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BDS2 BAMS > aetiology and pathogenesis of periodontal disease > Flashcards

aetiology and pathogenesis of periodontal disease Flashcards

1
Q

what is the leading cause in dental insurance cover

A

not getting periodontal disease treatment right

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2
Q

characteristics of healthy biofilm

A

Health promoting biofilm – symbiosis

Proportionate host response and action from complement and PMNs

Low biomass host and IMLP, antigens, bacterial DNA lead to acute resolution of inflammation

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3
Q

characteristics of gingivitis biofilm

A

Antibody, more PMNs and T & B Cells are proportionate host response to incipient dysbiosis

LPS, virulence factors and antigens lead to high biomass host having chronic resolution of inflammation

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4
Q

characteristics of periodontitis biofilm

A

Connective tissue and bone damage causes increased GCF and DAMPs

Hyperinflammatory (disproportionate host response) to frank dysbiosis (pathogenic biofilm) by antibodies, increased PMNs and plasma cells

High biomass host and antigens, gingipains and LPS leads to Failed resolution of inflammation

Cytokines, prostanoids, MMPs, oxidative stress leads to chronic non-resolving inflammation

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5
Q

plaque and periodontal disease

A

Plaque necessary but not sufficient of periodontal disease

Not good tooth brushing = plaque
- caries (if sugar there), gingivitis

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6
Q

what causes gingivitis

A

accumulation of plaque

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7
Q

what does gingivitis depend upon

A

factors

  • local
  • systemic
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8
Q

4 local factors of gingivitis

A
  • calculus
  • restoration margins
  • crowding
  • mouth breathing
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9
Q

2 systemic factors on gingivitis

A
  • sex hormones

- medication

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10
Q

gingival health description (3)

A
  • knife edge, scalloped gingival margin (well defined)
  • Stippling (in about 30%) at papilla

Pink
- Modified by habits (smoking) and racial pigmentation

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11
Q

healthy gingival barrier and environment

A

Intact barrier provided by junctional epithelium
- Not ulcerated

Epithelial barrier turns over quickly (4-5 days)

Shedding of oral epithelial cells
- Hard for bacteria to invade due to continuous shed

Flow of GCF
- Useful host defence – antibodies, complement, various proteins

Phagocyte function and lymphocyte infiltrate
- usual response in health 
Neutrophils
- Keep environment under control 
Lymphocytes regulate tissue
Complement activity
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12
Q

shedding of oral epithelial cells because

A

hard for bacteria to invade due to continuous shed

  • 4-5days
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13
Q

gingival margin and environment in gingivitis

A

Altered microbial colonisation

  • Key difference in appearance: red, inflamed margin, loss of stippling (shiny red appearance)
  • Microbiome change – more plaque of different composition

Increased flow of GCF

Influx of neutrophils, increased lymphocytes and monocytes

Plasma cell infiltrate

  • Immune system in health is amplified
  • More GCF, proteins and neutrophils etc

Proliferation and ulceration of epithelium
- Change in epithelium structure
- Ulcerate – bleed on probing
Holes in it

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14
Q

changes from health to gingivitis are

A

reversible

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15
Q

composition of immune cell infiltrate in normal healthy gingiva

A
  • Monocyte/macrophage
  • Lymphocyte
  • neutrophil
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16
Q

bacteria present in health

A

aerobes

gram positive

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17
Q

bacteria present in disease

A

anaerobes

gram negative

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18
Q

early gingivitis has an increase in….

A

immune cell infiltrate

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19
Q

what proliferates in early gingivitis

A

junctional epithelium

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20
Q

what cells increase in number in disease states?

