Dental Caries

Intoduction
• Loss of tooth substance may result from:

a) the action of oral microorganisms as in dental caries or

b) may be due to non-bacterial causes (attrition, abrasion, erosion

and pathological resorption).
Definition
• Dental caries is a progressive, irreversible bacterial disease of
the calcified tissues of the teeth, characterized by
demineralization of the inorganic components followed by
destruction of the organic substance of the tooth.
It is a complex and dynamic process involve a physicochemical
(movements of ions across ) ,as well a biological processes
(bacteria and the host defense mechanism).
 Theories of dental caries
• Worm theory.
• Chemical theory.
• Enzymatic theory.
• Acidogenic (chemico-parasitic) theory.
• Proteolysis theory.
• Proteolysis-chelation theory.
 Acidogenic (chemicoparasitic) theory.
Miller’s theory.

• States: “dental decay is a chemo-parasitic process

consisting of 2 stages, the decalcification of enamel
which also results in total destruction and decalcification
of dentin followed by dissolution of the softened organic
residue. The acid is derived from the fermentation of
starches and sugar lodged in the tooth surface.”
 Etiology of dental caries:
A) Risk factors (Major):
1. Bacterial dental plaque.
2. Sugar & carbohydrates.
3. Susceptible tooth surface.
4. Time.

B) Contributing factors:
1. Intrinsic factors.
2. Extrinsic factors.
 Bacterial
dental plaque

Sugars &
Carbohydrates.
Major Risk
factors
Susceptible
tooth surface.

Dental caries Time

Extrinsic
factors.
Minor Risk
factors
Intrinsic
factors.
Dental caries

Dental plaque

Sugar & Susceptible

carbohydrat tooth
es surface

Time
 Contributing factors:
Intrinsic factors:

1. Tooth composition: the content of calcium, fluoride, and other minerals

2. Tooth morphology: Deep, narrow pits and fissures favor the retention of plaque and
food

3. Tooth position: malaligned, out of the arch, rotated, etc. are more difficult to cleanse
which leads to accumulation of food and debris and eventually caries.

4. Enamel structure : Developmental enamel hypoplasia and hypomineralization may

affect the rate of progression but not the initiation of caries.
Extrinsic factors:

1. Saliva.
2. Diet.
3. Oral hygiene.
 Contributing factors
1- Saliva :
A. Composition: 1) minerals (calcium, fluoride, and mg) remineralization.
2) buffers neutralization of the acid formed

B. Quantity ( low flow rate as in xerostomia and during sleep causes more
caries susceptibility. )

C. Viscosity ( thick mucinous saliva is associated with caries.)

D. Anti-microbial property (contains antibodies, lactoferrin and lysosomes)

• Saliva prevents dental caries by:

1. Washing
2. Buffering
3. Anti-bacterial effect
4. Remineralization from salivary ca and fluoride.
 Contributing factors
2- Diet:

• Increase in sugar consumption is associated with increase risk of dental caries

• Balanced diet containing CHO and proteins and lipids
• Vitamin rich (vit. A , D , B)
• Containig minerals (eg. Fluoride and Calcium)

3- Oral hygiene:
• good oral hygiene prevents plaque formation.
Role of bacteria & dental plaque
 Role of bacteria:
• Germ-free animals never develop dental caries: bacteria is essential in
dental caries.

• 3 types are highly cariogenic bacteria e.g. mutans strep., lactobacilli,

actinomyces.
• Colonization of oral cavity of neonate (vagina, skin of breast, mother).
• S. salvarius colonizes oral cavity immediately after birth.

• S. sanguis colonizes tooth surfaces immediately at time of tooth eruption

(4-6 months).

• S. mutans colonizes tooth surface during the period 1.5 to 3 years of age
(window of infectivity).
What is the pellicle?
This is an adsorbed layer of glycoprotein that is become adherent to
the clean enamel surface

Dental plaque:
• It is a thin translucent biofilm consists of complex microbial
community, amorphous matrix derived from bacterial products &
salivary mucins, desquamated epithelia, leucocytes, & minerals.
• Matrix derived from bacterial products & salivary mucins >>
extracellular polysaccharide (Dextran) & intracellular polysaccharide
(amylopectin)
• Clinically classified into: Supra-gingival & sub-gingival
Dental plaque formation:
Acquired pellicle ---------------------(within seconds).

