Lecture 1 (28 March 07)
The Caries Process
Nature and character of dental caries
Disease pattern and civilization: Dental caries is an ancient disease. Interestingly, dental
caries follows the pattern of our civilization. The graph shows the percentage of carious teeth in
the English population. This first spike coincides with the Roman empire, probably due to the
increased use of cooked food. The second spike is a dramatic rise from the middle ages to the
last century, which relates to the industrial revolution and the easier access to refined
carbohydrate and sugar. By the 1950’s, dental caries has reached epidemic proportions affecting
more than 90% of the population in the developed world. Then there is a dramatic decline, the
main reason is one agent: F.
A little bit about epidemiology: A recent report by the US Surgeon General has identified
dental caries as the most prevalent infectious disease. Eventhough the prevalence of dental
caries in children has declined significantly in the last few decades, dental caries is 5 times more
common than childhood asthma and 7 times more common than hay fever.
Dental caries affects 85% of adults aged 18 or older in the US. Unfortunately, 80% of caries
occurs in 20% of the population, a group that is over-represented by individuals from lower
socio-economic classes.
A survey done in the late 80’s showed that in the US 75% of children aged 5-11 years old were
caries-free. But 70% of 12-17 years old had caries, and 94% of dentate adults (18 years or older)
had caries. The nature of caries has changed from a rapidly progressing childhood disease to a
slow but steadily progressing disease in adulthood.
Key features of caries: multifactorial, site-specific, and dynamic
Multifactorial: Traditionally, dental caries has been described as an outcome of host factors,
diet, and cariogenic bacteria in dental plaque. Caries cannot occur if there are no plaque bacteria
or fermentable carbohydrates. The host factors such as the tooth or saliva modifies the outcome.
This concept is easy to understand but it misses several significant players.
A modern concept of multifactorial causes is more complicated. Numerous biological factors
influence the outcome at a single site and in the individual as a whole. The etiological factor,
which is biofilm composition and metabolism, is determined by biological determinants (the
inner circle) that influence caries lesion at the tooth level. These biological determinants are
saliva (flow rate, composition, buffering capacity), diet (sugar, composition, frequency), and
others that we don’t know yet, including genetic factors. Genetics may impact tooth composition
and structure, morphology, saliva, endogenous microflora, and food preferences, for example.
In the outer circle are various behavioral and socio-economical factors which influence caries
development at the individual or population level.
Site-specific: Dental caries is the localized destruction of the tooth tissues, because it is an
outcome of the metabolism of microorganisms in biofilm (dental plaque). Tooth morphology
affects plaque accumulation. Compare to erosion which is more generalized destruction of tooth
tissues from internal or external acids. Dental caries occurs on the tooth surface where plaque
can accumulate undisturbed. Each site also represents a unique environment that influences
plaque composition, metabolic status, thickness, and diffusion properties. The access to dietary
substrates, saliva, and anticaries agents varies in different locations of the mouth.
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Dynamic: Dental caries is a dynamic process. Before caries can be detected by eyes or by x-ray,
there is a stage of sub-clinical initial lesion that is a battle between demineralization and
remineralization. This graph may be exaggerated, but let’s follow a daily activity of a person,
can be one of us. When we get up, we may be in the stage of demin from less salivary flow.
Although in some people it may not be the same way. Brushing stops the process of demin and
boost remin. Too bad we need breakfast, so plaque pH drops. When saliva neutralizes the pH,
we have a coffee break, then comes lunch, and snacks, and dinner. This poor person ends up
with a net mineral loss in a day, which means that the caries lesion will progress.
The brown spot or arrested lesion is a good example of the dynamic nature of dental caries. In
this case the gum line was higher when this tooth erupted, and the patient might not be able to
clean it well. When the tooth was fully erupted and plaque accumulation was reduced, there was
direct access to saliva, the conditions reversed in favor of repair or remineralization.
Development of early caries lesion in enamel
The concept of demineralization and remineralization: A short video about a general concept
of the demineralization and remineralization process, downloaded from a website of a company
that makes a milk derivative product called Recaldent. The video is very informative and
explains the carious process in lay language, great for patient education.
