Cariology – Study of Dental Caries

Def: A bacterial disease – of calcified tissues of teeth – involving demineralization of the inorganic structure – and destruction of organic substance – of the tooth.

Etiology of caries

1. Cariogenic bacteria:

  • S. Mutans
  • S. Sobrinus
  • S. Oralis
  • S. Sanguis
  • S. Mitis
  • Lactobacilli
  • Actinomyces

2. Susceptible tooth surface

3. Substrate

4. Time

NB: Acidogenic Theory: W. D. Miller 1889

  • Oral bacteria – ferment dietary CHO – form acid – decalcify tooth substance + destroy organic matrix

Experimental evidence: Role of S. Mutans in caries

1. Rapid generation of acid from sucrose

2. Synthesize extracellular polysaccharides

  • To promote adhesion to tooth
  • Increase plaque bulk

3. Synthesize intracellular polysaccharides – sustains acid production in the absence of sucrose

4. Present in high numbers in plaque associated lesions

5. Cariogenic and respond to immunizations in animal models

NB: This evidence is based on Koch’s postulates (1877)

  • 1. Isolate organism from pt with dx
  • 2. Culture organism outside the body
  • 3. Organism can cause dx in healthy susceptible animals
  • 4. Recover organism from inoculated animal. Pt’s serum contains antibodies to the organism.


  • Gnotobites + Cariogenic diet: No caries
  • Gnotobites + Cariogenic diet + Inoculated cariogenic bacteria: Caries develop

Etiology variables for caries progression

Intrinsic factors


  • Increased flouride conc. in enamel
  • Decreased enamel solubility


  • Enamel hypoplasia and hypomineralization
  • Deep pits and fissures
  • Misaligned teeth

Extrinsic factors

1. Saliva

  • Flow rate – High flow rate, decreased caries
  • Viscosity – Low viscosity, increased caries
  • Buffer (Ca2+ and Po42-)
  • Antimicrobial agents – Immunoglobulins, lysozyme, lactoferrous, thiocyanates

2. Diet

  • Presence of phosphates – Decreases caries
  • Fat – Increases caries
  • Trace elements (molybdenum, vanadium) – Decrease caries

Caries classification

1. Site of attack

  • Pit/fissure caries
  • Smooth surface caries
  • Cemental/root caries
  • Recurrent caries

2. Rate of attack

  • Rampant/acute caries
  • Slow/chronic caries
  • Arrested caries

Factors affecting outcome of caries

1. Nature of irritant – Bacterial type and load

2. Duration and severity of irritant – Bacterial virulence

3. Amount of bacterial substrate

4. Apical blood flow

5. Local anatomy of pulp chamber

6. Pre-existing state of pulp

7. Extent of other trauma

8. Microbial factors – Pathogenicity is the ability of a microbial species to produce dx = Virulence

  • Adhesion – Bacteria to tooth surface
  • Invasiveness – Spread to host tissue after infection
  • Toxigenecity – Endotoxin (cell wall), Exotoxin (excrete)
  • Communicability – Spread from one host to another

9. Host defenses

– Local

  • Epithelial lining – Physical barrier, IgA
  • Saliva
  • Colonization by normal flora

– Systemic

  • Humoral immunity – Ig A, D, E, M, G
  • Complement system & cytokines
  • Cell immunity – Lymphocytes (B & T), PMN’s

Spread of microbes from dento-alveolar complex

  1. Direct invasion/extension
  2. Lymphatic
  3. Haematogenous

Histopathology of enamel caries

Ground sections of teeth examined by:

  • Transmitted light
  • Polarized light
  • Microradiography
  • Electron microscopy (Microdissected pieces of enamel)
  • Biochemical studies (Microdissected pieces of enamel)

Phases of enamel caries:

  • The early (submicroscopic) lesion
  • Phase of non bacterial enamel crystal destruction
  • Cavity formation
  • Bacterial invasion of enamel
  • Undermining of enamel from below after spread into dentine

