Microbiology for Dentists Theme 2 Flashcards
1
Q
What is the autochthonous microbiotia ?
A
microorgansims characteristically found at a particular site
2
Q
What is the allochthonous microbiotia ?
A
microorganims transiently present at a site
they dont thrive at the site but may colonise transiently if the site becomes compromised.
3
Q
Where are archaea detected at increased levels ?
A
periodontal disease
4
Q
What are the most common type of virus found in the mouth ?
A
bacteriophages
5
Q
What is the most common viral pathogen in the mouth ?
A
HSV-1
6
Q
Which viruses are asymptomatic in the mouth so care is needed for cross infection ?
A
hepatitis B and HIV
7
Q
What is the most common fungus in the mouth ?
A
candida
8
Q
What are the most abundant bacteria in the mouth ?
A
oral streptococci
9
Q
What are the characteristics of oral streptococci ?
A
gram positive
alpha haemolytic
10
Q
Which diseases are bacteria responsible for ?
A
caries
periodontitis
abcesses
11
Q
What happens with oral streptococci and kiss plates ?
A
oral streptococci are alpha haemolytic - brownish colour change
12
Q
What is alpha haemolysis ?
A
produces hydrogen peroxide which bleaches haemoglobin - Fe changes transition states from Fe3+ to Fe2+
13
Q
How many species of bacteria naturally colonise the mouth ?
A
700 species- 13 phyla
14
Q
How many of the species in the mouth can be cultured ?
A
50%
15
Q
How long does it take to form mature dental plaque ?
A
1-4 minutes
16
Q
Where do bacteria live in the mouth ?
A
tongue
cheek
palate
teeth
17
Q
What are the lips, cheeks and palate like as a microbial habitat ?
A
have epithelial cells that are shed continually which get rid of bacteria
18
Q
What is the tongue like as a microbial habitat ?
A
highly papillated which creates an anaeorbic environment
tongue is reservoir for obligate anaerobes
19
Q
What are the teeth like as a microbial habitat ?
A
no shedding as no epithelial cell
prone to colonisation by bacteria
20
Q
What is the enamel pellicle ?
A
a protein film between enamel and bacteria that supports and inhibits bacterial adhesion. Prevents enamel dissolution
21
Q
Why do we culture microflora ?
A
understand physiology and biochemistry
link organism to disease
identify pathogenesis mechanisms
test antibiotics
22
Q
How can it be hard to culture certain microflora ?
A
some bacteria are dormant - not easily reactivated
some species are fastidious
23
Q
What are the culture independent methods of microbial analysis ?
A
PCR
Hybridisation
NGS- Metagenomics/targeted
24
Q
What are holobionts ?
A
we are superorganisms of our on cells and microbiotia - act as one biological unit
25
Which streptococci are enriched in dental plaque compared to soft tissues ?
gordonii and sanguinis
26
Is saliva sterile ?
it is only sterile when secreted but accumulates with bacterial cells
27
Are there more bacteria attached to epithelial cells than there are free in saliva ?
more attached to epithelial cells
28
How are bacteria removed from oral surfaces ?
sloughing epithelial cell
mechanical debridement
active release
29
What is the problem with sampling saliva to look at the oral microbiome ?
there are different amounts of bacteria in the plaque compared to the soft tissue
30
What is the core microbiome ?
13 phyla present in almost everyone
31
What is the peripheral microbiome ?
species present in some and not others
32
Why do some microbiomes form clusters in different individuals ?
differences in the metabolome
| this could be correlated with disease susceptibility
33
What does the acquired enamel pellicle do ?
it protects enamel
| protects against the dissolution of enamel by keeping calcium and phosphate together
34
How does saliva help control plaque accumulation ?
aggregating bacteria which are then swallowed
| having antimicrobial effects
35
Which salivary proteins bind to bacteria ?
MG2
Gp340
PRPs
Statherin
36
What are the roles of the salivary proteins ?
agglutinate
aggregate
inhibit
promote/inhibit microbial colonisation
37
What is aggregation/agglutination ?
occurs in the fluid phase
results in large clumps
large clumps removed in swallowing
38
What is adhesion ?
proteins in the saliva pellicle interact with bacteria resulting in the adhesion of bacteria to teeth
39
What is unique about salivary proteins ?
exhibit different bacteria binding proteins when in solution than on the surface
40
What are immunoglobulins present in saliva as ?
secretory IgA
41
What is the resting flow rate of IgA ?
33 mg/100 mL
42
What is the stimulated flow rate of IgA ?
6 mg/100 mL
43
What is the purpose of antibodies ?
to agglutinate bacteria - removed by swallowing
44
Which immunoglobulins are present in the GCF and what is their purpose ?
IgG and IgM
| activate complement and opsinisation
45
What are examples of host receptors that bind bacteria ?
PRPs
| Stahtherin
46
What are Proline rich proteins (PRPs) ?
they act in calcium phosphate stabilisation
| found in high concentrations in parotid and submandibular saliva
47
Why are PRPs cyptitopes ?
they change conformation and reveal binding sites that bacteria want to bind to
48
What are the fucntional domains of PRPs and what do they do ?
N term- binds to Hydroxyapatite
| C term binds to Actinomyces, Strep mutans and Sanguinis
49
What is statherin ?
main funcntion is calcium phosphate stabilisation
binds to hydroxyapatite and bacteria like actinomyces
secreted by parotid and submandibular glands
50
What does lysozyme do ?
cleaves bacterial cell walls
| causes no enzymatic cell degradation
51
Where can you find lysozyme ?
tears
saliva
sweat
52
What is the downside of lysozyme ?
not equally effective against all bacteria
| oral bacteria are more tolerant of it
53
What does lactoperoxidase do ?
catalyses the production of hypothiocynate from hydrogen peroxide ( by product of bacterial metabolism) and thiocyanate (in saliva)
54
What does hypothiocyanate do ?
uncharged so penetrates bacterial cell membranes
| inhibits bacterial glycolysis
55
What does lactoferrin do ?
binds iron and makes it unavailable
56
What is the acquired enamel pellicle ?
protein film that forms on the surface of enamel
contains salivary glycoproteins and bacterial products
eg. PRPs which allow bacterial adhesion
57
Which tooth surfaces are available for colonisation ?
fissures
smooth surfaces
approximal
gingival crevice
58
Is supragingival plaque aerobic or anaerobic ?
