Dental Pulp Quiz 10

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  1. Caries and pulpal infections share the same features, they are?
    1. caused by normal microbiota

    2. tissues are irreversibly damaged

    3. neither can undergo spontaneous remission

    4. neither can be treated by abx
  2. Prevalence of apical periodontitis?
    Before age 50 (30%)

    After age 50 (50%)

    Over 60 (62%)
  3. Define dental plaque?
    diverse community of microorganisms adhered to tooth a complex biofilm embedded in extracellular polymers
  4. Materia alba, define?
    bugs, leukocytes, desquamated oral epithelium
  5. Define biofilm?
    bug community, firmly attached to a substratum, interface, or each other, in polymer matrix produced by themselves, altered phenotypes
  6. Bacterial biofilms comprise what percentage of infections?
  7. Define planktonic?
    unattached MO cells
  8. Advantages of being a biofilm?
    1. Broader habitat for growth. Early colonizers setting stage for late.

    2. Increased metabolic diversity and efficiency (food chains and webs)

    3. Protection (from each other, host, environment)

    4. Enhanced ability to cause disease
  9. What is horizontal gene transfer?
    movement of genetic material between unrelated bacterial species

    (adv of biofilm)
  10. What is quorum sensing?
    bacteria communication via diffusing of signal molecules (autoinducers)
  11. What is pathogenic synergism?
    Bacteria working together to cause disease, diverse virulence traits
  12. Mechanism of abx resistance of a biofilm?
    1. Biofilm structure resists penetration (retained neutralizing enzymes in biofilm)

    2. Bacteria in stationary phases, if stationary then inactive and not growing, abx work on divding bacteria

    3. Subpopulation of persisters (survivors)
  13. Name two types of auto-inducers?
    Acyl homoserine lactones (-)

    Modified oligopeptides (+)
  14. What does quorum sensing regulate?
    1. virulence

    2. compentence of DNA uptake

    3. entry into stationary phase

    4. biofilm formation
  15. BF Formation (Stage 1) conditioning salivary film?
    (acquired pellicle) host and bacterial molecules coating enamel

    varies in thickness .1-.3 um
  16. BF Formation (Stage 2) transport of bacteria to pellicle tooth coated surface?
    bacteria in planktonic state brought into contact w/ tooth surface
  17. BF Formation (Stage 3) early reversible adhesion?
    early colonizers, weak interactions, initial adhesion
  18. BF Formation (Stage 4) stronger interactions?
    stronger interactions between bacterial adhesins and pellicle receptors

    irreversible attachment

    early colonizers grow and modify environment

    include s. mitis, s. oralis
  19. BF Formation (Stage 5) latecomers?
    Binding of latecomers (coaggregation)

    Between genetically different cells unlike agglutination or aggregation

    corncobs here
  20. BF Formation (Stage 6) multiplication of the attached bacteria?
    increased pop density
  21. BF Formation (Stage 7) detachment?
    Sessile ones produce enzymes that break adhesins and allow planktonic bacteria to colonize other surfaces.
  22. Caries can be categorized as follows:
    Occlusal (pit and fissure)



  23. Dental caries of enamel is first observed as:
    white spot lesions
  24. What is awhite spot lesion?
    demineralized subsurface enamel

    at biofilm

    white because of changes in refractive index

    50% mineral loss (as much as)
  25. What acid is formed in biofilms leading to caries?
    Lactic, formic, acetic, and propionic
  26. What promotes dissolution of tooth mineral?
    diffusing of hydrogen ion
  27. Describe remineralization?
    Lost calcium and phosphate and fluoride can diffuse back into noncavitated lesion forming mineral crystal surface

    much stronger than original carbonated hydroxyapatite
  28. Define the non-specific plaque hypothesis?
    caries develops by overall activity of plaque microbiota
  29. Define the specific plaque hypothesis?
    Only one or few species are responsible for caries
  30. Define the ecological plaque hypothesis
    shift in natural balance of the resident plaque microbiota

    significant change in environment changes the whoel community causing cariogenic bacteria to outcompete

    pH is this factor (s. mutans, lactobacilli)

    critical enamel pH is 5.5
  31. Who and what is the chemoparasitic theroy?
    Dayton Miller

    oral bacteria convert dietary carbohydrates to acids dissolving calcium phosphate of enamel
  32. Three properties common to cariogenic bacteria
    1. rapid transport of sugar

