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Mandal > Immunopathology of caries and host Immunity > Flashcards

Immunopathology of caries and host Immunity Flashcards

1
Q

inflammatory innate response at mucosal surface

A

via phagocytes: neutrophils, macrophages & esoinophils

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2
Q

dental caries and periodontal diseases caused by

A

endogenous microbes

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3
Q

regulation of commensal bacteria by

A

sIgA

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4
Q

carries characterized by

A
  • complex interactions
  • microbial products
  • salivary constituents
  • dietary carbs on tooth
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5
Q

formation of biolfims

A

dental plaque

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6
Q

caries eventually lead to

A

loss of mineralized tooth enamel

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7
Q

eclogical collision

A

infectious microbes and a lot of sugar in diet

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8
Q

immune regulation of oral commensals

mi

A
  • bacterial effects immune sytems
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9
Q

caries

description

microorganisms

A
  • decay of enamel and dentin (dental caries) or root carries
  • streptococcus Lactobacillus
  • Actinomyces (root caries)
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10
Q

Gingivitis

description

microorganisms

A
  • redness and swelling (inflammation) of gums
  • Actinomyces
  • Fusobacterium
  • Bacteroides
  • Prevotella
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11
Q

periodontitis

description

microorganisms

A
  • inflammation either rapid (aggressive) of slower (chronic) destruction of tissue supporting tooth
  • Aggregatibacter (rapid)
  • Porphyromonas
  • Treponema
  • tannerlla
  • fusobacterium
  • prevotella
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12
Q

Etiologic agents of dental carries

A
  • lactic acid bacteria
  • heterogenous family of bacteria
  • high pop. of S. mutans
  • GTF enzyme
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13
Q

lactic acid

A
  • ferminted sugar
  • chelates calcium
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14
Q

what facilitates bacterial adherence

A

glucosyltransferase (GTF)

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15
Q

Plaque Microbiota

A
  • streptococcus mutans sterotype C (main)
  • mom to child
    • gram positive coccus

other

  • streptoccus sorbinus
  • lactobacillus species
  • actinomyces
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16
Q

tooth with highest microbial diversity are more

A

susceptible to caries

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17
Q

gram+

A

promotes gingival health

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18
Q

promotes gingival health

A
  • plaque reduction
  • reduced inflmammation
  • low GCF flow
  • gram +
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19
Q

three types of dental carries

A

enamel

dentin

roots

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20
Q

enamel carries

A

smooth surface

  • S. mutans
  • S. salivarius

pit+fissures

  • S.mutans
  • Lactobacilli
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21
Q

Dentin carries

A
  • lactobacilli
  • anerobic gm+ rods
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22
Q

Root carries

A

Actinomyces

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23
Q

S. mutans fermentation

A
  • glucose is the most fermented
  • more acid production leads to larger drop in oral pH
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24
Q

Sucrose metabolism for S. mutans

A
  • glucosyltransferase (GTF) enzyme creates glucans & dextrans polymers
  • generates excess lactate
  • creates plaque
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25
Q

glucans and dextrins

A
  • sticky gelatinous
    • traps bacteria
    • feed plaque microbial community
    • attaches to tooth surface
26
Q

surface protein antigens of S. mutans

A

Antibodies against SA I/II prevent colonization of

S. mutans on teeth

27
Q

Polysaccharide antigens of S. mutans

A
  • antibodies against carb antigens are protective and prevent binding of GTF to cell prohibiting caries formation
28
Q

what is proposed as targets for caries vaccine antigen

A

GTF

29
Q

immunological control of cariogenic streptococcal and dental carries

A
  • Immunity to oral pathogens is principally mediated by sIgA in salivia
  • Systemic immunity cia IgG and IgM in GCF
30
Q

majority of pathogens invade via

(flu, HIV)