aerobix
59
Where is supragingival plaque present ?
in health on the teeth
| in cracks and fissures it can leads to caries
60
What is the nutrient source of supragingival plaque ?
saliva
61
Is subginigival plaque aerobic or anaerobic ?
anaerobic
62
What are significant amounts of subgingival plaque associated with ?
periodontitis
| ginigivitis
63
What is the nutrient source of subgingival plaque ?
gingival crevicular fluid
64
When does plaque accumulate faster ?
day
65
Where do pioneer colonisers attach to ?
salivary pellicle
66
What are environmental factors affecting plaque formation ?
diet
| smoking
67
What are bacterial factors affecting plaque formation ?
co aggregation
| bacterial adhesins that recognise the pellicle
68
What is the cyclic nature of plaque build up ?
initial colonisation- Streptococcus, Actinomyces, Veillonella
Microflora alteration phase- Fusobacterium and Prevotella
Lack of cleaning leads to dental caries and periodontitis
69
What is the role of the acquired enamel pellicle ?
primary colonising bacteria in plaque attach to it
70
What are the characteristics of the acquired enamel pellicle ?
```
1-3 micrometres thick
can permeate the outer layer of enamel
not easily removed
present on most enamel surfaces
a deposit of saliva proteins
```
71
How is the enamel pellicle formed ?
by the preceipitation of denatured saliva proteins
| it is selective- proteins with a high binding affinity bind to the tooth surface
72
As well as saliva proteins what else does the pellicle contain ?
components of the GCF
| oral mucosa and microbial cells
73
What are the functions of the enamel pellicle ?
lubricant
reduces mobility of calcium and phosphate ions - this stops the dissolution of enamel - demineralisation
prevents inappropriate crystal growth- stops dental calculus
contains enzymes
74
What is within the pellicle which prevents inappropriate crystal growth ?
statherin and PRPs
75
Which active enzymes are within the pellicle ?
```
amylase
lysozyme
peroxidase
carbonic anhydrase
glucosyltransferase
```
76
What does the pellicle do with bacteria ?
can inhibit and be a substrate for bacterial adhesion
77
What is within the pellicle that allows bacteria to adherer ?
the salivary proteins have receptors for bacteria
78
Name some salivary proteins in the pellicle ?
```
MGI
Amylase
PRPs
Statherin
Gp340
```
79
Which bacteria are present in initial plaque ?
50% of bacteria in initial plaque are streptococci
80
What are the human oral streptococci groups ?
mitis
anginosis
salivarius
mutans
81
What is the mitis streptococcus group ?
the most numerous in the mouth
82
What is the anginosis streptococcus group ?
commensal but found at abcesses
83
What is the salivarius streptococcus group ?
generally commensal but also used as probiotics
| also found elevated in dental caries
84
What is the mutans streptococcus group ?
associated with dental caries
| found in mature plaque and is not an early coloniser
85
What is the most abundant bacterium in initial plaque ?
Streptococcus Oralis
86
What are streptococcal adhesins ?
they are proteins on the surface of oral streptococci that can adhere to receptors on salivary proteins in the pellicle
87
What is an example of a streptococcal adhesin ?
antigen I/II
88
What is antigen I/II ?
a large multi domain protein on the surface of oral streptococci
mediates adhesion to the gp340 salivary agglutinin protein in the pellicle
89
What are the other functions of antigen I/II ?
can bind to to other bacteria like actinomyces
90
What structural properties allow antigen I/II to bind to other bacteria ?
it has a C-motif that covalently binds to peptidoglycan
91
What are the pioneer coloniser species ?
actinomyces
| veillonella
92
What are actinomyces ?
gram positive pleimorphic rods
facultative anerobes
harmless but can cause disease
93
What are veilonella ?
gram negative cocci
strict anaerobes
feed on lactate produced by other oral bacteria
94
Does veilonella cause disease ?
not associated with disease but elevated in caries
| found in supraginigival plaque although its aerobic
95
How does veilonella survive in supragingival plaque if its anaerobic ?
the surrounding aerobic bacteria use the oxygen so that the environment becomes anaerobic
96
What is the process of dental plaque formation ?
```
adhesion to the surface
coaggregation
coadhesion
mature biofilm with matrix
dispersal
```
97
What is the appearance of mature supragingival plaque ?
stratified
| gram positive cocci and short rods a tooth surface with filament towards the outer layers
98
What does supragingival mature plaque cause ?
causes a shift towards acidogenic/aciduric bacteria
99
Does the amount of plaque correlate with dental caries ?
no evidence to support correlation
100
What does accumulation of plaque at the gum line cause ?
irritates tissues and can lead to calculus formation
this leads to gingivitis (reversible)
can progress to periodontitis (irreversible)
accompanied with a change in oral microbiotia
101
What is present in the subgingival crevice in the mouth ?
few bacteria
anaerobic bacteria- not found elsewhere
asacchrolytic, proteolytic bacteria found here
102
What do early colonisers support the attachment of ?
bridging organsims
103
What are bridging organisms ?
they stick to perio pathogens and trigger inflammation of the gingiva
104
What is an example of a bridging organism ?
fusobacterium nucleatum
105
What is fusobacterium nucleatum ?
gram negative
proteolytic
anaerobic
long rods
106
What does fusobacterium nucleatum do ?
forms co aggregates with early coloniseres and later colonisers
invades host epithelial cells
present in high numbers in subgingival plaque
107
What is supragingival calculus a deposit of ?
saliva
108
What is subgingival calculus a deposit of ?
serum
109
What does the rough surface of calculus do ?
trigger inflammation
| leading to gingivitis and periodontitis
110
Where does calculus form ?
near salivary duct opening
111
What is calculus ?
mineralised plaque
112
What are sialoliths ?
form in salivary ducts
| they are supersaturated Calcium phosphate
113
What are the mechanisms of enamel loss ?
fracture
caries
erosion
abrasion
114
What is caries ?
loss of enamel due to bacterial acid production
115
What is erosion ?
loss of enamel due to dietary acids
116
What is abrasion ?
loss of enamel due to mechanical wear
117
What is the main component of enamel ?
biological appatite
118
What is biological appatite made from ?
