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Occlusal Caries: Pathology, Diagnosis and

Logical Management

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 C A R I O L O G Y C A R I O L O G Y

Occlusal Caries: Pathology, Diagnosis

and Logical Management
K.R. EKSTRAND, D.N.J. RICKETTS AND E.A.M. KIDD

realize, however, that diagnosis

Abstract: Occlusal caries now accounts for most of the lesions in children aged 8–15 precedes treatment planning. They are
years. This paper presents a ranked visual scoring system for occlusal caries diagnosis. not the same.
It relates the clinical appearance of the lesion to its activity, the level of infection of the
As far as carious lesions are concerned,
dentine and the histopathology. The appropriate management for each score is
suggested.
diagnosis implies deciding whether
demineralization is present, the depth of
Dent Update 2001; 28: 380-387 the lesion and whether it is progressing
rapidly or slowly (active caries) or whether
Clinical Relevance: Occlusal caries remains a problem for many young people. it is already arrested. Thus diagnosis is
This paper relates the chairside diagnosis of the lesion to its appropriate clinical
more than lesion detection: it should also
management.
consider lesion activity.

Why does this Terminology

Matter?

D ental caries is a dynamic process

taking place in the microbial
deposits on the tooth surface. It results
in a disturbance of the equilibrium
between the tooth surface and the
surrounding plaque fluid so that, over
time, the net result may be a loss of
mineral from the tooth surface.1 This
definition of dental caries has some
important implications:

Plaque formation cannot be totally
prevented even by toothbrushing.
These deposits are always
metabolically active. Thus plaque
formation is a physiological
phenomenon in an oral
environment.

Lesion formation reflects the
K.R. Ekstrand, DDS, PhD, Department of
Cariology and Endodontics, School of Dentistry,
Faculty of Health Sciences, University of
Copenhagen, Denmark, D.N.J. Ricketts, BDS, FDS
RCS (Eng.), PhD, MSc, Unit of Comprehensive
Restorative Care, Dundee Dental School, Dundee,
and E.A.M. Kidd, BDS, FDS RCS (Eng.), PhD,
Division of Conservative Dentistry, GKT Dental
Institute, Guy’s Hospital, London.
metabolic activity in the plaque.

At the crystal level the
demineralization and
remineralizations resulting from pH
fluctuations within the plaque fluid
cannot be prevented.

Thus the carious process itself
cannot be prevented; it is an
ubiquitous natural process.

The process can be active, rapidly
progressing, slowly progressing or
arrested.

The carious process is driven by
the activity of the plaque and
therefore modification of the plaque
will modify the process.

The disease can be controlled so
that lesion progression to the stage
of a white spot or frank cavity can
be prevented.
What is Diagnosis?
Diagnosis is a Greek-derived word
meaning decision. Diagnosis is not an
end in itself; it is a mental resting place
for prognostic considerations and
therapeutic decisions. It is important to
This distinction between detection and
diagnosis matters because the clinician
needs to know the activity of the lesion
in order to plan logical treatment. If the
lesion is active, preventive, and
possibly operative, treatment is
required to arrest lesion progression. If
the lesion is already arrested this would
be unnecessary.
EPIDEMIOLOGY
It is often said that occlusal pits,
fissures and grooves are particularly
susceptible to dental caries. Although
the caries experience of children aged
8–15 years has apparently declined,
studies have shown that occlusal caries
now accounts for the majority of
lesions in this age group.2–7
WHY DOES CARIES
APPEAR ON OCCLUSAL
SURFACES?
The dental tissues of the fissures and
grooves are not inherently caries-
prone. The surface is susceptible

