were found on mandibular premolars than mandibular

canines despite the fact that less premolars had occlusal

wear and unlike Radentz in common with other studies more

wedge-shaped lesions were found on the left than on the right

side of the mouth. No consistent association was found

between either attrition and or erosion and cervical wedge-

shaped lesions in the canines or premolars.

The hypothesis of site specificity is explained in terms of

salivary physiology. The labial surfaces of the maxillary teeth


are more prone to attack because the teeth tend to dry out

during breathing and the minor labial salivary glands do not

have good buffering capabilities. The lingual surfaces of the

mandibular teeth are protected by the secretions of the

sublingual salivary glands and only a few wedge-shaped

lesions (2%) were found in this area of the mouth. The authors

were however unable to explain why the mandibular

premolars and molars are less protected from occlusal erosion

and associated buccal cervical lesions.

They concluded that a hypothesis that wedge-shaped

lesions arise primarily due to the occlusal forces responsible

for attrition was unsustainable and the primary aetiology

should be regarded as being acid demineralisation at sites

unprotected by saliva, possibly involving stress corrosion as a

pathogenic mechanism or abrasion related to right- or left-

handed tooth brushing.

4.4. Experimental evidence

Whitehead et al.34 described an experiment to investigate the

effect of stress corrosion on intact enamel.34 An incidental

finding of this experiment was that 8% of the teeth subjected

to a combination of acid and cervical stress developed cervical

notch lesions. The low rate of occurrence lends weight to the

feeling that the development of this type of lesion is multi-

factorial and that not all factors are yet understood.

5. Treatment

One of the consequences of the unclear aetiology and

diagnosis of NCCTSL is a confused approach to clinical

management. Bader et al.35 reported this to be an area of

great professional uncertainty with no agreement between

practitioners on how to describe lesions or their aetiology.35

Even root caries did not have 100% agreement. The options

considered for restoration were:

� N
othing.
� R
estoration.
� R
estoration with occlusal adjustment.
The response to their survey showed 38% of practitioners

would restore a lesion they described as abrasion, 47% would

restore a lesion they described as an erosion and 49% would

restore a lesion they describe as ‘‘other’’ and is now commonly

called abfraction. Ninety nine percent would restore a root

caries lesion. The level of variation in treatment options was

almost a perfect split and indicated a maximum level of

disagreement.

Owen and Gallien36 suggested that active treatment is

required to prevent further stress concentration occurring

which may lead to pulpal exposure or tooth fracture.36 Grippo5

was strongly in favour of restoring these lesions and listed 19

reasons for doing so, ranging from decreasing the stress

concentration to enhancing the patients feeling of complete-

ness as listed below5:

� D
ecreases stress concentration.
� D
ecreases flexure.
� D
ecreases the progress of the abfraction.
� S
trengthens the tooth.
� P
revents pulp involvement.
� E
liminates acid dissolution or corrosion.
� P
revents tooth fracture.
� E
liminates stress corrosion.
� M
oderates the effects of piezo-electricity.
� P
revents root caries.
� P
revents toothbrushing abrasion.
� E
liminates cervical sensitivity.
� P
rovides comfort to the adjacent soft tissues.
� Im
proves aesthetics.
� P
rovides an area that is more easily cleaned by the hygienist.
� P
revents food collecting in these areas.
� Im
proves gingival health by providing food deflection.
� E
ases oral hygiene for the patient.
� P
rovides the patient with a feeling of good health or
completeness.

A contradiction which emerges from Grippo’s philosophy is

that the placement of resin composite restorations is

recommended to prevent tooth flexure. In contrast he records

a high rate of restoration loss which is thought to be due to

heavy functional loading forces causing further tooth flexure.

Braem et al.37 in their article on stress induced cervical

lesions, also pointed out that any restoration placed in one of

these lesions would be prey to the stresses and strains which

had caused it in the first place and therefore would make it

more likely to fail.37

Levitch et al.11 gave a list of indications which they felt

necessitated active treatment.11 They were:

� If
the structural integrity of the tooth is threatened.
� If
exposed dentine is hypersensitive.
� If
the aesthetics are unacceptable.
� If
pulpal exposure is likely.
� If
tooth shape modification is necessary to allow partial
denture design.

