biofilm 2 - periodontitis Flashcards
(36 cards)
1
Q
what are the different oral biofilm diseases
A
- caries
- endodontic infections
- oral malodour
- mucosal infections
- periodontal infections
2
Q
what are examples of mucosal infections
A
- thrush
- angular cheilitis
- denture stomatitis
3
Q
what can cause malodour
A
- infection from dorsal surface of tongue
4
Q
what host factors can influence on oral microflora
A
- systemic disease
- antibiotic use
- oral hygiene
- genetics
5
Q
how can diet influence oral microflora
A
- chemical composition
- physical consistency
- frequency of intake
6
Q
how can saliva infelucne oral microflora
A
- flow rate
- pH
- antimicrobial factors
7
Q
how can GCF influence oral microflora
A
- antimicrobial components and humeral immunity
8
Q
how can microbial interactions influence oral microflora
A
- competition and co-operation
9
Q
how can the gaseous environment influence oral microflora
A
- oxygen concentrations can determine which organisms are present
10
Q
what are the types of PD classification
A
- gingivits
- periodontitist
- necrotising periodontal disease
- peri-implantitis
11
Q
what are the two periodontitis sub categories
A
- chronic = adult related
- aggressive = spontaneous (genetic)
12
Q
what determines the health of gums
A
- balance between health and disease
- balance between beneficial bacteria, immune surveillance and tissue homeostasis, against pathogenic bacteria, disruption of tissue homeostasis and non-protective immune responses
13
Q
what are some host factors that cause perio
A
- smoking/tobacco use
- genetics
- pregnancy/puberty
- systemic disease
- nutrition
14
Q
how does periodontitis develop
A
- normal flora colonise
- proportion of periodontopathognic bacteria increases causing mild inflammation
- high concentration of periodontopathogenic bacteria causing severe inflammation and pocket formation
15
Q
what are the development phases of biofilm formation
A
- naked surface
- conditioning film
- linkning film = e.g. streptococcus
- coaggregation, re-conditioning film = e.g. actinomyces
- accumulation, shedding = e.g. fusobacterium
16
Q
how can you prevent disease progresion
A
- by controlling health organisms, won’t get disease progression
17
Q
what causes the destructive processes
A
- gram negative anaerobic cocci
18
Q
what are the important microorganisms in health
A
- streptococci
- actinomyces
- veillonela
- haemophilus
- neisseri fusobacterium
19
Q
what are the important microorganisms in gingivitis
A
- actinomycetes
- prevotella intermedia
- bacteriodes
- fusobacterium nucleate
20
Q
what are the important microorganisms in periodontitis
A
- P. gingivalis
- tannerella forsythia
- treponema denticola
- prevotella intermedia
- these produce toxins and proteases that destruct the tissues
21
Q
what model is used to distinguish which organisms are more problematic
A
- socranksy’s model
22
Q
what organisms cause competition microbial interactions
A
- metabolic products = acids, oxidants
- bacteriocins
- receptor antagonism
23
Q
what organisms cause co-operation microbial interactions
A
- metabolic products = saccharides, peptides, growth factors
- adhesion substrates
- immune avoidance
24
Q
how can environment modification cause disease
A
- if you have healthy plaque it is because you have things to prevent the nasty organisms getting in
- if you have environment modification it can radically change what happens and can now allow disease progression
25
what is difficult to prove with Koch's postulates
- culture, present in disease, actively identifying disease, animal models
26
what alternative criteria is sued for Koch's postulates
* Association with disease based on increased numbers of pathogen at site of disease
* Elimination or decreased numbers results in return to health
* Evidence of host response to pathogen based on humoral and cellular immunity
* Pathogenic potential based on animal models
* Possession of pathogen with demonstratable virulence factors that cause periodontal destruction
27
what is prophyromonas gingivalis
- 'keystone' oral pathogen
- gram negative non-motile rod, strict anaerobe
- black pigmented = when placed in blood agar is takes haem from blood
- 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
- has an array of virulence factors
28
what are the virulence factors of P gingivalise
- host cell tissue adherence and invasion = fimbriae
- elaboration of proteases = collagenase, fibrinolysis, phospholipase A, phosphatase (cocktail of degradative enzymes)
- endotoxin (LPS) = proinflammtory
- capsular polysaccharide and outer membrane vesicles
- tissue toxic metabolic by-products = hydrogen sulphide, ammonia, fatty acids
29
how does P. gingivalis adhere to surface
- fibrillar adhesins
- long fimbriae (FimA) = initial attachment and biofilm organisation
- short fimbriae (Mfa1) = cell to cell auto aggregation
30
what are gingipains
- provide peptides from haem = nutrition
- RgpA = arginine specific
- Kpg = lysine specific
- possess haemoglutanin domains = attachment
- activate MMPs
- not a good pathogen
31
how can P. gingivalis manipulate host defences
- biofilm lifestyle
- gingipains = degradation of innate receptors and cytokines
- induction of tissue destruction = MMPs
- subversion = intracellular and 'tricking' host immunity
32
what is A. actinomycetemomitans
- luekotoxin
- cytotoxin
- LPS
- Fc binding proteins
- membrane vesicles
- glycoprotein matrix
- fimbriae
- phase variation
- subvert host cell immunity
- does the same sort of things as P. gingivalis
33
what are the systemic implications
- oral cavity
- rheumatoid arthritis
- implanted biomaterials
- immunocompromised patients
- hospitalised individuals
- contaminated medical/dental equipment
- atherosclerotic plaques and CVD
- increased risk CVD = 1.2-3.9 fold
- increased risk diabetes = up to 6 fold
34
what is the clinical management of perio
- mechanical disruption
- chemotherapeutic
- probiotics
- vaccines
- surgery
35
why can't we give vaccines
- can't make them for specific organisms as then other ones will still be there and cause problems
36
how could prebiotics work
- could modulate the biofilm before any problems start