Primary colonizers ----------------- (within first 24 hours), mutans strep.

Secondary colonizers -------------- (within 3 days), cocci & bacilli.

Tertiary colonizers ------------------- (7-14 days), anaerobic filamentous

bacteria.
Dental plaque is imperceptible,
detected by disclosing agents
 Role of dental plaque:
1. It produces acid, mainly lactic acid, by fermentation of dietary sugars. (Acid

is the general product of bacterial metabolism).

2. Acid leads to drop in plaque pH by 2 units within 10 minutes.

3. At critical pH (5.5) demineralization of enamel occurs.

4. After 30-60 minutes the plaque pH slowly rises to original value (by

outward diffusion of acids and sugars, inward diffusion of saliva buffer).

5. At neutral pH re-deposition of minerals on enamel (facilitated by F).

Critical pH 5.5

Critical pH 5.5
When the dental plaque lead to dental caries??
1. Repeated demineralization of enamel with out enough time for
remineralization ( frequency of sugar intake).

2. Bulky dental plaque.

**Enamel caries progresses when the net rate of loss of ions due to
acid attack is greater than the net rate of gain due to
remineralization
Microbiology of dental plaque
• Dental plaque consists of more than 500 species.

• The most cariogenic bacteria are streptococcus mutans, lactobacilli

and actinomycetes.
Role of S. mutans:
play a key role in the initiation of caries (Factors affecting the
cariogenicity of bacteria) :-
1. Acidogenic (ferment sugar( Sucrose ) produce acid).
2. Aciduric ( survive & multiply in acidic medium).
3. Produce extra-cellular polysaccharides (mutan or dextran)>>
a- adhesion to the tooth.
b- increase in plaque bulk.
4. Production of intracellular polysaccharides (amylopectin) which
are used by the bacteria when there is deficiency in the dietary
CHOs (starvation ) .
Initiate dental caries.
Smooth surface caries.
 Role of lactobacilli:
The pioneer organisms in dentine caries

• Acidogenic.
• Aciduric.
• Progression of caries .
• Fissure caries.
Role of actinomyces
• Acidogenic.
• Root caries.
 Role of carbohydrates
Types Of dietary sugars:

1- Intrinsic sugars: mainly fruits ,and vegetables.

2- Extrinsic sugars: added sugar.

• According to the chemical structure the CHOs are classified into:

a) Monosaccharides.
b) Disaccharides.
c) Polysaccharides.
**Starch solutions applied to bacterial plaque don't reduce its pH significantly
 Sucrose
Sucrose is the most cariogenic CHO, why?

1. Low molecular weight and can diffuse rapidly into dental plaque.

2. Broken down rapidly by bacteria forming acid.

3. Dextran synthesis from sucrose is faster than from other sugars.

 Factors affecting the cariogenicity of carbohydrates
1. Chemical composition (di-saccharides(sucrose) & mono are more
cariogenic than polysaccharides).
2. Physical form (sticky is more cariogenic).
3. Frequency of intake ( in-between meals).
4. Route of administration ( oral route).
5. Presence of other food constituents ( presence of protein, fats, nuts,
phosphates reduces carcinogenicity).
Prevention of dental caries
Reduce sugar & carbohydrates intake by dietary
change & utilizing sugar substitutes:( xylitol)

Increase tooth resistance: Fluoride application &

Fissure sealants.

Control dental plaque: Mechanical cleansing &

antimicrobial agents: chlorohexidine.