Ca
Phosphate
hydroxyl ions
119
Is biological appatite soluble ?
sparingly soluble
| increased solubility at low pH
120
What happens to pH after a sugar rinse according to stephans curve ?
there is a drop in pH
121
What happens after the drop in pH ?
after the decrease in pH the pH tries to return to normal
| this is the time in which the enamel dissolved as it is exposed to a low pH
122
What is the critical pH ?
roughly 5.5
| this is the pH which under the enamel dissolves quicker
123
What happens if you rip water on enamel ?
enamel will eventually dissolve
an equilibrium isnt reached as water is always being replaced
fresh water doesnt have any calcium in it - calcium always leaving the tooth
124
Why doesnt saliva dissolve enamel ?
supersaturated calcium phosphate doesnt come into contact with the enamel as the statherin and PRPs bind to the ions maintaining the enamel
125
How do you calculate the solubility product ?
the ion concentrations multiplied
| the ion concentrations must be multiplied by their respective power
126
What is the ionic product ?
the same as the solubility product but in solution
127
If IP>SP ?
solution is supersaturated
| unless the ions are stabilised in some way like by stahterin etc
128
What if SP >IP ?
solution is unsaturated and you get dissolution
129
What are the 2 ways that calcium hydroxyapatite can dissolve ?
loss of hydroxide ions
| loss of phosphate ions
130
What happens with the loss of hydroxide ions ?
adding acid means hydroxyapatite dissolves phosphate and hydroxyl ions
increasing acid means hydroxyl ions must decrease - pulling out hydroxyl ions to maintain equilibrium
131
What happens with the loss of phosphate ions ?
hydrogen ions bind to phosphate ions - pulling out phosphate ions
IP drops and SP is higher - dissolution
132
What is the effect on the critical pH if someone has lower calcium and phosphate concentrations ?
leads to a higher critical pH of about 6.5- this means there is a greater range of pH over which dissolution can occur
133
The KSP of a sparingly soluble halids is 4x10^8 moles
| How many moles of each element will dissolve in a litre of water ?
square root
solubility product is the product of the ion concentrations.
2x10^4
134
in the global burden of diseases which is the most 2nd prevalent disease ?
Latent tuberculosis
135
What is the name for the total genetic information in a complex population ?
metagenome
136
Which of the following species is most strongly acidogenic ?
lactobacillus fermentum
137
The concept that the total amount of plaque is responsible for dental caries is ?
specific plaque hypothesis
138
Which of the following species belongs to the mutans group streptococci ?
Streptococcus Sobrinus
139
At the crtical pH of enamel what is the relationship of the KP to IP ?
KP=IP
140
In acidic conditions hydroxyapatite dissolves because ions are removed from solution. Which ions are likely to be removed ?
Hydroxide
| phosphate
141
What are the different types of caries ?
```
primary
secondary
residual
active v inactive
early childhood caries
```
142
What is early childhood caries ?
presence of one or more decayed missing or filled tooth surfaces in any primary tooth between birth and 71 months
143
Which type of caries are becoming prominent ?
occlusal, interproximal and EDJ caries ever since the late 19th century
144
Why is caries set to increase in global prevalence ?
greater longevity and population growth
145
Which bacteria are commonly acossiated with caries ?
mutans streptococci
lactobacillus
actinomyces
bifidobacterium - scardovia wigiassae
146
How are the streptococci broken up ?
broken into groups with each group containing differnt species
147
What bacteria does the mutans group contain ?
strep mutans
| strep sobrinus
148
What are the features of the mutans streptococci ?
gram positive
catalase negative
sacchrolytic
facultative anaerobes
149
What are the caries associated with streptococci ?
S mutans
S sobrinus
non mutans acossaited low pH streptococci
150
What are the characteristics of S mutans ?
acidogenic
aciduric
produces glucans from sucrose
151
What is different about S.Sobrinus comapred to S.mutans ?
more acidogenic
| more adherent
152
Why does Kochs postulates not match up with Strep mutans ?
organism must be present in all cases of disease and not in healthy individuals- this cannot be the case because strep mutans is in 96% of the population and the level rather than the presence is important
153
Which bacteria are acossiated with early childhood caries ?
bifidobacterium
scardovia wiggisae
they have been isolated on acid agar
154
What are the characteristics of Scardovia Wiggisiae ?
anaerobic
pleomorphic
gram positive bacilli
sacchrolytic - produces acetic and lactic acid
155
What is the problem with S mutans ?
it has a low predictive value- there are other species like Prevotella that have a higher predictive value
156
What are germfree animals ?
no microorganism present in them
| used to investigate microbial aetiology
157
What are examples of virulence factors ?
adhesins
acid production
aciduricity
158
What are examples of adhesins ?
antigen I/II
glucosyltransferases
aciduricity
159
How do bacteria remain aciduric ?
DNA repair proteins
| protective membrane proteins
160
How are carbohydrates utilised by bacteria ?
glucose and sucrose make acid and intracellular storage polymers
sucrose also makes exopolysaccharides
161
How do bacteria uptake sugar ?
polysaccharides are digested
| monosaccharides and disaccharides are imported
162
What is xylitol ?
a sugar substitute
| imported, metabolised and knocked out - futile cycle
163
How is glucose uptake described ?
constitutive
164
What happens in high sugar conditions ?
lactate is the major product
homolactic fermentation
intracellular polysaccharides are made
165
What happens in low sugar conditions ?
mixed acid fermentation - heterofermentation
lactate dehydrogenase is inhivited
Intracellular polysacchrides are digested
166
Why is oxygen important in fermentation ?
it is an important regulator
167
What are intracellular polysaccharides ?
produced via glucose 1 phosphate when carbohydrates are in excess
make a glycogen type glucan
they are broken down and used for glycolysis in starvation
168
How do you get greater acid tolerance ?
pre acidification results in greater acid tolerance
169
What are mechanisms of acid adaptation ?
reduced permeability of cell membrane to protons
induction of proton translocating ATPase
induction of alkali production systems
induction of stress proteins
170
What are the purpose of stress proteins ?
protect enzymes and nucleic acids from denaturation
171
What alkali systems are higher in caries free subjects ?
salivary arginine deaminase
| urease
172
What do strep gordonii and strep sanguinis do with urease ?
arginine breaks down to urea by arginase
| urea broken down to carbon dioxide and ammonia bu urease
173
What do strep salivarius and actinomyces do with arginine deaminase ?
