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BDS3 BAMS Microbiology and Oral Pathology > Biofilm II - periodontitis > Flashcards

Biofilm II - periodontitis Flashcards

1
Q

5 oral biofilm diseases

A

caries

oral malodour

mucousal infections

endodontic infections

periodontal infections

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2
Q

oral biofilm diseases caused by

A

complex microbial colonies attached to surfaces

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3
Q

caries sites

A

root surface

coronal

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4
Q

oral malodour biofilm inhabits

A

dorsal surface of the tongue

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5
Q

mucosal infections of oral biofilm (3)

A

thrush

angular cheilitis

denture stomatitis

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6
Q

endodontic infections caused by oral biofilm

A

root canal infection

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7
Q

periodontal infectsion caused by oral biofilm

A

gingivitis

periodontitis

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8
Q

6 categories of influences on oral microflora

A

host factors

diet

saliva

gingival cervicular fluid

microbial interactions

gaseous environment

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9
Q

3 examples host factors that influence oral microflora

A

systemic disease

antibiotics use

oral hygiene methods

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10
Q

3 diet factors that influence oral microflora

A

chemical composition

physical consistency

frequency of intake

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11
Q

3 saliva factors that influence oral microflora

A

flow rate

pH balance

antimicrobial factors

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12
Q

2 gingival crevicular fluid factors that influence oral microflora

A

antimicrobials components

humoral immunity

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13
Q

2 microbial interactions that influence oral microflora

A

competition

co-operation

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14
Q

a gaseous environment factor that influeneces oral microflora

A

oxygen concentrations

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15
Q

healthy periodontium

A

no periodontal plaque, OH regime good and maintain, no inflammation

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16
Q

moderate periodontal disease

A

Inflammation – receding gum line, blood, plaque present, OH regime not ideal, possible host factors as well

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17
Q

advanced periodontal disease

A

unchecked leading to irreversible damage – bone loss and loss teeth (osteoclastogenesis)

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18
Q

classifications of periodontal disease (4 classes)

A
  • Gingivitis
  • Periodontitis
    • Chronic periodontitis – adult related
    • Aggressive periodontitis – spontaneous (genetic?)
  • Necrotizing periodontal disease
  • Peri-implantitis
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19
Q

periodontal disease cause is microbiological or immunological?

A

balance of factors needed

can cause tip from disease to health

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20
Q

examples of host factors on periodontal microbiome

A
  • smoking/tobacco use
  • genetics
  • pregnancy/puberty - hormonal
  • systemic disease - CVD, diabetes etc
  • nutrition
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21
Q

development of periodontitis

A

Biofilm – community of organisms attached to surface/interface

  • e.g. enamel

Grow from supragingival, deep into gingival crevice

  • Further down get increased in harmful anaerobic bacteria
    • Go from health biofilm to disease

controllable by OH

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22
Q

sequential stages of development of perio

A

initial organisms attach to conditioning film (now linking film)

  • coaggregation of bacterium
    • dense biofilm

cycle - interrupted back to the beginning by mechnical interruption (OH)

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23
Q

change in biofilm causes

A

a new microorganism to be brought in

control health related organisms to prevent going to disease associated stage

  • many factors drive

more accumulate more likely to have disease causing organisms (red) and overwhelm health organisms (green)