Vaccination.
Classification of dental caries
 Classification of dental caries
I. According to the rate of progression:
1. Chronic caries.
2. Acute ( rampant caries).
3. Arrested caries.
II. According to the site of attack:
1. Pits & fissures caries.
2. Smooth surface caries.
3. Cementum caries.
4. Recurrent caries
III. According to the tissue type:
1. Caries of the enamel.
2. Caries of the dentine.
3. Caries of the cementum.
IV. According to the number of surface involved:
1. Simple , 2. Compound, 3. Complex
V. GV Black classification
 According to rate of progression
1- Rampant / Acute caries:

• This is rapidly progressing caries involving

many or all of the erupted teeth
• More common in children and young adults.
• The rapid coronal destruction and limited
time for the protective responses of the
pulpodentinal complex to occur lead to
early involvement of the pulp.
Examples: Nursing bottle caries, Rampant
caries.
 According to rate of progression
2- Chronic caries (slowly progressive) :

• Progresses slowly with dull pain.

• More common in adults.
• Initial lesion is a large open cavity so better access of
the buffering saliva to the lesion.
• slow progress allows time for defense reactions of the
pulpodentinal complex (sclerosis and reactionary
dentine formation) to develop.
According to rate of progression
3- Arrested caries.

• Static lesion with no further progression.

• No symptoms.

• Due to better cleansing and prevention

• Lesion looks dark brown to black and hard

 Classification of dental caries
II. According to the site of attack:
1. Pits & fissures caries.
2. Smooth surface caries.
3. Cementum caries.
4. Recurrent caries
 According to site of attack.
1- Pits & Fissures:
Early caries may be detected clinically by brown or
black discoloration of a fissure in which a probe
catch .
The enamel directly bordering the pit or fissure
may appear opaque, bluish-white.
Apparently clinically sound enamel can overlay
extensive dentine caries.
2- Smooth surface caries :
Proximal surfaces

Caries begins just below the contact point ???

Chalky-white opacity of the enamel

>>>> Pigmented yellow or brown and may extend

buccally and lingually.

The surface of the lesion becomes roughened

>>>>>> frank cavitation occurs.
3-Cementum caries:
This occurs when the root face is exposed to the
oral environment as a result of periodontal
disease.
Usually shallow, saucer-shaped, with ill-defined
boundaries.
4-Recurrent caries:

This occurs around the margin or at the base of a previously existing

restoration.
 Classification of dental caries
III. According to the tissue type:
1. Enamel caries.
2. Dentine caries.
3. Cementum caries.
 Classification of dental caries
IV. According to the number of surface involved:
1. Simple
2. Compound
3. Complex
 According to number of surface involved:
1. Simple :
Involved only one surface

2. Compound :
Involved two surfaces

3. Complex :
Involved three or more surfaces
 GV Black Classification 1908:
1- Class I:
• Pits, fissures and grooves :

i-Occlusal surface of the all posterior teeth

ii-Palatal surface of the upper anterior teeth
iii-Palatal groove & pit of upper post. Teeth
iv- Buccal groove & pit of lower post. Teeth
 2- Class II:
• Caries involving the proximal surfaces of molar and
premolars

3- Class III:
• Caries on the proximal surfaces of the anterior teeth BUT
not involving the incisal edges
4- Class IV:
• Caries on the proximal surfaces of the anterior teeth and involving
the incisal edges

5- Class V:
• Caries on the gingival third of the facial
or lingual surfaces of all teeth

Class VI:
• Any carious lesion that is not included in the previous GV Black
classes (eg. carious lesions of the incisal edges of anterior teeth and
cusp tips of canine and posterior teeth).
Histology of dental caries
 Enamel caries

Ground Section …
• A section of bone or tooth prepared by polishing until thin enough for
microscopic examination.
1. Early enamel caries
• Early enamel caries shows four
histological zones ( degree of
demineralization ): (from inwards
to outwards)
1. Translucent zone (1%).
2. Dark zone (2-4%).
3. Body of the lesion (5-25%).
4. Surface zone.

• Note: normal enamel has a

porosity of 0.1%.
A. Early pit and fissure caries:
1- Enamel caries is cone-shaped.
2- The base of the cone is towards the amelo-dentinal junction, and
the apex is to wards the enamel surface.
B. Early smooth surface caries:
1- Enamel caries is also cone-shaped.
2- The base of the cone on the enamel surface ,
and the apex towards the amelo-dentinal
junction.
 Zones of enamel caries
1-Translucent zone:

• The first recognizable histological change

• More pours than normal enamel(1% pores volume compared to 0.1%
in normal enamel)
• The pores are larger than those of normal enamel.
• Fall in magnesium and carbonate content (by dissolution).