380 Dental Update – October 2001


Figure 1. Microradiograph of a section
through a narrow fissure whose deeper part
would exclude a toothbrush bristle.
Demineralization is obvious on either side of
the fissure wall. The dotted line on the left-
hand side indicates the depth of the fissure
from its entrance (E) to its base (B). The
arrows divide the fissure into three equal
parts: outer, middle and bottom. The three
black lines on the right-hand side show the
depth of the lesion along the direction of the
enamel prisms in the entrance, middle and
bottom part of the fissure. The lesion is
deepest at the entrance to the fissure, where
metabolically active plaque is present.
because plaque is likely to remain
undisturbed in this area.
Owing to the minute dimensions of
the pits and fissures, a toothbrush
bristle cannot access the area to
disturb the micro-organisms. However,
there is evidence that the micro-
organisms in the deeper parts of the
narrow fissure may not be the major
players in lesion formation.8 Micro-
organisms in the upper parts of the
fissures and in the more open grooves
are metabolically active and lesion
progression rate is thus faster at the
entrance to the fissures than the
bottom part8 (Figures 1, 2). What really
matters as far as the patient is
concerned is that these areas can be
reached by a toothbrush. It is thus
potentially possible to access and
clean these fissure areas in just the
same way as a smooth surface. This is a
very important concept that has
implications for both diagnosis and
management of occlusal caries.
Dental Update – October 2001
C A R I O L O G Y
WHEN IS THE TOOTH MOST
SUSCEPTIBLE?
The tooth is most susceptible to
plaque stagnation during eruption.9
Molar teeth take some 12–18 months
to erupt and a 6- or even 12-year-old
child may need some help from a
parent to clean an erupting tooth
effectively. In contemporary
populations it is rare to see occlusal
caries on premolars. This may be due
to their short eruption time and their
accessibility to cleaning.
THE VISUAL APPEARANCE
OF OCCLUSAL CARIES
Since it has been shown that lesion
formation takes place in the plaque-
stagnation area at the entrance to the
fissure, it follows that the lesion should
be visible provided the plaque is
removed. A few years ago new visual
criteria for the detection of occlusal
caries were proposed.10 A ranked
scoring system was described (Table 1
and Figures 3–16) and a laboratory
study showed that this system was well
correlated with lesion depth as assessed
histologically.10
This means that a dentist, using this
visual system alone, will have a good
idea of the depth of the lesion
histologically.
Subsequent work extended the ranked
scoring system to differentiate active
from arrested lesions (Table 1).11 The
study was carried out on erupted
wisdom teeth destined for extraction.
This allowed the activity of the lesions
to be assessed both clinically and after
tooth extraction, thus validating the new
system.
A further investigation was carried
out to relate the ranked scoring system
to the level of infection of the dentine as
assessed using microbiological
culturing techniques (Table 1).12
When using this visual ranked
scoring system it is absolutely
essential that all plaque is cleaned from
the occlusal surface so that the dentist
can see the lesion clearly. This cleaning
should be preceded by disclosing so
that the dentist sees the plaque before
removing it with a brush. Figures 17
Figure 2. Microradiograph of a section
through a groove from the entrance (E) to the
base (B). The arrow divides the groove into
outer and bottom parts. The lines on the left,
following the direction of the enamel prisms,
indicate lesion depth and show similar depths
of lesion at the entrance and bottom part. This
is because grooves harbour metabolically
active plaque throughout their depth.
and 18 emphasize the importance of
this cleaning. The white spot lesion is
clearly visible in Figure 18 but
obscured by plaque in Figure 17. Notice
that in Figure 17 the tooth does not
look obviously plaque-covered and this
shows why it is important to disclose
and remove all stained plaque before
making the diagnosis.
Table 1 illustrates the clinical criteria,
the corresponding histological picture,
the likely activity of the lesion and its
level of infection.
A reasonable sequence for doing this
careful visual examination is as follows:
1. Disclose.
2. Brush off all plaque and rinse
thoroughly using the three-in-one
syringe.
3. Place cotton-wool rolls and a saliva
ejector. Leave the surface of the
tooth wet. Is there a white spot
(score 2) or a brown spot lesion
(score 2a)?
4. Does the wet tooth have a greyish
discoloration of the underlying
dentine? If so, the score is 3.
5. Dry the tooth with a three-in-one
syringe.
381
 C A R I O L O G Y

Table 1. Lesion appearances, activity, histopathology and level of infection.

Score Clinical Figures Activity Histopathology Figures Level of

appearance infection

0 No, or slight, Fig. 3 Probably none No enamel Fig. 4 0

change in demineralization or
enamel a narrow surface
translucency after zone of opacity
prolonged air- (edge phenomenon).
drying (>5 s)

1 Opacity (white) Fig. 5 Active Fig. 6

hardly visible on
the wet surface
but distinctly
visible after air-
drying

Enamel demineralization
limited to the outer
50% of the enamel
layer
1a Opacity (brown) Fig. 7 Arrested Fig. 8 0
hardly visible on
the wet surface,
but distinctly
visible after air-
drying

2 Opacity (white) Fig. 9 Active Fig. 10

distinctly visible
without air-drying

Demineralization
involving 50% of the
enamel and up to 1/3
of the dentine.
2a Opacity (brown) Fig.11 Arrested Fig.12 +
distinctly visible
without air-drying

