Dentin caries

Dentin caries
Whether or not an active, noncavitated carious lesion in enamel will progress into the
dentin and the rate of progression are determined by many factors:
1. The overall estimated caries risk (C1 to C3) of the individual
2. The rate at which the enamel lesion has developed
3. The size, depth, and site of the enamel lesion
4. The posteruptive age of the enamel
5. The future efficacy of self-care and supplementary needs-related preventive
On the approximal surfaces of the posterior teeth, the progression of a carious lesion
through the enamel into the dentin can easily be followed on serial bitewing
radiographs. However, the radiographs do not disclose whether the lesions are
cavitated or noncavitated. In an early study, Backer-Dirks (1966) showed that 50% of
enamel carious lesions on the mesial surfaces of the permanent first molars progressed
into the dentin from ages 11 to 15 years, 67% from 9 to 15 years, and 74% from 7 to
15 years. However, more recent studies on premolars and molars have shown that
only 14% of the approximal enamel carious lesions progressed into the dentin from
ages 13 to 15 years (Bille and Carsten, 1989), 30% to 40% from 14 to 18 years
(Lervik et al, 1990), and as low as 5.4% from 11 to 22 years in the most recent study,
which was based on prevention and remineralization rather then restoration (Meja`re
et al, 1999).
In this context, it is important to recognize that the two mineralized tissues of the
tooth crown¾the enamel and the dentin¾are different not only in origin but also in
composition. They therefore respond differently to stimuli such as chemicals (acids),
attrition, temperature, and so on.
The enamel is derived from the ectodermal component of the tooth germ, while the
pulpodentinal organ is developed from the mesenchymal component. The enamel is
avascular and acellular and cannot respond to injuries, whereas the dentin and the
dentinal cells, the odontoblasts, are integral parts of the pulpodentinal organ and are
vital tissues, with specific defense reactions to external insults. Because the enamel is
a microporous solid, stimuli from the oral cavity can permeate to the dentin and the
pulp. Changes in dentin during caries progression cannot be understood, therefore,
without taking into account the spread of the enamel lesion.
The most common defense reaction by the pulpodentinal organ is tubular sclerosis, ie,
deposition of mineral within the dentinal tubules. The earliest dentinal response to the
enamel lesion that can be detected by light microscopy is tubular sclerosis, at the site
where the central travers (CT) crosses the dentinoenamel junction (Fig 175). Enamel
demineralization increases enamel porosity and hence the permeability of the enamel,
and the first mild stimuli initiating the defense reaction reach the dentin underlying
the most porous part of the enamel lesion. The light microscope provides relatively
low magnification, and much earlier dentinal reactions have been detected using
biochemical and histochemical methods.
Initial tubular sclerosis can be detected before the advancing front of the enamel
lesion reaches the dentinoenamel junction. When contact is established between the
enamel lesion and the dentinoenamel junction, the first sign of dentinal
demineralization can be seen along the junction (Figs 175 and 176) as yellow or
brownish discoloration, depending on the aggressiveness of lesion formation. For
many years, it has been thought that demineralization of dentin progresses laterally
along the dentinoenamel junction, on the assumption that the anatomic discontinuity
between the two tissues facilitates penetration of destructive agents.
However, recent systematic investigations have concluded that discolored dentinal
demineralization never extends beyond the limits of the enamel lesion at the
dentinoenamel junction (Bjorndal, 1991). If the active enamel lesion is regarded as a
multitude of microlesions at different stages of progression, then the dentinal sclerosis
lateral to the demineralization may be interpreted as a reaction to stimuli in the
direction of the rods from the less advanced parts of the enamel lesion approaching
the dentinoenamel junction (see Figs 175 and 176).
At this stage of lesion progress, therefore, the lesion in dentin should not be
considered as an entity in itself, with a central and spreading focus of destruction, as
conventionally assumed. The dentinal changes merely represent a continuum of
pulpodentinal reactions to variations in acid challenge at the enamel surface, with
transmission of the stimulus through the enamel in the directions of the rods.