A

plasma cells (antibody making B cells)

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21
Q

how to reverse gingivititis

A

remove microbial challenge

control other factors as well

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22
Q

Periodontitis

A
  • Irreversible loss of attachment
  • Apical migration of junctional epithelium

predominance of plasma cells

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23
Q

how to clinically tell difference between gingivitis and periodontitis

A

BPE probe - 10mm pocket (probe disappears)

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24
Q

false pocket

A

Increase in pocket depth without loss of attachment

  • ‘local epithelium start to proliferate
  • Pocket and then bone still intact

Junctional epithelium not changed position

  • Become ulcerated
  • Inflammation causes pocket
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25
Q

true pocket

A

Apical migration of junctional

Loss of attachment and loss of bone

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26
Q

progression of periodontitis

A

Gingivitis does not always progress to periodontitis
- In many it does

Once periodontitis is intiated, progression of attachment loss may be episodic rather than continuous
- Hard to judge rate

Different sites within the same mouth may be affected to markedly varying extents

Progression of attachment loss is generally very slow (0.05-0.1 mm per year) but this is highly variable
- 0.1mm per year so in 10 years 1mm
- Can go to 2mm per year in some patients
Serious issue if miss these patients for a few years – tooth loss
- Depends on root health
Important to monitor and keep an eye on tooth health

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27
Q

progression of attachment loss is generally

A
  • 0.1mm per year so in 10 years 1mm
  • Can go to 2mm per year in some patients
    Serious issue if miss these patients for a few years – tooth loss
  • Depends on root health
    Important to monitor and keep an eye on tooth health
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28
Q

biofilm

A

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

29
Q

4 properties of biofilm

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

30
Q

what do you need to manage in order to manage periodontal diseaase

A

biofilm

31
Q

bacterial virulence is

A

Ability to colonise and compete in an ecological niche

Ability to evade the host defences
- Many features tailor them to work effectively and cause periodontal disease
>degrade host immunoglobulin and complement
>leucotoxin production
>tissue invasion
>inhibition of antibody synthesis

32
Q

evidence of bacterial causation for periodontal disease (5)

A

Presence in elevated numbers at diseased sites

Reduced numbers following periodontal therapy

Presence of an elevated specific immune response antibodies created

Production of virulence factors

Evidence from animal models in some animals, bone destruction around teeth

  • not one bacteria
  • complex of bacteria
33
Q

how do oral biofilms form and mature

A

lower - early colonisers, after teeth brushing

accumulate
changes occur
stick to each other

34
Q

keystone pathogen

A

Certain bacteria turn up and cause chaos

Presence in biofilm will change it

Use bacteria to create dysbiotic biolfilm
- Community goes bad after arrival
Manipulates it

Inflammation response
- exaggerates dysbiosis response, bacteria thrive

35
Q

mechanisms of host immune response (4)

A

Saliva

Epithelium

  • physical barrier
  • shedding of cells
  • production of inflammatory mediators

GCF

Inflammatory and Immune Responses

  • Selection of inflammatory and immune cells
  • Play key role in regulating what happens in patient with perio
36
Q

neutrophils role

A

Neutrophils generate reactive oxygen species which kill bacteria
- By stander damage to host also

NET neutrophil extracellular trap

  • Web of sticky DNA and other molecules
  • Trap bacteria
  • Release mediators which kill bacteria and damage host
37
Q

neutrophil features

A

Trilobe cells
Multi nucleate
In health but increase in periodontal

38
Q

change from normal flora to dysbiotic flora due to

A

Inflammatory response which includes neutrophils

39
Q

if flora is kept regulated and control

A

flora in check - gingivitis throughout life not progression
- Cellular response contains gingivitis

Exceed certain level will progress to periodontitis

40
Q

what is the initial periodontal lesion composed of mainly

A

T lymphocytes
- helper CD4 mainly

influence B cell production

41
Q

what cells predominate at a later stage in periodontal lesion

A

B cells and Plasma cells predominate at a later stage

  • Antibody is produced locally, but circulate in blood
  • Antibody is probably protective, but there is an argument if could be destructive
42
Q

protective functions of antibody (4)

