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BDS3 Caries Symposium II > Caries Microbiology - The basics > Flashcards

Caries Microbiology - The basics Flashcards

1
Q

pathogenesis of infection

A

When microbes find a new host and start to multiply – called colonisation

A balance can develop between colonised microbes and humans – will lead to ‘so called’ normal flora

If microbe causes disease – called an infection

If source of microbe is patient’s own flora – called an endogenous infection

If source of microbe is flora from outside the patient’s body – called exogenous infection

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2
Q

when microbes find a new host and start to multiple

A

colonisation

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3
Q

a balance can develop between colonised microbes and humans

A

so called ‘normal flora’

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4
Q

if microbe causes disease

A

infection

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5
Q

if source of microbe is patient’s own flora

A

endogeneous infection

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6
Q

if source of microbe is flora from outside the patient’ body

A

exogeneous infection

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7
Q

primary pathogens

A

alwyas cause disease in new susceptible humans

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8
Q

microbes that cause disease only in immunosuppressed individuals

A

oppurtunistic pathogens

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9
Q

opportunistic pathogens found in

A

normal flora

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10
Q

‘carrier state’

A

microbes can remain in the human body for some time after infection

The continued presence of an organism (bacteria, virus, or parasite) in the body that does not cause symptoms, but is able to be transmitted and infect other persons.

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11
Q

colonisation =

A

the presence of bacteria on a body surface (like skin, mouth, intestines, airway) without causeing disease in person

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12
Q

normal flora =

A

presence of bacteria normally found at specific body sites

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13
Q

infection =

A

invasion and multiplication of microorganisms in body tissues, especially that causing local cellular injury to competition

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14
Q

dental plaque

A
  • ‘a diverse microbial community (predominantly bacteria) found on the tooth surface, embedded in a matrix of polymers of bacterial and salivary origin’
    • Main aetiological agent associated with caries
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15
Q

main aetiological agent associated with caries

A

plaque

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16
Q

plaque develops

A

develops naturally on teeth, and forms part of the defence systems of the

host by helping to prevent colonisation of enamel by exogenous (and often pathogenic) microorganisms (colonisation resistance).

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17
Q

plaque beneficial role

A

colonisation resistance - forms part of host defence systems by helping prevent colonisation of enamel by exogenous microoganisms

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18
Q

plaque is a ….

A

biofilm

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19
Q

plaque preferentially found

A

at protected and stagnant surfaces on teeth

  • greatst risk of disease
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20
Q

mechanisms of plaque formation

A

attachment, growth, removal and reattachment of bacteria to the tooth surface is a continuous and dynamic process.

However, several distinct processes can be recognised:

  • Absorption of salivary proteins and glycoproteins, together with some bacterial molecules, to the tooth surface to form a conditioning film (the acquired pellicle).
    • Long-range (>5Onm), non-specific interaction of microbial cell surfaces with the acquired pellicle via van der Waals attractive forces.
    • Shorter-range (10-20nm) interactions, in which the interplay of van der Waals attraction forces and electrostatic repulsion produces a weak area of attraction that can result in reversible adhesion to the surface.
  • Irreversible adhesion can occur if specific inter-molecular interactions take place between adhesins on the cell surface and receptors in the acquired pellicle.
  • Secondary or late-colonisers attach to primary colonisers (coaggregation), also by specific inter-molecular interactions.

Cell division of the attached cells to produce confluent growth, and a bioflim.

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21
Q

oral microbiome

A

at least 700 bacterial species

predominately on hard tissues

  • also found on dorsum of tongue
  • can be found on soft tissues (shedding)

sterile at birth

  • via food, milk, water, mothers’ saliva
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22
Q

plaque composition and variation

A

Environmental conditions on a tooth are not uniform.

Differences exist in the degree of protection from oral removal forces and in the gradients of many biological and chemical factors that influence the growth of the resident microfiora.

These differences will be reflected in variations in the composition of the microbial community, particularly at sites so obviously distinct as the gingival crevice, approximal regions, smooth surfaces, and pits and fissures.

  • fissure plaque will be influenced more by saliva than other sites, whereas gingival crevicular fluid (GCF) has a greater impact on plaque in the gingival crevice.
  • gingival crevice also has a lower redox potential (Eh) and is colonised by higher numbers of anaerobes, especially proteolytic species which obtain key growth factors from the catabolism of host proteins and glycoproteins in GCF.
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23
Q

plaque structure

A

studied mainly by electron microscopy.

