Enamel And Dentine Caries

Front 1

Physical properties of human enamel and dentine

Back 1

Enamel:
96% mineral

3% water
1% protein

Dentine:
70% mineral
10% water
20% protein

Enamel = hard+ stiff

Dentine = flexible + compressible (to support enamel)

Front 2

Enamel structure

Back 2

HAP crystals (60-90nm width, 25-30nm depth) ordered into prisms/rods, Prisms almost perpendicular to amelo-dentinal junction.

Circadian rhythm in enamel production = regular, daily, cross-striation-roughly 5 micron periodicity

Incremental lines in periodicity = striae of retzius

Crystals in fully mature enamel = less regular as they grow to occlude all available space.

Front 3

Dentine structure

Back 3

Non-collagen proteins present e.g. dentine phosphoprotein, growth factors present e.g. BMP, IGF's.
When dentine is demineralised: above stimulate stem cells into odontoblast-like cells to create tertiary reparative dentine.

Tubules increase + become wider towards pulp

Superficial dentinal tubukes occupy 1% of dentine volume to 30% of deeper dentine

Hence deeper dentine = more porous + permeable to bacteria + chemicals

Front 4

Early Enamel Caries

White spot lesion

Back 4

Opaque white spot - sub-surface become porous as result of mineral dissolved by acid produced by plaque bacteria

As porosity increases - lesion may take up stain + eventually begin to cavitate.

Front 5

Physical processes of early enamel caries

Back 5

Ca10(PO4)6(OH)2 ⇌10Ca2++ 6PO43– +2OH–

Front 6

Enamel caries physical appearance

Enamel caries = Purely chemical process, dissolution of HAP by acid.

Back 6

1) Translucent zone

2) Dark zone = increase porosity, small holes inaccessible to imbibing fluid

3) Body of lesion = more porosity, large pores.

Front 7

Caries in dentine

Back 7

Caries in dentine (3 stages)

1) Mineral is removed by the bacterial acid

2) Ground substance is removed by enzymes

3) Enzymatic removal of the collagen

Front 8

How does dentine initially respond?

Back 8

- Production of peritubular dentine to occlude tubules (inhibit diffusion of bacterial acids + enzymes).

- This results in translucent + sclerotic dentine, the lesion will progress slowly here.

- Crown of younger tooth wont have time to do that. Odontoblasts will first try wall off the lesion with sclerotic dentine, if they don't have time theyll increase amount of dentine at pulpal surface, producing reactionary dentine.

However if lesion progresses rapidly then odontoblasts may be killed and replaced with more bone-like material (reparative dentine)

Front 9

What exists inside the pulp space

Back 9

Pulp dentine complex, dentine is vital tissue with cellular component that maintains the dentine structure, takes part in the innervation of the tooth as proprioception, allows defensive mechanism to be instigated.

Front 10

Defensive mechanism is 2 fold:

Back 10

1) Expression of chemicals that are antibacterial in nature combat bacterial contamination/infection of the dentinal tubules

2) Secretion of HAP by the odontoblasts to create + lay reactive or secondary dentine to close dentinal tubules from advancing noxious agent + protect the pulp

Front 11

What are the effects of bacteria upon pulp-dentine complex

Back 11

Loss of vitality + bacterial colonisation by proteolytic gram -ve facultative anaerobic bacteria of pulp space and dentinal tubules

Front 12

Pulp-dentine complex; response to invasion

Back 12

Odontoblasts - live in pulp/dentine interface and extend long cellular processes through dentinal tubules. Odontoblasts also exhibit features of innate immune cells including expression of TLRs

Can progress so you can identify 7 to 31 different species, associated with degradation of dentinal matrix and stimulation of odontoblasts.

Bacterial stimulation causes odontoblasts to undergo major functional adaptations; deposition of intertubular dentin and accelerated dentinal matrix deposition referred to as reactionary dentine.

Front 13

Spread of caries into dentine (smooth surface caries)

Stage 1

Back 13

Plaque layer forms on enamel surface, along with time + fermentable carbohydrates + lack of fluoride ions, causes release of organic acids. Lesion tends to progress down areas of high porosity + low mineral content

Front 14

Spread of caries into dentine (smooth surface caries)

Stage 2

Back 14

Acid dissolution of enamel prisms at prism boundaries and centre of prisms, loss of mineral, increased porosity + acid attack advances through enamel.

Front 15

Spread of caries into dentine (smooth surface caries)

Stage 3

Back 15

Spreads along ADJ laterally

Front 16

Spread of caries into dentine (Smooth surface caries)

Stage 4

Back 16

Dentinal tubules decrease in volume as intertubular dentine is laid down to become sclerotic and reactionary dentine on the pulpal wall

Front 17

Spread of caries into dentine (smooth surface caries)

Stage 5

Back 17

Enamel surface cavitates, plaque bacteria enters enamel and into dentine (infected dentine)

Front 18

Spread of caries into dentine: Occlusal/pit caries

Back 18

Spread of caries within dentine may produce large hidden lesion below smaller enamel lesion, sometimes called occult caries.

Can be called fluoride syndrome resulting from enamel having high fluoride content + being relatively resistant to caries.

Front 19

3 layers when caries process enters into dentine:
Infected dentine

Back 19

Coronal layer of dentine, exposed through open cavity, exposure to bacteria + saliva. Gross distribution of organic matrix, no recognisable dentinal tubules. Proteolytic bacteria consuming type 1 collagen

Front 20

3 layers when caries process enters into dentine:

Affected dentine

Back 20

Closer to pulp, recognisable dentine structure affected by waves of demineralisation. Dentine slightly demineralised as crystals are dissolved. Possible to see isolated bacteria in superficial zones of the affected dentine, not heavily infiltrated

Front 21

3 layers when caries process enters into dentine:

Normal dentine

Back 21

Normal dentine with tubules, tubules reduced in size as odontoblasts lay down secondary dentine inside tubules to form impenetratable layer. As caries gets closer to pulp layer gets thinner so risk of direct pulpal exposure.

Likely micro-pulpal exposure has occured before visible exposure.