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DENT 5302 TOPICS IN DENTAL BIOCHEMISTRY

DENT 5302 TOPICS IN DENTAL BIOCHEMISTRY

24 March 2008

The caries process

Dietary factor and cariogenic aspects of dental plaque
Plaque fluid and the caries process

Fluoride and dental caries

Anticaries mechanisms of fluoride
Objectives:

Fluoride metabolism

Nature and character of dental caries

Fluoride toxicity

Factors influencing the caries process

Application of fluoride (& Ca P) in caries control measures

Development of early caries lesion in enamel

Dentin caries

Outline

Carious
Teeth (%)

Nature of dental caries

History & Epidemiology

Epidemic

1950
Industrialize

20

Key features of dental caries

Multi-factorial

15

Site specific
Dynamic

Fluoride

Roman
10

Demineralization-Remineralization
Formation of early enamel lesion

Microscopic features of early enamel lesion

Caries free vs Caries controlled

Dentin caries

2000

1000

1000

2000

Percentage of carious teeth in English population

Nature and character of dental caries

Disease pattern and civilization: Dental caries is an ancient disease. 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 1950s, 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 fluoride.
Dental caries: the most prevalent infectious disease
5x > childhood asthma ; 7x > hay fever
Affects 85% of adults (>18 years old) in the US
80% of caries occurs in 20% of the population
www.surgeongeneral.gov/library/oralhealth/

Underprivileged population?

Less than high school

High school

At least some college

Total children

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 socioeconomic status.

Evans CA, Kleinman DV (2000).

The Surgeon General's report on
America's oral health: opportunities
for the dental profession.
J Am Dent Assoc. 131: 1721-8.

A survey done in the late 80s showed that in the US

75% of children aged 5-11 years old were cariesfree. Data from the latest National Health and
Nutrition Examination Survey (NHANES) 19992002 showed that 42% of children and adolescents
aged 6 -19 years, had caries experience in their
permanent teeth, and 91% of dentate adults aged >20
years had caries experience.

1980s: 75% of children aged 5-11 years old were caries-free

42% of children and adolescents aged 6 -19 years, had caries experience in
their permanent teeth
91% of dentate adults aged >20 years had caries experience
NHANES1999-2002

The nature of caries has changed:

Rapidly progressing childhood disease
Slow but steadily progressing disease in adulthood
Data from the National Health and Nutrition Examination Survey (NHANES)
1988-1994 vs 1999-2002:

The nature of caries has changed from a rapidly

progressing childhood disease to a slow but steadily
progressing disease in adulthood.

Dental caries in primary teeth of Children aged 2-5 years has increased!

Discussion

An interesting observation when compare data from

the current NHANES to the 1988-1994 survey is that
dental caries in primary teeth of children aged 2-5
years has increased!

From the current survey, what factors contribute to the

increase in caries experience?

Dental caries is multifactorial

Characters
of caries

Dental caries is multifactorial

Traditional
concept

Cariogenic
bacteria (dental
plaque)

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 dont
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.

Diet:
Fermentable
carbohydrate

Host factors:
Tooth
Saliva

Characters
of caries

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.

Dental caries is multifactorial

Social class

Modern
concept

Education
Saliva
Microbial
species Biofilm

Biological
determinants

Flow rate
Composition
Buffer

Income

Fluoride
Tooth
Genetic

Time
Behavior

Socioeconomical factors

Diet

Composition
Sugar
Frequency

Attitude

Knowledge

Characters
of caries

Dental caries is site specific

Dental caries: Localized destruction of tooth tissues

Erosion

Why localized?
Tooth morphology affects plaque accumulation
Metabolism of microorganisms in dental plaque (biofilm)
Microenvironment (plaque composition, thickness, diffusion properties)
Access to dietary substrates, saliva, anticaries agents

Characters
of caries

Dynamic: Dental caries is a dynamic process.

Before caries can be detected by eyes or by xray, there is a stage of sub-clinical initial lesion
that is a battle between demineralization and
remineralization.

Dental caries is dynamic

Mineral content

Demineralization vs Remineralization

breakfast coffee
break

This graph shows pH change during the day.

When we wake up, our teeth are in the stage of
demin from less salivary flow. Brushing stops
the demin and boost remin. Breakfast drops
pH. When saliva neutralizes the acid, we have
coffee break, then lunch, and snacks, and
dinner. This day ends up with a net mineral
loss, which means that the caries lesion
progresses.

Net
loss

lunch
snack

brushing

dinner
snack
brushing

am

on
no

pm

n
id

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). 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 anticariogenic agents
varies in different locations of the mouth.

h
ig

The brown spot or arrested lesion is an 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.

Brown spot (Arrested lesion)

Change in microenvironment
Reduced plaque accumulation
Access to saliva

A short video about de- and remineralization

process, downloaded from a website of a
company that makes a milk derivative product
called Recaldent.