arginine broken down citrulline releasing ammonia
| citrulline enters the carbomoyl phosphate cycle releeasing ammonia
174
What are the macromolecules that form the basic structure of the matrix ?
polysaccharides
proteins
nucleic acids
175
What do the macromolecules do ?
form a scaffolding
176
What are the small molecules that are trapped in the matrix ?
nutrients
signalling molecules
trace metals
177
What are exopolysaccharides ?
polymers made of sugar residues that are secreted by a microorganism into the environement
178
What are the 2 types of exopolysaccharides ?
glucans and fructans
179
What are glucans made by ?
glucosyltransferase
180
What are fructans made by ?
fructosyltransferases
181
What are glucans ?
polymer of glucose formed outside the cell using sucrose as the substrate
182
Why is sucrose the substrate for glucan synthesis ?
contains a high energy glycosidic bond
183
What are 2 examples of fructan polymers ?
inulins and levans
184
What are inulins ?
insoluble
contain beta 2,1 bonds
can be cross linked with beta 2,6 bonds
identical to a fructose polymer in vegetables- used as a long term carbohydrate storage rather than starch
185
Who synthesises inulins ?
streptococcus mutans
| steptoccus salivarius
186
What are levans ?
contain beta 2,6 bonds
water soluble
rotate polarised light to the left
187
Who makes levans ?
strep sanguinis
strep salivarius
strep sobrinus
188
What are the 2 examples of glucan polymers ?
mutans and dextrans
189
What is mutan ?
water insoluble
core is alpha 1-3 linked
70% of plaque exopolysaccharide is mutan
some can be mostly alpha 1-3 linked but with some alpah 1-6 links
190
What is dextran ?
```
soluble
almost all alpha 1-6 bonds
rotates polarised light to the right
synthesised by strep salivarius
many variations with alpha 1-3 linked glucose side chains
```
191
How do enzymes form glucans and fructans ?
enzymes make alpha 1,3 and alpha 1.6 links
192
What is special about enzymes that make glucans and fructans ?
they dont need a primer
| can add to preexisting glucan which induces a conformational change
193
How are GTFs made and secreted ?
they are secreted into plaque and are extracellular
| different bacteria secrete different enzymes
194
What do glucans act as ?
receptros for unrelated GTFs
195
What are the other enzymes present in the matrix ?
proteases
| dextrinases
196
What are some examples of GTFs ?
glucansucrase
dextransucrase
mutansucrase
197
What are some examples of FTFs?
fructansucrase
inuslosucrase
levansucrase
198
What does GTF-S cleave ?
water soluble dextran like glucans with an alpha 1-6 backbone
199
What does GTF-I cleave ?
insoluble glucans with alpha 1-3 backbone
200
What does GTF-SI cleave ?
partially soluble alpha 1-3 polymer
201
Which gene codes for GTF-I ?
gtfB
202
Which gene codes for GTF-SI ?
gtfC
203
Which gene codes for GTF-S ?
gtfD
204
How many types of FTFs are there ?
2- one synthesis an inulin like polymer and the other a levan
205
Which bacteria make fructans ?
strep mutans
| strep salivarius
206
What is mutan essential for ?
strep mutans biofilms
207
Which sugar produces a thicker biofilm matrix ?
bacteria grown in glucose produce a thicker matrix and bacteria grown in sucrose thicker matrix
208
What can mutanase potentially do ?
treatment with mutanase can potentially reduce biofilm formation
209
What will knocking out genes like gtfB do ?
reduce biofilm formation - thin biofilms
210
What do biofilms do with microcolonies ?
biofilms form mutan rich colonies- clusters of polysaccharides that have a low pH - acid is localised to certain areas- enamel degradation
211
What happens if you add sucrose to a culture of bacterial cells ?
the bacterial cells will clump as they will use sucrose to make glucans
bacteria have glucan binding proteins on the surface
aggregate
212
How are FTFs related to caries aetiology ?
FTFs are very active in plaque
however the amount of fructan in plaque is low
suggests that fructan is turned over rapidly and then used quickly as a short term energy store
213
How are FTFs thought to contribute to caries ?
they extend the fermentation time on plaque bacteria
214
What do glucans do with mutans streptococci ?
they help them to stick
215
What do soluble dextrans mediate ?
cell aggregation
216
What do insoluble glucans contribute to ?
cell adherence
217
How do other bacteria adhere to strep mutans ?
via glucan ridges
218
Which interactions do glucan bridges lead to ?
metabolite cycling
signalling
competition
219
What are amyloids ?
proteins that form robust fibrils that are hard to degrade
| they run perpendicular to the length of the fibril
220
What are fucntional amyloids ?
have a function in biofilm stabiliisation
melanin formation
innate antiviral immune response
221
Which bacteria produce large amiunts of the extracellualr DNA ?
p.Aureginosa
222
What does treatment with DNase lead to ?
disrupts biofilms temporarily
| can reduce periodontal pathogen colonisation
223
What re the functions of extracellular DNA ?
```
gene transfer
chelates metal ions
biofilm formation
antimicrobial protection
nutrient uptake
biofilm stability
```
224
What is plaque fluid ?
the fluid which fills spaces between bacteria in dental plaque
225
How much is the plaque fluid ?
30% of total plaque volume
226
What is the composition of plaque fluid ?
modified saliva
bacterial metabolites
gingival fluid
227
What is the function of the plaque fluid ?
acts as a buffer between saliva and tooth
maintains calcium, phosphate ans fluoride concentrations
can retain antimicrobials in tooth wash
228
What is periodontitis ?
spectrum of diseases
| affects tooth supporting structures
229
What happens to the junctional epithelium in periodontitis ?
junctional epithelium at base of gingival crevice migrates down root of tooth to form periodontal pocket
230
Migration of the junctional epithelium is a result of ?
direct microbial action but also a result of exaggerated host immune response
231
Changes in the microbiotia lead to ?
changes in the environmental conditions
232
What is the size of deep pockets ?
5mm +
233
What can recession be to the extent of ?
apical third of the tooth
234
What are some manifestations of periodontitis ?
loss of periodontal bone support
mobility
tooth loss
triangular shaped boe defects- intrabony periodontal pocket
235
What are some factors influencing periodontal disease ?
