caries microbiology Flashcards
1
Q
what is colonisation
A
- when microbes fine a new host and start to multiple
- the presence of bacteria on a body surface without causing disease in the person
2
Q
what is normal flora
A
- the presence of bacteria normally found at specific body sites
3
Q
what is infection
A
- invasion and multiplication of microorganisms in body tissues, especially that causing local cellular injury due to competitive metabolism, toxins, intracellular replication, or antigen-antibody response
4
Q
what is endogenous infection
A
- if source of microbe is patients own flora
5
Q
what type of infection is caries
A
- endogenous
6
Q
what is an exogenous infection
A
- if source of microbe is flors from outside the patients body
7
Q
what are primary pathogens
A
- microbes that always cause disease in a new susceptible human
8
Q
what are opportunistic pathogens
A
- microbes that cause disease only in immunocompromised patients
9
Q
what is the carrier state
A
- the continued presence of an organism = bacteria, virus or fungi
10
Q
what is dental plaque
A
- a diverse microbial community found on the tooth surface, embedded in a matrix of polymers of bacteria and salivary origin
- main etiological agent associated with caries
- develops naturally on teeth
11
Q
what does plaque do
A
- forms part of the defence systems of the host by helping to prevent colonisation of enamel by exogenous microorganisms
- colonisation resistance
- it is an example of a biofilm
12
Q
where is plaque mainly found
A
- protected and stagnant surfaces
13
Q
how does plaque form
A
- continued and dynamic process
- absorption of salivary proteins and glycoproteins, together with some bacterial molecules, to the tooth surface to form conditioning film
- interaction between microbe cell surfaces and pellicle via van Der Waals
- adhesion to the surface
- irreversible adhesion can happen if specific inter-molecular interactions take place between adhesions
- secondary colonisers attach to primary colonisers
- cell division forms the biofilm
14
Q
how many bacterial species are there
A
- around 700
- get 50-60 in your mouth
15
Q
where is the oral microbiome predominantly found
A
- hard tissues
- also on dorsum of tongue
- every part of mouth has its own microbiome
16
Q
what defines your microbiome
A
- you are sterile at birth
- attachments to people you are with for a long time will define your microbiome
17
Q
what are the 4 phases of plaque formation
A
1 = colonisation by pioneer bacteria 2= outgrowth 3 = secondary colonisation 4 = climax community
18
Q
what happens in the first stage of plaque formation
A
- the microbe is held by a weak force
- electrostatic and hydrophobic interactions
- may involve delicate structures called fibrils or fimbriae which project from he cell surface
19
Q
what happens in the second stage of plaque formation
A
- adhesion is rendered essentially irreversible by the synthesis of polymers
- polymers form part of matrix
- polymers comprise soluble and insoluble high molecular weight polysaccharides
- metabolism changes things which allow other bacteria to come in and form matrix glue which allows them to stick together
20
Q
what bacteria is important in early colonisation
A
- streptococcus
21
Q
what is the oral microbiome shaped by
A
- the environment
- how baby is delivered drives what bugs you get as well
22
Q
what in your mouth prevents species surviving
A
- bushing and flossing teeth clears some built up biofilm
- saliva, pH, temperature and immune system prevents many species from surviving
- oral antibiotics inhibit growth
23
Q
what is caries
A
- loss of mineralised surfaces of the tooth
- surfaces are permanently damaged
- underlying dentine is at risk or damaged
- it is a multifactorial disease
24
Q
what are typical features of a low caries risk person
A
- alkali producing bacteria such as S. Sanguines
- unstimulated saliva flow of >1ml/min
- infrequent sucrose consumption
- fluoride intake to levels allowing production of fluorapatite
25
what are the typical features of a high caries risk person
- acid producing bacteria such as mutant streptococci and lactobacilli
- unstimulated saliva flow of <0.7ml/min
- frequent sugar consumption
- little or no fluoride intake
26
what is the process of caries progression
- adhesion -> survival and growth -> biofilm formation -> complex plaque -> acid -> caries
- complex plaque is difficult to remove
27
what are the key pathogens linked to caries
- streptococco mutans
- lactobacillus acidophilus
- actinomyces viscosus
- Candida albicans
- nocardia spp
28
what is the principle cariogenic bacteria
- streptococcus mutans
29
how does demineralisation start
- take fermentable carbohydrates and as you feed sucrose, acid production is high leading to demineralisation
30
what are the key virulence factors of a prokaryotic cell
- capsule is sticky so can evade immune system and can help attach