Schematic illustration of steps in the formation of enamel lesion: Organic acids produced by
plaque bacteria diffuse into the enamel by the difference in concentration gradient. Then the
acids dissociate, providing H+. H+ attack the apatite crystals, break them down to calcium,
phosphate, and other ions. Calcium, phosphate, and other ions diffuse according to their
concentration gradients through microporosities of the carious. They can go in any direction. If
reaching saturated level, they can precipitate back. If the plaque fluid is undersaturated with
mineral ions, they will diffuse outward. In the body of the lesion the demineralization may
continue until as much as 70% of the mineral is dissolved. When more minerals are dissolved,
calcium and phosphate concentration increase. Also the ions in plaque fluid can diffuse inward
depend on the concentration gradient. At some point, the concentration of Ca/P at the surface is
high enough to precipitate. This leads to the formation of an 'intact' surface layer, about 20-40
m thick. Some of the calcium and phosphate diffuse inwards, therefore remineralization is also
observed in the dark zone under the body of the lesion. Fluoride in the aqueous phase promotes
the remineralization process by adsorbing onto the crystal surface and attracting calcium,
phosphate ions, leading to new mineral formation, similar to fluorapatite. The partially dissolved
crystals act as a core for reprecipitation.
Microscopic features of early enamel lesion: The lesion consists of several zones, better seen
under a polarized light microscope. These zones have different levels of porosities as shown in
the diagram here. The lesion is usually covered by an apparent intact surface layer.
1. Surface Zone: Intact surface 20-100 mm thick, <10% mineral loss
2. Body of the Lesion: Largest zone, 24 % mineral loss
3. Dark zone: very small pores, 6 % mineral loss
4. Translucent zone: advancing front, 1 % mineral loss
Clinically, early enamel caries lesion is seen as a white opaque area, so called ‘white spot lesion’.
This is a small area of subsurface demineralization beneath dental plaque. Although it is the first
clinical sign, the caries process has progressed for quite a while. Usually the lesion must
progress to a few hundred microns to be clinically visible. We see the subsurface
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demineralization as a white area because of many porosities under the surface. We emphasize on
early caries lesions because that is the stage where the carious process is reversible, and the
fluoride and preventive treatment is most effective.
Early carious lesions are reversible, as shown in a classic study from Baker-Dirks. They
followed carious lesions in children for 7 years. Only 9 of 72 white spot lesions became
cavitated. More than half regressed to ‘normal’ enamel. Note that this study was done in
community with water fluoridation.
Caries free vs Caries controlled: The dynamic of the caries process leads to a question on the
accuracy of the term ‘caries-free’. Traditionally, carious lesions refer to those that are clinically
detectable by explorer, which do not include initial or arrested lesions. If we include
demineralization and remineralization as part of the caries process, there is no caries-free
individual. The term caries-controlled is more appropriate.
Dentin caries
Progression of carious lesion: If more acids are produced and the dissolution is in favor over
the repair process, the lesion will progress through enamel into dentin. The progression of caries
process can be slow in population with good oral hygiene. For example, proximal lesions in
permanent teeth can take 3-4 years to progress through enamel. (Pitts, 1983) Studies from
Scandinavian found the median survival time of dentin lesions to spread in the outer half of
dentin to be about 3 years. In late teen Danish population (16-18 years old), of 100 lesions
present in the enamel, 9.2 progressed into the outer dentin per year. The transition into the inner
dentin was slower, only 2.3 surfaces per 100 surfaces per year However, the progression can be
much more rapid in caries active individuals. This picture of rampant caries in a Mountain Dew
drinker, a patient in our clinic, shows high caries activity that has to be controlled immediately.
Microscopic features of dentin caries are: zone of decomposed dentin, zone of bacterial
invasion, zone of demineralization, sclerotic dentin, and reparative dentin. Dentin caries
progresses by demineralization of inorganic substance, breakdown of the organic matrix by
proteolytic enzymes, and bacterial invasion. Clinically, these zones are not readily recognizable,
and the classic pathology does not guide how we should treat carious lesion. More practical way
is to divide the lesion into inner and outer carious dentin. (Note: The reparative dentin is the
reaction of pulp to protect itself.)
Two layers of carious dentin: Diagram shows a relationship between hardness, bacterial
invasion, intratubular crystals of different layers of carious dentin. The inner carious dentin is
the front line when acid attack. Dissolving calcium and phosphate ions fill dentinal tubules and
precipitate as new crystals with lower calcium content, seen as transparent layer or ‘sclerotic
dentin’. The inner carious dentin is uninfected and vital, and the crossband structure of collagen
undergo partially change. The odontoblastic process extends all the way through this layer.
With further attack, the organic substance and odontoblastic process degenerate, and bacteria
invade, it becomes outer carious dentin, which is necrotic and infected. The outer carious dentin
is non-remineralizable because the collagen crossbands are broken. Apatite crystals need the
crossband to attach in order to remineralize.
Practical use of this concept: The outer carious dentin should be removed before filling because
this layer is infected and cannot be remineralized. Because it is non-vital, there is no pain when
it is removed. The inner carious dentin should be kept to preserve natural tooth structure and
enhanced to remineralize. The inner carious dentin is vital, patient will feel pain when it is
touched.
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