The implication of this approach is that when acid production at the surface ceases,
because of regular disturbance or removal of the cariogenic microbial biomass, then
demineralization also ceases, arresting further progression of the lesion.
Figure 177 shows a cross section of an active carious lesion with a cavity into the
enamel and some spread of the lesion into the dentin along the dentinoenamel
junction. To the right is a detail (SEM) of the base of the enamel cavity, which is
covered by cariogenic plaque, predominantly cocci. Every single enamel prism can
still be seen, albeit the outer structure of some prisms is less mineralized.
A cross section of another carious lesion with microcavitation in the enamel and a
noncavitated lesion in the underlying dentin is shown in Fig 178. However, after
arrest of such a lesion, there is only very limited mineral uptake from saliva by the
enamel and the dentin, and both the demineralized enamel and the demineralized
dentin therefore persist, as scars in the tissue. Figure 179 shows a microradiograph of
a ground section through an inactive approximal carious lesion, with cavitation in the
outer part of the enamel and involvement of dentin; the caries has been arrested for
several years (Thylstrup and Fejerskov, 1994). In the enamel, some mineral
redeposition can be seen corresponding to the base of the cavity, whereas the
peripheral demineralized dentin remains unchanged after arrest of the lesion.
Conventionally, involvement of dentin has been regarded as the stage in caries
progression at which operative intervention becomes necessary to arrest further
destruction, and there have been many studies attempting to improve the radiographic
detection of this stage. The term dentinal involvement is, however, too vague to define
the continuum of changes occurring in the pulpodentinal organ during caries
progression and therefore serves no useful purpose as an indicator for operative
To understand the gradual exposure of the pulpodentinal organ during progressive
lesion formation, it is important to be aware that, although there has been some
mineral loss from the enamel and the lesion is thus characterized as porous, adequate
mineral remains to preserve the structural composition of the enamel (see Figs 146
and 147). The area below the surface zone is not an empty space, but highly
mineralized tissue, despite some degree of mineral loss. The first signs of surface
breakdown are therefore limited to the outermost enamel and are presumably caused
by mechanical trauma during mastication, microtrauma during interdental wear, or
iatrogenic damage from careless probing of approximal surfaces (see Fig 177).
If such areas are not kept relatively free of dental plaque, the process will continue,
because, all other matters being equal, the bacteria harbored in the microcavity will be
more sheltered than those on the surface, and this will favor an ecological shift toward
anaerobic and acidogenic bacteria (see chapter 1). The progressive destruction of the
enamel or the gradual enlargement of the cavity is therefore the combined result of
continued acid production in the protected microbial biomass and mechanical
As long as the base of the cavity is still confined to the enamel, massive bacterial
invasion of the dentin is unlikely. At this stage, the lesion can successfully be arrested
(see Fig 179). However, a persistently undisturbed active carious lesion will
eventually progress to cavitation of the dentin: Exposure of the dentin to the masses of
bacteria in the cavity will soon lead to decomposition of the most superficial part of
the dentin, as a result of the action of acids and proteolytic enzymes. This zone is
referred to as the zone of destruction (see Fig 175). Beneath this zone, tubular
invasion of bacteria is frequently seen (Fig 180).
If lesion progression is very rapid, it is not uncommon to see so-called dead tracts in
the dentin, indicating destruction of the odontoblastic processes without tubular
sclerosis. Such empty dentinal tubules are readily invaded by bacteria (Fig 181).
Between the zone of bacterial penetration and the sclerotic dentin, the translucent
zone, there is a zone of demineralization, caused by acids produced in the biomass of
anaerobic and aciduric bacteria in the cavity.