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24
Q

clinical result of periodontal disease

A

clinical attachment loss

alveolar bone resorbs

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25
health associated periodontal bacteria
gram positive aerobic immune system doesn't respond to them
26
disease associated periodontal bacteria
gram negative anaerobic
27
how often does biofilm need managed
daily if builds up = damage to host and hard to get under control again (damage will become irreversible if progress to bone loss)
28
important microorganisms in health
*Oral streptococci (variety), Actinomyces, Veillonella, Haemophilus, Neisseri, Fusobacterium*
29
important microogranisms in gingivitis
* Actinomyces, Prevotella intermedia, Bacteroides, Fusobacterium nucleatum* * *Anaerobic – have capacity to cause damage*
30
important microorganisms in periodontitis
*Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola, Prevotella intermedia, A.a, etc* * *Anaerobic – produce proteases and toxins that destroy tissue* * *Many organisms contribute to disease*
31
Socranksy's model
Study – culture, sequence * Identify in health and disease (perio) * red – amber – green Hard to demonstrate cause and effect * are they there due to disease? Do they cause the disease?
32
red organisms in Socranksy's model
p.gingivalis T.forsythia T.denticola
33
amber organisms in Socranksy's model
P.intermedia fusobacterium nucleatum P.nigrescens etc
34
green organisms in Socranksy's model
C. gingivalis C.spitigena S.sanguis
35
microobial competition
dominance * Metabolic products – acids, oxidants * Bacteriocins * Receptor antagonism
36
mirobial co-operation
integration * Metabolic products – saccharides, peptides, growth factors * Adhesion substrates * Immune avoidance
37
microbial interactions types
* competition * co-operation Hundreds MO interact Positive and negative affects Permutations of interactions is vast So hard to determine what ones are key
38
example microbial interactions describe
Streptococcus might attach particular fibrin on conditioning film, and another organism attach to it Or Organism attaches to fibrin on conditioning surface and it does or doesn’t like it so there’s a different ways can be viewed * May produce anitbiotics (e.g. streptomyces) – create spatial awareness * Exclude organisms Have cooperation or competition
39
healthy plaque role
has many microorganisms that prevent nasty pathogenic microorganisms penetrating
40
what causes healthy biofilm plaque switch to disease community
Environmental modification – *diet, hormonal, antibiotics* Change commensal community * allow pathogenic bacteria to thrive = disease Change microbiome back – hard * need harsh tools – chlorohexidine daily, antibiotics
41
how many species needed to form biofilm
more than one coaggregation and cooperation
42
issue with Koch's postulate
difficult to prove: culture, present in disease, actively identifying disease, animal models
43
alternative criteria to Koch's postulate (5)
* 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 taken together – used to determine what MOs are important
44
Porphyromonas gingivalis importance
‘Keystone’ oral pathogen IMPORTANT BUT NOT KEYSTONE * as biofilm will still be present even if destroyed 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 (bone loss) An array of virulence factors
45
porphymonas gingivalis characteristics
* Gram-neg non-motile rod, strict anaerobe (no O2 or CO2 – obligate) * Black pigmented (iron accumulation from hemin, when grown on blood agar – diagnostic differentiation)
46
porphymonas gingivalis virulence factors
* Host cell tissue adherence and invasion * Fimbriae * Elaboration of proteases – ‘cocktail of degradative enzymes’ *destroy cells* * collagenase * fibrinolysin * phospholipase A * phosophatases​ * Endotoxin (LPS) – pro-inflammatory * Capsular polysaccharide & outer membrane vesicles * Tissue toxic metabolic by-products * hydrogen sulfide * ammonia * fatty acids
47
role of virulence factors
cause disease agitate immune response
48
adhesion of P.gingivalise
**Fimbrillar adhesins** * Help invade membrane vesicle of host cells by binding to cellular integrins * Long fimbriae (FimA) * Long and peritrichous (all way round cell) * Initial attachment and biofilm organization * Short fimbriae (Mfa1) * Cell to cell autoaggregation * Microcolony formation Adherence mechanisms may vary according to substrate, may be multimodal. P. gingivalis _releases membrane vesicles containing functional adhesins that may also bind to the substrates shown_
49
gingipains in p.gingivalis
Provide peptides from heme - _nutrition to itself_ * RgpA (arginine specific) * Kpg (lysine specific) Possess haemaglutanin (HagA) domains - attachment Activate matrix metalloproteases (MMP’s)
50
manipulating host defences of P.gingivalis
Biofilm lifestyle Gingipains * Degradation of innate receptors * Degradation of cytokines – e.g. IL-8, ICAM-1 * Induction of tissue destruction – MMP’s Subversion – intracellular and ‘tricking’ host immunity
51
p.gingivalis pathway to perio disease
Subverts immune response * interferes with complement Dysbiosis of biofilm Activates complement * proinflammatory – bone destruction, PDL loss **Agitator** **Involved** **Important but not solely** has classical virulence factors of good pathogenic MO
52
virulence factors of A.actinomycetemcomintans (A.a) (9)
* Leukotoxin * Cytotoxin * LPS * Fc binding proteins * Membrane vesicles * Glycoprotein matrix * Fimbriae * Phase variation * Subvert host cell immunity similar pathogenicitiy to p.gingivalis - involved too
53
comparison of P.gingivalis and A.actinomycetemcomitans association
P. gingivalis - Increased in numbers in PD A. actinomycetemcomitans -Increased in numbers in LAP, and some chronic PD
54
comparison of P.gingivalis and A.actinomycetemcomitans elimation
P. gingivalis A. actinomycetemcomitans both Suppressed or undetectable levels in treated lesions Detectable in recurrent lesions
55
comparison of P.gingivalis and A.actinomycetemcomitans host response
P. gingivalis - Increased serum and crevicular fluid levels in subjects with PD A. actinomycetemcomitans - Increased serum and crevicular fluid levels in subjects with LAP
56
comparison of P.gingivalis and A.actinomycetemcomitans animal studies
P. gingivalis - Pathogenic potential demonstrated in rodent and non-human primitive models A. actinomycetemcomitans - Pathogenic potential demonstrated in rodent models of PD
57
comparison of P.gingivalis and A.actinomycetemcomitans virulence factors
P. gingivalis - Host tissue cells adherence and invasion, degradative, enzymes, endotoxin, metabolic by-products A. actinomycetemcomitans - Host tissue cell adherence and invasion, elaboration of leukotoxin, degradative enzymes, endotoxin, bone resorption-inducing factor
58
periodontal pathogenic bacteria are
Only grown in anaerobic condition – can be oxygenated if other bacteria drive it down to low cellular level
59
periodontal pathogenic bacteria cause
collateral damage - PDL and bone
60
chronic inflammation of periodontium effect on immune system
doesn't go unnoticed immune system creates lookalike autoantibodies
61
implications of chronic periodontium inflammation (8)
* Oral cavity * Implanted biomaterials - *joints for RA* * Immunocompromised pts - *IE risk* * Hospitalised individuals * Contaminated medical/dental equipment *Dysregulation of the oral mucosal immune system by biofilm manifests as destructive inflammation locally **AND systemically*** * Increased risk of cardiovascular disease - 1.2- 3.9 fold * Suggested increased risk of rheumatoid arthritis * Increased risk diabetes - up to 6 fold
62
dysbiotic microbiome is
harmful links to systemic body diseases from periodontal disease * CVD * rheumatoid arthritis * diabetes chronic inflammatory cause (initiated by more than one MO)
63
clincal management of periodontal biofilm (5 options)
* Mechanical disruption - brushing * Chemotherapeutic ? * periostat, damped immune response * Probiotics * Hard to repopulate a dysbiotic biofilm * Prebiotics is better – modulate existing before disease begins * Vaccines ? * cannot make of particular MO as others will fill space * Surgery

BDS3 BAMS Microbiology and Oral Pathology (6 decks)

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