```
tobacco
oral hygeine
medication
type 2 diabetes
stress
systemic
```
236
What is the development of periodontal disease ?
initial microbial homeostasis
change in environment leads to altered microbial population
exaggerated inflammatory response
damage to periodontium
237
What is the cementum colonised by ?
gram positive species like actinomyces and streps- early colonisers
bridging organisms- fusobactrium nucleatum allow microbial organisms to attach
environmental change can lead to co-aggregation and co-adhesion
238
What is microbial dysbiosis ?
conditions changing mean shift in bacteria becoming pathogenic - disease promoting microbiotia
239
Besides microbial dysbiosis what is also important in periodontits ?
hyper inflammatory host response
| individual patient
240
What type of microbiotia promotes periodontitis ?
synergistic
dysbiotic
shape the disease provoking microbiotia
241
Describe the microbial changes in periodontal disease ?
```
disordered collection
aggregation
interspecies interactions
structured heterogenic communties
keystone pathogens
dysbiosis
expression of virulence factors
```
242
How can we determine the subgingival microbiota ?
direct sampling from perio pockets
cultivation of samples
molecular techniques
243
What is the problem with trying to determine the species in subgingival plaque ?
most perio pathogens are anaerobic- when exposed to air cant culture
244
What is checkerboard hybridisation ?
DNA probes made for existing bacterial sequences
DNA taken from host and purified
probes used to identify which species are present
245
What does the intensity of the signal correlate with ?
the amount of organism
| semi quantatative
246
What is the red complex ?
frequently associated with severe periodontal disease
247
What are the 3 organisms of the red complex ?
Porphyromonas.gingivalis
Tannerela.forsytha
Trepnoma.denticola
248
Which organisms are the initial colonisers in periodontal disease ?
Streptococcus- commensal
249
Which organisms are bridging organisms ?
fusobacterium nucleatum
250
What are the characteristics of F. Nucleatum ?
gram negative
proteolytic
anaerobic
long rod shaped
251
What does F . nucleatum do ?
forms co-aggregates
with early colonisers- strep
late colonisers- T. denticola
inavdes host epithelial cells
252
What are the characteristics of red complex bacteria ?
gram negative
proteolytic - destroy proteins in GCF
fastidious anaerobe
253
What is Porphyromonas gingivalis ?
```
short rods
produces black/brown pigments using iron
highly proteolytic
adheres to oral streptococci
keystone
```
254
What are keystone pathogens ?
disproprotionately important role in causing disease
255
What is tannerella forsytha ?
short rods tapered
difficult to grow in monoculture
possess a glycosylated S layer- hide from immune system
256
Why doesnt Kochs postulates apply to periodontitis ?
not culturable
not present in all cases of disease
more than 1 species involved
level rather than presence more important
257
What is the TM7 phlyum ?
frequently detected in subgingival dental plaque
elevated in mild perio
can grow when co-cultured- actinomyces odontlyctus
small genome- reflects dependence on others for growth
258
What are the adhesins of P.gingivalis ?
major fimbriae- adhesion and invasion
| minor fimriae- coaggregation
259
What does the P.gingivalis capsule do ?
allows them to evade host immunity - phagocytosis and complement activation
260
What does the LPS of P.gingivalis do ?
it is potently inflammatory
261
What do P.gingivalis proteases do ?
extracellualr cysteine proteases-
cleave host proteins and collagens
major antigen in infection
262
What are the functions of Extracellular cysteine proteases ?
nutrition
processing
haemogluttinin
adhesion
263
What is AA ?
exception to the ecological plaque hypothesis
aggressive forms of periodontitis
facultative anaerobe
264
What is the function of AA ?
adhesion
impairment of host defence
tissue invasion
bone resorption
265
What is the function of AA adhesins ?
tight adherence by fimbriae and locii
| bind to epithelial cells and enhance receptor medaited endocytosis
266
What are leukotoxins ?
pore forming toxin
| targets immune cells expressing B2-integrin
267
What other AA toxins are there ?
cytolethal distending toxin
268
What is AA JP2 ?
clone associated with aggressive forms of periodontitis
storng leuukotixin activity
W.african adolescents
269
Are fungi eukaryotic or rokaryotic ?
eukaryotic
270
What are ascomycota ?
they can form ascospores
| candida doesnt even though it is part of the ascomycota
271
What are basidiomycota ?
can cause disease - cryptococcus
272
What is the morphology of fungi ?
they grow as branched tubes called hyphae
273
What is the relative size of fungi ?
they are smaller than human cells but bigger than bacteria
274
What is the structure of the fungi cell wall ?
thick rigid cell wall
made of ergesterol rather than cholesterol
divided into 2 layers
275
What is the outer layer of the fungi cell wall like ?
amorphous
glycoproteins
carbohydrates
mannans
276
What is the inner layer of the fungi cell wall like ?
glucans and chitin
277
Why is the fungi cell wall important ?
for adherence and antigenicity
278
What is the carriage rate of candida ?
35-55%
279
What is the most common fungi species in the mouth ?
fungi
280
What are some members of the genus candida ?
```
candida albicans
candida glaborata
candida kruvei
candida tropicalis
candida dublineisis
```
281
Is the genus candida pathogenic ?
most non pathogenic
282
What does it mean if candida are dimorphic ?
they can transition between yeast and hyphal form
283
What is the significance of hyphae ?
they can be disease causing and invade epithelium
284
What does it mean if candida is opportunsitic ?
change in the environment
| change in the gene expression and expression of virulence factors
285
What is the process of candida becoming pathogenic ?
normal commensals
change in environemntal conditions
candida proliferation
pathogenic and disease
286
What are the different morphologies of candida ?
hyphae
budding yeast
pseudohyphae and chlamydosphore
287
What is morphotype switching ?
swich between yeast and hyphal form
288
What is morphotype switching controlled by ?
```
osmotic shock
temperature fluctuations
pH
nutrients
oral bacteria
salivary factors- statherin
```
289
Where can you find candida ?
in mixed species biofilms
| amongst cocci and roda
290
How can bacteria influence candida ?
presence of bacteria can influence how they switch from hyphae to yeast
serum triggeres hyphae profuction
peptidoglycan can trigger hyphal formarion
291
How can Strep Gordonii influence hyphae ?
strep gordonii antigen I/II mediate binding to C.Albicans hyphae
292
How does Strep mutans influence hyphae ?
produces competence stimulating peptide which inhibits C.Albicans hyhae formation
293
What is competence stimulating peptide ?
allow transformation and DNA transfer
294
What type of relationships do oral bacteria have with C.Albicans ?
synergistic or competitive
295
Overall do Oral streptococci benefit or inhibit C.Albicans ?
benefit
296
Does lactobacillus inhibit or benefit oral bacteria ?
inhibit
297
What type of agar is Candida grown on ?
