Abfraction Lesions Where Do They Come From?

A Review of the Literature

John R. Antonelli, D.D.S., M.S., Timothy L. Hottel, D.D.S., M.S., M.B.A.,
Franklin Garcia-Godoy, D.D.S., M.S., Ph.D., Ph.D.
Introduction
Eccentric occlusal loading and
the subsequent flexing of teeth have
been cited as generating tensile
forces resulting in the breakdown of
enamel prisms in the form of noncarious cervical lesions (NCCLs).1,2
Non-carious cervical lesions are
characterized by the wedge-shaped
loss of hard tissue, predominantly
on the buccal or facial surfaces,
regardless of the teeth affected,
close to the cemento-enamel
junction (CEJ).3 In 1991, Grippo
coined the term abfraction as a new
classification of cervical lesions caused
by biomechanical loading forces, to
distinguish it from erosion and abrasion.4
During eccentric loading, flexing stresses
throughout the tooth produce tension on
one side and compression on the other in
the area of the fulcra, generally located at
or near the CEJ.1 The result over time is
the formation of a NCCL. Non-carious
cervical lesions are more commonly
associated with the loss of enamel;
exposure of dentin occurs much less
frequently, ranging between 2 and 6%.3
During parafunction, patients are

EXAM #43

ABSTRACT
The theory of non-carious cervical lesions (NCCLs) suggests that tooth
flexure arising from cyclic, eccentric occlusal forces causes their formation
and progression in vulnerable cervical regions of teeth. The etiology is still
controversial. Attrition, corrosion, abrasion and stress-corrosion might act alone
or in combination to initiate and perpetuate lesions. This review of the literature
provides the basis for the diagnosis that can be used in consideration of treatment
options.

capable of applying eccentric occlusal

loads of approximately 225 lbs. In an
exceptional case, a bite force of 443 kg
(975 lbs.) was recorded.5 To add to these
increased loads, total tooth contact time
for bruxers was found to range from
30 minutes to three hours in a 24-hour
period. Total tooth contact time for
non-bruxers was approximately ten
minutes.6 Working excursions were found
to produce cuspal deflections on the
order of 200 to 400 m compared with
deflections of only 20 m with centric
occlusion forces.7 Short-term, intermittent
vertical occlusal loads generally do not
produce pathologic effects as pulpal and

proprioceptive stimuli act to limit contact

forces. In bruxers, however, occlusal
contacts may be traumatic as they last
longer, are more frequent and occur in a
long stroke against cuspal inclines; the
magnitude of occlusal loading and cuspal
deflection are greatest toward the end of
a lateral excursion of the mandible. These
horizontal forces induce both tensile
and compressive stresses in the cervical
area, which might explain the higher
prevalence of NCCLs among bruxers.2,8-15
For example, in a study of occlusion in 91
university students, nearly two-thirds of
all NCCLs were found in sleep bruxers,
where lesions were nine times more

Figure 2

| Continuing Education Exam #43

Figure 1

T
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A

14

Journal of the Tennessee Dental Association 93-1

indicated that the teeth flexed within their

proportional limits.26
Seven finite element studies showed
that when vertical and parafunctional
contact loadsin the range of 170-250
N (38-56 lbs., or one-third to one-half of
maximum biting force)were applied
to premolar teeth, increased tensile
and shear stresses were recorded at or
near the CEJ.12,14,27-31 In a finite element
study, Rees and Hammadeh32 created
models of a maxillary central incisor,
canine and first premolar with an intact
DEJ and compared maximum principal
stress (MPS) concentrations generated
in enamel, 1.1 mm above the CEJ, with
identical tooth models showing varying
degrees of undermining in the cervical
DEJ. Incisal and occlusal loads of 100