    2. convert rapidly to acid

    3. do so under low pH

    ability to produce intra(more acid) extracellular polysaccharides (more adhesion)
  33. Acidogenic and aciduric?
    produce acid, and do so under low pH
  34. Who and when isolated s. mutans?
    1924 Clarke

    s. sobrinus now too
  35. Two methods of attachment of s. mutans to tooth surface?
    Sucrose independent and dependent

    Ind: adhere to salivary proteins, others, lectinlike interactions

    Dep: break sucrose into fructosyl (into cell) and glucosyl

    glucosyl polymerized into extracellular polysaccs glucans (mutan and dextran)

    mutan: higly branched insoluble biologic glue
  36. What role due lactobacilli play in caries formation?
    They do not form but propagate the lesion, their adherence is low

    not high producers of extracell polysaccs
  37. What species increase pH?
    Veillonella and Actinomyces
  38. What % of microbiota are yet to be id in caries lesion?
  39. What is the zone of destruction?
    Superficial layer of dentin decomposed by acid in a cavitated lesion
  40. What is the zone of demineralization?
    separates the infected dentin from sclerotic dentin
  41. What bugs predominate as carious lesion progresses?
    Lactobacilli and/or proteolytic anaerobic bacteria like prevotella
  42. What is responsbile for symptoms of a cavity?
    Ammonia and indole produced by anaerobic bacteria

    LPS from gram (-)
  43. What are some first line host defense antimicrobial systems in saliva?





  44. Primary mechanisms of fluroide?
    inhibits demineralization: adsorbes to surface of carbonated hydroxyapatite, resists acid dissolution

    enhances remineralization: by adsorbption it attracts calcium and phosphate ions, a fluorapatite like crystal forms

    inhibits bacterial metabolism: fluoride combins with hydrogen ions goes into cell and acidfy cell and fluoride interferes with bacterial enzymes
  45. What lines the dentinal tubules?
    Lamina limitans, sheathlike
  46. What is anachoresis?
    Theory, bacteria from gingival crevice or perio pocket reach the root canals through severed bloods vessels of periodontium during trauma
  47. Estimated number of bacterial cells in oral cavity? Species?
    10 billion

    700 taxa, 13 phyla

    50-60% remain to be cultivated
  48. What major ecological factors determine composition of root canal microbiota?
    • O2 tension
    • type and amount of nutrients

    bacterial interactions

    temp, pH, receptors for adhesins
  49. Main sources of nutrients for bacteria in root canal?
    1. necrotic tissue

    2. proteins and glycoproteins from tissue exudate via apical and lateral foramina

    3. components of saliva

    4. products from other bacteria
  50. What is amensalism?
    Seen as a negative interaction between bugs, production of substance inhibits other species
  51. C. Albican % in primary infection?
  52. Archae type detected in primary infections?
  53. Which viruses are detected in apical periodontitis?
    Epstein Barr and CMV
  54. Secondary intraradicular infections, cause?
    MO not present in primary infection, some time after professional intervention

    either during treatment, between appoint, or even after root canal filling
  55. Predominant MO in persistent or secondary infections?
    Gram positive or facultative anaerobics
  56. Persistent and secondary infections are a major cause of endo failure, why?
    1. inc risk of adverse tx outcome when bacteria are present in the canal at time of obturation

    2. most obturated teeth have been shown to harbor intraradicular infections
  57. What do residual bacteria have to do to cause persisten apical periodontitis?
    1. adapt to changed environment during treatment, antimicrobial effects of root filling

    2. reach critcal numbers for virulence

    3. unrestrained access to periradicular tissues

    4. induce host reponse
  58. E. Faecalis prevalence in endodontically tx teeth?

    9 times more likely
  59. Situations that permit Actinomyces or P propionicum to reach periradicular tissue?
    1. Apical extrusion of debri during instrumentation

    2. direct advance from the infected root canal into the lumen pocket cysts

    3. previous participation in acute apical abscesses, followed by persistence after acute response subsides
  60. Percent corresponding apical actinomycosis of apical perio?
  61. What are three potential antigens of s. mutans for vaccine development?
    Surface fibrillar adhesins (antigen I/II)


    Glucan binding proteins
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Dental Pulp Quiz 10
2013-09-22 19:29:35
Quiz 10

Dental Pulp
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