Sobarand dextrose agar
| selects agaisnt bacteria due to low pH
298
Which candida species have true hyphae ?
albicans
| dublineisis
299
Which differential agar is candida grown on ?
CHROMagar
| different species have different morphologies
300
How else can we identify Candida species ?
using different carbohydrates
| diff species have diff nutritional requirements
301
What are the virulence factors of candida ?
```
adherence
morphology
phenotype switching
hydrolytic enzymes
candidalysin
```
302
How does adherence work as a candida virulence factor ?
candida can adhere to epithelium or prostheses and resist saliva flow
produce adhesins
303
Which adhesins do candida produce ?
mannoproteins
fibrils
agglutinin like sequence proteins
hyphal wall protein
304
How does morphology act as a candida virulence factor ?
polymorphic/dimorphic
hyphae formation allows
oral epithelium invasion
evade pahgocytosis
305
Which factors are hyphae produced in response to ?
temperature
carbon dioxide
alkaline pH
306
How does phenotypic switching act as a candida virulence factor ?
change morphology in response to environmental stimuli
| influence antigenicity, adhesion and drug susceptibility
307
Which hydrolytic enzymes do Candida produce ?
Aspartyl proteinases
| phospholipases
308
What do aspartyl proteinases do ?
```
nutrtion
cell morphology siwtching
remove tissue barriers
cleave immune proteins
facilitate adherence
```
309
What do phsopholipases do ?
hydrolyse phospholipids leading to host cell membrnae damage
cell lysis
receptor exposure
310
What is candidalysin >
a lytic peptide that punches holes in epithelial cell
| allows penetration of host tissue
311
What are some manifestations of candidasis ?
denture stomatitis
biofilm formation on surface of dentures
damage arises due to hyphal formation
neutrophil damage
312
What are some local factors that can make patients predisposed to candidasis ?
dentures
inhaled corticosteroid inhalers
reduced salivary formation
rich carb diet
313
What are some systemic factors that can make patients predisposed to candidasis ?
```
medication
diabetes
nutritional deficiency
salivary gland hypofunction
HIV
age extermities
```
314
How can we diagnose oral candidosis ?
appearance- erethrema, white patches
| lab tests- blood tests, oral swab, biopsy and histology
315
What are the primary forms of oral candidosis ?
acute pseudomembreanous candidosis
acute erythemous candidosis
chronic erythemous candidosis
chronic hyperplastic candidosis
316
What is acute pseudmembranous candidosis ?
red mucosa
plaques can be scraped off hard palate and tongue
inhaler use
317
What is acute eryhtemous candidosis >
```
painful red patches
cracking of dorsum
loss of filiform papillae
due to antiobiotic sore mouth
antibiotic use removes bacteria but leads to candida overgrowth
```
318
What is chronic erythemous candidosis ?
denture stomatitis
poorly fitting denture
no hyphae invasion
lack of OH
319
What are the treatment methods for denture stomatitis ?
wash dentures in chlorhexidine/sodium hypochlorite
| leave dentures out as much as possible
320
What is chronic hyperplastic candidosis ?
```
candidal leukoplakia on sides of mouth
heavy smokers
can progress to malignancy
cant be scraped off
candidal hyphae invade epithelial layer
```
321
What are parasites ?
eukaryotic pathogens
322
Which parasites are part of the excavata group ?
leismania
| trichomonas tenax
323
Which parasites are part of the amoebozoa ?
entamoeba gingivalis
324
What is symbiosis ?
association between organisms from different species
325
What is mutualism ?
both partners benefit from interaction and are co-dependent for thriving
326
What is commensalism ?
one partner benefits whereas the other is neither harmed nor receives benefit
327
What is parasitism ?
one partner relies on the host for nutrients and shelter at cost to the host and leads to host damage
328
What are obligate symbionts ?
can only live together in symbiosis
highly adapted to body sites in one host
most parasitic protozoa are obligate symbionts and require a host to complete their life cycle
329
What are facultative pathogens ?
they dont cause disease all the time
330
What are opportunstic pathogens ?
cause pathologies when the host is compromised
331
In which situations can the host be compromised ?
AIDS
immunodeficinecy
malnutrition
chemotherapy
332
Which are the best adapted parasites ?
the ones that are least pathogenic and dont harm their host
333
Which 2 functions must the mucosa mediate ?
protect the individual from insults- microbial, chemical and physical
facilitate exchange
334
Which interactions are required for healthy mucosa ?
microbes interact with epithelial cells and with immune cells
335
What are supraorganisms ?
interactions between human and microbial cells
336
What is a eubiotic microbiotia ?
promotes health
337
What is a dysbiotic microbotia ?
promotes diseases
abnormal, micorbial and taxonomic structures lead to pathologies
even in the absence of pathogens
338
What are pathobionts ?
members of the microbiotia that have the potential to cause damage
339
What does monexenous mean ?
parasite requires a single host for life cycle completion
T.tenax
E.gingivalis
340
What does heteroxenous mean ?
two or more hosts required for completion
1 host is intermediate for development other is definite for sexual development
Leishmania
341
What does promiscuous mean ?
infect broad range of hosts
| T.tenax
342
What are zoonoses ?
human disease caused by animal parasites
| animals are reservoirs for human pathogens
343
Which archaea are in the oral cavity ?
methanobrevibacter
344
Which microbial eukaryotes are present in the oral cavity ?
fungi
| microbial parasites- T.tenx/E.gingivalis
345
What are autochtnous microbiotia >
characteristically found at a particular site
adapted to grow in the cavity
T.tenax and E.gingivalis
346
What are allocthnous micrbiota ?
transiently present due to host compromise
347
What is the route of transmission of Leishmania ?
sand flies
348
What are the 3 main pathobiologies of Leishmania ?
cutaneous leishmania- most common. skin lesions etc
visceral leishmania- fever, weight loss, spleen and liver
mucocutaeneous leishmania- destruction of mucous membranes- requires nose, mouth entry
349
What are 2 common microbial eukaroyotes assocaited with periodontitis ?