This is a very reasonable list of clinical situations requiring

intervention but does not go into detail of what treatment is

suggested.

Spranger38 described the genesis of angular NCCTSL and

went on to postulate that normal tooth to tooth contacts are

protected by the body’s proprioceptive mechanisms but these

are overridden by parafunctional activity which results in

excessive forces arising when eccentric loads occur on the

non-working side.38 The author’s conclusion was that occlusal

adjustment should be undertaken prophylactically to inter-

rupt the pathogeneic process along with the placement of a

resin composite restorations to resist the tensile and com-

pressive forces coupled with the use of bite guards if

necessary. However, there is no clinical evidence to sub-

stantiate this conclusion.

The advent of reliable dentine adhesive systems and

adhesive materials has increased the options available to

restore NCCTSL. Prior to this, practitioners were faced with

treating a loss of tooth substance by removing more tooth

substance to try and create a retentive preparation. Heyman


et al.39 in a study to examine the effects of tooth flexure on

restoration retention found that microfilled resins were better

retained than macrofilled resins, possibly due to their greater

flexibility, but that patients rated as having active bruxism had

statistically higher rates of restoration loss.39 No occlusal

adjustments had been carried out. A recent study by Carre and

Brunton40 of restoration retention rates for cervical lesions in

occlusally adjusted and non-adjusted teeth did not, however,

show a statistically significant difference between the two

groups, which suggests that occlusal adjustment is ineffective

as a means of prolonging retention of cervical restorations.

6. Discussion

The small number of prevalence studies suffer from several

limitations not least that the lesions are ill defined, some of the

studies have studied a small population and different studies

have classified lesions in a different way. The picture is further

complicated by the wide number of variables within a

population and even within a given individual mouth over a

period of time. It is therefore not surprising that a confusing

and unclear picture emerges from the accumulated preva-

lence data. Despite these limitations it is clear however that

the older the population the greater the percentage of lesions

found, the greater the number of lesions per individual and the

larger the lesions. This raises two important points namely

can this lesions be prevented or their progress arrested at an

earlier age with a view to preventing a future treatment need?

It would seem that when the intraoral distribution of

NNCTSLs is considered as with their prevalence in the general

population, that an unclear picture emerges where limited

conclusions can be drawn. This is possibly also related to the

confusing terminologies and variable diagnoses which have

been used in different studies at different times.

There appears to be no doubt that occlusal forces are

implicated in the formation of the majority of lesions. Whilst

this cannot explain the aetiology of all lesions, e.g. lingual

wedge-shaped lesions and isolated lesions in otherwise

healthy mouths which have never had an opposing occlusion

it seems to be a common factor that has been highlighted as a

probable cause in the majority of studies of lesions of this type.

This is reinforced by the fact that potentially destructive

tensile stresses do occur in the cervical regions of teeth due to

occlusal loading and the observation that eccentric loading

causes greater stresses than axial loads.

Other theories which have been postulated in relation to

lesion formation include the role of saliva, the site specificity

hypothesis, a possible association with a piezo-electrical

effect and experimental evidence of lesion formation when

teeth are subjected to vertical barrelling in an acidic environ-

ment. There is little or no evidence to support or refute these

theories and therefore it must be concluded that further

research is needed to establish the precise role, if any, of these

aetiological factors in lesion formation.

In terms of treatment for lesions, when operative inter-

vention is indicated, the situation is equally unclear which is a

direct reflection of the confusion around the aetiology of lesion

formation. This is supported by the conclusions of Bader

et al.’s study35 where practitioners showed considerable

confusion and variation in treatment planning for these

lesions. The reasons for restoration are generally accepted to

be similar to the list of indications proposed by Levitch et al.11

Poor retention rates for resin composite restorations placed in

such lesions are likely to be explained by continued tooth

flexure but also the modulus of elasticity of the material which

can make it unsuitable for the restoration of these lesions.

