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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
true pocket
Apical migration of junctional Loss of attachment and loss of bone
26
progression of periodontitis
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
27
progression of attachment loss is generally
- 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
28
biofilm
One or more communities of microorganisms, embedded in a glycocalyx, attached to a solid surface.
29
4 properties of biofilm
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
what do you need to manage in order to manage periodontal diseaase
biofilm
31
bacterial virulence is
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
evidence of bacterial causation for periodontal disease (5)
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
how do oral biofilms form and mature
lower - early colonisers, after teeth brushing accumulate changes occur stick to each other
34
keystone pathogen
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
mechanisms of host immune response (4)
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
neutrophils role
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
neutrophil features
Trilobe cells Multi nucleate In health but increase in periodontal
38
change from normal flora to dysbiotic flora due to
Inflammatory response which includes neutrophils
39
if flora is kept regulated and control
flora in check - gingivitis throughout life not progression - Cellular response contains gingivitis Exceed certain level will progress to periodontitis
40
what is the initial periodontal lesion composed of mainly
T lymphocytes - helper CD4 mainly influence B cell production
41
what cells predominate at a later stage in periodontal lesion
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
protective functions of antibody (4)
Inhibition of adhesion/invasion - Antibodies stuck on then harder to invade Complement activation Neutralistion of toxins Opsonisation and phagocytosis of bacteria
43
what to antibodies ultimately do
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
side effect of mouth breathing at night
Dry mouth Less saliva and distributed differently -Less defence mechanisms
45
Matrix Metalloproteinases
a family of zinc and calcium dependent proteolytic enzymes, which include collagenases Family of enzymes which breakdown connective tissue (collagen matrix)
46
what causes matrix degradation in periodontitis mainly
MMPs secreted by host inflammatory cells
47
drugs that inhibit bone destruction aim to inhibit
MMPs
48
2 pathways which converge to cause periodontitis progression
connective tissue bone metabolism by MMPs osteoclast activation
49
normal healthy bone level measure from ACJ
1-2mm (can vary)
50
how to work out bone loss
in connection to root length (proportion) | - root to ACJ is 100%, in periodontal disease approx 60% lost
51
horizontal bone loss
Level pattern of bone loss across all teeth Some places more than others - Not necessarily pathological on all sites
52
vertical (angular) bone loss
One side bone level higher than others
53
2 patterns of bone loss
horizontal vertical (angular)
54
angular bone loss regeneration potential
maybe | - use wall of bone to help regenerate
55
horizontal bone loss regeneration potential
none
56
how does vertical bone loss arise
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
treatment of furcation bone loss
hard
58
6 general risk factors for periodontal disease
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
3 general risk determinants for periodontal disease
Genetics Socioeconomic status Gender - Ambiguous – males are less likely to report
60
3 categories of local risk factors for periodontal disease
- anatomical risk factors - tooth position - iatrogenic risk factors
61
anatomical risk factors for periodontal disease (4)
Enamel pearls/projections Grooves Furcations Gingival recession
62
local risk factors for periodontal disease predispose
periodontal disease and loss of attachment
63
5 tooth position factors that predispose periodontal disease
Malalignment Crowding Tipping Migration Occlusal forces
64
4 iatrogenic risk factors which predispose periodontal disease
Restoration overhangs Defective crown margins Poorly designed partial dentures Orthodontic appliances
65
smoking as a risk factor for periodontal disaese
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
Periodontitis/gum disease linked to what other health conditions
Alzheimer’s association Arthritis Cardiovascular disease Poor pregnancy outcomes
67
what is the primary aetiological agent in inflammatory periodontal disease
microbial plaque
68
the extent and severity of periodontal disease is dependent on....
the interaction between microbe and host

BDS2 BAMS (54 decks)

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