DP04 aetiology, pathogenesis and histology of caries Flashcards
(37 cards)
What is the 1st theory of caries aetiology?
The proteolytic theory - proteolytic enzymes produced by bacteria
Microbial component to caries
What is the 2nd theory of caries aetiology?
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
What is the 3rd theory of caries aetiology?
Acidogenic theory
Fermentation of dietary carbohydrates
Acid demineralises enamel
Which theory is the most likely?
Mainly 3 and a little of 1
Proteolysis is involved in dentine caries
How does plaque form?
Clean tooth surface
Acquired pellicle (glycoproteins) from saliva
Colonisation of pioneer bacteria
Succession - modification of habitat
Climax communities eg approximal surfaces
What are the pioneer bacteria in oral flora?
95% streptococci
S sanguis, S mitis, Neisseria etc
What are the established bacteria?
Increase in filamentous rods at 14 days
What are the major pathogens in caries?
S mutans
Lactobacilli
Actinomyces
How is acid produced in dental plaque?
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
What is Stefan’s curve?
Shows the buffering of saliva
After 5mins the pH drops from 7 to 5.5
Raises again after about an hour`
What intrinsic factors cause susceptibility of a tooth surface to caries?
Enamel composition - fluorapatite
E structure - hypoplasia and hypomineralisation
Tooth morphology - pits and fissures might be deep
Tooth position - crowding
Iatrogenic PRFs
What extrinsic factors cause susceptibility of a tooth surface to caries?
Poor OH
Diet
Saliva
What things can affect saliva flow?
Alcoholics –> dehydration
Sjrogrens/radiotherapy –> affecting parotids
What factors of saliva affect its buffering capacity?
Flow rate
Non-specific host immunity (eg lysozymes)
Specific host immunity (secretory IgA deficiency –> susceptible)
What are the functions of saliva?
Digestive, lubricant, solvent, defence, buffers
What are the protective qualities of saliva?
→ Washing action
→ Regulation of pH - buffering
Increased flow rate -> increased [HCO3-]
→ Ca2+ and PO4- content
→ Non-specific and specific host immunity
How does fluoride affect tooth surface structure?
Reprecipitation into fluorapatite crystals
Concentrates in plaque
Inhibits bacteria metabolism
Inhibits synthesis of IC polysaccharides eg glycogen
How does arrested caries present and why?
Tooth structure remineralised and darker in colour - incorporates stain.
E - dark brown; dentine - dark brown/black
Describe enamel white spot lesions
Early enamel lesion
E surface demineralised then remineralised
Can be arrested
Usually found on contact points between posterior teeth
What are smooth surface caries?
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
Describe fissure caries
Lesion doesn’t occur at base of fissure but bilaterally in the walls of the fissure giving the appearance of 2 smooth surface lesions
What are the 4 zones of an enamel lesion histopathologically?
Translucent zone
Dark zone
Body of lesion
Surface zone
Describe the translucent zone
Advancing front of the lesion
Pore space 1%
Removal of Mg and carbonate
Describe the dark zone
2-4% pore space
Varying size of pores - small and large
Remineralisation