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BDS3 - caries symposium > caries microbiology > Flashcards

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

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2
Q

what is normal flora

A
  • the presence of bacteria normally found at specific body sites
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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
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4
Q

what is endogenous infection

A
  • if source of microbe is patients own flora
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5
Q

what type of infection is caries

A
  • endogenous
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6
Q

what is an exogenous infection

A
  • if source of microbe is flors from outside the patients body
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7
Q

what are primary pathogens

A
  • microbes that always cause disease in a new susceptible human
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8
Q

what are opportunistic pathogens

A
  • microbes that cause disease only in immunocompromised patients
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9
Q

what is the carrier state

A
  • the continued presence of an organism = bacteria, virus or fungi
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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
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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
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12
Q

where is plaque mainly found

A
  • protected and stagnant surfaces
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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
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14
Q

how many bacterial species are there

A
  • around 700

- get 50-60 in your mouth

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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
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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

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17
Q

what are the 4 phases of plaque formation

A 
1 = colonisation by pioneer bacteria 
2= outgrowth 
3 = secondary colonisation 
4 = climax community
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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
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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
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20
Q

what bacteria is important in early colonisation

A
  • streptococcus
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21
Q

what is the oral microbiome shaped by

A
  • the environment

- how baby is delivered drives what bugs you get as well

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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
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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
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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
Q

what are the typical features of a high caries risk person

A
  • 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
Q

what is the process of caries progression

A
  • adhesion -> survival and growth -> biofilm formation -> complex plaque -> acid -> caries
  • complex plaque is difficult to remove
27
Q

what are the key pathogens linked to caries

A
  • streptococco mutans
  • lactobacillus acidophilus
  • actinomyces viscosus
  • Candida albicans
  • nocardia spp
28
Q

what is the principle cariogenic bacteria

A
  • streptococcus mutans
29
Q

how does demineralisation start

A
  • take fermentable carbohydrates and as you feed sucrose, acid production is high leading to demineralisation
30
Q

what are the key virulence factors of a prokaryotic cell

A
  • capsule is sticky so can evade immune system and can help attach
  • fimbriae help attach
  • release an endotoxin from gram negative cell wall
31
Q

what is streptococcus mutant

A
  • 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
Q

what helps the virulence of strep mutans

A
  • 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
Q

what are adhesins

A
  • make up fibrillar layer of cell wall

- if have these then it can adhere to enamel more freely

34
Q

what are binding proteins

A
  • glucosyltranserases, frucosyltransferase

- take sugar and turn them into glucans

35
Q

what are some sugar modifying enzymes

A
  • fructanase

- dextranase

36
Q

what to polysaccharides do

A
  • protection = matrix

- storage = glycogen

37
Q

what are the virulence factors of strep mutans

A
  • adhesins
  • binding proteins
  • sugar modyfing enzymes
  • polysaccharides
  • acid tolerance and adaptation
  • range of virulence factors
38
Q

what happen with sucrose metabolism

A
  • 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
Q

what are the properties of water soluble glucans

A
  • readily degraded for energy source

- formation of lactic acid

40
Q

what are the properties of water insoluble glucans

A
  • sticky and hard = act as cement
  • promote accumulation of plaque
  • very resilient and difficult o remove
41
Q

what are 2 bacterial polysaccharides

A
  • GTF = glucosyl transferase

- GBP = glucose binding proteins

42
Q

what acids are produced

A
  • 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
Q

what pH does it have to fall below for demineralisation

A

below pH 5.5

44
Q

what does acid tolerance do

A
  • maintains pH balance
  • alters cell membrane
  • protection and repair mechanisms
45
Q

how does strep mutans maintain pH balance

A
  • extrusion of H+ ions through a proton translocating ATPase
  • maintain physiological pH levels
  • H+ ions go into bacterium then straight back out
46
Q

how does strep mutans alter cell membrane for acid tolerance

A
  • increase in the proportion of mon-unsaturated membrane fatty acids
  • decreased proton permeability
  • changes permeability by changing cell membrane
47
Q

what are strep mutans protection and repair mechanisms for acid tolerance

A
  • up regulation of molecular chaperones proteases and DNA repair mechanisms
48
Q

why is strep mutans a well-adapted pathogen

A
  • it is tolerant to acid

- maintains energy from feeding it sugars

49
Q

how can we interfere with strep mutans acid tolerance

A
  • 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
Q

what are the anti caries effects of fluoride

A
  • systemic effect
  • antimicrobial effect
  • topical effect
51
Q

what is fluoride systemic effect to prevent caries

A
  • incorporation of ingested fluoride into developing enamel as fluorapatite which reduces its solubility in acid and promotes remineralisation
52
Q

what is fluoride antimicrobial effect to prevent caries

A
  • fluoride inhibits plaque metabolism and is concentrated within plaque
  • activity increases at pH values <5 especially in case of strep mutans
53
Q

what is fluoride topical effect to prevent caries

A
  • the surface layer of enamel is converted into FA which reduces its solubility in acid and promotes remineralisation
54
Q

how does the mouth change into diseased biofilm

A
  • 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
Q

what is the effect of a high protein diet

A
  • few acidogenic organisms = ammonia produced
  • more gram-negatives
  • secondary metabolite = malodour
  • tend to support organisms associated with perio disease
56
Q

what is the effect of a high carbohydrate diet

A
  • metabolism reduces pH
  • acidic organisms thrive
  • streptococci and lactobacilli
  • resting pH would decrease
  • causes problems
57
Q

what is the effect of a high sucrose diet

A
  • plaque matrix would contain large amounts of extracellular polysaccharides of both the fructan and gluten variety
58
Q

what is the effect of a frequent carbohydrate diet

A
  • plaque would contain significantly increased numbers of highly acidic organisms such as strep mutans and lactobacilli
59
Q

how do we modify microbiome and manage caries microbiology

A
  • diet is key

- low saliva can be enhanced by chewing gum

BDS3 - caries symposium (6 decks)

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