Seventy-five
percent of retention
failures of Class V
bonded composite
restorations have
been attributed to
bruxism and/or other
forms of stressful
occlusion.
N (normal force), angled at 45 degrees,
were applied to the teeth. Maximum
stress levels were measured along a
labial/buccal horizontal plane in both
intact teeth and teeth in which defects
of varying vertical heights were created
at the cervical DEJ. At normal chewing
loads of 100 N, even the smallest cervical
defects resulted in a dramatic increase
in MPS in cervical enamela defect
height of only 0.37 mm was found to
produce MPS levels that exceeded the
failure stress level for enamel (80 MPa)
in all tooth types. When intact teeth were
subjected to normal loads, MPS levels
were well below the critical failure stress
value. When 100 N was applied to an

intact incisor, the highest MPS level (30.3

MPa) was registered at the cervical DEJ.
However, some bruxers can exert loads of
up to 1000 N; therefore, if one multiplies
the MPS value by 10, the stress value for
the incisor increases to approximately
300 MPa, well above the failure value for
enamel in an intact tooth.
Coronal cavity preparation was shown
to concentrate additional stress in the
region of the CEJ because of increased
cuspal flexing.12,23,27-31 In MOD cavity
preparations, cusps become cantilever
beams that deflect in response to occlusal
loading. As cavity preparation depths
increase, longer cantilever beams are
created. Deflection varies as the cube
of the length of the beam; therefore,
if the height of the cusp doubles as
the preparation deepens, then cuspal
deflection increases by a factor of eight.33
Rees12 found that peak tensile and shear
stresses were greatest along the cervical
plane farthest from the occlusal loading
point (0.3 mm above the CEJ), because
of the greater lever arm. Rees and
Jacobson34 applied loads of identical
magnitude and location to caries-free
mandibular premolars for which Class
V cavity preparations were prepared.
When occlusal cavity preparations
were added, stress forces around the
periphery of the Class V preparations
were magnified as the depth of the
occlusal preparations were increased.
Seventy-five percent of retention failures
of Class V bonded composite restorations
have been attributed to bruxism and/
or other forms of stressful occlusion.25
Stereomicroscopic photographs showed
evidence of cervical hydroxyapatite
crystal disruption resulting from tensile
stresses generated by mastication and
bruxism; the researchers maintained that
cervical debonding and leakage can result
when Class V restorations are subjected to
the same tensile forces that cause lateral
deformation of teeth.35 Also, compression
resulting from the barreling effect on a
tooth during centric loading might result
in retention failure through a squeezing
effect on the restoration.25,36 These
investigations strongly suggest a causal
relationship between axial and eccentric
occlusal forces and the formation on
NCCLs in teeth.
In one study of 50 extracted human
teeth, the margins of all NCCLs were

93-1 Abfraction Lesions Where Do They Come From? A Review of the Literature

Continuing Education Exam #43 |

prevalent than in the mouths of healthy

control subjects.15 The occlusal stress
theory postulates that the biomechanical
effects of eccentric, cyclic occlusal
loading are the principal factors that
initiate the formation of NCCLs.
Photoelastic studies, which provide
a visual display for the observation
and measurement of stress distribution
throughout tooth models, confirm that
when cusps are loaded obliquely, most
stresses are concentrated in cervical
areas.16-18 When loads were applied to
maxillary premolarsthe teeth most
frequently involved with NCCLs
moments of force were produced around
the centers of resistance (i.e., the alveolar
crest levels), which led to tooth flexing.
As the distance between buccal cusps
and their centers of resistance are longer
than that of lingual cusps, the same
amount of force applied to the cusps was
found to produce greater cervical stress
concentrations on the buccal sides, which
might explain the greater prevalence of
buccal side NCCLs.6
Buccal class V cavity preparations
made in maxillary first premolars and
central incisors exhibited changes in
cervical-occlusal dimension when the
teeth were subjected to occlusal/incisal
loading. Photographic evidence showed
that increasing occlusal loading was
responsible for changes in the occlusalcervical width of the Class V preparation
margins and the subsequent extrusion
of amalgam restorations. This suggests
that occlusion could play a major role in
the formation of NCCLs. Tensile stress,
generated by eccentric occlusal forces
during normal function and parafunction,
was found to be responsible for the
disruption of enamel bonds between
hydroxyapatite crystals and the eventual
separation of enamel from dentin.12,19-24
Heymann et al.,25 proposed that heavy
centric forces might generate compressive
stresses and vertical deformation of the
tooth (a barreling effect), which could lead
to cervical tooth flexure. The ability of
occlusal loads to initiate NCCLs through
tooth deformation was further validated in
an in vivo study, where miniature strain
gauges were bonded to cervical areas on
the labial surfaces of maxillary incisors
in healthy subjects. Large surface
compressive and tensile strains were
recorded in the cervical regions, which