T.tenax
| E.gingivalis
350
What are the types of Trichmonas ?
Trichomonas vaginalis
trichomonas gallinae
trichomonas tenax
351
Which eukaroyte is found in the periodontal pcoket ?
t.tenax
352
How is E.gingivalis transmitted ?
foecal oral route
353
What is the relationship between E.gingivalis and periodontits ?
could target homeostatic bacteria
| direct contributor to inflammation
354
What are the 4 types of anti fungal drugs ?
polyenes
azoles
5-flucoytosine
echinocadnins
355
What are polyenes ?
nystain
disrupt fungal cell membranes by interacting eith ergesterol and making the membrane leaky
topical
356
What are azoles ?
miconazole
inhibit ergesterol biosynthesis
topical and systematic
357
What is 5-flucocytosine ?
inhibt DNA and protein synthesis
| systematic
358
What are echinocardins ?
inhibt Beta 1-3 D-glucan aynthesis
intravenous
microfungin
359
What must be considered with anti-fungal medication ?
fungi are slow growing- long course of treatment
| consider other drugs being given
360
What are dental abscesses ?
collection of pus which is walled off by a barrier of inflmmatory reaction
361
How can abscesses develop ?
confined space that bacteria can gain entry to and multiply
362
What is a dentoalveolar abscess ?
pulp death due to bacterial invasion as a result of dental caries
363
What are the routes of infection for a dentoalveolar absecess ?
```
exposed dentine tubules
pulp exposure
bacteremia
root fracture
endodontic infection
```
364
What is an endodontic infection ?
infected pulp
365
What does root canal treatment do ?
clean out the canals and seal them to prevent bacterail access
366
Which chemicals are used to clean out root canals ?
sodium hypochlorite
chlorhexdine
calcium hydroxide
iodine
367
Which species are resistant to root canal treatment ?
enterococcus faecialis
| result in flare ups
368
What is a periodontal abscess ?
differentiated from dentoalveoalr due to a vital pulp
369
How does periodontal abscess develop ?
foreign material in an estabished periodontal pocket
| leads to swelling, eryhtrema and pus at gingival margin
370
Species associated with periodontal abscesses ?
porphyromonas
fusobacterium
actinomyces
haemolytic strep
371
How can we treat a dentoalveoalr abscess ?
local measures- RSI and scaling
irrigation of root canal
antispetics - chlorhexidine mouthwash
extraction
372
Which bacteria are present in dental abscesses ?
usually anaerobes- facultative and strict
373
Which facultative anaerobes can you find in dental abscesses ?
viridans strep
saphy
strep anginosus
374
Which obligate anaerobes can be found in dental abscesses ?
fusobacterium
preveotella
T. denticola
375
What are factors that can affect bacterial populations in abscesses ?
oxygen tension
availability of nutriets like proteins
bacterial interactions
376
Why might you find bacterial popualtions with 3/4 species ?
multiple infection but only certain species survive
| one species infects and paves the way for others
377
What does coaggregation lead to ?
coinvasion of epithelial cells or dentine tubules
378
What is an example of coinvasion into epithelial cells ?
Fusobacterium nucleatum aggreagates with S.cristatus into cells
379
What is an example of coinvasion into dentine tubules ?
P.gingivalis and S.gordonii
380
What are localsied spreads of infection ?
soft tissue abscesses
| cellulities- inflammation spreads through connetive tissue
381
What are extreme spreads of infection >
sinuses
osteomyelitis
adjacent fascial layers
maxillary sinus
382
What is osteomyelitis ?
inflammation of the medullary bone - maxill and mandible
| posterior extension to the cortical bone and the periosteum
383
What are typical isolates found in osteomyelitis ?
obligate anaeroboes
| actinomyces
384
What are treatment optiond for osteomyelitis ?
local debridement
topical antispetic
antibiotics
385
Give some examples of tissue sapces ?
pterygomandibualr space
lateral pharyngeal space
sublingual, submandibular, submental
386
Where can infection from 1-6 go ?
sublingual space
387
Where can infection from 1-3 go ?
submental space
388
Where can infection from 6-8 go ?
buccal space
389
Where can infection from an 8 go ?
```
submasseteric space
pterygomandibular space
lateral pharyngeal space
retropharyngeal space
mediastinum
```
390
How can we treat dental abscesses ?
```
local measures
drain pus
tooth extraction
drain root canals
devride infected periodontal pocket
irrigate operculum
```
391
When do you prescribe antibiotics ?
evidence of spreading infection
| systemic involvement
392
When is there evidence of spreading infection ?
lymph node involvement
swelling
lockjaw
393
When is there evidence of systemic involvement ?
fever
dysphagia
malaise
temp over 38
394
What are warning signs ?
```
raising of tongue
elevated floor of mouth
neck swelling
fever
voice hoarosness
breathing difficulty
```
395
Which antibiotics can be presribed for infections ?
metronidazole
| amoxicillin
396
What is ludwigs angina ?
progression of dentoalveolar infection to tissue spaces
neck swelling
difficulty breathing
to mediastinum
397
Which bacteria are involved in Ludwigs angina ?
prevotella
porporymonas
fusobacterium
anaerobic strep
398
What is pericoronitis ?
superficial infection of operculum
usually lower 8s
local sprea of infection
infection in space between tooth and overlying tissue
399
Which anaerobic bacteria are involved in pericoronitis ?
p.intermdium
anaerboc streptococci
fusobacterium
A.actinomycecomitans
400
How can we manage pericoronitis ?
locla measures
irrigation
extraction
metronidazole if systemic
401
What is cerviofacial actinmycosis ?
opportunsitic infectin caused by Actinomyces- A.isrealii
submandibular swelling/ angle of mandible swelling
thick yellow pus granules - sulphur granules
402
What are the visible granules in C.actinomycosis ?
calcified aggregates of actinomyces filaments
403
What is ANUG ?
poor OH, stress, immunocompromised, smokers
grey pseudomembrane - superficial infection of gingival margin
treponema and prevotella
404
How can we treat ANUG ?>
OHi improvement
remove supra/subgingival plaque dpeosits
scaling
ultrasonic debridment
405
What are seocndary forms of oral candidosis ?
