Biofilm II - periodontitis Flashcards
5 oral biofilm diseases
caries
oral malodour
mucousal infections
endodontic infections
periodontal infections
oral biofilm diseases caused by
complex microbial colonies attached to surfaces
caries sites
root surface
coronal
oral malodour biofilm inhabits
dorsal surface of the tongue
mucosal infections of oral biofilm (3)
thrush
angular cheilitis
denture stomatitis
endodontic infections caused by oral biofilm
root canal infection
periodontal infectsion caused by oral biofilm
gingivitis
periodontitis
6 categories of influences on oral microflora
host factors
diet
saliva
gingival cervicular fluid
microbial interactions
gaseous environment
3 examples host factors that influence oral microflora
systemic disease
antibiotics use
oral hygiene methods
3 diet factors that influence oral microflora
chemical composition
physical consistency
frequency of intake
3 saliva factors that influence oral microflora
flow rate
pH balance
antimicrobial factors
2 gingival crevicular fluid factors that influence oral microflora
antimicrobials components
humoral immunity
2 microbial interactions that influence oral microflora
competition
co-operation
a gaseous environment factor that influeneces oral microflora
oxygen concentrations
healthy periodontium
no periodontal plaque, OH regime good and maintain, no inflammation
moderate periodontal disease
Inflammation – receding gum line, blood, plaque present, OH regime not ideal, possible host factors as well
advanced periodontal disease
unchecked leading to irreversible damage – bone loss and loss teeth (osteoclastogenesis)
classifications of periodontal disease (4 classes)
- Gingivitis
- Periodontitis
- Chronic periodontitis – adult related
- Aggressive periodontitis – spontaneous (genetic?)
- Necrotizing periodontal disease
- Peri-implantitis
periodontal disease cause is microbiological or immunological?
balance of factors needed
can cause tip from disease to health
examples of host factors on periodontal microbiome
- smoking/tobacco use
- genetics
- pregnancy/puberty - hormonal
- systemic disease - CVD, diabetes etc
- nutrition
development of periodontitis
Biofilm – community of organisms attached to surface/interface
- e.g. enamel
Grow from supragingival, deep into gingival crevice
- Further down get increased in harmful anaerobic bacteria
- Go from health biofilm to disease
controllable by OH
sequential stages of development of perio
initial organisms attach to conditioning film (now linking film)
- coaggregation of bacterium
- dense biofilm
cycle - interrupted back to the beginning by mechnical interruption (OH)
change in biofilm causes
a new microorganism to be brought in
control health related organisms to prevent going to disease associated stage
- many factors drive
more accumulate more likely to have disease causing organisms (red) and overwhelm health organisms (green)
clinical result of periodontal disease
clinical attachment loss
alveolar bone resorbs
health associated periodontal bacteria
gram positive aerobic
immune system doesn’t respond to them
disease associated periodontal bacteria
gram negative anaerobic
how often does biofilm need managed
daily
if builds up = damage to host and hard to get under control again (damage will become irreversible if progress to bone loss)
Socranksy’s model
Study – culture, sequence
- Identify in health and disease (perio)
- red – amber – green
Hard to demonstrate cause and effect
- are they there due to disease? Do they cause the disease?
red organisms in Socranksy’s model
p.gingivalis
T.forsythia
T.denticola
amber organisms in Socranksy’s model
P.intermedia
fusobacterium nucleatum
P.nigrescens
etc
green organisms in Socranksy’s model
C. gingivalis
C.spitigena
S.sanguis
microbial interactions types
- competition
- co-operation
Hundreds MO interact
Positive and negative affects
Permutations of interactions is vast
So hard to determine what ones are key
example microbial interactions
describe
Streptococcus might attach particular fibrin on conditioning film, and another organism attach to it
Or
Organism attaches to fibrin on conditioning surface and it does or doesn’t like it so there’s a different ways can be viewed
- May produce anitbiotics (e.g. streptomyces) – create spatial awareness
- Exclude organisms
Have cooperation or competition
healthy plaque role
has many microorganisms that prevent nasty pathogenic microorganisms penetrating
what causes healthy biofilm plaque switch to disease community
Environmental modification – diet, hormonal, antibiotics
Change commensal community
- allow pathogenic bacteria to thrive = disease
Change microbiome back – hard
- need harsh tools – chlorohexidine daily, antibiotics
how many species needed to form biofilm
more than one
coaggregation and cooperation
Porphyromonas gingivalis importance
‘Keystone’ oral pathogen IMPORTANT BUT NOT KEYSTONE
- as biofilm will still be present even if destroyed
Increased numbers in PD
Suppressed or undetectable in successfully treated lesions
Increased serum of GCF in PD
Pathogenesis demonstrated in murine and non-human primates (bone loss)
An array of virulence factors
porphymonas gingivalis characteristics
- Gram-neg non-motile rod, strict anaerobe (no O2 or CO2 – obligate)
- Black pigmented (iron accumulation from hemin, when grown on blood agar – diagnostic differentiation)
porphymonas gingivalis virulence factors
- Host cell tissue adherence and invasion
- Fimbriae
- Elaboration of proteases – ‘cocktail of degradative enzymes’ destroy cells
- collagenase
- fibrinolysin
- phospholipase A
- phosophatases
- Endotoxin (LPS) – pro-inflammatory
- Capsular polysaccharide & outer membrane vesicles
- Tissue toxic metabolic by-products
- hydrogen sulfide
- ammonia
- fatty acids
adhesion of P.gingivalise
Fimbrillar adhesins
- Help invade membrane vesicle of host cells by binding to cellular integrins
- Long fimbriae (FimA)
- Long and peritrichous (all way round cell)
- Initial attachment and biofilm organization
- Short fimbriae (Mfa1)
- Cell to cell autoaggregation
- Microcolony formation
Adherence mechanisms may vary according to substrate, may be multimodal.
P. gingivalis releases membrane vesicles containing functional adhesins that may also bind to the substrates shown
gingipains in p.gingivalis
Provide peptides from heme - nutrition to itself
- RgpA (arginine specific)
- Kpg (lysine specific)
Possess haemaglutanin (HagA) domains - attachment
Activate matrix metalloproteases (MMP’s)
manipulating host defences of P.gingivalis
Biofilm lifestyle
Gingipains
- Degradation of innate receptors
- Degradation of cytokines – e.g. IL-8, ICAM-1
- Induction of tissue destruction – MMP’s
Subversion – intracellular and ‘tricking’ host immunity
p.gingivalis pathway to perio disease
Subverts immune response
- interferes with complement
Dysbiosis of biofilm
Activates complement
- proinflammatory – bone destruction, PDL loss
Agitator
Involved
Important but not solely
has classical virulence factors of good pathogenic MO
periodontal pathogenic bacteria are
Only grown in anaerobic condition – can be oxygenated if other bacteria drive it down to low cellular level
periodontal pathogenic bacteria cause
collateral damage - PDL and bone
implications of chronic periodontium inflammation (8)
- Oral cavity
- Implanted biomaterials - joints for RA
- Immunocompromised pts - IE risk
- Hospitalised individuals
- Contaminated medical/dental equipment
Dysregulation of the oral mucosal immune system by biofilm manifests as destructive inflammation locally AND systemically
- Increased risk of cardiovascular disease - 1.2- 3.9 fold
- Suggested increased risk of rheumatoid arthritis
- Increased risk diabetes - up to 6 fold
dysbiotic microbiome is
harmful
links to systemic body diseases from periodontal disease
- CVD
- rheumatoid arthritis
- diabetes
chronic inflammatory cause (initiated by more than one MO)