15

| Continuing Education Exam #43

16

located below the CEJ, extending from the

CEJ to root surface, with all enamel above
the CEJ intact.37 The authors concluded
that without the loss of cervical enamel,
there was insufficient evidence to support
the theory of NCCLs based on tooth
flexure. They cited erosion and abrasion as
the primary factors responsible for lesion
development. However, the location of
lesions on root surfaces is frequently
associated with gingival recession or loss
of attachment, either concurrent with or
prior to NCCL formation. Kuroe et al.,17
showed that with decreasing periodontal
support, stress concentration was shifted
away from the CEJ and toward apical
dentin. Non-carious cervical lesions have
been reported in 20.4% of the mouths
of subjects with periodontitis.38 An
epidemiological evaluation determined
that 77% of teeth with lesions showed
recession on the buccal aspects.39 In a
veterinary study, lesions were reported in
virtually all cats with plaque and various
levels of gingivitis and/or periodontitis.40
The level of supporting alveolar bone,
the orientation of forces (occlusal versus
oblique), and the location of occlusal
contacts will ultimately determine the
shape and position of NCCLs. For
example, as occlusal tooth morphology
is irregular, with asymmetric points of
loading, lesions may be asymmetrically
located on the buccal surface, angled
either toward the mesial or distal.41
Therefore, to discount tooth flexure as
an important factor in the genesis of
lesions, based solely on lesion location,
seems premature. It is more likely that
the pathologic mechanism involves stress
corrosion and acid demineralization
acting concurrently on relatively
unprotected tooth sites.21
Recently, laser scanning microscopy
provided additional evidence to support
the theory that hyperfunction or
malocclusion plays a role in the formation
of microfractures in enamel and dentin
at the CEJ.42 In a study of 309 teeth
with NCCLs, the greatest association
(94.5%) was the coexistence with wear
facets; 77% of the lesions were found
in patients lacking canine disocclusion
and 73.5% of the teeth with lesions
were in group function (GF); balancing
side prematurities were associated with
20% of the lesions.38 An early scanning
electron microscopic study of cervical

lesions, which placed heavy emphasis on

occlusal loading in their pathogenesis,
determined that two mechanisms of action
were responsible for cervical corrosion:
occlusal stress was associated with
wedge-shaped lesions, which comprised
68% of the samples examined, and
rounded formsassociated with physical
abrasioncomprised the remainder.43
Occlusal loading may have a
fundamental role in the initiation of
NCCLs; however, its role may not be
central to their eventual formation.14
The degree to which occlusal loading
and tooth flexure influence the
formation and propagation of NCCLs is
unknown. The pathogenesis of NCCLs
is considered to be multifactorial, with
occlusal loading, corrosion and abrasion
acting synergistically rather than in

The pathogenesis of
NCCLs is considered
to be multifactorial,
with occlusal
loading, corrosion
and abrasion acting
synergistically rather
than in isolation.
isolation.37,44-46 Dental erosion, as defined
by Imfeld44 and Grippo,47 is the painless
loss of solid tooth surface primarily by
acid, without bacterial involvement. The
loss of substrate in erosion is a physical
process involving the flow of a substance
by a stream of liquid or gas, with or
without solid particles. As no forceful
stream of liquid occurs in the mouth to
produce enough friction to cause tooth
surface loss, Grippo et al.,48 subsequently
proposed deleting the term erosion from
the dental nomenclature in favor of the
more appropriate term corrosion to denote
the chemical dissolution of teeth. They
proposed several combined mechanisms
to explain tooth wear, which included
attrition-abfraction, abrasion-abfraction,

