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22 Cards in this Set
- Front
- Back
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What are the 3 factors required for caries? |
Key microorganisms Susceptible host Environmental factors - poor diet, poor OH, low saliva flow |
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Confounding factors of dental caries |
Diverse microbiota Fluoride availability non-specific virulence traits |
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Evidence that caries are an infectious disease |
gnotobiotic (sterile) animal studies Human epidemiology studies - cross sectional and longitudinal Vaccinations in rodents and primates |
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Microorganisms that cause caries |
Strep. mutans c,e,f - main culprits, collectively know as mutans streptococci Strep. sobrinus d,g Actinomyces naeslundi A. ondontolyctus Lactobacilli - advanced lesions Bifidobacteria |
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Describe the microorganism implicated with caries |
Strep. mutans - cocco-bacilli (cocci or short rods) colonise hard non-shedding surfaces, implicated with initiation of caries Actinomyces - g+, branched rods, common in plaque, some species implicated in root surface caries, opportunistic, Lactobacillus - G+, rod, implcated in advanced caries Bifdobacteria - G+, rod, branched cells, recently implicated |
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Difficulty in determining the aetiology of dental caries |
Diverse range of microbiota - not simple single species "pathogens" are present in normal microbiota - normally in small amounts - therefore presence isn't diagnostic Lesions can remineralise Difficult to correlate microbiota to enamel status (microsampling and early diagnosis) - sample will take organisms from health and disease area Pathogenic traits are relatively non-specific Multi-factorial nature of caries |
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Koch's postulates for a pathogen |
1 - microbe should be found in all disease sites (MS not found in all) 2 - the microbe should be grown on a media for several subcultures (difficult as 50% non-culturable) 3 - pure subculture should produce disease in a susceptible animal new postulate 4 - high titre of antibodies should be detected during infection |
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Alternative version of Koch's postulates for caries and perio |
1 - microbe should be present in sufficient numbers to cause disease 2 - high level antibody response should be detected 3 - microbe should produce specific virulence factors 4 - removal of microbe should cause clinical improvement |
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Explain the different hypotheses for the aetiology of caries |
(model answer pg 104 Oral Microbiology) 1 - Specific - disease arises when certain species are present (ie Strep. mutans). Good points: focused efforts on controlling and removing certain species. Bad points: disease could occur when these species weren't present. Obviously this hypothesis didn't cover everything which led to ... 2 - Non-specific - no specific species required to be present, disease is the outcome of the total microflora. Good points: considers it may be a polymicrobial infection. Bad points: microbes can be present and there is no disease so disease must occur when there is a specific ecology which leads on to.. 3 - Ecological - disease is a result of a shift in the balance of the local microbiota as a result of a change in the local environmental conditions. Ie regular suger intake = more acid = lower pH = increased in acid-producing and acid-tolerant species = more acid = further demineralisation |
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Describe the types of study used for caries and perio, give their benefits and disavantages |
Cross-setional - a study of a pre-determined surface on many individuals at a single point in time. The microflora sampled is correlated with the status of the tooth surface. Benefits: Large population can be sampled, covering many types, social groups, genders etc. Disadvantages: microbiota sampled cannot be identified as causing the inflammation or decay or arising because of it, only "associations" can be made, sites cannot be identified as progressing, arrested or healing and the microflora may be different for each type. Longitudinal - initially healthy sites are sampled multiple times over a period of time, sites are selected from evidence from previous studies that show the sites are likely to be affected by disease. Microflora is compared before and after diagnosis of disease and between sites that remained healthy and sites that became diseased. Benefits: a true cause and effect relationship can be identified. Disadvantages: for practical reasons (cost and effort) only a small sample can be studied. |
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General findings of studies |
Cross-section - Greater MS proportion at caries sites. Inverse reltationship between MS and strep. sanguinis (present in health) - 71% of fissure caries had >10% MS - 70% of caries free had no detectable MS Longitudinal - increase in MS proportion and isolation frequency - MS can occur after the first signs of demineralisation - caries can occur in the absence of MS - role of other bacteria in caries progression (lactobacilli in advanced lesion) |
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Role of other bacteria |
Acidogenic/low pH isolates - S. mitis, S. oralis - studies of the rate of acid production at different pHs shows that some strains os MS are worse acid producers than other species Lactate utilising species - Veillonella - convert lactate to weaker acid Base-generating - S. salivarius, S. sanguinis, A. naeslundii - convert either urea or Arginine to ammonia - raises pH |
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Classic bacteria of other types of carie |
Early childhood - MS, lactobacilli Root surface - Actinomyces (early studies), MS & lactobacilli (later studies), diverse microbiota - Actinomyces israelii, A. gerencseraie, MS, G- rods (recent studies) |
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Characteristics of cariogenic bacteria |
- rapid sugar transport and uptake - out compete other bacteria - Acidurity - can metabolise sugars and produce acid at low pH - Produce extracellular polysccharide - contributes to adhesion and structure of plaque matrix - Produce intracellular polysaccharide - storage, can still produce acid with no intake of sugar BUT: these characteristics are quite general - no simple toxin to identify |
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Stages of microbiota shift from health to cariogenic |
Stress - increased sugar frequency = more frequent acid production
cause Environmental - neutral pH -> low pH changes selection pressure Ecological shift - S. sanguinis, S. gordonii --> MS, lactobacilli, bifidobacteria |
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List approaches for controlling caries |
Plaque control FLuoride Sugar substitutes Antimicrobials & anti-plaque agents Replacement therapy Vaccination Passive immunisation |
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Effects of flouride |
Enamel - remineralisation - lower critical pH - fluorapatite - harder to be demineralised Microorganism - acidify cell interior - slow cell processes - inhibit IPS synthesis - reduce glycolysis - inhibits enolase - above remove competitive opportunity for MS |
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Sugar substitutes |
- bulking agents - sorbitol, xylitol - intense sweetners - saccharin, aspartame - not or weakly metabolised to acid - stimulate saliva flow - buffering - weak antimicrobial activity - xylitol & S. mutans |
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Antimicrobial and anti-plaque agents |
- toothpastes and mouthwashes - chlorhexdine is gold standard - others: triclosan, metal salts, plant extracts, enzymes - kill some bacteria at high conc and persist at low conc and subdue bacteria |
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Replacement therapy |
Use genetically engineered strain to outcompete cariogenic strains dairy strains - problem: don't colonise mouth - may have systemic effect - swallowed and trigger immune response? GM s. mutans - remove function of lactate production, increase production of inhibitor - will affect non GM strains |
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Vaccination |
Vaccinate against known cariogenic bacteria (ie MS) protection achieved in rodents and primates, no human trials - difficult to convince for vaccination of non lethal disease |
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Passive immunisation |
Probably best option Easier to pass than vaccination -make antibodies outside of body (plants) - after clean coat surfaces with antibodies - blocks adhesins and formation on biofilm - reduces MS colonisation - primates and human trial - safe, acceptable, non-invasive, targeted |