3 Localized enamel Fig.13 Active Demineralization Fig.14 ++

breakdown in involving the middle
opaque or 1/3 of the dentine
discoloured
enamel and/or
greyish
discoloration from
the underlying
dentine

382 Dental Update – October 2001


Score Clinical Figures
appearance
4 Cavitation in Fig.15
opaque or
discoloured
enamel exposing
the dentine
6. Does the tooth surface appear
sound (score 0)? Is there now a
white (score 1) or brown (score 1a)
spot lesion?
7. Is there an obvious cavity? If so
gently use a probe to check whether
there is exposed dentine at its base
(score 4). Alternatively, can you see
localized enamel breakdown in
opaque or discoloured enamel? This
may look like a hole made by a
woodworm or a slightly enlarged
fissure. These appearances are
microcavities (score 3).
Notice that the probe is used only to
check there is dentine at the base of
the cavity in score 4.
WHY DOES AIR-DRYING
HELP?
Demineralized enamel is more porous
than sound enamel and this is the key
to understanding some of the visual
changes. A white spot lesion that is
obvious on a wet tooth surface is more
porous and deeper than one that is
visible only after thorough air-drying.
This is due to the differing refractive
indices of enamel (1.62) water (1.33)
Figure 17. Erupting first permanent molar with
its occlusal surface covered by plaque.
Dental Update – October 2001
C A R I O L O G Y
Activity Histopathology
Active Demineralization
involving the inner
1/3 of the dentine
and air (1.0). The pores in the
demineralized tissue fill with a watery
medium and the difference in refractive
index between this and sound enamel
results in the lesion looking white. If
the dentist dries the tooth, the water
will be replaced with air. The difference
in refractive index between air and
enamel is greater than between water
and enamel, which means that a lesion
becomes more obvious after air-drying
and a less porous lesion can be
detected.
THE SHAPE OF THE LESION
The spread of the enamel lesion is
guided by prism direction. Caries on
occlusal surfaces does not involve the
entire fissure system (groove-fossa
system) with the same intensity but
occurs as a localized phenomenon where
plaque accumulates. These are the areas
best protected against functional wear –
the deepest part of the groove fossa
system (Figure 19).
It is important to remember that the
lesion is developing in three
dimensions. It is often initiated in the
fossae, which are the depressions where
two or more interlobular grooves meet.
Thus several surfaces are involved in
the initial dissolution9 and the lesion,
following the enamel prisms, assumes
the shape of a cone with its base
towards the enamel–dentine junction
(Figure 20). The dentine reaction occurs
beneath this, and it is this anatomy
which gives the occlusal lesion its
apparently undermining character. This
explains why such a small cavity
becomes a surprisingly large hole when
the dentist accesses the demineralized
Figures Level of
infection
Fig.16 ++++
area to remove the soft, infected dentine
(Figure 19).
Once into dentine the lesion follows
the direction of the dentinal tubules but
there is some discussion as to what
happens at the enamel–dentine junction
(EDJ). It has been suggested that caries,
even in precavitated stages, spreads
laterally along the EDJ owing to the
lower resistance of the mantle dentine,
and that this lateral spread undermines
the sound enamel. Recent study seems
to show that lateral spread is associated
with an advanced stage of the carious
process where the enamel is
cavitated.13,14 At this stage the dentine
is soft to probing and heavily infected.
On an occlusal surface these
anatomical considerations explain why a
lesion may look like a small cavity on the
surface of the tooth but represent a
great deal of destruction once the
dentist removes the undermined enamel.
THE DEFENCE REACTIONS
OF THE DENTINE–PULP
COMPLEX
There are two important defence
Figure 18. The same tooth as in Figure 17 after
cleaning the fissure with a brush. A white spot
lesion is now visible.
383
 C A R I O L O G Y

new visual system there was no hidden

a b caries. In other words, caries in dentine
that was sufficiently extensive to show
on a bitewing radiograph was not
missed in the visual examination but was
scored as 2, 3 or 4 (Table 1).
This is likely to be due to very careful
cleaning of the teeth and the new visual
criteria. However, this was a laboratory
study where the teeth were easy to see:
it does not imply that radiographs are
not useful in the diagnosis of occlusal
caries clinically. Whenever a bitewing
radiograph is available, it should always
be carefully examined for occlusal caries
in dentine. Without meticulous cleaning
c d and drying, quite advanced lesions are
still easy to miss clinically.

