Diagnosis of occlusal caries
It might be expected that occlusal carious lesions would be fairly easy to diagnose, because unlike approximal and subgingival root surfaces, these surfaces are readily accessible for visual inspection. However, clinically (visual or visual-tactile by probing) or radiographically, diagnosis of occlusal lesions is a delicate problem, because of the complicated three-dimensional shape of the occlusal surfaces, incorporating fossae and grooves with a great range of individual variations.
Disease progression
It is a common clinical observation that caries on occlusal surfaces does not involve the entire fissure system with the same intensity but is a localized occurrence. Viewed in a stereomicroscope or SEM, the occlusal surface of a permanent molar appears as a convoluted landscape, with high mountains separated by valleys, some that are deep rifts and others that resemble open river beds (Fig 201).
Each tooth type in the dentition has its own specific occlusal surface anatomy, and caries is usually detected in relation to the same specific anatomic configuration in identical tooth types. In maxillary molars, for example, the central and the distal fossae are sites that typically accumulate plaque and hence also the sites at which caries most often occurs. In general, occlusal caries is initiated at sites where bacterial accumulations are well protected against functional wear (see Figs 20 and 174).
Thus, two factors have been considered of importance for plaque accumulation and caries initiation on occlusal surfaces: (1) stage of eruption or functional usage of teeth, and (2) tooth-specific anatomy. This explains why almost all molar occlusal caries is initiated during the extremely long eruption period (12 to 18 months) and why occlusal caries is uncommon in premolars, with an eruption time of only 1 to 2 months. This was confirmed in a 2.5-year longitudinal study by Mansson (1977), who examined first molars every 3 months from the start of eruption and found that
development of caries occurred, on average, within 11 months of the start of eruption, ie, during eruption (most had decayed within 3 to 9 months). On the other hand, there was virtually no further initiation of occlusal caries beginning 15 months after the start of eruption.
Monitoring for and measures to prevent the development of occlusal caries should be intensified during the eruption period (high-risk period). If the teeth have erupted into natural chewing function without developing occlusal caries, then the risk is over; examinations can be more cursory and less frequent. Nor is there any indication for application of fissure sealant.
In cross section, most molar fissures have a relatively wide opening (entrance) followed by a narrow cleft, approximately 1.0 mm deep and 0.1 mm wide, almost to the dentinoenamel junction (see Fig 116). The carious lesion usually starts in the enamel on either side of the entrance to the fissures and is visible as a noncavitated white-spot enamel lesion. Gentle probing with a sharp explorer will damage the surface zone of such a lesion and initiate cavitation to the lesion body. A rule of thumb is to use sharp eyes and a blunt probe (or no probe at all) and to arrest the
lesion by plaque control and fluoride.
Most clinical and scientific concern with respect to occlusal caries has been over the possible events in deep and inaccessible fissures. However, caries always starts in the surface enamel, from the metabolic activity of bacterial accumulations on the surface.
It is reasonable to assume that evolution of plaque with cariogenic potential requires space that, in this context, is available only above the entrance to the narrow fissures, the grooves. This assumption is supported by ultrastructural studies indicating that, in contrast to the vital bacteria found at the entrance, nonvital bacteria or different stages of calculus formation are usually harbored by the depths of the fissures (Ekstrand, 1988; Theilade et al, 1976).
Fewer than 10% of fissures are atypically flask shaped, with a narrow neck and a
bulbous base: The carious lesion can start at the entrance as well as at the base of the
fissure (see Fig 117). These fissures should be regarded as at risk. Fortunately, from a
diagnostic point of view, there is a strong correlation between steep cuspal inclination
and such sticky risk fissures.
Figure 202 shows an unusually wide, shallow fissure, full of stagnant, cariogenic
plaque and an associated noncavitated enamel lesion around the entire fissure. Figure
203 shows a so-called risk fissure with stagnant, cariogenic plaque in the entrance as
well as at the base of the fissure. In this case, localized, noncavitated enamel lesions
have developed on both sides of the entrance and around the bulbous base of the
fissure. However, even extreme risk fissures, with irregularities such as horizontal
tunnels, can be maintained free of caries (see Fig 118).
Progressive destruction of the occlusal surface thus begins as a local process in the
deepest part of the groove-fossa system, as a result of accumulation of bacterial
plaque. In this area, which is already sheltered from physical wear, the formation of a
microcavity further improves the potential for bacterial attachment and colonization.
This accelerates demineralization and destruction, further enhancing local conditions
for bacterial growth.
Figures 204a, 204b, and 204c show different stages of localized progressive occlusal
lesions in a mandibular molar with a discolored, cavitated lesion in the distal fossa.
The cross section of the lesion in the fossa shows superficial enamel breakdown with
cavitation into about 50% of the enamel but no cavitation into the dentin; ie, there is
no bacterial invasion of the dentinal tubules, and the lesion could be arrested (Fig
204b). However, the enamel lesion (demineralized area) is approaching the
dentinoenamel junction and there is demineralized dentin in the contact area,
corresponding to the direction of the rods. The anterior fissure in Fig 204a is shown in
cross section in Fig 204c. There is no progressive demineralization.
Figure 205a shows a localized cavity in the central fossa of a maxillary first molar.
The cross section of the lesion shows that the cavity is truncated and that the
superficial zone of destruction and the zone of dentinal demineralization are confined
to the involved enamel (Fig 205b). The cross section of the fissures shows that these
are filled with calcified material, indicating total absence of cariogenic plaque (Fig
205c). It is therefore assumed that the dark brown cavity is arrested or stagnant.
In people living in communities without dental health care, the natural progression of
occlusal caries is rapid, because of the particular anatomic configuration of the
occlusal surface where caries is initiated. Occlusal caries usually begins in a fossa, ie,
a depression where two or more interlobal grooves meet. Several surfaces are
involved in the initial dissolution, and the process is therefore three-dimensional.
Because enamel demineralization always follows the rods, the enamel lesion initiated
in a fossa gradually assumes the shape of a cone, with its base toward the
dentinoenamel junction. The response by the dentin corresponds to the direction of
the involved enamel rods. A section through such a lesion has the two-dimensional
appearance of two separate, independent lesions, but the lesion is three-dimensional
and actually cone shaped. Although textbooks have traditionally emphasized the
undermining character of occlusal or so-called hidden caries, the pattern of lesion
growth in these areas is not particularly surprising in the context of the structural
arrangement of rods in the occlusal groove-fossa system.
As enamel destruction proceeds, a true cavity forms, the outline reflecting the
arrangement of rods in the areas: The cavity has the shape of a truncated cone. The
particular anatomic configuration of the occlusal surface at the site of caries initiation
explains why the openings of occlusal cavities are always smaller than the base. The
“closed” nature of the process obviously favors undisturbed growth of bacteria and
hence accelerated destruction of the tissue. Occlusal enamel breakdown is the result
of further demineralization from an initially established focus, rather than general
demineralization involving the entire fissure system.
Figure 206 illustrates the progressive stages of lesion formation in an occlusal fossa,
from the earliest noncavitated enamel lesion to cavitation into the dentin with a zone
of bacterial invasion and dentin destruction, where excavation and restoration are
indicated. However, at the second-to-last stage (E), no such invasive intervention is
indicated, despite a considerable zone of demineralized dentin and a sclerotic and
translucent zone into the pulp. The method of choice would be placement of a fissure
sealant or a minimally invasive sealant restoration, using a resin-based glass-ionomer
material or compomer.
