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BDS2 Periodontology > Periodontitis: aetiology and pathogenesis > Flashcards

Periodontitis: aetiology and pathogenesis Flashcards

1
Q

What are the risk factors for periodontitis?

A
  • behavioural
  • environmental
  • genetic
  • epigeneitc
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2
Q

What is the inflammation like in clinical health, gingivitis and periodontisis

A

clinical health- acute resolution of inflammation
gingivitis - chronic resolution of inflammation
periodontisis - chronic non-resolving inflammation

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3
Q

What is the role of plaque in periodontal disease

A

plaque is NECESSARY but NOT SUFFICIENT for periodontal disease

plaque will cause gingivitis but not always periodontal disease

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4
Q

What is the pathogenesis of gingivitis

A

Microbial challenge (plaque)
- local plaque retention factors e.g. calculus, restoration margins, crowding, mouth breathing
- systemic modifying factors e.g. sex hormones, medication
Clinical disease (gingivitis)

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5
Q

What does gingival health look like

A
  • knife edge, scalloped gingival margin
  • stippling (about 30%)
  • pink
  • oral epithelial cells shed continuously
  • flow of GCF (antibodies inside)
  • cellular immune response is small and regulated
  • intact barrier provided by the junctional epithelium
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6
Q

What does gingivitis look like

A
  • red margins, inflamed, no stippling
  • increase plaque and change in its composition
  • increased GCF, increased immune cells
  • proliferation and ulceration of epithelium (bleeds)
  • predominance of plasma cells

(all increases as gingivitis becomes more established)

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7
Q

What happens to gingivitis when you remove the microbial challenge

A

return to health

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8
Q

What does periodontitis look like

A
  • bone loss (irreversible)
  • apical migration of the junctional epithelium
  • plasma cells >50%
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9
Q

How can we tell the difference between gingivitis and periodontitis

A

by using a BPE probe

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10
Q

Why can smokers gingiva be misleading

A

they have paler gingiva and look healthy but can have deep pockets

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11
Q

Does gingivitis always progress to periodontitis

A

not always

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12
Q

Once periodontitis is initiated, how does attachment loss progress

A

episodic rather than continuous

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13
Q

Do all regions of the mouth progress to periodontitis at the same rate

A

no, can be very different within the same mouth

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14
Q

How quickly does attachment loss happen

A

generally very slow (0.05-0.1mm per year) but this is highly variable

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15
Q

What is a big factor as to how fast patients are to periodontitis

A

their microbiome/ immune response

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16
Q

what is a biofilm

A

one or more communities of microorganisms, embedded in a glycocalyx, attached to a solid surface

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17
Q

What are the properties of biofilms?

A
  • provide protection for colonising species from competing organisms and environment (host defences, antibiotics etc)
  • facilitate uptake of nutrients and removal of metabolic products
  • development of appropriate physiochemical environment e.g. pH, O2 concentration
  • communication between bacteria
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18
Q

What is bacterial virulence

A
  • ability to colonise and compete in an ecological niche

- ability to evade the host defences

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19
Q

How can we work out whether specific bacteria cause periodontal disease

A
  • presence in elevated numbers at diseased sites
  • reduced numbers following periodontal therapy
  • presence of an elevated specific immune response
  • production of virulence factors
  • evidence from animal models
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20
Q

Is there any proved causative microorganisms in periodontal disease

A

no, none satisfy koch’s postulates

- complexes are more likely

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21
Q

what is a key stone pathogen

A

will change to make the whole community bad

22
Q

What are the 3 microorganisms at the ‘top’ of the periodontal disease pyramid

A
  • P. gingivalis
  • B. forsythus
  • T. denticola
23
Q

Periodontitis is a synergistic infection what does this mean

A

plaque ecology is important

there are other host and environmental factors which modify the disease

24
Q

What mechanisms does the host immune response have against periodontal disease

A
  • saliva
  • epithelium (physical barrier, shedding of cells, production of inflammatory mediators)
  • GCF
  • inflammatory and immune responses
25
Q

How do neutrophils protect against bacteria but contribute to host damage

A
  1. reactive oxygen kills bacteria but damages host
  2. NETs kill bacteria but damages host

Some people, neutrophils keep inflammation in check so won’t progress to periodontitis but others will

26
Q

How does the cytokine response to pathogenic biofilm contribute to periodontitis.