- fimbriae help attach
- release an endotoxin from gram negative cell wall
31
what is streptococcus mutant
- key organism associated with caries
- gram positive coccus
- 8 serotypes
- adhesion and biofilm formation = has chains, good at forming biofilm as sticky
- metabolises dietary sucrose to form insoluble polymers of glucose that stick to surface
- survive in low pH environments
32
what helps the virulence of strep mutans
- glucans, adhesion and acid
- glucans help it to adhere and the more it adheres the more it colonises
- lots of strep mutant makes an acidic pH
33
what are adhesins
- make up fibrillar layer of cell wall
| - if have these then it can adhere to enamel more freely
34
what are binding proteins
- glucosyltranserases, frucosyltransferase
| - take sugar and turn them into glucans
35
what are some sugar modifying enzymes
- fructanase
| - dextranase
36
what to polysaccharides do
- protection = matrix
| - storage = glycogen
37
what are the virulence factors of strep mutans
- adhesins
- binding proteins
- sugar modyfing enzymes
- polysaccharides
- acid tolerance and adaptation
- range of virulence factors
38
what happen with sucrose metabolism
- if feed sugar, then particular enzymes will produce fructans or glucans and these are both very sticky
- as a by-product things that allow glycolysis which cause CO2 which is important for driving acid
39
what are the properties of water soluble glucans
- readily degraded for energy source
| - formation of lactic acid
40
what are the properties of water insoluble glucans
- sticky and hard = act as cement
- promote accumulation of plaque
- very resilient and difficult o remove
41
what are 2 bacterial polysaccharides
- GTF = glucosyl transferase
| - GBP = glucose binding proteins
42
what acids are produced
- all pathways fundamentally end with a by-product of acid that's from input of sugars
- formic acid
- acetic acid
- lactic acid
- butyric acid
43
what pH does it have to fall below for demineralisation
below pH 5.5
44
what does acid tolerance do
- maintains pH balance
- alters cell membrane
- protection and repair mechanisms
45
how does strep mutans maintain pH balance
- extrusion of H+ ions through a proton translocating ATPase
- maintain physiological pH levels
- H+ ions go into bacterium then straight back out
46
how does strep mutans alter cell membrane for acid tolerance
- increase in the proportion of mon-unsaturated membrane fatty acids
- decreased proton permeability
- changes permeability by changing cell membrane
47
what are strep mutans protection and repair mechanisms for acid tolerance
- up regulation of molecular chaperones proteases and DNA repair mechanisms
48
why is strep mutans a well-adapted pathogen
- it is tolerant to acid
| - maintains energy from feeding it sugars
49
how can we interfere with strep mutans acid tolerance
- externally, fluoride ions interact with hydrogen ions forming HF
- internally HF dissociate and F- inhibits ATPase
- fluoride can interact with H ions to form hydrogen fluoride so can't get into bacteria
- fluoride is anti-bacterial
50
what are the anti caries effects of fluoride
- systemic effect
- antimicrobial effect
- topical effect
51
what is fluoride systemic effect to prevent caries
- incorporation of ingested fluoride into developing enamel as fluorapatite which reduces its solubility in acid and promotes remineralisation
52
what is fluoride antimicrobial effect to prevent caries
- fluoride inhibits plaque metabolism and is concentrated within plaque
- activity increases at pH values <5 especially in case of strep mutans
53
what is fluoride topical effect to prevent caries
- the surface layer of enamel is converted into FA which reduces its solubility in acid and promotes remineralisation
54
how does the mouth change into diseased biofilm
- generally we have a healthy mouth
- when there is a modification (host or environmentally derived) that will lead to changes
- if an organism is fed foods that will make it abundant it will take over
55
what is the effect of a high protein diet
- few acidogenic organisms = ammonia produced
- more gram-negatives
- secondary metabolite = malodour
- tend to support organisms associated with perio disease
56
what is the effect of a high carbohydrate diet
- metabolism reduces pH
- acidic organisms thrive
- streptococci and lactobacilli
- resting pH would decrease
- causes problems
57
what is the effect of a high sucrose diet
- plaque matrix would contain large amounts of extracellular polysaccharides of both the fructan and gluten variety
58
what is the effect of a frequent carbohydrate diet
- plaque would contain significantly increased numbers of highly acidic organisms such as strep mutans and lactobacilli
59
how do we modify microbiome and manage caries microbiology
- diet is key
| - low saliva can be enhanced by chewing gum