ELECTRICAL
CONDUCTANCE AND
LASER FLUORESCENCE
MEASUREMENTS
This article would be incomplete without
mentioning the enormous research effort
that has been put into making it easier
for the dentist to detect occlusal carious
lesions.
Carious lesions can be detected on
Figure 19. (a) A molar tooth before plaque removal. The cavitation in the central the basis of their increased electrical
fossa is just visible. (b) The tooth has been cleaned with a brush and dried. Now the conductivity. The change in electrical
cavity is obvious, but it looks small. (c) The dentist has started to gain access to the
infected and demineralized dentine. (d) Further access has been gained prior to final
conductivity has been explained by the
excavation. Notice how large the cavity is in relation to (a). This is purely a factor of fact that the porosities, formed during
anatomy. demineralization, fill with saliva to form
conductive pathways. The technique
involves a digital readout and has been
shown to detect carious lesions and
reactions of the dentine–pulp complex: THE CONTRIBUTION OF identify teeth that are caries-free.10,17,18
tubular sclerosis and reactionary THE RADIOGRAPH TO These machines are not commercially
dentine. These were well reviewed by DIAGNOSIS available in the UK.
Massler as early as 1967.15 He pointed It was in the early 1980s that Recently, a laser-based instrument
out that the response of the pulp to the practitioners first alerted the profession (KaVo Diagnodent) has been produced
carious process is productive, not in the UK to the problems of occlusal and marketed. This uses a technique of
degenerative, unless the pulp is actually caries diagnosis and advised colleagues illuminating the tooth with laser light
invaded by micro-organisms. The pulp– to examine radiographs very carefully. (wavelength 655 nm), which is absorbed
dentine complex has a remarkable The phenomenon of ‘hidden caries’ by both inorganic and organic tooth
healing potential and treatment of an (defined as an occlusal carious lesion substance. Some of this light is emitted
advanced lesion should be directed that is missed on a clinical examination as near-infra-red fluorescent light and,
towards promoting arrest of the but subsequently found as an obvious as the carious lesion progresses, an
infection and healing of the dentine by lesion in dentine on a bitewing increase in emitted fluorescent light
sclerosis and repair. Massler advocated radiograph) was described.16 occurs; this is detected by the
removing only infected dentine initially, The laboratory study that first instrument and presented to the
avoiding over-instrumentation and described the ranked visual scoring operator as a digital readout.19 This
placing temporary restorations so that system for occlusal caries took technique, like electrical conductance,
natural repair could take place. radiographs of all the teeth. Using the shows great promise. Both will detect

