The Developing Caries Lesion

Content
• Concepts Of Caries
• Embryology and Histology of Enamel
• Physical and Microscopic Features of Incipient Caries
• Pore Spaces of the Different Zones
• Direct Connection of the Bacterial Plaque to the Body of
the Lesion
• Cariogenic Bacteria
• Bacterial Adhesion
• Coronal Dentin Caries
• Root Caries
• Prevention of Root Caries
Concepts of Caries

• Balance between de- and remineralization

maintains homeostasis  intact tooth
• Demineralization > Remineralization 
cavitations
 Theories of Caries

Barber-surgeon Era Late 1700 Robertson, England,

1835

Theory of Vital Theory

‘tooth worm’ Food impaction +
fermentation  caries

Caused by worms Inflammation within a

living in the center of defective tooth  surface
the tooth lesion

G.V. Black W.D.Miller,

Germany,1890

Chemico-parasitic Theory
Source of acids: gelatinous
microbic plaque
extraction of ‘lime salt’ from
bacterial acidogenesis 
First step of dental decay
Areas of caries occurence

• Pit and Fissure caries

– Occlusal surface of posterior teeth
– Lingual pits maxillary incisors
– Buccal surfaces of lower molar
• Smooth-surface caries
– On intact smooth surfaces other than pit & fissure
• Root-surface caries
– Involves any surface of the root
• Secondary or recurrent caries
– On tooth surface adjacent to existing restoration
 Factors of Caries Occurrence

Host
Caries

Substrate Agent

Time
 Embryology and Histology of Enamel

Billions of Crystal Millions of Individual Rods Enamel

• Keyhole-shaped structure • 95% inorganic material

• Structure of head and tail • 5% organic material

and water
• Ø : 6-8 microns
• One ameloblast from DEJ to
tooth surface Porosity  network
of channels

• Permit physiological
remineralization Diffusion of ions and
small mollecules
• Cushion intense biting pressure
• Conducting plaque acids to cause
demineralization
 Exquisite genetic control of enamel tissue building

Odontoblastic Secretory of Penetrates into predentin

Deposition – Initial Pre-dentin
ameloblast + subjacent odontoblast
event of secretory

Octacalcium laid down Forming matrix – Use Proteins Ameloblast retreat

acellular+avascular to surface

Approaching
Hidroxyapatite Pre-eruptive stage – Reduced enamel
Eruption stage -
crystal matrix degraded epithelium
ameloblast

Eruption stage –
Dental Plaque Acquired Pellicle reduced enamel
epithelium
disappeared
Physical and Microscopic Features of
Incipient Caries
• Earliest stage of caries development
• Extremely important  carious process can be
arrested or reversed
• Difficult to recognized and diagnosed clinically
• Macroscopically  area of opacity  white spot
lession
• Microscopically
– interproximally  small lucency gingival to the contact
point
– fissure caries  billaterally at two surfaces at orrifice
of fissure, coalesces at the base
Zones of Incipient Lesion

• Surface zone
• Body of the lesion
• Dark zone
• Translucent zone
Pore Spaces of the Different Zones
• Translucent zone-deepest zone  50% of carious
lesions  slight demineralization  1% pore space

• Dark zone  95% of carious lesion  2-4% pore space

 suggested as remineralization site  wider dark zone
 greater remineralization

• Main body of the lesion  peripheral to dark zone  5%

pore on the fringe of lesion, 25% in the center

• Surface zone  1% pore space  suggested as

remineralization site
Direct Connection of the Bacterial Plaque to the
Body of the Lesion

• Demineralization of enamel surface  ragged profile 

in optimum condition  repaired by body defenses +
man made strategies

• Speed of caries progression depends on  ion

concentration, pH, saliva flow, buffering actions

• The initial acid attack  dissolves magnesium and

carbonate ion  removal of less soluble calcium,
phosphate, other crystal ions
Cariogenic Bacteria
• Mutans streptococci
– Able to produce extracellular glucans from sucrose
– Able to produce lactic acid
– Able to produce intracellular polysaccharides (energy)
stores
– Able to adhere to tooth surfaces
– Acid tolerance
– Founded by J.K.Clarke in 1924  more oval than
streptococcus
– Found largely in the plaque occurring immediately
over developing smooth-surface lesion, more
populated in teeth destined to become carious (ex.
white spot lesions)
Cariogenic Bacteria