*** The translucent zone is sometimes absent or very narrow.

2-Dark zone:

• Contain 2-4% by volume of pores.

• Some pores are larger ,but others are smaller than those in the
translucent zone suggesting that some remineralization has occurred.

• It is narrow in rapidly advancing lesions ,and wider in slowly

advancing ones when there is more remineralization.
3- Body of the lesion:
• Has a pore volume of 5-25%.

• Contains more apatite crystals than in normal enamel.

• These large crystals suggesting that some reprecipitation of minerals

dissolved from deeper layers.

• But with continuous acid attack there is more dissolution of mineral

from both the periphery and the core of the crystals
4- Surface Zone

• This is layer shows little change in early lesion.

• The surface of normal enamel differs in composition from deeper
layers:
a- more mineralized.
b-contain more fluoride
• The surface layer remains normal ,because it is an area of
reprecipitaion of ions derived from plaque and from deeper layers.
Surface zone

Body of the
lesion
2. Late enamel caries:
• When caries reach DEJ spreads laterally along the junction leading to
separation of enamel from dentine & become undermined.
• Ultimately to cavitation and loss of surface zone.
Histo-pathogenesis of enamel caries Clinical aspect

1. Subsurface translucent zone Unrecognized

1. dark zone develops in centre of translucent zone Unrecognized

1. the body of the lesion develop in the center of Chalky white spot.
dark zone.

1. stained by exogenous pigments from food, brown spot.

tobacco, and bacteria

1. DE junction it spreads laterally bluish-white margin

1. Undermining and breaks down of enamel form a cavity

 Dentine caries
• Caries of the dentin develops from enamel caries when the lesion reaches
the amelo-dentinal junction (A.D.J).

• Dentine differs from enamel in that:

a) It is a living tissue >>>>> Respond to caries attack.
b) It contain high organic content (in the form of collagenous protein) -20% of its
weight.
• Responses of the dentino-pulpal complex to dental caries:
1. Sclerosis of dentinal tubules.
2. Sealing of dead tracts.
3. Reparative ( reactionary) dentine.
 Reactionary or (tertiary) dentin
1- A layer formed at the pulp surface deep to the carious dentin.

2- It differs from normal dentin:

a- Tubules are irregular, tortuous and fewer in number.

b- Hyperminerlized ,compared to normal dentin.

c- Its formation increases the bulk of the tissue between the

carious dentin and the pulp.
In rapidly progressive lesions the defense reaction is overtaken by the
carious process.

The early lesion is cone- shaped with the base at the (A.D.J).
Steps of dentin caries:
a) acid demineralization.
b) bacterial invasion.
c) collagenous destruction.
The pathogenesis of dentin caries involve:
a- defense reaction of the pulpodental complex:
1- sclerosis ( in dentinal tubules).
2- reactionary dentin formation.
3- sealing of the dead tracts.
*** The defense reaction begins before the carious process reaches the
dentin.

b- bacterial destruction:
1- demineralization
2- proteolysis
 Zones of dentin caries
1- The sclerotic or translucent zone :
Is a vital reaction of odontoblasts to irritation
is located beneath and at the sides of the lesion.
Two mechanisms are suggested for this sclerosis to occur:
a. acceleration of the normal physiologic process of deposition of peritubular dentin-
>>>>> eventually occludes the tubules.
b. or minerals first appears in the cytoplasmic processes of odontoblasts , and the
tubule is occluded by calcification of the odontoblastic processes it self.
2- Dead tracts
They result from death of odontoblasts at an earlier stage in the
carious process.
Obviously not undergo sclerosis.
They provide ready access of bacteria and their products to the pulp.
To prevent this the pulpal end of a dead tract is occluded by a thin
layer of hyaline calcified material derived from pulp cells.

** beyond this here is often irregular reactionary dentine following

differentiation of odontoblasts
 3-Zone of deminerlization
• The intertubular dentin affected by acid production by a wave
of acid diffusing a head of the bacterial front.

