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Stage 2 > MFD Theme 2a > Flashcards

MFD Theme 2a Flashcards

1
Q

what are autochthonous microbiota

A

characteristically found at a site
adapted to survive and grow at that site
colonise the mouth and form dental plaque

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2
Q

what are allochthonous microbiota

A

transiently present at the site

do not thrive at site but may colonise transiently

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3
Q

what are the resident oral microbiota

A

archaea, viruses, fungi, bacteria

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4
Q

what are archaea and when are they commonly detected

A

part of prokaryotes, separate from bacteria

detected in periodontal disease

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5
Q

what is the most common virus

A

herpes simplex type 1 (HSV-1)

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6
Q

how can HIV and Hept B be carried

A

symptomatically

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7
Q

what infects bacteria and is the most common virus in the mouth

A

bacteriophage viruses

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8
Q

what is the most common fungi in the mouth

A

candida spp

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9
Q

what are the most abundant bacteria in the mouth

A

oral streptococci

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10
Q

what oral diseases are streptococci responsible for

A

caries, periodontitis, abscesses

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11
Q

what haemolysis does oral streptococci cause

A

a-haemolysis

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12
Q

what occurs in alpha haemolysis

A

H202 is produced which bleaches the haemoglobin - greenish brown appearance

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13
Q

what occurs in beta haemolysis

A

complete clearing of the agar

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14
Q

what haemolysis does staphylococcus cause

A

gamma haemolysis

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15
Q

what occurs is gamma haemolysis

A

no haemolysis

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16
Q

why might there be a greenish tinge on the kiss plate

A

viridan (oral) streptococci

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17
Q

what the difference between a core and peripheral microbiome

A

everyone has a core microbiome but the peripheral microbiome varies from individual to individual

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18
Q

what bacteria live on the tongue

A 
streptococcus (salivarius/mitis group) 
veillonella 
actinomyces 
haemophilus 
prevotella
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19
Q

what bacteria live on the cheek

A

streptococcus (mitis group)
haemophilus
simonsiella

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20
Q

what bacteria form supragingival plaque

A

streptococcus
actinomyes
haemphilus

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21
Q

what bacteria form subgingival plaque

A 
streptococcus 
actinomyces
peptostreptococcus
fusobacterium 
porphyromonas
aggregatibacter
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22
Q

what bacteria are almost exclusively found in dental plaque

A

streptococcus gordonii

streptococcus sanguinis

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23
Q

what can saliva samples tell us about the bacteria in the mouth

A

gives us an average but doesn’t tell us the location of the bacteria

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24
Q

what can cause halitosis

A

anoxic bacteria and the bottom of the mouth

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25
Q

what are the microbial habitats in the mouth

A

lips, cheeks, palate
tongue
teeth

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26
Q

what are the characteristics of the lips, cheeks and palate

A

epithelial cells, continually shed (desquamation)

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27
Q

what are the characteristics of the tongue

A

highly papillated
reservoir for obligate anaerobes (perio.pathogens)
tonsils may also harbour perio pathogens

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28
Q

what are the characteristics of teeth

A

non-shedding
many different surfaces with different microbial populations
covered with acquired enamel pellicle

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29
Q

how can the pellicle be removed

A

by acid

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30
Q

what does the pellicle do

A

covers enamel

prevents enamel dissolution but can also help bacteria

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31
Q

how can you culture the microflora

A

isolate bacteria

  • understand basic physiology/biochem
  • link organism to disease
  • identify pathogenesis mechanisms
  • test antibiotics
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32
Q

how can you count the no of different species of bacteria in a clinical sample

A

culturing and count colonies

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33
Q

what is the problem with the technique of culturing bacteria to estimate species

A
  • some bacteria aren’t easily cultured
  • viable count cultures fewer cells
  • dormant bacteria
  • some species fastidious /grow easier suggesting more abundant
  • 50% oral bacteria isolated
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34
Q

what is culture independent microbial analysis

A

based on the comparison of DNA sequences from different bacteria

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35
Q

what are the 2 ways culture independent microbial analysis works

A

sequencing of the 16S to work out the species present or sequences the whole DNA to work out gene functions

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36
Q

does culture independent microbial analysis require isolation of the organism

A

no

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37
Q

what does PCR do

A

looks at all bacteria, may find ‘new’ species

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38
Q

what does hybridisation do

A

quantifies sequences already discovered

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39
Q

what does next generation sequencing do and how

A

identifies all DNA present

- target (16S rRNA ‘microbiome’ analysis) OR Full sequence (‘metagenomics’)

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40
Q

does saliva have bacteria in when secreted

A

no, its sterile when secreted and accumulates bacteria after

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41
Q

are there more bacteria attached to epithelial cells or free in saliva

A

3 times more attached to epithelial cells

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42
Q

how are bacteria removed from oral surfaces

A 
sloughing of epithelial cells 
mechanical debridement 
active release (possibly)
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43
Q

what are the limitation of sampling saliva as a reflection of the overall oral microbiome

A
  • proportions of microbial species are different from plaque/soft tissue biofilms
  • care is required when sampling to ‘standardise’
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44
Q

what microbiome is present in almost everyone

A

core microbiome of 13 phyla

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45
Q

what microbiome is present in some and not others

A

peripheral microbiome

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46
Q

what are clusters of the microbiomes

A

associated with differences in metabolome

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47
Q

what is the main source of the enamel pellicle

A

saliva

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48
Q

what is the difference between saliva and enamel pellicle

A

they have the same organisms but in different proportions

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49
Q

how can salivary compounds help to control plaque accumulation

A

through:

  • aggregating bacteria which are then swallowed
  • antimicrobial effects
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50
Q

why is saliva important for bacteria

A

its a key nutrient for them

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51
Q

what are the antimicrobial components of saliva

A 
cystatins 
VEGh
Lactoperoxidase
Lysozyme 
Chitinase 
Histatins 
Defensins 
Lactoferrin
Calprotectin
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52
Q

what are the microbial adhesion components of saliva

A 
Gp340
Mucins 
PRPs
Amylase
Statherin 
S-lgA
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53
Q

what are the surface protection and maintenance components of saliva

A 
mucins 
ca2+
phosphate 
bicarbonate
PRPs
statherin
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54
Q

what are some salivary molecules(proteins) that bind to bacteria

A

MG2 (muc7)
Salivary Agglutinin (gp340), PRPs
Statherin

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55
Q

what do the salivary molecules do

A

bind to bacteria and teeth
agglutinate or inhibit bacteria
promote or inhibit microbial colonisation

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56
Q

how have bacteria adapted to survive in the mouth

A

by sticking to the salivary pellicle

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57
Q

when does aggregation/agglutination occur and what does it result in

A

in the liquid phase

results in large clumps which adhere poorly and are swallowed

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58
Q

how do bacteria adhere

A

due to proteins in the saliva pellicle and adhesion of bacterial cells to teeth

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59
Q

what are immunoglobulins and what do they do

A

a key feature of the immune system and are present in saliva, they agglutinate bacteria

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60
Q

what is the rate of secretory IgA at rest and stimulated flow

A

33mg/100mL resting flow

6mg/100mL stimulated

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61
Q

what are the immunoglobulins present in gingival fluid and what do they do

A

IgG, IgM

they activate complement/opsonisation

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62
Q

what are the three modes of gp340 recognition

A

aggregation and adherence
aggregation &laquo_space;adherence
aggregation&raquo_space; adherence

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63
Q

what are proline-rich proteins (PRPs)

A

host receptors which are acidic/basic/glycosylated proteins

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64
Q

where are PRPs found

A

high conc in parotid and submandibular saliva

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65
Q

what is the main function of PRPs

A

calcium phosphate stabilisation

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66
Q

what is the c-term for PRPS

A

a cryptitope- becomes an epitope after change in structure allowing antibodies to bind

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67
Q

what does the N-term in PRPs bind

A

hydroxyapatite

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68
Q

what does the C-term in PRPs bind

A
  • Actinomyces spp.
  • Streptococcus mutans
  • Streptococcus sanguinis
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69
Q

what is statherin and its function

A

host receptor thought to be involved in calcium phosphate stabilisation (with PRPs)

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70
Q

what does statherin bind

A

hydroxyapatite, porphyromonas gingivalis and actinomyocytes spp.

