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PREVENTION II
“CARIOLOGY’
HISTORICAL OVERVIEW
• General understanding of cause of dental caries
has not changed since Miller developed the
chemoparasitic theory over 100 years ago:
– Acid is produced by metabolism of dietary
carbohydrates by oral bacteria.
– Acid dissolution of the mineral phase of the
tooth.
– Secondarily, the organic phase of enamel and
dentin is broken down.
KEY FEATURES
• Dental caries has a multi-factorial
causation.
• Dental caries is an oral infection.
• Dental caries is a dynamic process.
• Dental caries can be modified by
protective factors.
MULTI-FACTORIAL PROCESS
• Involves the interaction of host factors (tooth
surface, saliva, acquired pellicle), diet, and dental
plaque (biofilm).
• Caries does not occur in the absence of either
plaque or dietary fermentable carbohydrates.
• Therefore, caries must be considered a
dietobacterial disease.
• Dental caries can be conceptualized as an
interaction between genetic and environmental
factors, in which the biopsychosocial components
are expressed in a highly complex, interactive
manner.
MULTI-FACTORIAL PROCESS
BIOLOGICAL FACTORS
CARIES IS AN
ORAL INFECTION
• Germ free rats that were fed high sucrose
containing diets did not develop dental caries.
• When the same animals were infected with
specific strain of micro-organisms, caries
developed.
• Experiments also document that micro-organisms
could be recovered from a carious lesion, isolated,
cultured, and used to infect caries- free animals,
resulting in caries.
• Antibiotics have been shown to reduce the
incidence and severity of caries in experimental
animals.
GENETICS
• In the past the importance of genetic factors has been
minimized primarily because the disease was essentially
present in the entire population, thus not allowing genetic
differences among individuals to manifest themselves.
• Genetic factors relate to:
– tooth composition and structure
– tooth morphology
– arch form
– tooth alignment
– saliva flow rate and composition
– oral physiology
– endogenous microflora
– food preferences
– personality traits
TEETH
• Location, morphology, composition,
ultra-structure, and post-eruptive
age of the tooth.
• Teeth have a high resistance to
caries, as evidenced by the low caries
prevalence in primitive humans.
• Modern humans have challenged this
natural resistance by modifying our
diets.
ENAMEL SOLUBILITY
• Theoretically, if one could decrease the acid
solubility of enamel, this would decrease the
caries susceptibility of a tooth.
• However, studies have shown that even pure
fluorapatite, which is the least acid-soluble form
of calcium-phosphate species, demineralizes in the
presence of a strong acid challenge.
• While enamel is composed mostly of mineral in the
form of hydroxyapatite, it also contains other
inorganic and organic components.
MAJOR COMPONENTS
OF ENAMEL
ENAMEL COMPOSITION
• Enamel composition reflects the composition of
the physiologic fluid surrounding the developing
tooth.
• Enamel composition at the surface also reflects
the fluids of the oral environment as well.
• Evidence suggests that trace element composition
in enamel, such as the amount of fluoride present
as fluorapatite, is of relatively minor importance in
the clinical expression of dental caries.
ENAMEL STRUCTURE
• Factors other than enamel composition affecting
enamel solubility are crystal size and shape, and
the proximity of the crystals.
• Enamel is composed of long, thin, crystallites,
approximately 40 nanometers (billionth of a
meter) in diameter, that are bundled together to
form enamel rods or prisms, approximately 4
microns (millionth of a meter) in diameter running
from the dentin to the outer enamel surface.
• An organic matrix surrounds the prism, forming
the prism sheath; this organic material composes
about 5% of tooth enamel by volume.
STRUCTURAL
RESISTANCE
• The larger and more uniform the crystals, the less
the specific surface area and reactivity
(solubility).
• The more closely packed the crystals, the less
space for water and thus diffusion pathways
between crystals.
• Because of the spaces between crystals, enamel is
a micro-porous material. Water between the
crystals serves as a diffusion channel in which
acids can diffuse into those spaces to attack the
crystals. Therefore, the more closely packed the
crystals, the less soluble the enamel.
POST-ERUPTIVE MATURATION
• Caries susceptibility is greatest immediately subsequent to
eruption, and tends to decrease with age.
• Teeth undergo a post-eruptive maturation process that
involves changes in the composition of the surface enamel.
• This is related to the demineralization-remineralization
dynamic which will be discussed subsequently.
• During the demineralization process, the more soluble
carbonate-rich apatite is preferentially lost and replaced by
apatite lower in carbonate and higher in fluoride, assuming
fluoride exists in the oral environment.
• These reprecipated crystals eventually grow to be larger
than the original crystals, creating hypermineralized areas
of enamel.
• This response of the enamel explains the decreased
susceptibility to caries that occurs with age.
• The effectiveness of fluoride in caries prevention can be
largely attributed to its ability to enhance the
remineralization process.
SALIVA
• Salivary flow rate and composition are well
recognized as important host factors that modify
the caries process.