A

Inhibition of adhesion/invasion
- Antibodies stuck on then harder to invade

Complement activation

Neutralistion of toxins

Opsonisation and phagocytosis of bacteria

43
Q

what to antibodies ultimately do

A

Prevents progressive infection and, therefore, potentially serious systemic consequences
- Inadvertent local tissue damage (bystander damage) combined with attempts at repair

Immune response protects you but causes bone damage as it does

  • Want to keep pathogenic biofilm out of systemic circulation
  • Natural retreat of body tissue away from biofilm
44
Q

side effect of mouth breathing at night

A

Dry mouth

Less saliva and distributed differently
-Less defence mechanisms

45
Q

Matrix Metalloproteinases

A

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

Family of enzymes which breakdown connective tissue (collagen matrix)

46
Q

what causes matrix degradation in periodontitis mainly

A

MMPs secreted by host inflammatory cells

47
Q

drugs that inhibit bone destruction aim to inhibit

A

MMPs

48
Q

2 pathways which converge to cause periodontitis progression

A

connective tissue bone metabolism by MMPs

osteoclast activation

49
Q

normal healthy bone level measure from ACJ

A

1-2mm (can vary)

50
Q

how to work out bone loss

A

in connection to root length (proportion)

- root to ACJ is 100%, in periodontal disease approx 60% lost

51
Q

horizontal bone loss

A

Level pattern of bone loss across all teeth

Some places more than others
- Not necessarily pathological on all sites

52
Q

vertical (angular) bone loss

A

One side bone level higher than others

53
Q

2 patterns of bone loss

A

horizontal

vertical (angular)

54
Q

angular bone loss regeneration potential

A

maybe

- use wall of bone to help regenerate

55
Q

horizontal bone loss regeneration potential

A

none

56
Q

how does vertical bone loss arise

A

Presumed to be down to bone shape to begin with
- Narrow then horizontal bone loss

Destruction at most apical point of plaque (how far biofilm in pocket) 2mm down get immune response tissue destruction

  • Occupies whole width = horizontal
  • Bone fatter = get vertical
57
Q

treatment of furcation bone loss

A

hard

58
Q

6 general risk factors for periodontal disease

A

Smoking

Diabetes
- Poorly controlled = more susceptible

Stress - less well defined

Drugs

Systemic disease - less well defined

Nutrition - less well defined

  • Micronutrient deficiency – low fruit and veg intake
  • Obesity
59
Q

3 general risk determinants for periodontal disease

A

Genetics

Socioeconomic status

Gender
- Ambiguous – males are less likely to report

60
Q

3 categories of local risk factors for periodontal disease

A
  • anatomical risk factors
  • tooth position
  • iatrogenic risk factors
61
Q

anatomical risk factors for periodontal disease (4)

A

Enamel pearls/projections

Grooves

Furcations

Gingival recession

62
Q

local risk factors for periodontal disease predispose

A

periodontal disease and loss of attachment

63
Q

5 tooth position factors that predispose periodontal disease

A

Malalignment

Crowding

Tipping

Migration

Occlusal forces

64
Q

4 iatrogenic risk factors which predispose periodontal disease

A

Restoration overhangs

Defective crown margins

Poorly designed partial dentures

Orthodontic appliances

65
Q

smoking as a risk factor for periodontal disaese

A

most well defined

Effect on subgingival plaque is uncertain

Vasoconstriction of gingival vessels and increased gingival keratinisation

Impaired antibody production

Depressed numbers of Th lymphocytes
- Smoking has impact on immune system operation – change in response of bacteria in mouth

Impaired PMN function

Increased production of pro-inflammatory cytokines

3-6 times more likely to get disease

66
Q

Periodontitis/gum disease linked to what other health conditions

A

Alzheimer’s association

Arthritis

Cardiovascular disease

Poor pregnancy outcomes

67
Q

what is the primary aetiological agent in inflammatory periodontal disease

A

microbial plaque

68
Q

the extent and severity of periodontal disease is dependent on….

A

the interaction between microbe and host

BDS2 BAMS (54 decks)

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