A

mucosal structures

31
Q

Salivia antibodies

A
  • majority
    • IgA
  • GCF
    • IgG
    • IgM
32
Q

gingival crevice antibodies

A
  • lymphocytes
  • macrophages
  • PMN
33
Q

caries are associated with which antbodies

for S.mutans

A

increased sIgA

(reseach has not confirmed)

34
Q

Development of sIgA specific to S. mutans

newborn-infant

1 year

10 years

A
  • newborn-infant
    • no Ab to S. mutans
  • 1 year
    • start developing Ab against S. mutans
  • 10 years
    • IgA levels = to an adult
35
Q

correlation of sIgA or serum IgG or IgM

A

correlate levels of sIgA or IgG and IgM Abs to S. mutans with resistance to dental caries

36
Q

Immunological host defenses in caries

A
  • production of slgA
    • not understood well
    • salivary abs interact with bacterial surface proteins
    • bacteria opsonize bacteria
37
Q

immune response to root suface carries

A

complement-IgG-PMN immune activation

  • IgG-complement activation via classical pathway
    • C3a, C5a generation
    • Inflammation-phagocyte PMN
38
Q

root surface bacteria

A

Actinomyces , S. mutans , lactobacillus

39
Q

goal for vaccination against caries

A
  • prevention of attachment
  • reduce number of pathogens
  • interfere with metabolic activity
40
Q

dental vaccination approaches targetins specific pathogen

A

S. mutans

(difficult to get sIgA to generate long term response)

41
Q

problems with vaccine against carries

A

development of rheumatic fever, acute glomerulonephritis

42
Q

vaccine identification candidate

A

GTF or GTB

generate sIgA or serum IgG protective

43
Q

Dental caries and periodontal diseases are the resilt of an

A

ecological imbalance between resident microbiota and host immunoity

44
Q
  • what provudes host defense in the oral cavity
A

innate and adaptive immunity

45
Q

Innate immunity is primarly imparted via

A

mucosal and dental barriers

46
Q

soluble antimicrobial mactors in saliva and GCF make up

A

the first line of defense (innate immunity)

47
Q

saliva flushes

A

mucosal and dental surfaces of the mouth

48
Q

GCF flushes the

A

oral cavity

49
Q

inflammatory innate response at the mucosal surface is rendered by phagocytes

A

neutrophils. macrophages, and eosinophils

50
Q

what provides adaptive immunity

A
  • sIgA in saliva
  • IgG and IgM in GCF
  • effector T lymphocytes
51
Q

diveristy and richness of microbial communites of the tooth surface directly releate to

A
  • caries risk
  • more diverse more at risk to caries
52
Q

with established caries acid environment reduces the

A

diversity and richness of local microbiota

53
Q

plaque accumulation triggers

A

inflammatory host response

54
Q

change in the local environment condition favoring growth of proteolytic

A

gram-bacteria

55
Q

host dendenses in caries

A

not understood well

56
Q

bacteria in mouth…

(steps)

A
  1. swallow bacteria
  2. stimulation of b cells in peyer’s patch in gut-assoicated lymphoid tissue
  3. gereration of plasma cells in salivary glands
57
Q

production sIgA

(6 effects)

A
  1. salivary Abs interact with bacterial surface proteins
  2. interfere with bacterial adhesion, colonization and caries formation
  3. Abs opsinize bacteria
  4. promote phagocytosis by PMNs and macrophages
  5. release of chemokines and trigger inflammation
  6. activation of lymphocytes
58
Q

vaccine against caries

A
  • whole pathogen vaccination with S.mutans in humans does not work
59
Q

S.mutans Ag is crossreactive with

A
  • S. pyogenes Ag molecular mimicry
  • can induces Abs cross reactive to human heart, joints and kidney tissues
60
Q

Bad effect of vaccine against caries

A
  • generation of auto antibodies
  • induction of autoreactive T cells to myocardium , heart valves, joint, blood vessels and kidney
61
Q

what is a possible type of caries vaccine ?

A

synthetic vaccine without epitopes shared with human Ag is a possibility

Mandal (7 decks)

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