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71
Q

when does statehrin not bind bacteria

A

when in the soluble state- only when its stuck to the surface

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72
Q

what are the important antibacterial enzymes in saliva that inhibit bacterial growth

A

lysozyme
lactoperoxidase
lactoferrin

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73
Q

what do lysozymes do

A

cleaves bacterial cell wall peptidoglycan, can cause non enzymatic cell degradation triggering autolysis when not active

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74
Q

what does lactoperoxidase do and what are reaction products

A

targets peroxide produced bacteria. producing hypothiocyanite plus some cyanosulphurous acid and cyanosulphuric acid

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75
Q

what is the acid base eqm in the thiocynate reactions

A

HOSCN->

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76
Q

what effect the does the pK for HOSCN/OSCN- being 5.3 have on the reaction and what does this do to bacteria

A

more acid favours HOSCN which penetrates bacterial cell envelopes

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77
Q

what produces lactoperoxidase

A

produced by host and bacteria

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78
Q

what does lactoferrin do

A

binds iron and makes it unavailable and some bacteria produce iron-binding proteins called siderophores to complete for host iron

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79
Q

which toothpastes contain components of saliva

A

those targeted to specialist markets

  • dry mouth
  • pets
  • children
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80
Q

what dental product contains lysozyme, lactoperoxidase, and lactoferrin

A

BioXtra toothpaste

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81
Q

what dental product contains a dual enzyme system

A

Biotene toothpaste

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82
Q

what are the tooth surfaces available for colonisation

A

fissure
smooth surfaces
approximal
gingival crevice

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83
Q

what are the characteristics of supragingival plaque

A

present in health
mainly aerobic
fairly easily removed from smooth surfaces

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84
Q

what is the nutrient source for supragingival plaque

A

saliva

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85
Q

what are the characteristics of subgingival plaque

A

periodontal pockets become anaerobic
significant plaque associated with gingivitis/periodontitis
difficult to remove

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86
Q

what is the nutrient source for subgingival plaque

A

gingival crevicular fluid

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87
Q

what are the environmental factors affecting dental plaque accumulation

A

diet/smoking

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88
Q

what are the host factors affecting dental plaque accumulation

A

saliva amount/composition

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89
Q

what are the bacterial factors affecting dental plaque accumulation

A

adhesins that recognise pellicle/congregation

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90
Q

how fast does dental plaque start to accumulate and how

A

within mins of tooth cleaning, faster at day than night.

pioneer colonisers attach to saliva pellicle

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91
Q

what binds to the pellicle

A

only selective organisms due to receptors on its surface

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92
Q

how to bacteria attach to teeth

A

primary colonising bacteria attach to the pellicle (the conditioning layer)

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93
Q

what are the characteristics of the enamel pellicle

A

1-3 micro metres thick (exceptionally 10)
may permeate the outer layer of enamel
not easily removed
deposit of saliva proteins

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94
Q

how does the pellicle form

A

precipitation of denatured salivary proteins

selective adsorption of salivary proteins: molecules bind in proportion to their affinity for a substrate

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95
Q

where do additional components in the formation of the pellicle originate from

A

GCF
oral mucosa
microbial cells

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96
Q

what is the importance of the pellicle

A

lubricant-reduce tooth wear
bicarbonate-buffer
reduces calculus formation
reduces mobility of calcium and phosphate ions
prevents inappropriate crystal growth (statherin and PRP)
active enzymes

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97
Q

what is the importance of the pellicle reducing the mobility of calcium and phosphate ions

A

diffusion barrier and binding to PRP

reduces enamel demineralisation (erosion and caries)

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98
Q

what is the importance of the pellicle preventing inappropriate crystal growth

A

Statherin and PRP

ensuring hydroxyapatite crystal doesn’t dissolve but also that we don’t want more on top

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99
Q

what active enzymes does the pellicle contain

A 
amylase-receptor for bacteria 
lysozyme 
peroxidase
glucosyltransferase-produced by bacteria 
carbonic anhydrase
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100
Q

what inhibits s.mutans biofilm formation

A

mucin MG1

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101
Q

what salivary proteins in the pellicle act as receptors for bacteria

A 
MG1
amylase
PRP
Statherin
Gp340 (salivary agglutinin)
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102
Q

what are the 4 main types of human oral streptococci

A

mitis
anginosus
salivarius
mutans

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103
Q

what are mitis group streptococci

A

most numerous

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104
Q

what are anginosus group streptococci

A

generally commensal but are associated with abscesses

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105
Q

what are salivarius group streptococci

A

generally commensal (some investigated as probiotics)

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106
Q

what are mutans group streptococci

A

associated with dental caries

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107
Q

what is antigen I/II

A

large protein on the surface of many oral streptococci (binds bacteria)

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108
Q

what does antigen I/II do

A

binds to receptors in the pellicle

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109
Q

what does antigen I/II mediate

A

adhesion to salivary agglutinin gp340 in fluid phase or in pellicle

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110
Q

what are the multi domain proteins on antigen I/II

A 
N-terminal domain
Alanine-rich repeats
Variable region
Proline-rich repeats 
Carboxy-terminal domain, containing motif for wall anchoring
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111
Q

what is actinomyces spp.

A

gram positive pleimorphic rods
facultative anaerobes
mostly harmless, can cause disease
interact with streptococci and colonise surfaces

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112
Q

what are examples of actinomyces spp.

A

A. naeslundii, A. oris, A. israelii

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113
Q

what is veillonella spp.

A

gram negative cocci
strict anaerobes
feed on lactate streptococci produce .
elevated caries

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114
Q

what are examples of veillonella spp.

A

V.atypica, V.dispar

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115
Q

how does dental plaque form

A 
adhesion to salivary pellicle 
coaggregation -> growth
coadhesion 
mature biofilm 
dispersal
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116
Q

what are the characteristics of mature supragingival dental plaque

A 
contains 10^11 microbial cells/gram
stratified appearance (gram-positive cocci and short rods at tooth surface; filaments towards outer layers)
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117
Q

what problems can mature supragingival dental plaque cause

A

caries follows a shift towards acidogenic/aciduric bacteria

gingivitis occurs when plaque grows below the gum line

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118
Q

what happens when there is failure to control dental plaque

A

accumulation of plaque at gum margins directly irritates gum tissue, or form calculus which in turn irritates the gums
gingivitis -> periodontitis

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119
Q

roughly how many bacteria are in the subgingival crevice

A

relatively few

10^3 to 10^6 CFU/crevice

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120
Q

what bacteria are found in the subgingival crevice

A 
anaerobic bacteria (found here or on dorsal surface of tongue)
asaccharolytic, proteolytic bacteria, but not the same as in perio disease
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121
Q

what are the characteristics of fusobacterium nucleatum

A

gram negative, proteolytic, anaerobic, long rod-shaped cells
Can be present in high numbers in subgingival plaque

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122
Q

what does fusobacterium nucleatum coaggregate with

A

early colonisers (e.g. Streptococcus spp.) and late colonisers (e.g. T.denticola)

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123
Q

what is dental calculus

A

mineralised plaque

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124
Q

what is supragingival calculus a deposit from

A

saliva

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125
Q

what is subgingival calculus is a deposit from

A

serum

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126
Q

what is subgingival calculus also known as

A

serumnal calculus

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127
Q

what do rough surfaces of calculus trigger

A

inflammation -> gingivitis -> periodontitis

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128
Q

what are the 2 types of calculus

A

gross, very gross

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129
Q

where does calculus form

A

preferentially near salivary duct openings

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130
Q

what is the epitactic agent in calculus formation

A

probably a bacterium

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131
Q

where do sialoliths form and how

A

in salivary ducts

Supersaturated calcium phosphate
High pH

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132
Q

what is an important bridging organism between early and late colonisers

A

F.nucleatum

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133
Q

what are the types of caries

A 
anatomicals sites 
primary vs recurrent caries
residual caries 
cavitated vs non cavitated 
active vs inactive
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134
Q

what are the anatomical sites of caries

A

pits and fissures, smooth surfaces (enamel caries or root caries, which starts on exposed cementum/dentin)

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135
Q

what is recurrent caries

A

occurs after treatment/restoration

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136
Q

what is residual caries

A

insufficient treatment

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137
Q

what appears in early non cavitated caries

A

white spot lesion

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138
Q

what is early childhood caries

A

the presence of one or more decayed (non-cavitated or cavitated lesions), missing (due to caries) or filled tooth surfaces in any primary tooth in an age between birth and 71 months of age

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139
Q

what are the theories that caries is the result of microbial sugar fermentation

A 
worms 
chymical theory 
parasitic theory 
chemico-parasitic theory (most important) 
proteolytic theory 
proteolysis-chelation theory
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140
Q

what are the 2 stages of the chemico-parasitic theory (chemical and bacteria)

A

1- decalcification of enamel

2- dissolution of enamel

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141
Q

what is the chymical theory

A

food putrefaction released unidentifued chemical agent which dissolved teeth

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142
Q

what is the parasitic or septic theory

A

filamentous parasite in plaque responsible

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143
Q

what is the proteolytic theory

A

microbes invade enamel lamellae and initiate caries by proteolysis

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144
Q

what is the proteolysis-chelation theory

A

microbial proteolytic destruction of the organic matrix

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145
Q

what is the ecological plaque hypothesis

A

disease as an imbalance

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146
Q

what is the specific plaque hypothesis

A

caries aetiology

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147
Q

what are the bacteria commonly associated with caries

A

mutans streptococci
lactobacillus spp.
actinomyocenes spp.
bifidobacterium spp. and related

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148
Q

what are the virulence factors for bacteria linked to caries

A 
acid production from sugars
acid tolerance 
intracellular storage granules 
extracellular polysaccharides 
adhesins
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149
Q

what are the mutans streptococci found in humans

A

s. mutans
s. sobrinus

streptococci is broken down into 4 groups, one is the mutans streptococci

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150
Q

wha are the characteristics of the mutans streptococci

A

gram-positive, catalase-negative, saccharolytic, facultive anaerobes

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151
Q

which mutans streptococci is generally more acidogenic and adherent

A

s.sobrinus (less frequently carried)

