DP04 aetiology, pathogenesis and histology of caries Flashcards

(37 cards)

1
Q

What is the 1st theory of caries aetiology?

A

The proteolytic theory - proteolytic enzymes produced by bacteria
Microbial component to caries

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2
Q

What is the 2nd theory of caries aetiology?

A

The proteolysis-chelation theory
Products of proteolysis chelate and remove Ca2+
Most efficient at neutral pH - we know teeth are vulnerable to caries at a lower pH so this theory has been disproven

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3
Q

What is the 3rd theory of caries aetiology?

A

Acidogenic theory
Fermentation of dietary carbohydrates
Acid demineralises enamel

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4
Q

Which theory is the most likely?

A

Mainly 3 and a little of 1
Proteolysis is involved in dentine caries

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5
Q

How does plaque form?

A

Clean tooth surface
Acquired pellicle (glycoproteins) from saliva
Colonisation of pioneer bacteria
Succession - modification of habitat
Climax communities eg approximal surfaces

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6
Q

What are the pioneer bacteria in oral flora?

A

95% streptococci
S sanguis, S mitis, Neisseria etc

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7
Q

What are the established bacteria?

A

Increase in filamentous rods at 14 days

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8
Q

What are the major pathogens in caries?

A

S mutans
Lactobacilli
Actinomyces

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9
Q

How is acid produced in dental plaque?

A

Ingestion of sugar –> fall of pH due to acid production of bacteria –> pH 5.5 critical with liberation of Ca and PO4 ions –> pH increases with deposition of Ca and PO4 ions

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10
Q

What is Stefan’s curve?

A

Shows the buffering of saliva
After 5mins the pH drops from 7 to 5.5
Raises again after about an hour`

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11
Q

What intrinsic factors cause susceptibility of a tooth surface to caries?

A

Enamel composition - fluorapatite
E structure - hypoplasia and hypomineralisation
Tooth morphology - pits and fissures might be deep
Tooth position - crowding
Iatrogenic PRFs

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12
Q

What extrinsic factors cause susceptibility of a tooth surface to caries?

A

Poor OH
Diet
Saliva

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13
Q

What things can affect saliva flow?

A

Alcoholics –> dehydration
Sjrogrens/radiotherapy –> affecting parotids

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14
Q

What factors of saliva affect its buffering capacity?

A

Flow rate
Non-specific host immunity (eg lysozymes)
Specific host immunity (secretory IgA deficiency –> susceptible)

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15
Q

What are the functions of saliva?

A

Digestive, lubricant, solvent, defence, buffers

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16
Q

What are the protective qualities of saliva?

A

→ Washing action
→ Regulation of pH - buffering
Increased flow rate -> increased [HCO3-]
→ Ca2+ and PO4- content
→ Non-specific and specific host immunity

17
Q

How does fluoride affect tooth surface structure?

A

Reprecipitation into fluorapatite crystals
Concentrates in plaque
Inhibits bacteria metabolism
Inhibits synthesis of IC polysaccharides eg glycogen

18
Q

How does arrested caries present and why?

A

Tooth structure remineralised and darker in colour - incorporates stain.
E - dark brown; dentine - dark brown/black

19
Q

Describe enamel white spot lesions

A

Early enamel lesion
E surface demineralised then remineralised
Can be arrested
Usually found on contact points between posterior teeth

20
Q

What are smooth surface caries?

A

Lesion usually coned shape w apex at CEJ (Unlike dentine lesions - spread at ADJ)
On reaching the enamel dentine interface, spread of caries is along ADJ, giving a broad base to the dentine lesion

21
Q

Describe fissure caries

A

Lesion doesn’t occur at base of fissure but bilaterally in the walls of the fissure giving the appearance of 2 smooth surface lesions

22
Q

What are the 4 zones of an enamel lesion histopathologically?

A

Translucent zone
Dark zone
Body of lesion
Surface zone

23
Q

Describe the translucent zone

A

Advancing front of the lesion
Pore space 1%
Removal of Mg and carbonate

24
Q

Describe the dark zone

A

2-4% pore space
Varying size of pores - small and large
Remineralisation

25
Describe the body of lesion
5-25% pore space Large apatite crystals Reprecipitation of mineral dissolved in deeper zones
26
Describe the surface zone
More highly mineralised due to reprecipitation of ions
27
How does destruction of dentine occur?
Acid demineralisation Proteolytic breakdown of matrix by bacterial enzymes
28
How does dentine caries spread?
Lateral spread of caries at ADJ Slows down towards pulp, increased fluoride exchange with pulp
29
What are the 4 zones of dentine caries?
Zone of destruction (closest to tooth surface) Zone of bacterial invasion Zone of demineralisation Zone of sclerosis
30
What is the histology of the zone of destruction?
Gross proteolytic breakdown of tissue Liquefaction foci enlarge - small areas of proteolytic breakdown where organic component is broken down Transverse clefts - when liquefaction foci join up and get bigger, tear perpendicularly to tubules
31
What occurs in the zone of bacterial invasion?
Acidogenic organisms at front: lactobacilli Mixed organisms - acidogenic and proteolytic behind Elliptical areas of proteolysis developing
32
What is in the zone of demineralisation?
Wave of diffusing acid No bacteria
33
What is the histology of the zone of sclerosis?
Lamina of tubules become plugged with mineral crystals in centripetal manner (pulp is responding) Pulp also responds directly as OD processes are retracting Calcification of OD process 'Dead tracts of fish' - empty space
34
What are the 2 types of tertiary dentine?
Reactionary and reparative (close to pulp)
35
Which tertiary dentine is mainly formed in response to caries?
Reactionary - upregulation of ODs --> more organic matrix moves pulp away from assault
36
What do root caries require?
Loss of attachment
37
When does secondary caries occur?
Around iatrogenic intervention