384 Dental Update – October 2001

 C A R I O L O G Y
a b
Figure 20. (a) An extracted tooth with a lesion slightly larger than in Figure 19. (b) A hemi-
section of the tooth through the cavity emphasizing how much destruction is present beneath a
relatively small hole. It shows: the cone shape of the enamel lesion as it follows prism direction;
lateral spread of the lesion along the EDJ; and spread of the lesion into dentine along the dentinal
tubules.
demineralization and provide a
quantitative readout.
There is thus the potential to measure
lesion progression or arrest. It should be
remembered, however, that these are
machines and they do not have brains!
Both may be confused by areas of
hypomineralization, which they will
interpret as caries. In addition, the laser-
based instrument is totally confused by
staining, such as a stained fissure,
interpreting this colour change as caries
in dentine. Neither can these machines
assess the activity of the lesion if used
on a single occasion. They have the
potential, however, to monitor lesion
progression or arrest if used on several
occasions.
LOGICAL MANAGEMENT
It is now possible for the clinician to
make a good diagnosis of occlusal
caries; both the degree of
demineralization and the activity of the
lesion. This diagnosis must be set in the
context of a complete clinical and
radiographic examination of all surfaces
of all teeth. The dentist can then define
the current caries activity of the patient
and plan appropriate preventive, non-
operative treatment including oral
hygiene instruction with a fluoride
toothpaste, diet analysis and advice and
further fluoride supplementation, if
appropriate. This paper will now
concentrate on the management of
occlusal surfaces.
Sound teeth (score 0) and arrested
386
lesions (scores 1a, 2a) require no
treatment. Active lesions where the
tooth surface is intact (scores 1, 2) may
be managed by plaque control alone.
The plaque that is causing the
demineralization is on the tooth surface
and accessible to a brush. It has been
shown that these lesions can be
controlled by intensive patient
education and professional tooth
cleaning.20 It would seem likely therefore
that occlusal caries can be controlled by
twice-daily plaque removal with a
fluoride toothpaste.
The problem with the erupting tooth is
that it lies below the level of the other
teeth in the arch, and the brush misses
the occlusal surface unless it is
specifically brought over that tooth
surface with the brush head at right
angles to the other teeth (Figure 21).
The parent should stand behind the
child to assist. A hygienist or oral health
educator should show children and
parents how to clean these erupting
surfaces and see children and their
parents monthly until the surface is
either being correctly cleaned or a failure
to motivate is established.20 The latter is
an indication for administration of a
fissure sealant.
If caries is to be prevented, good
plaque control is also required once the
tooth has erupted, but again this should
be monitored. Topical application of
fluoride varnish or solution is an
important treatment while plaque control
is being perfected but should only be
used if there is active caries. The
application will delay lesion progression
in this critical period.21 The use of a
chlorhexidine and thymol varnish has
also been suggested22 and its use during
the time of eruption of first and second
molar teeth has been researched.
Results appeared promising.
Some form of operative treatment is
indicated once the occlusal surface is
cavitated (score 3, 4). These lesions are
active because now the patient cannot
remove the cause of caries (the plaque)
with a toothbrush.
The accepted management for the
microcavity (score 3) is a sealant
restoration but the possibility of fissure
sealing alone should be borne in mind.
Approximately 40% of these teeth will
have no radiolucency on a bitewing
radiograph and will be minimally
infected.12 Handelman reviewed his
extensive work on this subject in 1991.
Even if the lesion is visible in dentine on
a bitewing radiograph,23 microbiological
study showed a reduction in cultivable
bacteria 2 weeks after fissure sealing. It
is even more important to note that the
demineralization did not progress over 4
years in these sealed teeth.
The cavitated lesion, where dentine is
exposed (score 4), requires operative
intervention so that the patient can
clean. In deep cavities where the dentist
fears an exposure, there is much to be
said for accessing the carious dentine,
which will be heavily infected, soft and
wet, and placing a temporary
restoration, perhaps an acid-etched
composite resin24 or a glass ionomer
cement.25 This allows the pulp-dentine
complex to mount the defence reactions
of tubular sclerosis and reactionary
Figure 21. The correct position of the toothbrush
on an erupting second permanent molar.
Dental Update – October 2001

dentine and guards against unnecessary
exposure. Before this treatment, the
dentist should check that these teeth are
vital and without symptoms of
irreversible pulpitis.
Whether the dentist should
subsequently re-enter to remove all the
soft dentine has to be under dispute.
There is now 10-year clinical data24
pertaining to large occlusal lesions
where soft, infected carious dentine was
sealed in place with no apparent
detriment. Caries did not progress; the
pulps did not become non-vital. This
suggestion runs contrary to
contemporary teaching in the UK and
Denmark but consideration of the
evidence demands that we re-evaluate.
Further research work is urgently
needed in this area.
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BOOK REVIEW
Paediatric Dentistry. 2nd edn. Richard
Welbury, ed. Oxford University Press,
Oxford, 2001 (£35.00). ISBN 0-19-263186-1.
This is the second edition of an extremely
important book in paediatric dentistry, not
only for undergraduate and postgraduate
dental students, but also general dental
practitioners. The first edition was
published in 1997, and it has subsequently
become very popular and I am quite sure
that it is on most Dental Schools’ reading
lists. The editor, Richard Welbury, brings
together a wealth of information from 16
well-known authors, mainly within the
specialty of paediatric dentistry,
supplemented with authors from oral
surgery and restorative dentistry. There
are 17 chapters, which cover all aspects of
Dental Update – October 2001
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paediatric dentistry from craniofacial
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basic and advanced restorative
techniques, and treating the medically
compromised patient. The chapters are
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armamentarium and numbered technique
rather like a recipe.
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25. Bjørndal L, Larsen T,Thylstrup A. A clinical and
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has been included on the management
of dental caries in the pre-school child.
It outlines the ways of managing
behaviour in this potentially difficult
group of children, as well as sensible
advice on treatment planning.
In summary, this is an excellent book,
which I would thoroughly recommend
not only for the newly emerging
specialists in paediatric dentistry, but for
all clinicians that see and treat children.
It is a comprehensive book covering all
aspects of paediatric dentistry. This
latest edition addresses the previous
omissions. I find it an easy to read book,
which makes it very useful for quick
reference in the surgery. I suggest it is
well worth the money and should be on
everyone’s bookshelf.
Victoria Clark
Birmingham Children’s Hospital
387