A heterogeneous and a colonial type of sub-structure have been observed in sections of smooth surface plaque.

  • heterogeneous type is associated with pallisaded regions where filaments and cocci appear to be aligned in parallel at right angles to the enamel surface.
    • Micro-colonies, presumably of single populations, have also been observed.
    • In addition, horizontal stratification has been described.

The early stages of development results in a condensed layer of apparently a limited number of bacterial types.

From 7 to 14 days, the bulk layer forms which shows less orientation but a higher morphological diversity.

This layering has been attributed directly to bacterial succession

In mature plaque, organisms have been seen in direct contact with the enamel due to enzymic attack on the pellicle. Electron microscopy has confirmed the presence of an inter-bacterial matrix of polysaccharide.

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24
Q

barriers to wide variety of microbes that enter the oral cavity regularly

A
  • saliva
  • pH
  • temperature
  • immune system

initally prevent many species from surviving

then brushing and flossing teeth clears up some built up biofilm

oral antibiotics inhibit growth

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25
Q

what forms a barrier for incoming bacteria

A

Symbiosis of the oral microbes that are able to survive these conditions form an elaborate scaffold that lives on the tooth enamel and at the interface with the gums. It forms a barrier for incoming bacteria

26
Q

caries is

A
  • loss of mineralised surfaces of the tooth
  • surfaces are premanently damaged
  • underlying dentine is at risk or damaged
  • multi-factorial disease
    • microbial biofilms
    • acidity - sugar metabolism
27
Q

Low caaries risk, risk factors

A
  • alkalia producing bacteria such as S.sanguinis
  • unstimulated saliva flow of >1ml/min
  • infrequent sucrose consumption
  • fluoride intake to levels allowing production of Fluroapatite
28
Q

high caries risk, risk factors

A
  • acid producing bacteria such as mutans streptococci and lactobacilli
  • unstimulated saliva flow of <0.7ml/min
  • frequency consumption of high levels of sucrose and other fermentable carbohydrates
  • little or no F intake
29
Q

caries progression

A
  • adhesion
  • survival and growth
  • biofilm formation
  • complex plaque
  • acid
  • caries

https://www.youtube.com/watch?v=incvTfw6FyA

30
Q

key pathogens that cariogenic bacteria

A
  • Streptococcus mutans
  • Lactobacillus acidophilus
  • Actinomyces viscosus
  • Candida albicans
  • Nocardia spp.

Many others – 16S sequencing

31
Q

what drives demineralisation

A

microbial metabolism drives demineralisation

32
Q

caries is disease of what tissue

A

hard

33
Q

what is a key determinant in caries

A

microbial plaque

34
Q

components of Prokaryotic Cell

A

*

35
Q

factors related to the cariogenicity of S.mutans

A
  • produces water solube and insoluble extracellular polysaccharides from sucrose which help in the colonisation of tooth surfaces by consolidating microbial attachment
  • ability to initiate and maintain microbial growth and to continue acid production in sites with low pH
  • rapid metabolism of sugars to lactic acid and other organic acids
  • can attain the critical pH for enamel demineralisation more rapidly than other common plaque bacteria
  • produces intracellular polysaccharide which can act as food store for use when dietary carbohydrate is low
  • sig correlation in jumans between S.mutans counts in saliva and plaque with prevenalence and incidence of caries*
  • S.mutans can be isolated from precise sites on the tooth surface before the development of caries*
  • Correlation betweeen the progression of lesion and S.mutans counts*
36
Q

key virulent factor for S.mutans in caries

A

produces water solube and insoluble extracellular polysaccharides from sucrose which help in the colonisation of tooth surfaces by consolidating microbial attachment

37
Q

Koch’s postulate - the Germ Theory of Disease

A
  • The microbe must be present in every case of the disease
  • The microbe must be isolated from the diseased host and grown in pure culture
  • The disease must be reproduced when a pure culture is introduced into a susceptible host
  • The microbe must be recovered from an experimentally infected host
38
Q

sterptococcus mutans

A

Gram-positive coccus

8 serotypes

Adhesion and biofilm formation

Metabolizes dietary sucrose to form insoluble polymers of glucose – stick to surfaces

