aetiology and pathogenesis of periodontal disease Flashcards
what is the leading cause in dental insurance cover
not getting periodontal disease treatment right
characteristics of healthy biofilm
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
characteristics of gingivitis biofilm
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
characteristics of periodontitis biofilm
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
plaque and periodontal disease
Plaque necessary but not sufficient of periodontal disease
Not good tooth brushing = plaque
- caries (if sugar there), gingivitis
what causes gingivitis
accumulation of plaque
what does gingivitis depend upon
factors
- local
- systemic
4 local factors of gingivitis
- calculus
- restoration margins
- crowding
- mouth breathing
2 systemic factors on gingivitis
- sex hormones
- medication
gingival health description (3)
- knife edge, scalloped gingival margin (well defined)
- Stippling (in about 30%) at papilla
Pink
- Modified by habits (smoking) and racial pigmentation
healthy gingival barrier and environment
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
shedding of oral epithelial cells because
hard for bacteria to invade due to continuous shed
- 4-5days
gingival margin and environment in gingivitis
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
changes from health to gingivitis are
reversible
composition of immune cell infiltrate in normal healthy gingiva
- Monocyte/macrophage
- Lymphocyte
- neutrophil
bacteria present in health
aerobes
gram positive
bacteria present in disease
anaerobes
gram negative
early gingivitis has an increase in….
immune cell infiltrate
what proliferates in early gingivitis
junctional epithelium
what cells increase in number in disease states?
plasma cells (antibody making B cells)
how to reverse gingivititis
remove microbial challenge
control other factors as well
Periodontitis
- Irreversible loss of attachment
- Apical migration of junctional epithelium
predominance of plasma cells
how to clinically tell difference between gingivitis and periodontitis
BPE probe - 10mm pocket (probe disappears)
false pocket
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
true pocket
Apical migration of junctional
Loss of attachment and loss of bone
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
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
biofilm
One or more communities of microorganisms, embedded in a glycocalyx, attached to a solid surface.
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
what do you need to manage in order to manage periodontal diseaase
biofilm
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
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
how do oral biofilms form and mature
lower - early colonisers, after teeth brushing
accumulate
changes occur
stick to each other
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
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
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
neutrophil features
Trilobe cells
Multi nucleate
In health but increase in periodontal
change from normal flora to dysbiotic flora due to
Inflammatory response which includes neutrophils
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
what is the initial periodontal lesion composed of mainly
T lymphocytes
- helper CD4 mainly
influence B cell production
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
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
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
side effect of mouth breathing at night
Dry mouth
Less saliva and distributed differently
-Less defence mechanisms
Matrix Metalloproteinases
a family of zinc and calcium dependent proteolytic enzymes, which include collagenases
Family of enzymes which breakdown connective tissue (collagen matrix)
what causes matrix degradation in periodontitis mainly
MMPs secreted by host inflammatory cells
drugs that inhibit bone destruction aim to inhibit
MMPs
2 pathways which converge to cause periodontitis progression
connective tissue bone metabolism by MMPs
osteoclast activation
normal healthy bone level measure from ACJ
1-2mm (can vary)
how to work out bone loss
in connection to root length (proportion)
- root to ACJ is 100%, in periodontal disease approx 60% lost
horizontal bone loss
Level pattern of bone loss across all teeth
Some places more than others
- Not necessarily pathological on all sites
vertical (angular) bone loss
One side bone level higher than others
2 patterns of bone loss
horizontal
vertical (angular)
angular bone loss regeneration potential
maybe
- use wall of bone to help regenerate
horizontal bone loss regeneration potential
none
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
treatment of furcation bone loss
hard
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
3 general risk determinants for periodontal disease
Genetics
Socioeconomic status
Gender
- Ambiguous – males are less likely to report
3 categories of local risk factors for periodontal disease
- anatomical risk factors
- tooth position
- iatrogenic risk factors
anatomical risk factors for periodontal disease (4)
Enamel pearls/projections
Grooves
Furcations
Gingival recession
local risk factors for periodontal disease predispose
periodontal disease and loss of attachment
5 tooth position factors that predispose periodontal disease
Malalignment
Crowding
Tipping
Migration
Occlusal forces
4 iatrogenic risk factors which predispose periodontal disease
Restoration overhangs
Defective crown margins
Poorly designed partial dentures
Orthodontic appliances
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
Periodontitis/gum disease linked to what other health conditions
Alzheimer’s association
Arthritis
Cardiovascular disease
Poor pregnancy outcomes
what is the primary aetiological agent in inflammatory periodontal disease
microbial plaque
the extent and severity of periodontal disease is dependent on….
the interaction between microbe and host