• Lactobacilli
– Cariogenic, acidogenic, aciduric
– Once considered the essential bacteria
causing caries
– Low pH environment of LB  suppress-
eliminates the MS colonization  LB establish
a monopoly of the environment
Bacteria Adherence

• Mutans streptococci able to attach by:

– Through extracellular protein (adhesins)
located on the fimbriae (fuzzy coat)
– Sucrose-dependent mechanism, require
sucrose to produce sticky glucans
Coronal Dentin Caries

• Objective of ameloblast  form future surface of tooth

• Objective of odontoblast  form the border of the dental

pulp

• Tubuli dentinalis  contain fluid from pulp chamber 

via secondary tubules + canaliculi  communication and
fluid transport

• Lesion approaching DEJ  tubules dead tracts +

calcified  sclerotic dentin (barrier to advancing caries)

• Without overt cavity  remineralized (slowly)

Root Caries
• Greatest risk: mandibular molar
• Least risk: mandibular incisor
• Risk factors:
– Age
– Gender
– Fluoride exposure
– Systemic illness
– Medications
– Oral hygiene
– Diet
• Plaque + salivary concentration of MS correlated
positively with root caries
Root Caries vs Coronal Caries

• Tissue affected:
– Enamel  highly mineralized
– Root 
• low mineral content, high organic content 
progress by acid demineralization and protheolysis
• Cavitation spread laterally, depth 0,5-1mm
• Dark-brown coloration
• Bacterial invasion
– Root  occurs earlier (cementum+dentin)
Physical Characteristic of Arrested Root Caries

• An outer barrier of hypermineralized surface dentin

• A sclerotic inner barrier between carious and sound

dentin

• Mineralization occurring within the dentinal tubules

• Dark and hard in appearance

• Smooth, hard and glassy feel in tactile examination

Prevention of Root Caries

• Best for elderly  prevention of periodontal disease in middle-age

or earlier

• Daily mechanical and chemical plaque control

• Severe restriction of refined carbohydrates

• Routine professional dental attendance for preventive office

identification of risks and counseling on self-care needs

• Chlorhexidine  very effective MS control agent

• Biological repair of root lesion can be achieved (with professional

guidance + patient cooperation)
Secondary/recurrent caries

• Starts with small imperfections of restoration or

tooth-colored filling with higher affinity to plaque

• Bacteria sheltered from protective effect of saliva

and self-care efforts

• Lesion develops between cavity margin and the

restoration
Measuring Plaque pH, the Stephan Curve

• Plaque fluid determines the eventual caries

status

• Plaque fluid supersaturated with calcium and

phosphate ion at a given pH plaque adjacent to
the tooth  no demineralization

• pH range for demineralization  5,5 to 5

(combine with sufficient time of exposure)
The Stephan Curve
Principles of De- and Remineralization of Teeth

• Demineralization caused by plaque acids  dissolution of tooth

minerals for calcium, phosphate and hydroxyl crystal

• Remineralization  requires availability of same ions + fluoride as

catalyst to support reconstruction damaged rods

• Crystals + fluoride compound involved in the process 

hydroxyapatite (HAP), fluorhydroxyapatite (FHA) and calcium
fluoride (CaF2)

• Fluoride incorporated into HAP  FHA  firmly bound (ex. Water

fluoridation)

• CaF2 adsorbed onto surface of HAP and FHA crystal  loosely

bound
The Relationship Between HAP, FHA and CaF2

• Attack of plaque acid  CaF2 dissolved  HAP dissolved  FHA

dissolved

• Dissociated ions  increase fluid saturation  slow crystal

dissolution  arrest crystal solution

• pH return to normal  crystal re-form  maintain homeostasis

• Frequent & prolonged acid attacks  homeostasis system

breakdown

• Some studies indicate remineralization existed in inner enamel and

dentin (very slowly)