corrosion-abfraction and biocorrosion

(caries)-abfraction; however, the relative
contributions of the various processes
remain unclear.45
Some investigators believe that the loss
of cervical enamel and dentin, and the
subsequent formation of NCCLs, might
be influenced by factors other than cuspal
flexure from mechanical overloading.
An analysis of the composition of dental
enamel revealed great variability in
the mineral and protein content of the
surface and subsurface; very high mineral
contents were detected at the surface
and very low values were found near the
dentinoenamel junction (DEJ).49 Lower
mineral contents and greater pore volumes
were generally detected in cervical
enamel, which might make enamel in this
region more prone to demineralization
than occlusal enamel.50 Microscopic
studies have detected enhanced porosity
in cervical enamel compared with
enamel in other areas.51,52 Rees suggested
that erosive agents could enter enamel
through internal pore channels to weaken
cervical enamel, thereby contributing
to the development of NCCLs.22 Despite
the greater porosity of cervical enamel,
it was determined that the post-eruptive
influences of saliva and crevicular fluid
minimize potential lesion formation
and make it unlikely that differences in
enamel solubility from different regions
of the crown account for why the majority
of cervical lesions appear on the labial and
buccal surfaces.53 The rarity of NCCLs
on the lingual surfaces of teeth might be
attributed to a greater flow of saliva and
greater clearance of acidic substances
along lingual tooth sites than along buccal
sites, and the protection afforded by the
tongue and the pooling of saliva in the
floor of the mouth that results in greater
opportunities for remineralization.
When human premolars were
subjected to an acid environment that
mimicked weak acid in plaque (pH
4.5) and to cyclic loads of 100 N at
frequencies equivalent to 2.4 and 6
months of chewing, pitting and cracking
was observed in the cervical enamel of
loaded specimens, with exposure of the
underlying enamel.54 By contrast, uniform
dissolution of cervical enamel at the CEJ
was noted in unloaded specimens. Mean
volumetric loss of enamel in the cervical
thirds of areas subjected to tensile

Journal of the Tennessee Dental Association 93-1

freshman college students and reported

a prevalence of only 2%. Brady and
Woody43 examined 900 dentists and
reported 5.3% with lesions. Bernhardt
et al.,39 examined 2,707 subjects (mean
age 40.6 11.1 years) and reported
a prevalence of 24.7%. According
to Estafan et al.,57 prevalence among
dental students (mean age 28.9) was
33.1%. Khan et al.,11 found 49% of
dental patients (mean age 33.46 years)
with NCCLs. A much higher occurrence
(85%) was reported among 250 subjects
examined by Bergstrom and Eliasson,58
where ages ranged from 2160 years.
Recently, an anthropological study of
NCCLs examined 3,927 teeth from 259
individuals from the Copper and Middle

A recent study of
2,849 maxillary and
mandibular incisors,
canines, premolars
and molars reported
maxillary and
mandibular first
premolars most
frequently affected
by NCCLs.
Ages and 6,145 teeth from 238 modern
subjects.59 The most remarkable finding
was the absence of NCCLs in the large
sample of skeletons from prehistoric
and Medieval remains, compared with
a prevalence of 26% among modern
subjects from the same geographic area,
perhaps attributable to a much shorter life
span in prehistoric man.
The prevalence of NCCLs within the
dentition is well documented. A recent
study of 2,849 maxillary and mandibular
incisors, canines, premolars and molars
reported maxillary and mandibular first
premolars most frequently affected by
NCCLs.39 Maxillary and mandibular

