PREVENTION II

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PREVENTION II

• CARIOLOGY

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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.

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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.

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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.

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MULTI-FACTORIAL PROCESS
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BIOLOGICAL FACTORS
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CARIES IS AN ORAL INFECTION

• Germ free rats that were fed high sucrose
  containing diets do 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.

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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

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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.

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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.

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MAJOR COMPONENTS OF ENAMEL
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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.

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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 nm in diameter) that are
  bundled together to form enamel rods or prisms
  (approximately 4 microns 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 the tooth enamel by volume.

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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.

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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-reminerali
  zation 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.

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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.

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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.

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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.

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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).

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SUCROSE

• The cariogenicity of sucrose is partly attributed
  to its contribution to the plaque bacterias
  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
  glucose-grown 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.

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THE PROCESS DIAGRAMMATICALLY
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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.

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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.

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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.

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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.

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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.

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PHOTOMICROGRAPH OF WHITE SPOT LESION
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RADIOMICROGRAPH OF WHITE SPOT LESION
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WHITE SPOT LESION

• 1 SURFACE ZONEOne 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.

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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.

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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.

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WHITE SPOT LESION

• 3 DARK ZONE
• This zone is very porous, and has experienced
• a mineral loss of about 6.

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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.

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DEMINERALIZATIONREMINERALIZATION

• 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 clinical 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.

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DEMINERALIZATIONREMINERALIZATION

• 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

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DEMINERALIZATIONREMINERALIZATION
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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 bite-wing
  radiograph
• At this stage the lesion is observed on the
  radiograph as a small triangular region of
  radiolucency in the outer enamel.

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RADIOGRAPH VERSUS HISTOLOGY
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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.

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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 bite-wing
  radiograph has probably already advanced into the
  dentin. This is especially true in the primary
  dentition.

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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.

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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.

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CARIES PROGRESSION IN A FISSURE
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DEMINERALIZATIONREMINERALIZATION
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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.