• Salivary tooth protection mechanisms include
mechanical cleansing action, dilution and buffering
plaque acids, anti-microbial properties, and
providing inorganic and organic components that
inhibit tooth demineralization and assist in the
remineralization and repair process.
• Reduced or loss of salivary function is associated
with dramatic increases in caries activity.
ACQUIRED PELLICLE
• The acquired pellicle, which is an acellular, essentially
bacteria-free organic film of mucopolysaccrides that is
deposited on teeth, occupies a critical position between the
enamel surface and the biofilm which we refer to as the
dental plaque.
• The formation of biological films, such as the pellicle, is
ubiquitous in nature and precedes the formation of all
biofilms.
• The pellicle is formed mainly by selective adsorption of
salivary glycoproteins and proteins. These organic
components of saliva have a high affinity for the enamel
surface and rapidly adsorb to a clean (pumiced) enamel
surface.
• The pellicle adheres to the enamel and acts as a diffusion
barrier to protect the enamel from acid exposures of short
duration, as in ingestion of acidic foods.
ACQUIRED PELLICLE
• If removed (by dental polishing) the pellicle
requires a maturation period (7 days) before it
becomes maximally protective against acids.
• The use of abrasive toothpastes and whitening
products, as well as the abrasion from rubber cup
prophylaxis, removes the pellicle, and can have an
adverse effect on exposed tooth surfaces in
increasing the probability of loss of tooth enamel
by demineralization.
DIET
• The frequency of eating fermentable
carbohydrates has been strongly associated with
dental caries.
• Factors associated with diet and dental caries
include the relative retentiveness of the food; the
presence of protective factors in food, such as
calcium, phosphate, and fluoride, and the type of
carbohydrate.
• Complex carbohydrates (starches) are less
cariogenic than simple carbohydrates (sucrose,
glucose, and fructose).
SUCROSE
• The cariogenicity of sucrose is partly attributed to its
contribution to the plaque bacteria’s ability to synthesize
extracellular polysaccharides, which favors the accumulation
of more bacteria.
• In studies using mutans Streptococci, plaque prepared from
sucrose-containing cultures was found to have a markedly
enhanced demineralization potential compared with glucosegrown plaque.
• The effect was attributed to an alteration of the diffusion
properties of plaque due to the water-insoluble extracellular
matrix (the glucan) synthesized from sucrose.
• The glucan permits greater penetration of dietary
carbohydrates into the plaque.
THE PROCESS DIAGRAMMATICALLY
PLAQUE
• A number of endogenous oral microorganisms
found in dental plaque can contribute to the caries
process:
– mutans streptococci (S. mutans, and S. sobrinus
– S. sanguis and salivarius, and other non-mutans
species
– Lactobacilli species
– Actinomyces species
– yeast
• It is important to remember that even in a caries
free mouth, 1 ml of saliva contains 10-100,000
endogenous microorganisms.
PLAQUE
• Initial colonization of the plaque biofilm on a tooth surface
is predominately S. sanguins and S. salivarius.
• Shortly after initial adherence to the tooth, Streptococcus
mutans becomes a major component of the biofilm.
• Streptococcus mutans is generally considered the most
virulent of the organisms that participate in dental caries.
• Through time there is a maturation of the plaque
characterized by a shift from a predominated aerobic Gram
positive cocci to anaerobic Gram negative rods.
• If a lesion progresses to cavitation, and particularly as it
advances into the dentin, lactobacilli seem to be favored
because they thrive in this sheltered, highly acidic
environment.
• Thus the process of enamel demineralization and eventual
cavitation is related to bacterial succession, in which one
organism initiates or pioneers the plaque, while subsequently
another organism takes over.
PLAQUE pH
• The pH of dental plaque is normally close to
neutrality.
• When a fermentable carbohydrate (such as
sucrose) is ingested, the plaque bacteria produce
acids which causes a drop in the pH level.
• pH levels lower than 5.5 can initiate
demineralization and after a sucrose rinse, the pH
value can fall to as low as 4.0.
• At these low pH levels, calcium and phosphate ions
begin to dissolve out of the enamel and will
continue to do so as long as the environment
remains sufficiently acidic.
STEPHAN CURVE
Approximately twenty minutes after ingestion of sucrose, and once the
supply of fermentable nutrients is exhausted, the bacterial will cease to
produce acids and the plaque pH will gradually return to a slightly
alkaline resting level.
DYNAMIC NATURE OF
CARIES
• The earliest macroscopic evidence of caries of a
smooth enamel surface is a small opaque white
region; referred to as a white spot lesion.
• Its presence is an indication that there is a
localized decrease in mineral content of the
enamel, although the surface is still hard when
examined with a dental explorer. In ground section
of a white spot lesion, viewed under polarized light
microscopy, four different zones can be
identified.