second premolars and canines were the

second and third most frequently affected,
respectively. The data showed a nearly
equal distribution of lesions among the
maxillary and mandibular teeth. In
another study, maxillary posterior teeth
appeared more prone to NCCLs, and first
premolars had the highest prevalence
followed by first molars, second premolars
and canines.60 Unfortunately, investigative
methods and sample criteria vary, making
it difficult to correlate results.
All studies that sorted patients into
multiple age groupings reported that the
prevalence of NCCLs increased with
increasing age.39,60-63 Crazing and vertical
microfracturing may be more common
in older enamel, resulting in a loss of
rigidity and a greater propensity for
lesion formation. The age phenomenon
observed may be secondary to greater
occlusal stress as tensile stresses created
during tooth flexure disrupt chemical
bonds between hydroxyapatite crystals.21
Older subjects who lack canine guidance
as a result of tooth wear may be the
victims of greater occlusal stresses
produced by lateral forces transmitted
to posterior teeth, which may lead to the
development of NCCLs. Older patients
with multiple missing teeth may have a
higher incidence of lesions as remaining
teeth bear greater occlusal loads and are
subjected to greater stresses.36 A higher
incidence of dry mouth and diminished
quality and buffering capacity of saliva
among older subjects might play a role
in the prevalence of NCCLs within this
population.60,64,65
A 6-year study of risk factors for
NCCLs found age and toothbrushing
frequency to be the two most significant
risk factors for the progression of
NCCLs.65 In general, as age is associated
with longer periods of toothbrushing,
reduced periodontal attachment and
greater exposure of vulnerable root
surfaces to acid attack, it is considered
to be directly associated with increased
incidences of NCCLs. Unfortunately, the
study did not assess the role of occlusal
stress in lesion formation or progression.
Bergstrom et al.,62 uncovered the
strongest associations between NCCLs
and brushing technique (58% of lesions
were linked with horizontal brushing)
and brushing frequency (more than 69%
of subjects who brushed at least twice

93-1 Abfraction Lesions Where Do They Come From? A Review of the Literature

Continuing Education Exam #43 |

stresses and an acid environment was

2.5 times greater than areas in enamel
that were in compression. Volumetric
loss of cervical enamel in areas under
tension was 3.5 times greater than all
areas in the cervical third of unloaded
teeth. The loads applied experimentally
more closely resembled normal function.
Parafunctional loads would apply greater
and more irregular cycles of force and,
therefore, over many years the frequency
of cervical enamel loss would be greater.
In the acid environment, enamel was
eroded to depths of 50-200 m. Cervical
enamel subjected to prolonged cyclic
loads in an acid environment exhibited
significantly greater loss while in tension
than cervical areas in compression. These
studies provide additional data to support
the primary role of occlusal loading in the
destruction of cervical enamel and dentin.
Perikymata, which are elevations
between imbrication lines of Pickerill
in enamel, are continuous around teeth
and parallel to the CEJ and to each other.
Perikymata are more pronounced, and
more exposed cervically and become
shallower toward the incisal; therefore,
pitting in cervical perikymata predisposes
these areas to acid penetration. As
weaker mechanical bonds exist between
enamel and dentin cervically than in
other areas of the DEJ, the combined
structural and chemical differences
unique to cervical enamel may account
for its enhanced susceptibility to
cracking and, subsequently, to corrosion,
demineralization and lesion formation.54
Another intrinsic factor that could lead
to cervical tooth loss is the presence of a
concavity on the DEJ in the occlusal third
of functional (buccal) cusps of mandibular
premolars and molars and in the nonfunctional (buccal) cusps of maxillary
premolars and molars.55 Enamel thickness
abruptly decreases cervical to these
sites and their locations correspond to
areas where NCCLs are most commonly
located. When the contour of the
concavity in the DEJ was slightly altered
in a finite element model, the patterns of
stress in the cervical area was altered.28
These data inferred a strong association
between DEJ contour, stress patterns and
the development of NCCLs.
Reports about the prevalence of
NCCLs have varied widely. Shulman
and Robinson56 examined 1,345 male