Survive in low pH environments – enamel dissolution

Combined Virulence: Glucans, Adhesions and Acid

39
Q

s.mutans virulence factors

A
  • Adhesins
    • SpaP (AgB, AgI/II, PI) – makes up fibrillar layer of cell wall
  • Binding proteins
    • glucosyltransferases, frucosyltransferases, glucan binding protein
  • Sugar modifying enzymes
    • Fructanase, dextranase
  • Polysaccharides
    • Protection (matrix) and storage (glycogen)
  • Acid tolerance and adaptation
    • ATPase (F1F0 ATPase or H+ ATPase)
40
Q

sucrose metabolism

A
41
Q

2 types of glucans

A

water soluble

water insoluble

42
Q

water soluble glucans

A

readily degraded for energy source

formation of lactic acid

43
Q

water insoluble glucans

A

sticky and hard - acts as cement

promote accumulation of plaque

44
Q

bacterial polysaccharides

A

?

GBP = Glucan Binding Protein

GTF = Glucosyl Transferases

45
Q

acids produced in oral cavity

A
  • lactic acid - strongest (pH3.5)
  • formic acid
  • acetic acid

pH drops below 5.5 -> demineralisation

46
Q

de and re mineralisation balance

A
47
Q

acid pathways in oral cavity

A
48
Q

3 roles of acid tolerance

A
  • maintains pH balance
  • alters cell membrane
  • protection and repair mechanisms
49
Q

acid tolerance - mainatains pH balance

A

extrusion of H+ ions through a proton translocating F1-F0 ATPase (maintains phsyiological pH level)

50
Q

acid tolerance - alters cell membrane

A

increase in the proportion of mono-unstaurated membrane fatty acids - decreased proton permeability

51
Q

acid tolerance - protection and repair mechanisms

A

up-regulation of molecular chaperones, proteases and DNA repair mechanisms

52
Q

what happens if acid tolerance is interfered with

A

externally = fluoride ions interact with hydrgen ions = HF

internally = HF dissociate = F- inhibits ATPase

53
Q

3 anit caries activities of F

A
  1. systemic effect
  2. topical effect
  3. antimicrobial effect
54
Q

systemic effect of F

A

incorpartion of ingested F into developing enamel as FA - reduces its solubility in acid and promotes remineralisation

F present in water (naturally or artificially at 1ppm), certain foods, tablets or added to milk

55
Q

topical effect of F

A

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

F containing toothpastes, gels and certain restorative materials (GIC)

56
Q

antimicrobial effect of F

A

F inihibits plaque metabolism and is concentrated within plaque

activity increases at pH values <5

esp in case of S.mutans

inhibiting mechanisms include - reducing glycosis, indirectly inhibiting sugar transport, interfereing with bacterial permeability and inhibiting the synthesis of glycogen for intracellular storage

57
Q

environmental fluctuations due to

(healthy and disease biofilms: ecological plaque hypothesis)

A
  • high protein diet
  • high carbohydrate diet
  • high sucrose
  • frequent carbohydrate
58
Q

high protein diet effect on oral biofilm

A
  • Few acidogenic organisms -> ammonia produced
  • More Gram-negatives
  • Secondary metabolites - malodour
59
Q

high carbohydrate diet effect on oral biofilm

A
  • Metabolism reduces pH
  • Aciduric organisms thrive
  • Streptococci and lactobacilli
60
Q

high sucrose diet effect on oral biofilm

A

plaque matrix would contain large amounts of extracellular polysaccharides of both the fructan and glucan variety.

61
Q

frequent carbohydrate effect on oral biofilm

A

eg snacking on confectionary

then the plaque would contain significantly increased numbers of highly aciduric organisms such as Streptococcus mutans and lactobacilli.

62
Q

managing caries microbiology

A

diet - no sucrose = inhibition of glucan production

Fluroide - enamel remineralisation; inhibtion of bacterial metabolism

Polyol gum - increase saliva flow

Probiotics - antagonise S.mutans and other cariogenic taxa

Vaccines - in animals - generate secretor IgA against S.mutans

Antimicrobial peptides/STAMPS/small molucles/phage - tageted killing of S.mutans and other cariogenic taxa

BDS3 Caries Symposium II (7 decks)

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