PHOTOMICROGRAPH OF
WHITE SPOT LESION
RADIOMICROGRAPH OF
WHITE SPOT LESION
WHITE SPOT LESION
#1 SURFACE ZONE
One of the the fascinating features of this initial lesion of caries is
that most of the demineralization begins to occur at a subsurface
level, leaving the surface zone relatively unaffected.
WHY SUBSURFACE?
• It is theorized that the mineral dissolved from
this subsurface zone is pumped toward the
surface and acts to remineralize the surface zone
by precipitation of minerals from this underlying
layer.
• The surface layer of enamel is also more highly
mineralized than the subsurface layer to begin
with, and thus may be more resistant to acid
attack.
• Although the surface layer is relatively
unaffected, it is more porous at this stage than it
was before the lesion was initiated.
WHITE SPOT LESION
#2 BODY OF THE LESION
This is the largest portion of carious enamel in the white spot lesion.
It has often lost one-quarter of its original mineral content.
WHITE SPOT LESION
#3 DARK ZONE
This zone is very porous, and has experienced
a mineral loss of about 6%.
WHITE SPOT LESION
#4 TRANSULENT ZONE
This is the advancing front of the enamel lesion. It is more porous than
sound enamel but less porous than the dark zone.
DEMINERALIZATION:REMINERALIZATION
• Eventually, the relatively unaffected surface zone becomes
demineralized and the rate of the progress of the lesion
increases rapidly.
• This surface zone appears to control, to a large extent, the
rate of progression of a lesion.
• If the surface layer above a lesion can be ‘strengthened’
through fluorides or mineralizing solutions, the lesion can
become arrested, and the process reversed.
• Or if the surface area becomes and remains plaque-free,
then the saliva itself, being supersaturated with regard to
calcium and phosphate, can remineralize the initial lesion as
well.
• The average time for the dynamic carious process to
proceed from the stage of a white spot lesion to clinically
detectable caries is approximately two years.
• A high frequency of exposure to sucrose could greatly
accelerate the process of demineralization, while exposure
to fluorides may favor remineralization.
DEMINERALIZATION:REMINERALIZATION
• The enamel surface is in a state of dynamic
equilibrium with its local oral environment (plaque
fluid and saliva) that involves the constant
movement of ions in and out.
• As the pH of plaque drops, a point is reached
where the mineral phase of enamel begins to
dissolve.
• This critical point is estimated to be between 5.0
and 6.0
DEMINERALIZATION:REMINERALIZATION
IMPLICATIONS FOR
RADIOGRAPHIC DIAGNOSIS
• Laboratory studies demonstrate that
histologically the lesion must penetrate
just into the dentin before evidence of a
carious lesion is observed on a routine bitewing radiograph
• At this stage the lesion is observed on the
radiograph as a small triangular region of
radiolucency in the outer enamel.
RADIOGRAPH VERSUS HISTOLOGY
PRIMARY TEETH
• In the primary dentition, this understanding of the carious
process suggests a significant problem.
• Primary molars tend to have broad, flat contact areas in
contrast to the contact ‘points’ in the permanent dentition.
• This exposes a large interproximal area of primary teeth to
stagnation which favors bacterial colonization.
• Additionally, primary enamel thickness is about one-half that
of permanent enamel, and the pulp chamber is relatively
larger.
• Studies indicate that the rate of progression of a lesion
through primary enamel is much faster compared with an
equal distance through permanent enamel.
CLINICAL IMPLICATIONS FOR
CARIES DIAGNOSIS
• A carious lesion which could not be
detected by explorer or radiographically,
has already penetrated halfway through
the enamel.
• A lesion which can be observed on a bitewing radiograph has probably already
advanced into the dentin. This is especially
true in the primary dentition.
CARIES PROGRESSION
• Although the enamel surface is clinically intact when the
lesion reaches the enamel-dentin junction, acids can diffuse
into the dentin via carious enamel and, together with other
clinical stimuli, can cause the dentin and pulp to respond.
• Lateral spread along the enamel-dentin junction produces a
broad-based lesion that follows the curvature of the
dentinal tubules so its narrow apex approaches the pulp.
• In the dentin there is a zone of sclerosis walling off the
lesion from the surrounding normal dentin.
• The pulp also reacts to the advancing lesion by laying down a
region of reparative dentin.
CARIES PROGRESSION
• The body of the dentinal lesion may at first be
uninfected, since bacteria cannot gain access until
a cavitation forms in the surface enamel.
• At this stage, if preventive measures are
instituted, the lesion can remain static or even
regress.
• Once the enamel lesion becomes cavitated,
bacteria can penetrate into the tissue, and the
rate of progression of the dentin lesion increases.
• At this time, proteolytic enzymes of the bacteria
destroy the organic collagenous matrix of the
enamel and dentin, and the characteristic dental
cavity exists.
CARIES PROGRESSION
IN A FISSURE
DEMINERALIZATION:REMINERALIZATION
SUMMARY
• Dental caries has a multi-factorial
causation.
• Dental caries is an oral infection.
• Dental caries is a dynamic process.
• Dental caries can be modified by
protective factors.