There is still some uncertainty concerning the degree of pulpal response to various
stages of caries development. Reactionary (tertiary) dentin may form even before
bacterial invasion of the dentin: Reactionary dentin is less mineralized and contains
irregular dentinal tubules. When demineralization of the dentin approaches within 0.5
to 1.0 mm of the pulp, an inflammatory response may be seen in the subodontoblastic
region. This does not constitute true infection of the pulp, however; the inflammatory
cell reactions are believed to occur in response to bacterial toxins.
From a treatment perspective, it should be noted that there is no true indication for
invasive intervention until the cavity has reached the dentin: until then, the lesion can
be arrested, and even softened dentin is not infected by bacteria. These principles
apply particularly to buccal and lingual surfaces but should also be valid for most
approximal and occlusal surfaces.
Actively progressing dentin caries is soft and yellowish in color. The purpose of
excavation is to remove infected and necrotic tissue but to avoid cutting into the
underlying sound tissue, destroying thousands of odontoblastic processes. The most
appropriate method of excavation is the use of hand instruments or slowly rotating
burs, allowing the operator to recognize the interface between the relatively hard
translucent zone and the demineralized dentin. After excavation, although there may
be no marked discoloration and the dentin is hard on probing, some microorganisms
may still remain in open dentinal tubules (see Fig 180). Microbiologic investigations
indicate that about 25% of excavated teeth still harbor bacteria, and histologic
techniques have demonstrated microorganisms (Reeves and Stanley, 1966) in one or
more tubules in 30% to 50% of teeth. On average, there are 45,000 dentinal tubules
per 1 mm2 and some may be dead tracts with remaining microorganisms (see Fig
181). However, under a well-sealed, retentive restoration, they are denied access to
substrate and will do no harm.

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Articles for theme “caries”:
ArrestFluoride and plaque controlArrest of enamel carious lesions is a reality, as shown in the studies by Backer-Dirks (1966) and von der Fehr et al (1970). In vitro as well as in vivo studies have shown that carious lesions in enamel can successfully be arrested by plaque control or topical use of fluoride. The most efficient means is a combination of both, as exemplified in Fig 156. On the left is an active, noncavitated enamel lesion on the mesiolingual surface of a mandibular second molar.
Development of Carious LesionsEnamel cariesDevelopmentThe physicochemical integrity of dental enamel in the oral environment is entirely dependent on the composition and chemical behavior of the surrounding fluids: saliva and plaque fluids. The main factors governing the stability of enamel apatite are pH and the free active concentrations of calcium, phosphate, and fluoride in solution.  The development of a carious lesion in enamel involves a complicated interplay among a number of factors in the oral environment and the dental hard tissues.
Development and Diagnosis of Carious LesionsIntroductionA carious lesion should be regarded not as a disease entity, but as tissue damage or a wound caused by the disease dental caries. The coronal lesion begins as clinically undetectable subsurface demineralization of enamel, visible only at microscopic level, and gradually progresses, first to visible demineralization of the enamel surface and to cavitation of the dentin, and finally to complete destruction of the tooth crown despite restoration, but without prevention (Fig 145).
ConclusionsCaries riskFrom a cost-effectiveness aspect caries-preventive measures should be applied strictly according to predicted caries risk. In populations with very high caries prevalence and caries incidence (where almost everyone develops new lesions every year) the traditional whole population strategy would be cost effective. The number of such populations is dwindling, however, particularly in the industrialized countries where caries prevalence was high 20 to 30 years ago.
Cariogram ModelA new model, the Cariogram, was presented in 1996 by Bratthall for illustration of the interactions of caries-related factors. The model makes it possible to single out individual risk or resistance factors. A special interactive version for the estimation of caries risk has been developed.The original Cariogram was a circle divided into three sectors, each representing factors strongly influencing carious activity: diet, bacteria, and susceptibility. The development of the model was based on a need to explain why, in certain individuals, carious activity could be low in spite of, for example, high sucrose intake, poor oral hygiene, high mutans streptococci load, or nonuse of fluorides.