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152
Q

what are non-mutans low-pH streptococci

A

a typical member of other species

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153
Q

why can koch’s first postulate not be applied in the case of bacteria associated with dental caries

A

microbes present in healthy individuals
even if you measure the amount of organisms present how do you do this? saliva will always be present and culture based approaches cannot distinguish between s.mutans and s.sobrinus

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154
Q

in a longitudinal study which cultured bacteria with early childhood caries, what were the bacteria most associated

A

s.mutans
scardovia wiggsiae

anaerobic, pleemorphic gram positive bacilli

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155
Q

what do sacchorytic bateria produce

A

acetic and lactic acid

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156
Q

what are the virulence factors of mutans streptococci

A

adhesins
acid production
acid resistance

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157
Q

what are the adhesins important in mutans streptococci important for colonisation

A

antigen I/II protein
glucosyltranferases (GTFs)
glucan binding proteins

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158
Q

what is involved in acid producing virulence factors in mutans streptococci

A

F-ATPase

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159
Q

what is involved in acid resistance (acidurity) in mutans streptococci

A

dna repair proteins

protective membrane proteins

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160
Q

what are the health promoting factors of non-mutans streptococci

A

adhesins of commensal bacteria - antigen I/II protein (streptococci)
alkali production

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161
Q

how can carbohydrates be utilised by caries associated bacteria

A

acid production

high energy bond in sucrose harnessed to produce polysaccharide

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162
Q

why is sucrose more cariogenic than glucose

A

only sucrose leads to the production of glucans therefore is more cariogenic

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163
Q

how do sugars get into bacterial cells e.g polysaccharides

A

transporters
polysaccharides can be digested
mon/disaccharides can be imported

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164
Q

why does xylitol import into cells lead to a futile cycle

A

its gets phosphorylated then dephosphorylated which can drain strep of energy and inhibit it

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165
Q

how is sugar uptake into cells regulated in high sugar

A

lactate is the major product and glycolysis is accelerated

IPS are made

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166
Q

how is sugar uptake into cells regulated in low sugar

A

mixed acid fermentation- lactate hydrogenase is inhibited

IPS are degraded

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167
Q

why is O2 an important regulator if fermentation

A

it inhibits pyruvate formate lyase

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168
Q

what is the importance of intracellular polysaccharides in bacterial cells

A

storage
glycogen-type glucan
broken down and used for glycolysis in starvation

(produced via glucose-1-phosphate when carbs in excess)

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169
Q

what is the importance of food webs in bacterial cells

A

bacteria rarely work in isolation
end products of metabolism can be recycled by other bacteria
several different bacteria na utilise lactate, lactate helps strep mutans

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170
Q

what does preacidification result in

A

greater acid tolerance, particularly in bacteria that are relatively acid sensitive

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171
Q

what are the mechanisms of acid adaptation

A

reduced permeability of cell membranes to H+
induction of H+ translocating ATPase (expels protons from cells)
induction of alkali production systems (arginine deiminase or urease)
induction of stress proteins that protect enzymes and nucleic acids from denaturation

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172
Q

what are the 2 ways we can make alkali in the mouth

A

arginine deaminase pathway

urease pathway

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173
Q

when is salivary deaminase and urease higher

A

in caries free subjects

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174
Q

whats involved in the plaque biofilm matrix

A

macromolecules and smaller molecules that may be trapped within the matrix

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175
Q

what are the macromolecules in the plaque biofilm matrix

A

polysaccharides
proteins
nucleic acids

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176
Q

what are the small molecules in the plaque biofilm matrix

A

nutrients
metals
signalling molecules
water channels

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177
Q

what are the 2 basic exopolysaccharides and what are they made by

A

glucans- glucosyltransferase

fructans- fructosyltransferase

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178
Q

what are expopolysaccharides made from

A

sucrose outside the cell

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179
Q

what are expopolysaccharides responsible for on sucrose containing agar

A

crystalline colony appearance

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180
Q

why is sucrose the substrate for expopolysaccharides

A

high energy in the glycosidic bond between the disaccharide

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181
Q

what can the energy released from glycosidic bonds be used for

A

to synthesis polymers

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182
Q

what do anomeric carbons give rise to

A

isomers

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183
Q

what are the types of fructan polymers

A

inulins (beta-2,1 bond type)- 96%

levans (beta-2,6 bond type)- 5%

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184
Q

what are fructan polymers (inulins) synthesised by

A

strep.mutans and some strains of strep.salivarius

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185
Q

what are fructan polymers (levans) made by

A

strep. sanguinis
strep. salivarius
actinomycesnaeslundii
some strep sobrinus

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186
Q

what are fructan polymers (levans) not made by

A

strep mutans

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187
Q

what are the two basic types of glucan polymers

A 
water insoluble (mutan)- alpha 1,3 linked 
water soluble (dextran)- alpha 1,6 linked
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188
Q

what is water insoluble (mutan) formed from

A

strep sobrinus

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189
Q

what are water soluble (dextran) formed from

A

strep salivarius

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190
Q

what is the variation of dextran formed from

A

strep sobrinus

191
Q

how can dextran be identified

A

rotates polarised light to the right

192
Q

what is the structure of the variant of dextran

A

numerous side chains of a-1,3 linked glucose (short) , every 15 backbone residues

193
Q

what are similar dextran-like polymers produced by

A

other strains e.g. strep mutans

194
Q

what is the structure of similar dextran-like polymers

A

side chains twice as numerous but shorter

comprises of single glucose residue linked alpha-1.3 to the branch residue

195
Q

what can form polymers comprising of both both α-1,3 and α-1,6 bonds

A

GTF enzyme of S. gordonii

effect on the local enviro
do not need primer

196
Q

how does exogenous glucan accelerate the reaction of polymer formation of both α-1,3 and α-1,6 bonds

A
  • binds to a site remote from catalytic site

- conformational change

197
Q

how do GTFs affect the environment

A

extracellular- secreted into complex enviro

198
Q

what can glucans act on for unrelated GTFs

A

acceptors

semi-processive reaction

199
Q

what is in the glucan soup

A

GTF

200
Q

what are other enzymes except those in the glucan soup

A

proteases -may modify GTF

dextranases

201
Q

what do GTFs and FTFs do

A

cleave sucrose or add glucose/fructose to an existing chain

202
Q

what do GTF-S produce

A

produce water soluble dextran-like glucans with an α-1,6 linked backbone

203
Q

what do GTF-I produce

A

an insoluble α-1,3 backbone polymer

204
Q

what do GTF-SI produce

A

a partially soluble α-1,3 backbone polymer

205
Q

what is the primer independent GTF called

A

GTFSi

206
Q

where are GTF-I, GFT-SI & GFT-S are enzymes found

A

s.mutans

207
Q

what is gtfA

A
  • sucrose phosphorylase (transfers glucose from sucrose to a phosphate)
  • bears little resemblance structurally to the GTFs
208
Q

what two types of FTFs have been found

A

one that synthesises an insulin like polymer and one a levan

209
Q

what bacteria is FTF absent from

A

strep.sobrinus

210
Q

what is essential for s.mutans biofilms

A

mutan

211
Q

how do biofilms grown in glucose and sucrose vary

A

glucose- thin with little or no matrix
sucrose- thicker (mutanase reduced biofilm)

Knockout mutants lacking gtfBor gtfC form thin biofilms

212
Q

what pH are mutan-rich microcolonies at

A

low pH

213
Q

what are glucan binding proteins (GBP)

A

proteins that bind glucans and mediate aggregation

214
Q

what are the types of GBP

A

some are bacterial surface proteins and some are secreted

215
Q

how do GBPs differ

A 
in size, strength of bond formed with glucan 
function i.e. adhesion/aggregation
216
Q

what do GBPA deficient mutans produce

A

flatter but more even biofilms

217
Q

what do GBPC deficient mutans of strep mutans produce

A

thicker biofilms than the parent strain

218
Q

what is the caries aetiology of FTFs

A

more active in plaque than GTFs
short term energy store
extend the fermentation time of plaque bacteria (caries)
improves survival of strep rather than directly affecting acid production

219
Q

the total amount of fructan in plaque low, what does this suggest

A

fructans are overturned rapidly

220
Q

how is fructan degradation achieved

A

by the enzyme fructanase

221
Q

what is the caries aetiolgy of GTFs

A

mutan streps cannot adhere well to teeth and glucans help them stick

222
Q

how are soluble dextrans involved in GTFs interactions

A

mediate cell to cell interaction (aggregation)

223
Q

how are insoluble dextrans involved in GTF interactions

A

mediate cell-surface interactions (adherence)

224
Q

what do glucan bridges allow for

A

other bacteria to adhere to s.mutans

225
Q

what interspecies interactions will cell-cell adhesion enhance in plaque biofilms

A

Metabolite cycling
Competition
Signalling

226
Q

what are functional amyloids

A

proteins in the biofilm matrix that form robust fibrils with with β-strands running perpendicular to the length of the fibril.