• The softened dentin in the base of a cavity is therefore sterile.

 4-Zone of bacterial invasion
The bacteria enter and multiply within the dentinal tubules.
The bacterial invasion probably occurs in two waves :
a- The first wave: is the acidogenic bacteria mainly lactobacilli which
produce acid >>> demineralized zone.
b- The second wave: is the proteolytic bacteria that attack the
demineralized matrix.

The peritubular dentin is compressed>>>> Intertubular compressed>>>

areas of proteolysis-liquefaction foci.
 5-Zone of destruction

The liquefaction foci enlarges and increase in number.

Cracks or cleft containing bacteria and necrotic tissue.

Bacteria are no longer confined to the tubules >>>> invade both the
peritubular and intertubular dentine

In acute caries ,the necrotic dentin is soft and Yellowish-white, where as

in chronic caries it is leathery and brownish-black in color.
 Root caries
• The primary tissue affected in the root caries is the cementum.

• It follows exposure of the root to the oral environment due to a

periodontal disease followed by bacterial colonization ,mainly Actinomyces
species, but also Lactobacilli and Mutans st.

• Histopathology shows:
a. Hypermineralized surface layer.
b. Demineralization of the subsurface layer that extend into the dentin.

• Root caries is detected clinically by softening and brownish discoloration.

Non-Bacterial tooth surface loss

Tooth wear
 Tooth wear
• Progressive loss of the tooth surface due to actions other than those
cause dental caries.

• The tooth wear is a normal physiologic process that occurs with aging.
• Tooth wear is considered pathological when the degree of destruction
creates functional, aesthetic, or dental sensitivity problems.
• Tooth wear is caused by four phenomena:
1. Erosion
2. Attrition
3. Abrasion
4. Abfraction

***in many individuals tooth surface loss is multi-factorial and a

combination of these processes is present.
 Erosion
A progressive loss of tooth substance by non bacterial

chemicals or acids.

Etiology:
1. Excessive consumption of carbonated drinks and fruit

juices with high levels of acidity (most common cause).

• Commonly seen in teenagers and young adults.

• Typically, the labial enamel is thin and shiny, sometimes with

exposure of the underlying dentine.

2. Gastro-oesophageal reflux disease or bulimia: affects the palatal

enamel more severely

3. Individuals with a low salivary flow rate

 Attrition
A progressive loss of dental hard tissue caused by the action of tooth to
tooth contact (mastication or grinding between opposing teeth).

Etiology:

1. Mild attrition is normal (normal physiological process that increases

with age)

2. Habitual clenching or grinding of the teeth (bruxism) may also result in

severe attrition pulp exposure.
 Abrasion
A progressive loss of tooth surface caused by mechanical actions of
substances other than tooth-to-tooth contacts.
Etiology:
1. Abrasion is commonly associated with inappropriate tooth brushing
technique, typically resulting to cervical notching
2. Abrasion may result from use of teeth as a tool to remove bottle tops
or hold pins, clips, or nails.
3. Oral piercing with the long-term use of intra-oral jewellery may also
cause tooth abrasion and gingival injury.
 Abfraction
• Loss of tooth structure from occlusal stresses that create
repeated tooth flexure with failure of enamel and dentin
at a location away from the point of loading.

• The term is derived from the Latin words ab and fractio,

which respectively translate into away and breaking.
 Pathogenesis:
• Dentin is able to withstand greater tensile stress
than enamel. When occlusal forces are applied
eccentrically to a tooth, the tensile stress is
concentrated at the cervical fulcrum, leading to
flexure that may produce disruption in the chemical
bonds of the enamel crystals in the cervical areas.
• Once damaged, the cracked enamel can be lost or
more easily removed by erosion or abrasion.
• appears as wedge-shaped defects limited to the cervical area of the teeth and
may closely resemble cervical abrasion or erosion.
Clues to the diagnosis
1. defects that are deep, narrow, and V-shaped (which do not allow the toothbrush
to contact the base of the defect) and often affect a single tooth.
2. subgingival lesions, a site typically protected from abrasion and erosion.
 ☺
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