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1. periodontal disease finals > Periodontal disease- microbiology > Flashcards

Periodontal disease- microbiology Flashcards

1
Q

what is a plaque biofilm?

A

complex microbial community found on the tooth surface

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2
Q

how is plaque part of the host defence?

A

it aims to exclude exogenous pathogenic bacteria through process called colonisation resistance

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3
Q

what is the first stage of plaque formation?

A

within seconds a pellicle forms on the tooth surface

bacteria do not directly adhere to enamel - they adhere to pellicle

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4
Q

what is the pellicle derived from?

A
  • salivary glycoproteins
  • proteins
  • enzymes
  • lipids
  • GCF fluid
  • minerals
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5
Q

what are the functions of the pellicle?

A
  • lubrications
  • protection against acids
  • attatchment
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6
Q

what happens after the pellicle forms on the tooth?

A

within minutes pioneer species begin attaching to the pellicle via adhesins

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7
Q

what are the early plaque pioneer species known as?

A

streptococcus species- gram positive facultative anaerobes- cocci

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8
Q

give examples of early streptococcus species

A

oralis
sanguis
mites

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9
Q

what are other early colonisers?

A

as micro colonies form and the diversity and complexity of the biofilm increases- other species including actinomycete, haemophillus and neisseria species attach

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10
Q

what are the properties of:

actinomyces
haemophillus
neisseria

A
  • gram + filamentous facultative anaerobes
  • gram - facultative anaerobes cocci
  • gram - aerobic bacteria cocci
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11
Q

what species dominates within 24 hrs?

A

gram + streptococci

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12
Q

what happens as plaque matures?

A

within one week- as plaque matures within an aerobic environment - aerobic bacteria consume 02 which reduces the redox potential which causes a shift to favour an anaerobic environment favouring the growth of GNABs- actinomycete and GNABS increase

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13
Q

what GNABs begin to colonise the biofilm?

A

prevotella intermedia
fusobacterium nucleatum
porphoramonas gingivalis

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14
Q

what does it mean when plaque matures and becomes more organised?

A

within 7-28 days
supra gingival plaque- streptococci dominate surface of tooth and as plaque thickens and matures- GNABs dominate the outer surface of plaque

sub gingival plaque- organised structure with GNAB motile spirochetes found at base of pocket, GNAB found within pocket and anaerobic bacteria attached to surfaces within pockets.

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15
Q

what are the differences between surpagingival and sub gingival plaque ?

A

supra- variable env, 02 env, influenced by diet, streptococcus dominate, GNAB increase as plaque increases

subgingival- constant env, influenced by GCF, anaerobic env, streptococcus dominates, GNAB more abundant

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16
Q

what happens if this biofilm is not disrupted?

A

gingival inflammation will occur

17
Q

where is GCF derived from and what are the constituents?

A

derived from blood serum
- immune cells such as neutrophils, macrophages
- immunoglobulins such as IgA, IgG, IgM
- complement
-enzymes

18
Q

what is seen histopathologically with gingival health?

A
  • little inflammatory infiltrate- mainly neutrophils
  • neutrophils at low levels are part of physiological immune surveillance
  • neutrophils leak through JE to address plaque
19
Q

how do you remain at clinical gingival health?

A

plaque builds initially at the gingival margin- when this is regularly disrupted with sufficient OH- there is a balance between the plaque bacteria and IR.

20
Q

where is the junctional epithelium in health?

A

attached at the ACJ- up to the base of the pocket

21
Q

what causes gingivitis?

A

dysbiosis caused by the accumulation of plaque which tips the balance causing a dysbiotic relationship between IR and plaque bacteria

22
Q

what is gingivitis ?

A

inflammation of the gingival tissues

23
Q

what happens to the JE during gingivitis?

A

JE is replaced by pocket epithelium which is not attached to the tooth. It becomes ulcerated and leaky at the base of the pocket. But the JE attachment remains at the ACJ- no LOA

24
Q

why is JE not good?

A

JE is leaky as it has intracellular spaces- therefore bacteria and bacterial products leak through triggering inflammation

25
Q

what must be done with patients to reverse gingivitis?

A

good OH- using TIPPS behaviour model

  • use disclosing tablets
  • PMPR if needed
26
Q

what do you get with gingivitis?

A
  • false pocketing- where the PPD > than the actual loss of attachment
  • BOP
  • oedema
  • erythema
  • plaque normally seen at gingival margin
  • overfilled ID space
  • loss of stippling
  • rolled margins
27
Q

what experimental evidence is there that plaque accumulation causes gingivitis?

A

harold Lowes experiment

  • 12 dental student
  • excellent OH- S+P
  • OH stopped
  • plaque indices measured
  • gingival indices measured
  • 10-21 days clinically obvious gingivitis observed
  • OH re-established- return to clinical gingival health
28
Q

what were the results from Lowes gingivitis experiment?

A
  • increase in plaque causes gingivitis
  • change in composition of plaque with gingivitis i.e more filament bac and spirochetes
29
Q

how do we know these results (return to health) weren’t due to mechanical stimulation of the gingivae?

A
  • repeated experiment with chlorahexidine
  • produced same results
30
Q

what do age studies on plaque accumulation show?

A

children with lots of plaque- minimal inflammation

elderly with minimal plaque- lots of inflammation

susceptibility to plaque increases with age

31
Q

does everyone respond to plaque gingivitis in the same way?

A

no- response depends on your susceptibility to plaque and presence of RFs. The amount of plaque that causes gingivitis varies between individuals. always want to treat gingivitis to avoid potential progression to periodontitis.

32
Q

if a person is susceptible, when would gingivitis become periodontitis?

A

exact cause is unknown- and it cannot be predicted but those who are susceptible and do not have good OH or appropriate tx can go on to develop periodontitis

33
Q

what is periodontitis?

A

inflammation of the periodontium leading to irreversible damage and desctruction of supporting periodontal tissues

34
Q

where is the JE in periodontitis?

A

migrates apically from ACJ onto root surface due to underlying PDL destruction - ideal pocket for GNABS
= loss of attachment

35
Q

what percentage of damage is done by the HR?

A

80%

36
Q

do RF’s cause disease?

A

no- they increase the probability of disease occurring, and if disease is present they can make it more severe. But their presence does not always mean disease.

37
Q

how do we know that plaque causes periodontitis?

A

moore and moore- tested periodontal pockets and found certain bacteria associated with disease- including red complex, prevotella intermedia, fusobacterium nucleatum, aggregatorbacter

socranksy used dna-dna hybridisation to identify 40 species- found particular species to be grouped together - formed 5 clusters- green, purple, yellow, orange, red- red were the most destructive bacteria and found grouped in deeper pockets.

38
Q

what animal studies show plaque causes periodontitis?

A

unethical study on dogs and monkeys
- ligature placed around tooth neck
- plaque accumulated
- lead to LOA and bone resorption

study on gnotobiotic animals (rats) where they are born in sterile environment- there microbiome is well known- inoculated with periopathogens- developed periodontal disease.

39
Q

name perio pathogens?

A

GNABs

  • fusobacterium nucleautm
  • prevotella intermedia - orange
  • porphoramonas gignivalis
  • treponema Denticola
  • tanarella forsythia - red
  • agregatorbacter actinomycetemcomitins- purple

1. periodontal disease finals (11 decks)

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