227
Q

what is the role of functional amyloids

A

biofilm stabilisation
melanin formation
initiation of innate antiviral immune response

228
Q

what produces large amounts of extracellular DNA and how can the biofilm be distrupted

A

P.aeruginosa

DNase I

229
Q

what are the functions of extracellular DNA

A

bacteria exchange genes (transformation)

source of nutrients

230
Q

where is eDNA present

A

subgingival plaque

231
Q

how DNase enzyme be used NucB

A

inhibits plaque formation

reduced colonisation by periodontal pathogens

232
Q

what is plaque fluid

A

fluid which fills the spaces between bacteria in dental plaque

233
Q

what is the composition of plaque fluid

A

saliva (modified)
bacterial metabolites/waste
material leeched from the tooth
gingival fluid

234
Q

what are the functions of plaque fluid

A

buffer between saliva and tooth
maintaining Ca2+, PO43-, F(which are reduced in conc when sucrose is present)
can retain antimicrobials or other components in mouthwash

235
Q

what are dental abscesses

A

Collection of pus, which is walled off by a barrier of inflammatory reaction (contained)

236
Q

what is the pathogenesis of abscesses

A

Abscesses can develop in any confined space to which bacteria can gain access and multiply

237
Q

what is the difference between a periodontal abscess and dentoalveolar

A

the tooth of periodontal abscess has a vital pulp

238
Q

what are the signs and symptoms of periodontal abscesses

A

swelling and erythema

pus likely to discharge from gingival margin

239
Q

what it the microbiology of periodontal abscesses

A

Associated with

Porphyromonas species

Prevotella species

Fusobacterium species

haemolytic streptococci

Actinomyces species and spirochaetes

240
Q

how can periodontal abscesses be managed

A

can be managed by local measures- scaling, root surface to clean out infection and drain the area

drainage and irrigation- antiseptic mouthwash- 0.2% CHX

extraction- if its occurred to the tooth before

antibiotics- if spreading and system involvement

241
Q

what are the routes of infection for dental alveolar abscesses and periapical abscesses

A

Bacteria gets in to the tooth via Dental caries

Exposed dentinal tubules- Bacteria cells can travel through dentine tubules

direct pulp exposure – bacteria enter and progress to the pulp.

spread out through apical fo

242
Q

where may you get swelling in a dentoalveolar abscess / periapical abscess

A

swelling in the sulcus adjacent to the tooth affected

243
Q

what is the most common endodontic infection

A

Infected pulp

244
Q

what does root canal treatment involve

A

cleaning out canals and sealing to prevent bacterial access - disinfect and sterilise the pulp

245
Q

what is commonly used to kill residual bacteria in endodontic infections

A

Sodium hypochlorite, chlorhexidine, calcium hydroxide and iodine

246
Q

what are the microbial species in abscess formation

A

facultative and strict anaerobes

247
Q

what are the facultative anaerobes in abscess formation

A

Oral (viridans) streptococci

Streptococcus anginosus group

Staphylococcus spp.

248
Q

what are the obligate anaerobes in abscess formation

A
  • Fusobacterium species
  • Prevotella species
  • Porphyromonas
  • Tannerella forsythia
  • Treponema denticola
  • Clostridium
  • Actinomyces
249
Q

what are the Factors affecting bacterial population in abscesses

A

Oxygen tension (selects for anaerobes)

Availability of nutrients (selects for proteolytic bacteria)

Bacterial interactions (selects for mutual co-operation)

250
Q

what are the POSSIBLE EXPLANATIONS FOR SELECTING A BACTERIAL POPULATION OF 3-4
SPECIES:

A

Multiple infection but only certain species survive

One species infects and prepares the way for appropriate others

251
Q

what can coaggregation between different bacteria lead to

A

Coinvasion of epithelial cells

Coinvasion of dentine tubules

252
Q

how does infection spread in periodontal abscesses (locally)

A

Soft-tissue abscess
mouth/skin

Sinus linking main abscess cavity with mouth/skin

Through soft tissue (cellulitis)
diffuse inflammation in connective tissue causing a inflammatory response

253
Q

how can infection spread further in PA

A 
Into adjacent fascial spaces
If progresses into deeper layers (osteomyelitis)
Into maxillary sinus
Indirect spread: 
-	Lymphatic routes
-	Haematogenous routes
254
Q

what is osteomyelitis

A

Inflammation of the medullary bone within the maxilla or mandible with posterior extension into the adjacent cortical bone and overlying periosteum

255
Q

when is osteomyelitis more common and what species are involved

A

if reduced vascularity

When infection present typical isolates include obligate anaerobes and Actinomyces species

256
Q

how is Osteomyelitis treated

A

based on local debridement, topical antiseptic on exposed areas, antibiotics as required

257
Q

when is there a risk of sepsis associated with PA

A

when infections spread into the lymphatic system or via haematogenous in the body this can lead to a metastatic abscess and a risk of sepsis

258
Q

how does infection spread from a lower molar tooth infection

A

the apices of the lower molars may be below the mylohyoid line/muscles and infection could spread into the buccal sulcus leading to swelling adjacent to the tooth

259
Q

how does infection spread from a upper molar tooth infection

A

infections can track up the maxillary sinuses

260
Q

what tissue spaces can dental infections spread into

A
  • Pterygomandibular space
  • Lateral pharyngeal space
  • Retropharyngeal space
  • Submasseteric space
  • Buccal space
  • Vestibular space
  • Sublingual space
  • Submandibular space
  • Submental space
261
Q

where do abscesses from mandibular premolars spread and why

A

into the sublingual space because the root apices lie below the mylohyoid line

262
Q

where do abscesses from mandibular molars spread

A

to submandibular space

263
Q

where do abscesses from mandibular wisdom teeth spread

A

infection in the lateral pharyngeal space

264
Q

where do abscesses from maxillary teeth spread

A

into the buccal space

265
Q

what are steps in the management of dental abscesses

A

Signs and symptoms

Assess the patient

Define location, nature and extent swelling

Systemic symptoms?

Identify cause of infection- radiograph , clinical signs and systemic indications

Diagnosis

Treatment

266
Q

what are local measures taken to treat dental abscesses

A

Drain pus if present

Tooth extraction

Access and drain through root canals

Soft tissue pus drain by incision

Debride infected periodontal pockets

Irrigate / debride infected operculum

267
Q

when is antibiotic prescription indicated

A

Evidence of spreading infection

  • Lymph node involvement
  • Swelling
  • Persistent swelling despite local treatment
  • Trismus-cant open the mouth due to worsening infection

Systemic involvement

268
Q

what are the warning signs for abscesses

A
  • Swelling, pain and raising of the tongue
  • Elevated floor of mouth
  • Malaise- systemically unwell
  • Fever
  • Swelling of the neck
  • Swelling of tissues of the submandibular and sublingual spaces
  • Hoarseness of the voice
  • Dysphagia
  • Stridor
  • Difficulty breathing
269
Q

what occurs in ludwigs agina

A

progression of dental alveolar infection to cause widespread swelling of tissue spaces

swelling of the neck, difficulty in breathing

spread of infection through fascial spaces to the mediastinum

270
Q

what are the species involved in the microbiology of ludwigs angina

A
  • Prevotella species
  • Porphyromonas species
  • Fusobacterium species
  • Anaerobic streptococci
271
Q

what is periocoronitis

A

superficial infection of operculum
infection in the space between the tooth and overlying soft tissue
pain and swelling

associated with wisdom teeth issue

272
Q

what bacteria is pericoronitis associated with

A
  • P. intermedia
  • Anaerobic streptococci
  • Fusobacterium species- greater abundance in patients with clinical symptoms
  • T. forsythia
  • A. actinomycemcomitans
273
Q

how can pericoronitis be managed

A

Local measures – mouthwash etc
Irrigation

(extraction- not local)

274
Q

what bacteria does metronidazole target

A

anaerobes

275
Q

what antibiotic is prescribed for pericoronitis if there is spreading infection and systemic involvement

A

metronidazole

276
Q

what causes cervicofacial actinomycosis

A

Opportunistic infection caused by members of the Actinomyces genus

  • A. israelii (90% of cases)
  • A. bovis
  • A. naeslundii
277
Q

what symptoms does cervicofacial actinomycosis present superficially

A

submandibular swelling

swelling at angle of mandible

278
Q

what is likely to precipitate infection in cervicofacial actinomycosis and why

A

Tooth extraction or trauma with bacterial species reaching deeper tissues

279
Q

as swelling develops in cervicofacial actinomycosis what can occur

A

multiple sinuses develop which are painful and slow growing
associated with thick yellow pus (‘sulphur granules’)
pus can persistently spread through tissue space

280
Q

what can cause acute necrotising ulcerative gingivitis (ANUG)

A

Poor oral hygiene, poor plaque control
Often immunocompromised
Poor diet and poor general health, stress
Smokers

281
Q

what are the signs of (ANUG)

A

Ulceration of the gingivae

Necrotising inflammation of the papillae between the teeth

Pain and halitosis

Superficial infection of the gingival margins

282
Q

what bacteria is ANUG associated with

A

fuso-spirochaetal bacteria

others:
- Treponema species
- Prevotella intermedia

283
Q

what are the local treatment measures of ANUG

A

• OHI and improvement in oral hygiene
• Removal of supra and subgingival deposits, scaling / ultrasonic debridement
Risk factor identification

284
Q

if there is spreading infection associated with ANUG, what drug should be prescribed

A

metronidazole

285
Q

what are some fungal soft tissue infections (secondary forms of oral candidosis)

A

Angular cheilitis (fungal and bacteria)

Median Rhomboid Glossitis

Chronic Mucocutaneous Candidosis

286
Q

what is angular cheilitis

A

inflammation of one or both corners of the mouth.