Histological Zones:

Histological zones of enamel caries

NB: Due to absence of cellular sensors in enamel – there is no defense reaction

1. Surface zone: 40 um thick

  • Little change in early lesion
  • Highly mineralized: Fluoride and Magnesium
  • Increased proteins
  • Surface of enamel is resistant to acid attack due to its structure, therefore subsurface demineralization occurs
  • Reprecipitation of minerals from:
    • Plaque
    • Minerals dissolved from deeper layers of lesion

2. Body of lesion: 2-25% pore volume

  • Reprecipitation of minerals (from deeper zones) – form larger apatite crystals
  • Continuous acid attack – more destruction of minerals – replaced by unbound water and organic matter from saliva and microbes
  • Increased prominence of striae of Retzius: White spots

3. Dark zone: 2-4% pore volume

  • Some remineralization concurrent with destruction
    • Narrow zone: Rapidly advancing lesion
    • Wide zone: Slow advancing lesion
  • Reprecipitation occurs from translucent zone

4. Translucent zone: 1% pore volume = size of H2O molecule

  • Normal enamel has 0.1% pore volume, therefore more porous than normal enamel
  • 1st recognizable change at advancing edge of lesion
  • Selective dissolution of Mg2+ and CO3-2 – Occurs at junctional areas btwn prismatic and interprismatic areas

NB: White spots stained with exogenous pigments (food, tobacco, bacteria) become brown spots

Histopathology of dentine caries

Defense reaction mediated by pulpo-dentinal complex

  • Sclerosis
  • Reactionary dentine
  • Sealing of dead tracts

Caries destruction involves interacting processes

  • Demineralization (acid always in advance of bacteria)
  • Proteolysis of matrix

NB: Defense reaction of dentine may occur before caries reach dentine due to irritation of odontoblasts – tertiary dentine

NB: Circumpulpal dentine more resistant to carious attack due to increased F diffused into from pulp

Histopathology of dentine caries

1. Zone of sclerosis (Translucent zone)

  • Sclerosed dentine = Increased mineral content
  • 2 patterns of mineralization:
    • 1) Centripetal deposition of peritubular dentine – therefore occlude tubule
    • 2) Minerals appear in cytoplasmic process of odontoblast – tubule occluded by odontoblastic processes
  • Dead tracts: Opaque, seen in sclerotic zone
    • Empty tubules + air + degraded odontoblastic processes
    • Occluded at pulpal end of EBURNOID (thin layer of hyaline calcified material)

2. Zone of demineralization

  • Wave of acid from bacteria in this zone
  • No bacteria in this zone

3. Zone of bacterial invasion

  • Bacteria multiply and extend within tubule
  • Acidogenic organisms eg. lactobacilli – occupy tubules at periphery of lesion and produce acids
  • Acidogenic + proteolytic organisms – attack demineralized matrix, therefore soften walls of tubules

Increased bacteria + Compression of inter and peritubular dentine = Break down of dentinal tubules – Liquefaction area (elliptical area)

The liquefaction areas are called liquefaction foci – which enlarge, increase in number and coalesce

Liquefaction area/foci dentinal tubules

4. Zone of destruction

  • Cavitation at amelodentinal junction
  • Transverse clefts (cracks) appear in dentine – perpendicular to the direction of dentinal tubules
  • Contain bacteria and necrotic tissue
  • Bacteria invade peri and intertubular dentine

5. Reactionary/Tertiary dentine

  • Beneath lesion in pulp
  • Pre-odontoblasts differentiate – lay down tertiary dentine to protect pulp

Histopathology of cementum caries

  • Recession of gingiva – cementum exposed to oral environment – cementum more homogenous and laminated – therefore when attacked – caries produce saucer shaped lesions
  • Prominent microbes:
    • Strep. mutans
    • Actinomycosis viscosus

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