Application

www.recaldent.com

Formation of early enamel lesion

plaque

saliva

Development of early caries lesion in enamel

sound enamel

Organic acids produced by plaque bacteria diffuse

into the enamel by the difference in concentration
subsurface
lesion
gradient. Then the acids dissociate and provide
acid diffuse & dissociate H+ + apatite
protons (H+). H+ attack the apatite crystals, break
H2O
OHthem down to calcium, phosphate, and other ions.
32+
Ca2+
Ca + PO4 + OH
Calcium, phosphate, and other ions diffuse
HPO42- PO43according to their concentration gradients through
Fmicroporosities of the carious enamel. They can go
surface zone (repair)
in any direction. For example, diffusing outward
when plaque fluid is undersaturated.
When more minerals are dissolved, calcium and phosphate concentration increase. 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. In the body of the lesion the demineralization may continue until as much as 70% of the
mineral is dissolved. Some of the calcium and phosphate diffuse inwards, therefore remineralization is also
observed in the 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

1
2
3

34

1. Surface Zone

Intact surface 20-100 m thick, <10% mineral loss

2. Body of the Lesion

Largest zone, highest mineral loss (24%)

3. Dark zone

Very small pores, <10% mineral loss

4. Translucent zone

Advancing front, 1% mineral loss

Clinical appearance: White spot lesion

First clinical sign of enamel caries lesion
300 500 m depth to be visible
Subsurface demineralization
Surface intact

At early stage, caries lesion is subsurface

Why are we interested in early caries lesion?
At this stage the lesion is reversible
Fluoride and preventive treatment are most effective at this stage

Microscopic features of early enamel lesion:

Early enamel lesion consists of 4 zones with different
levels of porosities.
1. Surface Zone: Intact surface 20-100 m thick,
<10% mineral loss
2. Body of the Lesion: Largest zone, highest mineral
loss
3. Dark zone: very small pores due to reprecipitation.
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
demineralization as a white area because of many
porosities under the surface. Early caries lesions with
intact surface are critical stage because the carious
process is still reversible, and preventive treatment and
control (such as fluoride) is effective.
4

Early carious lesions are reversible

Age 8

Age 15

Sound enamel

93

White spot

72

Cavitated lesion

19

74
37
15
26
4
9
19

111 sound enamel

41 white spots
32 cavitated lesions

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.

(Baker-Dirks, 1966)

Study done in community with water fluoridation

Only 9 of 72 white spot lesions became cavitated after 7 years
More than half of early lesions regressed to normal enamel

Discussion: (Pair)

caries-free vs caries-controlled

Is there a caries-free individual?

Q1 Do you have any cavities or fillings

Q2 Do you think you have demin-remin periods?

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.
Progression of Carious Lesion
How long?
Proximal lesions in permanent
teeth can take 3-4 years through

enamel, unless in caries active

individuals. (Pitts, 1983)
Median survival time from
stage 2 to 3 was ~ 3 years
Late teen Danish population
From 2 3: 9.2 surface % per year

Rampant caries in Mountain Dew drinker

From 3 4: 2.3 surface % per year

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.
5

Dentin caries

Microscopic features of dentin caries

Microscopic features carious dentin

A = zone of decomposed dentin

B = zone of bacterial invasion
C = zone of demineralization
D = sclerotic dentin
E = reparative dentin

Dentin caries progresses by demineralization of inorganic

substance and breakdown of the organic matrix by
proteolytic enzymes. Then bacteria invade dentin.

Outer carious dentin

Inner carious dentin

Dentin caries consists of zone of decomposed dentin, zone of

bacterial invasion, zone of demineralization, and sclerotic
dentin. Reparative dentin is the reaction of pulp to protect
itself. Clinically, these zones are not readily recognizable. It
is more practical to divide into inner & outer carious dentin.

Progression of dentin caries

Demineralization of inorganic
substance
Breakdown of organic matrix
by proteolytic enzymes
Bacterial invasion

Dentin caries

Knoop Hardness Number

Two layers of carious dentin

70 -Outer carious dentin
60 -

Inner carious dentin

infected

uninfected

nonremineralizable

remineralizable

50 - nonvital
insensitive
40 -

Sound dentin

vital
sensitive

30 20 Turbid
layer

10 -

DEJ

1000

Transparent
layer

Subtrans
parent
layer

Pulp
wall

3000 m

2000

Crystals in tubule lumen

Bacteria
Odontoblast

Fusayama T, Okuse K, Hosoda H. J Dent Res. 1966;45:1033-46.

Relationship between hardness, discoloration, and microbial invasion in carious dentin.

This 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. Then the bacteria invade
and the tissue becomes outer carious dentin which is necrotic and infected. The outer carious dentin is nonremineralizable because the collagen crossbands are broken. For the remineralization process, apatite
crystals need the crossband to attach to.
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.
Recommended references

Discussion
What do you learn today that can be used in future practice?

1. Clarkson BH. Introduction to Cariology. Dent Clin North Am

1999;43(4):569-578.

1. Why underprivileged population have more caries?

2. Zero DT. Dental Caries Process. Dent Clin North Am

1999;43(4):635-664.
3. Featherstone JD. The science and practice of caries prevention. J
Am Dent Assoc 2000;131:887-899.

2. What should we do with white spot lesion?

4. Gordon Nikiforuk. Understanding Dental Caries 1. Etiology and

Mechanisms, Basic and Clinical Aspects. Basel; New York: Karger
1985. Chapter 10.
5. Gao W, Smales RJ, Yop HK. Demineralisation and remineralisation
of dentine caries, and the role of glass-ionomer cements. Int Dent J
2000;50:51-56.

3. How much carious dentin should be removed?

6. Fejerskov O. Changing paradigms in concepts of dental caries:

Consequences for oral health care. Caries Res 2004;38:182-191.