17

| Continuing Education Exam #43

18

daily using a horizontal technique had

lesions). Bristle stiffness and abrasiveness
of dentifrice were weak. Other studies
found no significant relationship to link
toothbrushing frequency, technique,
toothbrush type or abrasiveness of
dentrifrice with NCCLs.3,38,58,62,66,67
Many lesions are found in patients who
are non-compliant with oral hygiene
recommendations.38 No data is available
to explain the presence of isolated lesions
in healthy mouths, lingual lesions that
are difficult to access with a toothbrush
or multiple lesions on the same tooth.
In a large sample of NCCLs, almost
33% were subgingival, which probably
excludes etiologic factors such as
toothbrushing, exogenous or endogenous
acids.38,68 Recently, non-carious cervicallike lesions at the CEJ were reported in
domestic cats.40,69 Thought to be caused
by chronic occlusal overload from a hard
diet and subsequent chipping away of
cervical enamel, the authors contended
that the evidence appeared to support the
occlusal theory of Lee and Eakle,2 which
maintained that teeth lacking protection
from canine guided disocclusion received
lateral forces that transmitted tensile
stress that led to development of cervical
erosive lesions. It is well-known that all
omnivores, including cats, share canine
guided protection.70 As toothbrushing
is not an issue in cats, toothbrushing
alone cannot explain the development of
NCCLs.
Many clinical studies that have
attempted to investigate the role of
occlusal stress in NCCL formation have
focused only on the presence or absence
of canine disocclusion, wear facets and/or
evidence of bruxism. In vitro studies that
have investigated the effect of eccentric
loads on cervical stress were inconclusive
as the loads applied were point rather
than sliding contacts in a variety of
directions.71 Most of the evidence
supporting the association between
occlusal stress and cervical lesions comes
mainly from finite element analysis
and laboratory studies. Direct data that
confirms this association clinically is
scarce. An exception was found recently
in a randomized controlled trial, in which
teeth with NCCLs and in group function
(GF) were tested to determine whether
or not selective occlusal adjustments to
reduce loading during working excursions

impacted on the rate of development

of lesions.72 Follow-up examinations
after 6, 18 and 30 months failed to show
statistically significant differences in the
rate of lesion progression between teeth
that were adjusted and those that were
not. The authors acknowledged that a
deficiency in their study was the inclusion
of only teeth that contacted in GF in
working excursions. Data supporting
a strong association between GF and
NCCLs are available.11,14,39,73 For example,
two studies ascertained that more than
60% of patients with NCCLs exhibited
GF.60,74 In a study of 111 patients recently
published in the Journal of Prosthetic
Dentistry, there was a strong relationship
between the presence of NCCLs and
occlusal loading.75 Unfortunately,
information to compare this data in
healthy subjects with controls is lacking.
An additional study is being conducted
by the authors using patients that exhibit
GF on one side and cuspid rise on the
other so that any NCCLs present have the
same patient as a control. This research
should be able to state, with some reason
of accuracy, what extent occlusion plays
in the formation of abfraction lesions the
common thread throughout the current
literature.
Disclosure. The authors did not report
any disclosures.
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John R. Antonelli, D.D.S., M.S., Professor,

Section of Prosthodontics; Director of Fixed
Prosthodontics Courses, Nova Southeastern
University, Ft. Lauderdale, Florida. Adjunct
Professor, Department of Prosthodontics,
College of Dentistry, University of Tennessee
Health Sciences Center, Memphis, Tennessee.
Timothy L. Hottel, D.D.S., M.S.,
M.B.A., Professor and Dean, Department
of Prosthodontics, College of Dentistry,
University of Tennessee Health Sciences
Center, Memphis, Tennessee. thottel@uthsc.
edu
Franklin Garcia-Godoy, D.D.S., M.S.,
Ph.D., Ph.D., Professor and Senior Executive
Associate Dean for Research; Chair,
Department of Bioscience Research; Director,
Bioscience Research Center, College of
Dentistry, University of Tennessee Health
Sciences Center, Memphis, Tennessee.

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movements on the progression of abfraction lesions. Oper Dent
2009;34(3):273-279.

Continuing Education Exam #43 |

93-1 Abfraction Lesions Where Do They Come From? A Review of the Literature

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