287
Q

what causes angular cheilitis

A

it can be fungal or bacterial in origin depending on the cause . e.g. dentures (fungal), not dentures like orthodontic appliance (bacterial)

  • candida
  • Streptococcus or Staphylococcus
288
Q

how can angular cheilitis be treated in patients with dentures

A

antifungal cream e.g. miconazole

289
Q

what is the reservoir for infection for angular cheilitis in

  1. denture patients
  2. non denture patients
A
  1. likely caused by candida so reservoir is the mouth

2. likely staphylococcus so anterior part of the nose

290
Q

how can angular cheilitis be treated in patients where its likely bacterial in origin

A

Sodium fusidate (fusidic acid) ointment

291
Q

what is Median Rhomboid Glossitis

A

Chronic infection (asymptomatic) Symmetrical-shaped area in the midline of the dorsum of the tongue

292
Q

what causes Median Rhomboid Glossitis

A

Atrophy of the filiform papillae

293
Q

what is Median Rhomboid Glossitis infection strongly associated with

A

smoking and Use of inhaled steroids

294
Q

what is Chronic Mucocutaneous Candidosis

A

immune disorder of T cells, it is characterized by chronic infections with Candida that are limited to mucosal surfaces, skin, and nails

295
Q

what is Chronic Mucocutaneous Candidosis associated with and what is a predisposing factor

A

rare congenital disorders

impaired cellular immunity against Candida

296
Q

what are the Treatment of Oral Candidosis

A

Rectify any local factors e.g unclean/ poor fitted denture, steroid inhaler

If locals fail - Antifungal medication (topical and systemic)

297
Q

what do polyenes (nystatin, amphotericin) do

A

disrupt fungal cell membrane (topical)

298
Q

what do azoles (fluconazole, clotrimazole, miconazole, ketocanazole, itraconazole) do

A

inhibits ergosterol biosynthesis (interfere with lanosterol demethylase)

topical or systemic

299
Q

what is periodontology

A

area of dentistry that deals with pd (supporting structures of the teeth as well as the diseases that affect them )

300
Q

what is the periodontnum

A

the supporting tissues of the teeth: gingivae, alveolar bone, cementum and pdl

301
Q

what is pd

A

Spectrum of conditions that are polymicrobial in origin (can be irreversible/ reversible) affecting the supporting structures of the teeth

302
Q

what are the types of PD

A

reversible- gingivitis
irreversible- periodontitis
necrotising (NUG, NUP, NUS(stomatitis))
periodotal abscesses

303
Q

what are 3 division of pd in the new 2017 classification

A

periodontal health, gingival diseases and conditions

periodontitis

other conditions affecting the periodontium

304
Q

what is the disease process for PD

A

junctional epithelium migrates down the root of the tooth forming a periodontal pocket - due to direct action by microorganisms

exaggerated and deregulated inflammatory response by the host

305
Q

how do pd pockets form

A

bone has shrunk the back- tooth is not supported

microorganisms in the crevice, inflammatory response

306
Q

what is looked at in a clinical examination of PD

A

clinical attachment loss

interproximal loss

307
Q

what are the details of periodontal pocket chart

A 
deep pockets >5mm around the teeth 
recession
loss of periodontal bone support 
mobility 
tooth loss
308
Q

once calculus is on the root surface what occurs

A

bacteria have a surface which they can colonise
inflammatory cells recruited
attachment loss and formation of pockets

309
Q

the development of pd is caused by a change in environmental conditions, what does this cause

A

it disrupts microbial homeostasis causing an altered microbial population- this causes an exaggerated inflammatory response damaging the supporting tissues of the teeth

310
Q

what are the environmental changes that occur in the periodontal pockets during the disease process

A 
flow of gingival crevicular fluid 
nutrition 
temperature 
pH
oxygen and oxidation 
aerobic to anaerobic
311
Q

what is the function of the GCF

A
  • bathes the gingival crevice
  • it increases with inflammatory response (some bacteria rinsed away)
  • humoral and cellular defence factors which can combat microbes that are there
312
Q

what are the problems that GCF can cause

A

it also provides proteins and glycoproteins which can serve as substrates for bacterial metabolism- the conditions in the niche favour bacteria for disease

313
Q

how does the GCF act as a substrate for bacteria

A

they are asaccharolytic (cant metabolise carbs) but they are proteolytic (can metabolise proteins) so the glycoproteins and proteins in the GCF act as a substrate

314
Q

how does the temp change in pd pockets during the disease process

A

increases due to inflammation

315
Q

how does the pH change in pd pockets during the disease process

A

proteolysis leads to pH going from neutral to slightly alkali

316
Q

how does the oxygen and oxidation potential change in pd pockets during the disease process

A

anaerobic enviro selecting for anaerobic bacteria

317
Q

what is the subgingival biofilm colonised by

A

gram negative bacteria

  • early colonisers (streptococcus and actinomyocenes)
  • bridging organisms like fusobacterium
  • periodontal pathogens attach by coaggregation /coadhesion
318
Q

what are the 3 component that contribute to the disease process in PD

A

microbial dysbiosis
individual patient
hyper-inflammatory host response

319
Q

what is the concept of microbial dysbiosis

A

change in biofilm which promotes changes towards the disease.

320
Q

what is the polymicrobial synergy and dysbiosis (PSD) model of PD

A

synergistic interactions among contributing bacteria, give rise to a dysbiotic community able to flourish

321
Q

how can you determine the subgingival microflora

A

Direct sampling from periodontal pockets using paper points

Cultivation of samples – identify bacteria present

however periodontal pocket is anaerobic, you’re exposing it to aerobic bacteria. Bacteria you want to detect won’t be present

Molecular methods- DNA approaches

322
Q

what is checkboard hybridisation used for and how is it done

A

detect periodontal pathogens
which microbes present at higher levels in disease

Specific DNA probes developed
DNA take from samples in patients and purified
DNA used to corelate which DNA from samples matched with probes
Look for particular organism

323
Q

what are the microbial changes that occur in subgingival plaque

A

tooth surface colonised by streptococcus
fusobacterium nucleatum act as bridging organisms and stick to streptococcal cells
red complex organisms bind

324
Q

what is fusobacterium nucleatum

A

gram negative, proteolytic, anaerobic, long rod-shaped cells
coaggregate with early colonisers (strep) and late colonisers (t.denticola)

325
Q

what are the characteristics of ALL red complex bacteria

A

fastidious gram-negative, proteolytic anaerobes

the can adhere to strep with no bridging organisms

326
Q

what are the 3 red complex bacteria

A

Porphyromonas gingivalis

Tannerella forsythia (Bacteroides forsythus)

Treponema denticola

327
Q

what are the characteristics of Porphyromonas gingivalis

A
  • Short rods.
  • Produces black and brown porphyrin (haem- containing) pigments.
  • Highly proteolytic.
  • Adheres to certain oral streptococci.
328
Q

what are the characteristics of Tannerella forsythia

A
  • Short rods with tapered ends.
  • Difficult to grow in monoculture – growth facilitated by other bacteria.
  • Possesses a glycosylated S-layer on the outside, which hides cells from the immune system.
329
Q

what are the characteristics of Treponema denticola, which PD is it a major cause of

A
  • Spirochaete, related to Treponema pallidum (causes syphilis).corkskew shape
  • Highly motile – flagellum is located in the periplasm and winds around the cell.
  • Major cause of necrotising PD
330
Q

why doesn’t kochs postulates apply to PD

A

more than one organism

organism may not be isolated in pure culture

331
Q

what is TM7 phylum

A

large group of bacterial species frequently detected in subgingival dental plaque (Elevated in mild periodontitis )

332
Q

what is used to track TM7

A

Axenic culture obtained using Fluorescence in situ hybridization (FISH)

333
Q

what happens when TM7 is co cultured

A

grows as long rods or short cocci, depending on partner organism

Some bacteria that couldn’t be previously grown can be when they’re co-cultured, partner organisms.

334
Q

what is the genome of TM7

A

Small genome (<1 Mbp), may reflect a dependence on other bacteria for growth

335
Q

what are the virulence factors of P. gingivalis (gram negative)

A
  • Adhesins/invasins - facilitate infection of host cell
  • Capsule - capsulated strains are more virulent – hide cell from immunity
  • LPS - can evoke inflammatory response
  • Haemagglutinins
  • proteases
336
Q

what are the P. gingivalis proteases

A

Cysteine proteases :
- Arg-Xaa specific protease (RGP)
-Lys-Xaa specific protease (KGP)
These are major antigens in infections.

