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BDS3 - Microbiology and Oral Pathology > biofilm 2 - periodontitis > Flashcards

biofilm 2 - periodontitis Flashcards

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1
Q

what are the different oral biofilm diseases

A
  • caries
  • endodontic infections
  • oral malodour
  • mucosal infections
  • periodontal infections
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2
Q

what are examples of mucosal infections

A
  • thrush
  • angular cheilitis
  • denture stomatitis
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3
Q

what can cause malodour

A
  • infection from dorsal surface of tongue
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4
Q

what host factors can influence on oral microflora

A
  • systemic disease
  • antibiotic use
  • oral hygiene
  • genetics
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5
Q

how can diet influence oral microflora

A
  • chemical composition
  • physical consistency
  • frequency of intake
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6
Q

how can saliva infelucne oral microflora

A
  • flow rate
  • pH
  • antimicrobial factors
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7
Q

how can GCF influence oral microflora

A
  • antimicrobial components and humeral immunity
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8
Q

how can microbial interactions influence oral microflora

A
  • competition and co-operation
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9
Q

how can the gaseous environment influence oral microflora

A
  • oxygen concentrations can determine which organisms are present
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10
Q

what are the types of PD classification

A
  • gingivits
  • periodontitist
  • necrotising periodontal disease
  • peri-implantitis
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11
Q

what are the two periodontitis sub categories

A
  • chronic = adult related

- aggressive = spontaneous (genetic)

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12
Q

what determines the health of gums

A
  • balance between health and disease
  • balance between beneficial bacteria, immune surveillance and tissue homeostasis, against pathogenic bacteria, disruption of tissue homeostasis and non-protective immune responses
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13
Q

what are some host factors that cause perio

A
  • smoking/tobacco use
  • genetics
  • pregnancy/puberty
  • systemic disease
  • nutrition
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14
Q

how does periodontitis develop

A
  • normal flora colonise
  • proportion of periodontopathognic bacteria increases causing mild inflammation
  • high concentration of periodontopathogenic bacteria causing severe inflammation and pocket formation
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15
Q

what are the development phases of biofilm formation

A
  • naked surface
  • conditioning film
  • linkning film = e.g. streptococcus
  • coaggregation, re-conditioning film = e.g. actinomyces
  • accumulation, shedding = e.g. fusobacterium
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16
Q

how can you prevent disease progresion

A
  • by controlling health organisms, won’t get disease progression
17
Q

what causes the destructive processes

A
  • gram negative anaerobic cocci
18
Q

what are the important microorganisms in health

A
  • streptococci
  • actinomyces
  • veillonela
  • haemophilus
  • neisseri fusobacterium
19
Q

what are the important microorganisms in gingivitis

A
  • actinomycetes
  • prevotella intermedia
  • bacteriodes
  • fusobacterium nucleate
20
Q

what are the important microorganisms in periodontitis

A
  • P. gingivalis
  • tannerella forsythia
  • treponema denticola
  • prevotella intermedia
  • these produce toxins and proteases that destruct the tissues
21
Q

what model is used to distinguish which organisms are more problematic

A
  • socranksy’s model
22
Q

what organisms cause competition microbial interactions

A
  • metabolic products = acids, oxidants
  • bacteriocins
  • receptor antagonism
23
Q

what organisms cause co-operation microbial interactions

A
  • metabolic products = saccharides, peptides, growth factors
  • adhesion substrates
  • immune avoidance
24
Q

how can environment modification cause disease

A
  • if you have healthy plaque it is because you have things to prevent the nasty organisms getting in
  • if you have environment modification it can radically change what happens and can now allow disease progression
25
Q

what is difficult to prove with Koch’s postulates

A
  • culture, present in disease, actively identifying disease, animal models
26
Q

what alternative criteria is sued for Koch’s postulates

A
  • Association with disease based on increased numbers of pathogen at site of disease
  • Elimination or decreased numbers results in return to health
  • Evidence of host response to pathogen based on humoral and cellular immunity
  • Pathogenic potential based on animal models
  • Possession of pathogen with demonstratable virulence factors that cause periodontal destruction
27
Q

what is prophyromonas gingivalis

A
  • ‘keystone’ oral pathogen
  • gram negative non-motile rod, strict anaerobe
  • black pigmented = when placed in blood agar is takes haem from blood
  • increased numbers in PD
  • suppressed or undetectable in successfully treated lesions
  • increased serum of GCF in PD
  • pathogenesis demonstrated in murine and non-human primates
  • has an array of virulence factors
28
Q

what are the virulence factors of P gingivalise

A
  • host cell tissue adherence and invasion = fimbriae
  • elaboration of proteases = collagenase, fibrinolysis, phospholipase A, phosphatase (cocktail of degradative enzymes)
  • endotoxin (LPS) = proinflammtory
  • capsular polysaccharide and outer membrane vesicles
  • tissue toxic metabolic by-products = hydrogen sulphide, ammonia, fatty acids
29
Q

how does P. gingivalis adhere to surface

A
  • fibrillar adhesins
  • long fimbriae (FimA) = initial attachment and biofilm organisation
  • short fimbriae (Mfa1) = cell to cell auto aggregation
30
Q

what are gingipains

A
  • provide peptides from haem = nutrition
  • RgpA = arginine specific
  • Kpg = lysine specific
  • possess haemoglutanin domains = attachment
  • activate MMPs
  • not a good pathogen
31
Q

how can P. gingivalis manipulate host defences

A
  • biofilm lifestyle
  • gingipains = degradation of innate receptors and cytokines
  • induction of tissue destruction = MMPs
  • subversion = intracellular and ‘tricking’ host immunity
32
Q

what is A. actinomycetemomitans

A
  • luekotoxin
  • cytotoxin
  • LPS
  • Fc binding proteins
  • membrane vesicles
  • glycoprotein matrix
  • fimbriae
  • phase variation
  • subvert host cell immunity
  • does the same sort of things as P. gingivalis
33
Q

what are the systemic implications

A
  • oral cavity
  • rheumatoid arthritis
  • implanted biomaterials
  • immunocompromised patients
  • hospitalised individuals
  • contaminated medical/dental equipment
  • atherosclerotic plaques and CVD
  • increased risk CVD = 1.2-3.9 fold
  • increased risk diabetes = up to 6 fold
34
Q

what is the clinical management of perio

A
  • mechanical disruption
  • chemotherapeutic
  • probiotics
  • vaccines
  • surgery
35
Q

why can’t we give vaccines

A
  • can’t make them for specific organisms as then other ones will still be there and cause problems
36
Q

how could prebiotics work

A
  • could modulate the biofilm before any problems start

BDS3 - Microbiology and Oral Pathology (7 decks)

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