What cytokines do this

A

modulate bone resorption (pockets forming)

MMPs, TNFa, prostaglandins, interluekins

27
Q

What part of the immune response is the initial periodontal lesion composed of

A

T lymphocytes

28
Q

What follows the intiial periodontal lesion of T cells?

A

B cells and plasma cells

- antibody is produced locally and probably protective

29
Q

What are the protective functions of antibody

A
  • inhibition of adhesion/invasion
  • complement activation
  • neutralisation of toxins
  • opsonisation and phagocytosis
  • prevents progressive infection, and therefore, potentially serious systemic consequences
  • inadvertent local tissue damage (bystander damage) combined with attempts at repair
30
Q

What do MMPs do

A

enzymes which break down connective tissue

31
Q

What are MMPs

A

Matrix metalloproteinases are a family of zinc and calcium dependent proteolytic enzymes, which include collagenases

32
Q

What is the role of MMPs in periodontitis

A

matrix degradation is largely a result of MMP’s secreted by host inflammatory cells

33
Q

What causes bone loss in periodontitis

A
  • osteoclast activation
34
Q

What is the normal bone level measured from the ADJ

A

1-2mm

35
Q

How is bone loss usually measured?

A

by percentage

root = 100%

36
Q

What is the pattern of bone loss like in periodontitis?

A

vertical and/or horizontal

37
Q

How does the pattern of bone loss affect how you treat periodontitis

A

Vertical/angular = may regenerate as you can use the wall still there to pack against

Horizontal = nothing to pack against

38
Q

How does vertical bone loss arise?

A

?

Maybe to do with where the biofilm is

39
Q

What can also complicate treatment of periodontitis

A

furcation bone loss (can get probe through)

40
Q

Risk factors of periodontisis

A
  • smoking
  • diabetes
  • stress
  • drugs
  • systemic disease
  • nutrition
41
Q

Risk determinants of periodontitis

A
  • genetics
  • socioeconomic status
  • gender
42
Q

Local risk factors - Anatomical

A
  • enamel pearls
  • grooves
  • furcations
  • gingival recession
43
Q

Local risk factors - tooth position

A
  • malalignment
  • crowding
  • tipping
  • migration
  • occlusal forces
44
Q

Local risk factors - Iatrogentic risk factors

A
  • restoration overhangs
  • defective crown margins
  • poorly designed partial dentures
  • orthodontic appliances
45
Q

In what ways is smoking a risk factor for periodontitis

A
  • effect on subgingival plaque is uncertain
  • vasoconstriction of gingival vessels and increased gingival keratinisation
  • impaired antibody production
  • depressed numbers of Th lymphocytes
  • impaired PMN function
  • increased production of pro-inflammatory cytokines
46
Q

What general health condition is a risk factor for periodontitis

A

diabetes

47
Q

How does periodontitis affect general health

A 
Heart - promotion of atherosclerosis
Liver - systemic inflammation 
Gut - dysbiosis
Pregnancy - inflammation induced pregnancy complications
- altzheimers?
- RH arthritis?
- CVS

(if you have inflammation it’s not just limited to the mouth)

48
Q

What is the primary aetiological agent in inflammatory periodontal diseases

A

microbial plaque

49
Q

What is the extent and severity of periodontal diseases dependent upon

A

the interaction between microbe and host

50
Q

What conveys susceptibility to periodontal diseases

A

risk factors which interfere with host defenses

BDS2 Periodontology (9 decks)

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