337
Q

what is the role of P. gingivalis proteases

A

These are major antigens in infections.
Roles in nutrition and processing bacterial proteins
Cleave host proteins in connective tissue
Secondary functions: haemagglutination & adhesion.
Multiple roles in evasion of host immune responses

338
Q

what is Aggregatibacter actinomyctemcomitans (A. a)

A

an exception to the ecological plaque hypothesis

Facultative anaerobe

Gram –ve, capnophilic (likes co2), coccobacillus, related to Haemophilus.

Implicated in localized aggressive PD

Depth of PD pockets more rapid

Can cause systemic disease

339
Q

what are the virulence factors of A.a

A 
Adhesins/invasins- fimbriae and gene products 
LPS
Leukotoxin- targets immune cells 
Cytolethal distending toxin
Proteases (trypsin-like)
340
Q

what isActinomycetemcomitans JP2

A

one particular clone- Derived from West Africa

strongly haemolytic
strong leukotoxin activity.
Rapid progressive form of PD in adolescence

341
Q

how is pd linked to systemic disease

A

• Periodontal bacteria can get into the blood stream and infect other part of the body where periodontal pathogens can trigger the immune response affecting other body systems

342
Q

how are subgingival bacteria and proinflammatory molecules able to enter circulatory system and potentially affect sites and systems elsewhere in the body

A

• Periodontium is highly vascular

343
Q

what are the diseases Linked with PD

A 
cvs- atherosclerosis
respiratory system- pneumonia 
endocrine- diabetes
muscular- rheumatoid arthritis
GI- cancers, oral, pancreatic, colonic 
reproductive system- adverse pregnancy outcomes
344
Q

how is pd linked to adverse pregnancy outcomes

A

linked preterm birth
F. nucleatum and P. gingivalis- F. nucleatum documented as most prevalent species in amniotic fluid from pregnancies complicated by preterm birth

345
Q

how is pd Associated with diabetes mellitus

A
  • Increased perio disease in patients with poorly controlled diabetes
  • Increased problems with diabetes
  • disease may affect glycaemic control
  • effect on insulin resistance (inflammation)
  • Virulence factors have ability to cause infection at sites distant from the oral cavity
346
Q

how is pd Associated with cvs

A
  • Increased infectious/inflammatory burden and maybe cardiovascular events
  • Association with atherosclerosis
  • P. gingivalis, F. nucleatum and A. actinomycetemcomitans detected within atheromatous plaques
347
Q

how is pd Associated with rheumatoid arthritis

A

Both conditions show some similarities in that they are associated with a similar host-mediated chronic inflammatory response

348
Q

what are fungi, outline their structure

A

Simple eukaryotes
Some can form multicellular structures
Some transition between yeast and hyphal forms e.g. Candida spp

larger than bacteria
membrane bound nucleus
mitochondria
cell wall- chitin

349
Q

what are the 2 phylums of fungi

A

Basidiomycota and Ascomycota

350
Q

what are basidomycetes (refer to spore production) and what is an ex of one that can cause disease in humans

A

the spores are produced EXTERNALLY,- septate hyphae and spores borne on a basidium

Basidiomycota- Basidiospores with one haploid nucleus

Example: Cryptococcus (pathogenic) can cause disease in humans

351
Q

what are ascomycetes (refer to spore production) and what is an example

A

form ascospores in sacs called asci INTERNALLY during sexual reproduction

Example: Candida

352
Q

what are fungal cells

A 
slow growing cells 
grow as branched tubes 
similar to mammalian cells of human host 
at least twice size of bacterial cells 
different cell wall structures
353
Q

what is the structure of fungal cells

A

3-6mm diameter
thick, rigid cell wall (2 layered)
-ergesterol rather than cholesterol
- outer amorphous layer of glycoproteins
-inner layer of polysaccharides e.g. glucans/chitin

(genetically similar to human cells so antifungals target features unique to fungi)

354
Q

why is the cell wall in fungal cells important

A

in terms of antigenicity and adherence to host cells

355
Q

what is the most common fungi in the mouth

A

candida species specifically candida albicans

356
Q

which candida species is more resistant to antifungals

A

candida globrata

357
Q

what is the genus of candida

A

ascomycota (do not produce ascospores)
400 diff species mostly non-pathogenic
c.albicans accounts for >80% of oral isolates
dimorphic fungi (yeast & hyphal forms)

358
Q

what form of candida albicans are most oral infections associated with

A

hyphal form of candida albicans

359
Q

outline the candida species associated with oral infections

A

c. albicans
c. glabrata
c. krusei
c. tropicalis
c. guilliermondii
c. dubliniensis

360
Q

why is the genus candida referred to as an ‘opportunistic infection’

A

infection is dependant on some underlying predisposition (‘disease of diseased’)

361
Q

outline how a candida infection can become pathogenic

A

harmless commensals

change in environmental or systemic conditions

conditions favour candida proliferation

pathogenic disease causing infection

362
Q

outline candida morphology

A

can exist as yeast form or hyphae

pseudohypahae

363
Q

what occurs when candida transitions from yeast to hyphae

A

hyphal form invades epithelia
certain cell surface receptors

only present in hyphae

morphotype switching is under complex regulatory circuit

serum can trigger hyphal production

purified peptidoglycan triggers hyphae (oral bacteria can trigger hyphae)

364
Q

what is the morphotype switching under the control of

A

Osmotic shock

Temperature fluctuations- elevated

pH of environment- alkaline

Nutrients

Cell density (farnesol) or adjacent cells in biofilm

Salivary factors (e.g. statherin)

Oral bacteria (peptidoglycan can trigger hyphal production)

365
Q

how is candida affected when in a mixed species biofilm

A

hyphae long structures associated with rods

serum trigger hyphal production

oral bacteria trigger hyphae due to peptidoglycan

366
Q

which protein Promotes C. albicans Hyphae Formation

A

S. gordonii Antigen I/II

367
Q

what protein Inhibits C. albicans Hyphae Formation

A

S. mutans Competence Stimulating Peptide

368
Q

overall, do oral streptococci appear to benefit Candida spp

A

yes

369
Q

how do Lactobacillus spp. affect Candida spp.

A

they tend to inhibit Candida spp.

370
Q

how can candida be grown and identified

A

Culture on Sabouraud Dextrose Agar (sometimes with antibiotics) selects for Candida over bacteria due to low pH.

Microscopy is helpful for identification. e.g. germ tube test

371
Q

how can multiple candida species from the same infection be determined

A

CHROMagar Candida

Biochemical tests are also useful, especially carbohydrate utilisation 9API strips)

molecular methods ( Sequencing of ribosomal RNA, PCR )

372
Q

how does adherence acts as a virulence factor in c.albicans

A

Adherence to oral epithelium or surfaces of prosthetic devices (dentures)

Cell surface hydrophobicity interactions

adhesins: mannoproteins, fibrils, 8 ALS proteins, Agglutinin-like sequence proteins (ALS), hyphal wall protein (Hwp1)

373
Q

how does morphology acts as a virulence factor in c.albicans

A

Hyphae formation

  • Promotes invasion of oral epithelium
  • Reduces likelihood of phagocytosis
  • Allows phagocytosed yeast to escape phagocyte
  • Mutants unable to form hyphae are less virulent
374
Q

how does Phenotypic switching acts as a virulence factor in c.albicans

A

Ability to rapidly change cell morphology

Responsive to environmental stimuli

Associated with altered gene expression affecting
	Antigenicity
	Adhesion 
	Phagocyte resistance
	Drug susceptibility
375
Q

how does Aspartyl Proteinases acts as a virulence factor in c.albicans

A
  • Nutrition, adapting cell morphology, break down tissue barriers, cleave immune proteins and facilitate adherence
  • Degrade host immune cells
  • Host cell and extracellular matrix damage
376
Q

how do Phospolipases Proteinases acts as a virulence factor in c.albicans

A

Hydrolyse phospholipids (membranes)

Damage host cells - Host cell membrane damage, promoting cell lysis or exposure of receptors to facilitate adherence

377
Q

what is candidalysin

A

Virulence Factor protein that break up into peptides

it helps candida albicans penetrate epithelial cells

378
Q

what is the host response to oropharyngeal candidiasis

A

c.albicans hyphal penetration and secretion of proteolytic enzymes, the host responds with Th1 and Th17 adaptive immune response

379
Q

what is the host response to denture stomatitis

A

c.albicans biofilm formation on dentures, hyphal invasion of host tissue. further damage mediated and propagated by the host innate immune response, predominantly neutrophils

380
Q

what is the host response to hematogenously disseminated candidiasis

A

induced by biofilm formation on tissue or abiotic surfaces, c.albicans hyphal invasion and secretion of proteolytic enzymes causes damage. Th1 and Th17 adaptive immune response

381
Q

what is the host response to gastro-intestinal candidiasis

A

induced by c.albicans overgrowth in GI tract, in immunocompromised host. damage mediated by mucosal invasion and disruption of the epithelial barrier .

c.albicans may be a predisposing factor for inflammatory diseases of the GI tract, such as colitis

382
Q

what is the host response to intra-abdominal candidiasis

A

onset of infection triggered by a c.albicans invasion of abdominal organs resulting in the formation of abscesses

383
Q

what is the host response to vulvovaginal candidiassis

A

c.albicans hyphal transition and invasion of vaginal mucosa, triggering innate immune response. damage propagated by host response , predominantly neutrophils

384
Q

what oral candidosis

A

oral thrush
Not a single infection
Could be a marker for an underlying systemic condition e.g, immune level testing, diabetes

385
Q

what local factors may contribute to oral candidosis

A

Denture wearing

Inhaled corticosteroids e.g. asthmatic patients

Reduced salivary flow

Carbohydrate-rich diet

386
Q

what medications are associated with oral candidosis and who is more likely to be affected ?

