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

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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.

NB:

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

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Etiology variables for caries progression

Intrinsic factors

Advantageous:

• Increased flouride conc. in enamel
• Decreased enamel solubility

Disadvantageous:

• 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 Po₄^2-)
• Antimicrobial agents – Immunoglobulins, lysozyme, lactoferrous, thiocyanates

2. Diet

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

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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

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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

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Spread of microbes from dento-alveolar complex

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

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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:

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

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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

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

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

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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

• Demineralization and proteolysis – in direction of Sharpey’s Fibers

• Prominent microbes:
  • Strep. mutans
  • Actinomycosis viscosus