Further robust studies are required to investigate the ideal

material for restorations of lesions of this type.

Adjusting the occlusion to prevent lesion progression or to

improve the retention of restorations cannot be supported as

there is no evidence that occlusal adjustment is helpful in

terms of slowing down lesion formation or improving the

retention of restorations when placed to restore lesions of this

type. This suggests however that occlusal forces whilst

implicated in the formation of most lesions cannot be the

single aetiological factor in lesion formation.

7. Conclusions

Despite the paucity of research in this area, a number of

conclusions can be drawn:

1. T
he older the population the greater the percentage of
lesions found, the greater the number of lesions per

individual and the larger the lesions.

2. N
CCTSLs are more common on the facial aspects of teeth
than the lingual, more common in premolars than canines,

and it would seem more common in the buccal segments of

the mouth than in the labial.

3. O
ral hygiene habits, and the right or left-handedness of the
patient when tooth brushing, affects the prevalence and

distribution of NCCTSL.

4. T
he formation of NCCTSL appears to be multifactorial. The
shape of a cervical lesion is not an accurate guide to its

aetiology.

5. A
combination of occlusal load and an acid environment
can create cervical notch lesions in vitro.

6. T
he use of a resin composite with an appropriate modulus
of elasticity in conjunction with a dentine adhesive system

can be an effective and non-destructive means of restoring

NCCTSL.

7. O
cclusal adjustment cannot be supported to prevent lesion
progression or to improve restoration retention.

r e f e r e n c e s

1. Black GV. A work on operative dentistry, vol. 1. Chicago:Medico-Dental Pub. Co; 1908. 39–59.

2. Miller WD. Experiments and observations on the wasting oftooth tissue variously designated as erosion, abrasion,chemical abrasion, denudation etc. Dental Cosmos 1907;XLIXNo. 1:123; XLIX No. 2:109–124; XLIX No. 3:225–247.

3. Ferrier WI. Clinical observations on erosions and theirrestoration. Journal of the California State Dental Association1931;7:187–96.

4. Kornfeld B. Preliminary report of clinical observations ofcervical erosions, a suggested analysis of the cause and thetreatment for its relief. Dental Items of Interest 1932;54:905–9.


5. Grippo JO. Non-carious cervical lesions: the decision toignore or restore. Journal of Esthetic Dentistry 1992;4:155–64.

6. Lee WC, Eakle WS. Possible role of tensile stress in theetiology of cervical erosive lesions of teeth. Journal ofProsthetic Dentistry 1984;52:374–9.

7. Grippo JO. Abfractions: a new classification of hard tissuelesions of teeth. Journal of Esthetic Dentistry 1991;3:14–9.

8. Lambert RL, Lindenmuth JS. Abfraction—a new name for anold entity. Journal of the Colorado Dental Association1994;73:31–3.

9. Shulman EH, Robinson HG. Salivary citrate content anderosion of teeth. Journal of Dental Research 1948;27:541–4.

10. Bergstrom J, Eliasson S. Cervical abrasion in relation totoothbrushing and periodontal health. Scandinavian Journalof Dental Research 1988;96:405–11.

11. Levitch LC, Bader JD, Shugars DA, Heymann HO. Non-carious cervical lesions. Journal of Dentistry 1994;22:195–207.

12. Radentz WH, Barnes GP, Cutright DE. A survey of factorspossibly associated with cervical abrasion of tooth surfaces.Journal of Periodontology 1976;47:210–3.

13. Xhonga FA. Bruxism and its effect on the teeth. Journal ofOral Rehabilitation 1977;4:65–76.

14. Graehn G, Berndt C, Staege B. Zur Epidemiologie keilformigeDefekte. Deutsche Stomatologie 1991;41:210–3.

15. Rees JS. A review of the biomechanics of abfraction.European Journal of Prosthodontics and Restorative Dentistry2000;8:139–44.

16. Rees JS, Hammadeh M, Jagger DC. Abfraction lesionformation in maxillary incisors, canines and premolars: afinite element study. European Journal of Oral Sciences2003;111:149–54.