A

Systemic corticosteroids, immunosuppressants, cytotoxics, broad-spectrum antibiotics

Extremes of age
Endocrine disorders – Diabetes mellitus o Anaemia
Patients with nutritional deficiencies
Salivary gland hypofunction
Immunosuppression
387
Q

serious systemic disease associated with reduced immunity are associated with oral candidosis?

A

Blood dyscrasias o Leukaemia
Malignancy
HIV

388
Q

how is Oral Candidosis diagnosed

A

Clinical appearance
- Can white plaques be scraped off, size, colour, surrounding redness

Laboratory tests (rinse with salt water and spit into pot)
-Blood tests (anaemia)
-Microbiology (Oral rinse
Oral swab)

Histology
-Biopsy

389
Q

what are the 4 primary forms of Oral Candidosis?

A

Acute pseudomembranous candidosis

Acute erythematous Candidosis

Chronic erythematous Candidosis

Chronic hyperplastic Candidosis

390
Q

which oral candidosis is the most common (produces pseudomembrnae – the white layer) and which one is the most common associated with dentures

A

Acute pseudomembranous candidosis

Chronic erythematous Candidosis (dentures)

391
Q

what is Acute pseudomembranous Candidosis and what is it associated with

A

Oral thrush

Acute- can be easily removed e.g. rinse mouth after inhaler

White patches that can be scraped off, irregular or oval shaped

Red and inflamed

Seen Inhaler users and immunosuppressed patients (HIV)

Could progress to oesophageal issues

392
Q

what is Acute erythematous Candidosis and what is it associated with

A

Antibiotic sore mouth / antibiotic stomatitis

Cracking of the dorsal surface of the tongue and loss if filiform papillae

Associated with treatment of broad spectrum antiobiotic – can reduce the bacterial community in oral environment allowing candida can progress

Seen in inhaler users

393
Q

what is Chronic erythematous Candidosis and what is it associated with

A

Denture Stomatitis
-Use of dentures

Redness if mucosa above the fitting surface of the denture

Asymptomatic

Develops under intraoral appliance

Seen on the palate

Result of inadequate oral hygiene

Management by a local measure

394
Q

how can denture stomatitis be managed

A

initially via local measures:

  • Clean dentures thoroughly
  • Soak dentures in chlorhexidine mouthwash or sodium hypochlorite for 15 mins twice daily
  • Chemical and mechanical cleansing of dentures twice daily
  • Leave dentures out as often as possible during treatment
  • Denture replacement or adjustment

Antifungal therapy if condition persists after management with local measures

395
Q

what is Chronic hyperplastic Candidosis and what is it associated with

A

Candida leukoplakia (less common)

  • seen in heavy smokers and alcohol
  • white patch at the sides of the mouth – CANNOT BE RUBBED OFF
  • Can be speckled – white and red, more prone to malignant transformation
  • rare
  • asymptomatic
  • 5-10 % patients with this can progress to hyperplasia and oral cancer
396
Q

in which candida infection can the white patches be scraped off

A

Acute pseudomembranous Candidosis

397
Q

how can Chronic hyperplastic Candidosis (Candidal leukoplakia) be diagnosed

A

need biopsy to diagnose

Hyphae invading epithelial cells

398
Q

what are Other Secondary Forms of Oral Candidosis

A

Angular Cheilitis

Median Rhomboid Glossitis

Chronic Mucocutaneous Candidosis

399
Q

what is Angular Cheilitis caused by and what is used as a treatment

A

infection with:

  • Candida
  • Streptococcus or Staphylococcus

Treatment (Consider the cause)

  • Miconazole cream
  • Sodium fusidate ointment
400
Q

what is Median Rhomboid Glossitis and what is it associated with

A

Symmetrical-shaped area in the midline of the dorsum of the tongue
Chronic infection
Atrophy of the filiform papillae

Infection strongly associated with smoking
Use of inhaled steroids

401
Q

what is Chronic Mucocutaneous Candidosis and what is it associated with

A

affects Skin, mucous membranes and nails

Associated with rare congenital disorders

Key predisposing factor impaired cellular immunity against Candida

402
Q

what are antifungal mediations

A

Topical antifungal medications
-Suspension, gel, lozenges

Systemic antifungal medications
-Tablets

403
Q

what is the main source of halitosis and what % is it

A

oral

85-90%

404
Q

what are the sources of halitosis (give the %)

A

oral 85-90%
5-10% nose (sinusitis)
3% tonsils (putrefaction)
1% other- bronchial and lung infections, kidney failure, carcinomas, stomach, protein rich diet

405
Q

what are the oral sources of halitosis

A

Poor oral hygiene

Gingivitis & periodontal disease

Oral infections, Candidosis

Faulty dental work

Unclean dentures

Dental abscesses

Putrefaction of post-nasal drip-

Xerostomia- dry mouth

ANUG, ANUP

Smoking

406
Q

what are the Intra-oral spaces where halitosis originates

A

Bacterial niches

  • Posterior tongue dorsum
  • Periodontal tissue sites
  • E.g. ANUG, ANUP, abscesses

Oral Candidosis

Oral tumours

407
Q

why are tongue dorsum thought to be major source of halitosis

A

Tongue coating
Numerous depression
Deep fissures
Anaerobic environment in tongue fissures - thickened tongue coating

408
Q

what are the Gram negative anaerobes in halitosis

A

Treponema denticola

Porphyromonas gingivalis

Bacteriodes forsythus (Tannerella forsythia)

Fusobacterium

Veillonella

Haemophilus

409
Q

what are the Gram positive anaerobes in halitosis

A

Stomatococcus mucilaginous

410
Q

what are the most active bacteria in halitosis

A

Porphyromonas gingivalis
Treponema denticola
Tannerella forsythia

These are the ones correlated with PD

411
Q

what is Halitosis primarily caused by

A

microbial degradation of both sulphur-containing and non-sulphur containing amino acids(cystine) derived from proteins

412
Q

what is the source of proteins degraded in halitosis

A

exfoliated human epithelial cells and white blood cell debris, or present in plaque, saliva, blood and tongue coatings

413
Q

which substances produce volatile sulphur compounds (VSC)

A
  • Bacteriodes melaninogenicus
  • T. denticola
  • P. gingivalis
  • P. intermedia
  • Bacteriodes loescheii
  • B. forsythus (T. forsythia)
  • Centipeda periodontii
  • Eikenella corrodens
  • Fusobacterium peridonticum
414
Q

what are the VSC associated with halitosis

A

Hydrogen sulphide H¬2S

Dimethylsulphide (CH¬3)2S

Diethylsulphide (C¬2H¬5)2S

Dimethyldisulphide (CH¬3)2S¬2

Diethyldisulphide (C¬2H¬5)2S¬2

Methyl mercaptan CH¬3S

415
Q

how are sulphur compounds released

A

due to proteolysis of amino acids

416
Q

how is skatole produced

A

Tryptophan metabolism

417
Q

how is Cadaverine produced

A

Protein breakdown

418
Q

how is Putrescine produced

A

Protein breakdown

419
Q

how is Isovaleric acid produced

A

Metabolite

420
Q

how can halitosis be diagnosed by Nasal appraisal

A

Self-assessment

  • Wrist licking
  • Smelling expectorated saliva
Subjective organoleptic analysis by confidant (SOAC) smelling another person’s breath
Assess the smell of
o	Breath
o	Floss
o	Tongue scrape

Gas chromatography

421
Q

how can halitosis be diagnosed by Instrumental sniffers

A

Very sensitive to H2S
Low sensitivity to mercaptan

Benzoyl Arginine Naphthylamide (BANA)

422
Q

how is Benzoyl Arginine Naphthylamide (BANA) used to detect halitosis

A

Rapid and simple diagnostic test for periodontal pathogens

Hydrolysis of BANA

Paper BANA assay are highly correlated with Treponema denticola, Porphyromonas gingivalis and Bacteroides forsythus (Tannerella forsythia)

Ability of subgingival plaque to hydrolyze BANA (Perioscan®) correlated with the CPITN score

Cystatin is a potent cysteine proteinase inhibitor

423
Q

what are the arguments for Relationship between halitosis and periodontal disease

A

Halitosis primarily caused by Gram-negative microorganisms associated with
periodontal disease

Halitosis commonly found in patients suffering from periodontitis

Elevated concentrations of volatile sulphur compounds in subjects with probing depths of ≥4 mm

Volatile sulphur compounds are toxic to gingival tissues

Hydrogen sulphide in periodontal pocketing

424
Q

what are the arguments against Relationship between halitosis and periodontal disease

A

Periodontally healthy patients can have halitosis

Tongue coatings are the major cause of halitosis

PD patients can be affected by halitosis

Periodontal pockets are partially sealed and the mass transfer of gases is low

Tongue cleaning reduces volatile sulphur compounds by more than 70%

425
Q

what is halitosis caused by

A

microorganisms that complete metabolic degradation of sulphur-containing amino acids

426
Q

what can Treatment strategies for halitosis include

A

masking the malodour- mouthwash

mechanical reduction of intraoral nutrients, substrates and microorganisms.

chemical reduction of the oral microbial load

rendering malodorous gases non-volatile

chemical degradation of the malodorous gases-

427
Q

what Improvements in oral hygiene can be used to manage halitosis and what are the issues with this

A

Tongue brushing and scraping

  • Possibility of damage to tongue
  • Difficult due to deep fissures

Effective tooth brushing
Interdental cleaning
Management of gingivitis and PD
Address defective restorations or restore carious lesions

428
Q

what are other way halitosis can be managed

A

Avoidance of dry mouth
Gum chewing- larger saliva volumes
Oxidation of VSCs (volatile sulphur compounds
Mouthrinses

429
Q

what is the Systematic review conclusion of the efficacy of mouthrinses in reducing halitosis

A

Mouthrinses containing antibacterial agents (chlorhexidine and cetylpyridinium chloride) or those containing chlorine dioxide and zinc can reduce halitosis to some extent

430
Q

what is the Critical summary assessment. of the efficacy of mouthrinses in reducing halitosis

A

Although antibacterial mouthrinses can reduce halitosis, the extent of effectiveness is uncertain owing to incomplete reporting, possible study bias and variation in patients’ characteristics and assessment methods.

431
Q

what do parasites act as

A

eukaryotic pathogens

pathogenic symbionts, infectious agents- includes viruses, bacteria and eukaryotes

432
Q

what are Parasitic protozoa

A

pathogenic microbial eukaryotes – protists

433
Q

what are exavata

A

Euglenozoa: Leishmania spp. Parabasalia: Trichomonas tenax

434
Q

what are Amoebozoa

A

Archamoebae: Entamoeba gingivalis

435
Q

what are Amoebozoa

A

Archamoebae: Entamoeba gingivalis

436
Q

what is symbiosis

A

the association between organisms from different species – different types of association can be defined, briefly there are three major categories: Mutualism, Commensalism, Parasitism

437
Q

what is mutualism

A

both partners benefit from the interaction and they are co-dependent for thriving

438
Q

what is Parasitism

A

one partner relies on a host for nutrients and shelter and there is a potential cost to the host – it is a potential pathogen causing pathologies (damages)

439
Q

what is Parasitism

A

one partner relies on a host for nutrients and shelter and there is a potential cost to the host – it is a potential pathogen causing pathologies (damages)

440
Q

what are facultative pathogens

A

they don’t cause disease all the time – blurring the distinction between parasites ,commensals and mutualists (Some parasites)

441
Q

what are facultative pathogens

A

they don’t cause disease all the time – blurring the distinction between parasites ,commensals and mutualists (Some parasites)

442
Q

what are Opportunistic pathogens

A

those that cause pathologies when the host is compromised – e.g. due to immunodeficiency (as in AIDS, due to malnutrition or chemotherapies)

443
Q

how do parasites interact with their host

A

highly adapted to one or more body sites of the host(s) that they require to progress through their life cycle

The best(optimally)adapted parasites are the least pathogenic, they don’t kill their host (evolve towards commensalisms?)

Many parasite-host relationships are long-term, chronic, highly intimate

444
Q

what are the 2 key contradictory functions Mucosal surfaces must mediate simultaneously

A

Protect the individual from microbial, chemical and physical insults

Facilitate exchanges between outside and inside our body

445
Q

where are the members of the mucosal microbiota are intimately associated with both of these functions

A

respiratory, digestive and urogenital tracts

446
Q

what is eubiosis

A

Microbiota taxonomic and functional structures that lead to homeostasis/health

447
Q

what is dysbiosis

A

abnormal Microbiota taxonomic and functional structures that lead to pathologies – even in the absence of overt pathogens

Peritonitis :anaerobic, less diversity, composition simplified and enriched in anaerobes

448
Q

what are pathobionts

A

members of the microbiota that have the potential to cause damage/pathologies

Some mucosal microbial parasites could be considered as pathobionts

449
Q

what are monoxenous parasites

A

Parasite requiring a single host for completing their life cycle

450
Q

what are heteroxenous parasites

A

Parasite requiring two or more hosts for completing their life cycle

451
Q

what are promiscuous parasites

A

they are capable of infecting a broad range of hosts (e.g. Trichomonas tenax, Leishmanis spp.) -common in cats and dogs

452
Q

what are zoonoses

A

Human diseases caused by animal parasites, the animal hosts represent reservoirs for the human pathogens

453
Q

what are the resident oral microbiota

A

Archaea- Methanobrevibacter oralis

Bacteria-responsible for oral diseases

Microbialeukaryotes

  • fungi- Protozoa-Microbial parasites
  • protists- Protozoa-Microbial parasites

Viruses

454
Q

what are Autochthonous microbiota

A

micro-organisms characteristically found at a particular site

These organisms are adapted to survive and grow at a given site (e.g. oral cavity

455
Q

what are Two common oral • Autochthonous microbial eukaryotes associated with periodontitis

A

Trichomonastenax

Entamoeba gingivalis

456
Q

what are Allochthonous microbiota

A

micro-organisms transiently (non specific) present at a given site.

These organisms are not specific to the site, but may colonise transiently, or if the site becomes compromised due to injury or immunodeficiency

457
Q

what is the most common Allochthonous microbiota

A

Leishmania species: most commonly (i) cutaneous can become (ii) systemic or (iii) mucocutaneous (including the oral-skin interface)

458
Q

what is the Leishmania species a member of

A

Euglenozoa, Excavata

Not possible to have Leishmania without sand flies

459
Q

where are the most common places for infection with the Leishmania species

A

on the arm, face etc. not in the oral cavity e.g. mucutaneous Leishmaiasis

460
Q

what are the effects of Trichomonas vaginalis

A

Infect Humans

Genitourinary tract

Associated with HIV, bacterial vaginosis, Pelvic Inflammatory Disease and low birth weight

461
Q

what are the effects of Trichomonas gallinae

A

Infect birds

Common among pigeons/columbiform

Can causes epidemics and high mortality rates

462
Q

what are the effects of Trichomonas tenax

A

Periodontitis

Infects humans, dogs and cats

Oral cavity, upper gastrointestinal tract and lungs

Associated with periodontitis (35% PP)

Identified in the urethra of MSM

463
Q

what is Trichomonas vaginalis pathobiology

A

Interactions between bacteria and viruses affects mucosal surface

Damage and facilitates HIV

464
Q

what are the Different way the Trichomonas vaginalis parasite contributes

A

Inflammation

Dysbiosis - profiling of microbiota changes, becomes more complex

Epithelial cells -damage them

This combination contributes to more fragile susceptible mucosa to infections

465
Q

What is the molecular basis of Trichomonas spp. mucosal life style and pathobiology?

A

Set of enzymes thought to target bacteria which encode a range of peptidases and cadidase lysosomes (breaks peptidoglycan) - combinations of enzymes do the same j bans the lysozyme in saliva it cleaves the peptidase that brings the sugars together

466
Q

what are the characteristics of Trichomonas spp.

A

Cell surface proteins involved in parasite-microbiota/host

interactions, (ii) metabolic enzymes and (iii) enzymes targeting other microbes

467
Q

which enzymes does Trichomonas spp. candidate peptidoglycan (PG) target and what is the role of the enzymes

A

NlpC/P60, GH19 and GH25

These enzyme play a key role in trigminomas bacteria interactions

468
Q

what is Entamoeba a member of

A

Amoabozoa

469
Q

what is The Entamoeba gingivalis (and E. histolytica) transmission like

A

Classical oral transmission that uses a cyst form

470
Q

what is the Entamoeba histolytica pathobiology

A

Most asymptomatic parasite is able to get through mucus layer and modify microbiota composition

471
Q

How could Trichomonas tenax and Entamoeba gingivalis contribute to periodontitis?

A

reduced microbial diversity

Keystone pathogen in combination with bacteria

Contribute to dysbiosis

Can trigger inflammation response

Factors involved in perio and which elements are relevant to parasites

472
Q

how can Trichomonas tenax and Entameoba gingivalis Contribute to dysbiosis

A

they feed on bacteria and change the inflammatory tone of the tissue

excessive diversity
pathobiont expansion
loss of mutualists
reduced diversity

473
Q

what else can Trichomonas tenax and Entamoeba gingivalis contribute to

A

Likely contribute directly and indirectly to the inflammation characteristic of periodontitis

Contribute at boosting local neutrophil population

Stage 2 (16 decks)

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