17. Rees JS. Biomechanics of abfraction. Personal communication;2004.

18. Sognnaes RF, Wolcott RB, Xhonga FA. Dental erosion. Journalof the American Dental Association 1972;84.

19. Zipkin I, McLure FJ. Salivary citrate and dental erosion.Journal of Dental Research 1949;28:613–26.

20. Khan F, Young WG, Shahabi S, Daley TJ. Dental cervicallesions associated with occlusal erosion and attrition.Australian Dental Journal 1999;44:176–86.

21. Pegoraro LF, Yelles DM, Pereira JC. Prevalence of non-carious cervical lesions in dental students and itsrelationship to occlusal aspects. Journal of Dental Research1999;78:474. (Abstract 2945).

22. Thresher RW, Saito GE. The stress analysis of human teeth.Journal of Biomechanics 1973;6:443–9.

23. Selna LG, Shillingburg HT, Kerr PA. Finite element analysisof dental structures—axisymmetric and plane stressidealizations. Journal of Biomedical Materials Research1975;9:237.

24. Yettram AL, Wright KWJ, Pickard HM. Finite element stressanalysis of the crowns of normal and restored teeth. Journalof Dental Research 1976;55:1004–11.

25. Picton DCA. On the part played by the socket in toothsupport. Archives of Oral Biology 1965;10:945–55.

26. Goel VK, Khera SC, Ralston JL, Chang KH. Stresses at thedentino-enamel junction of human teeth—a finite elementinvestigation. Journal of Prosthetic Dentistry 1991;66:451–9.

27. Spears IR. A three-dimensional finite element model ofprismatic enamel: a re-appraisal of the data on the Young’sModulus of enamel. Journal of Dental Research 1997;76:1690–7.

28. Rees JS. The role of cuspal flexure in the development ofabfraction lesions: a finite element study. European Journal ofOral Sciences 1998;106:1028–932.

29. Chen KK, Miyake K, Terashita M. Cervical strains induced byocclusal loading. Journal of Dental Research 1999;78:474.(Abstract 2947).

30. Nohl FS, McCabe JF, Walls AWG. The effect of load angle onstrains induced in maxillary premolars in vitro. Journal ofDental Research 1999;78:1059. (Abstract 200).

31. Hammadeh M, Rees JS. The erosive susceptibility of cervicalversus occlusal enamel. European Journal of Prosthodontics andRestorative Dentistry 2001;9:13–7.

32. Rees JS, Hammadeh M. Undermining of enamel asmechanism of abfraction lesion formation: a finite elementstudy. European Journal of Oral Sciences 2004;112:347–52.

33. Braden M, Bairstow AG, Beider I, Ritter BJ. Electrical andpiezo-electrical properties of dental hard tissues. Nature1966;212:1565–6.

34. Whitehead SA, Wilson NHF, Watts DC. Development of non-carious cervical notch lesions in vitro. Journal of EstheticDentistry 1999;11:332–7.

35. Bader JD, Levitch LC, Shugars DA, Heymann HO, McClure F.How dentists classified and treated non-carious cervicallesions. Journal of the American Dental Association 1993;124:46–54.

36. Owen BM, Gallien GS. Non-carious dental abfraction lesionsin an aging population. Compendium of Continuing Education inDentistry 1995;16:552. 554, 557, 558.

37. Braem M, Lambrechts P, Vanherle G. Stress-induced cervicallesions. Journal of Prosthetic Dentistry 1992;67:718–22.

38. Spranger H. Investigation into the genesis of angular lesionsat the cervical region of the teeth. Quintessence International1995;26:149–54.

39. Heyman HO, Sturdevant JR, Bayne S, Wilder AD, Sluder TB,Brunson WD. Examining tooth flexure effects on cervicalrestorations. Journal of the American Dental Association1991;122:41–7.

40. Carre C, Brunton PA. A study of occlusal factors in relation to therestoration of non-carious cervical lesions with resin composite.MPhil thesis. University of Manchester; 2003.

non-carious cervical tooth surface loss: a literature review

Documents