angualr cheilitis
median rhomboid glossitis
chronic mucocutaenous candidosis
406
What causes angualr cheilitis ?
candida
staph
strep
407
What is angualr cheilitis ?
lesions that affect the angles of the mouth
bilatera
soreness
eryhthema
408
What causes denture related angualr cheilitis ?
candida from mouth
409
Where do staphylocci originate in angualr cheilitis ?
anterior part of nose
410
If angualr cheilitis is fungal how do we treat ?
miconazole cream
411
If angualr cheilitis is bacterial how do we treat ?
sodium fusidate
412
What is median rhomboid glossitis ?
shape on dorsum of tongue
atrophy of filiform papillae
smoking and inhaled steroids are cause
413
What is chronic mucocutanous candidosis ?
imapired cellular immunity agaisnt candida
| assocaited with rare congenital disorders
414
What is the relationship between diabetes mellitus and periodontal disease ?
increased periodontal disease with diabetes
| periodontal inflammation may impact glycaemic control
415
What is the relationship between periodontal disease and adverse pregnancy reactions ?
periodontal disease linked with preterm babies
| F.nucleatum and P.gingivalis found in preterm baby amniotic fluid
416
What is the association between cardiovascualr disease and Periodontitis ?
periodontal disease leads to increased inflammation
| atheroscleorsis - P. gingivalis and F.nucleatum maintain inflmmation sites like plaque
417
What does inflammatory periodontal disease lead to ?
cytokine production
| LPS exposure
418
What are the sources of Hallitosis ?
85-90% oral
5-10% nose
3% tonsils
1% other
419
What are oral causes of halitosis ?
```
poor OH
gingivitis and periodontal disease
oral infections
unclean dentures
xerostomia
smoking
dental abscesses
```
420
What are the causes of xerostomia ?
```
mouth breathing
fasting
prolonged talking
stress
salivary gland hypofucntion
```
421
What are some bacterial niches where halitosis can originate ?
posterior dorsum of the tongue
gingival sulcus
pockets
interdental spaces
422
Where else can halitosis originates ?
oral candidosis and oral tumours
423
Why is the tongue a bacterial niche ?
tongue coating has deep fissures
bacteria can adhere and avoid saliva flushing
create anaerobic environment
424
What type of bacteria are prominent with hallitosis ?
gram negative anaerobes
425
What are the most active bacteria in hallitosis ?
P.gingivalis
T.denticola
Tannerella Forsythia
426
What is hallitosis primarily caused by ?
degradation of sulfur containing amino acids derived from proteins from exofoliated epithelial cells, plaque or blood.
427
What are some VSCs ?
hydrogen sulphide
| dmethylsulphide
428
What are some non sulfur compounds that dont cause hallitosis ?
skatole
| cadaramine
429
How can we assess halitosis ?
assess smell of breath, floss and tongue scrapes
use gas chromatography- sensitive to hydrogen sulphide
use BANA - detect periodontal pathogens
430
What arguments are for an association between peridontal disease and halitosis ?
gram negative microorganisms that cause hallitosis are associated with periodontal disease
Halitosis found in those with periodontitis
elevated VSCs in pockets 4mm+
431
What are the arguents against relationship between periodontitis and halltosis ?
periodontally healthy patients have hallitosis
tongue dorsum is main cause
periodontally pockets are partially sealed which prevent gas transfer
tongue cleaning reduces VSCs
432
How can we treat hallitosis ?
mask the malodour
reduced the bacteria mechanically and nutrients
chemical reduction of microbe load- mouthwashes
oxidising agents like chlorine dioxide which degrade VSCs and make them non volatile
433
What is FAA agar ?
cultivation of fastiduous anaerobic microorganism
| selective if you add antiobiotics vancomycin and neomycin
434
Why is there a low level of glucose in FAA agar ?
prevents alcohol and acid production
| also essential growth factor for anaerobes
435
What does reduced transport fluid do ?
provides anaerobic conditions acting as a reducing agent
436
Is FAA selective or indicative ?
indicative
| selective if you add antibiotics
437
What is MSB ?
with tellurite omitted it is selective for S.Mutans and sobrinus
indicative as well
438
What is TYCS ?
tryptone
yeast
cysteine
sucrose
439
What does TYCS do ?
used to differentiate strep mutans from sanguis
| uses high sucrose content to promote glucan formation by S Mutans which will form distinctive colonies
440
Is TYCS selective or indicative ?
both
| seletive for mutans but indicative of mutans and salivarius
441
What is blood agar ?
nutrient rich non selective medium
442
Which bacteria are common around mouth and nose ?
staphylococci- non haemolytic
443
What is alpha haemolysis ?
green colour change as hydrogen peroxide vlrach the heaemoglobin in the blood agar
444
What is beta haemolysis ?
complete lysis of RBCs
| light colour
445
What is gamma haemolysis ?
no haemolysis
446
What is chlorhexidine mouthwash used for ?
reduces potentially pathogenic flora to a minimum to allow re establishment of a healthy balance
used in periodontal patients and pre surgery
447
What does the snyder test detect ?
acidogenic and aciduric bacteria
| potential indicative caries test
448
What does the snyder medium contain ?
2% glucose and bromescol green
449
Which bacteria are detected in the snyder test ?
lactobacilli - found in carious lesions as there is a low pH in carious lesions- selective
450
Which carbohydrate do bacteria ferment in the snyder test ?
glucose into lactic, acetic and formic acid
451
Why does P.gingivalis form dark colonies on blood agar ?
contains porphoryn pigments that contain haem
| prevotella also does this
452
The antibiotics vancomycin and neomycin added to FAA are selective for which bacteria ?
fusobacterium
453
What is the selective agent in MSB agar ?
bacitracin- selective for S.mutans
454
How do you work out CFU/ml ?
number of colonies x dilution factor/ volume of culture plate
455
Why is CFU not the same as number of cells in a culture ?
CFU contains dead cells
| multiple cells can make a CFU
456
What is staph agar ?
selects for staphylococci by having a high NaCl concentration
457
What is McConkey agar ?
selects for enterobacteria like e.coli
| high concentration of bile salts
458
What is candida agar ?
low pH , chloramphericol
| selects for canddia as they tolerate a low pH in the mouth and vagina
459
What is bacictracin ?
an antibiotic
| s.sonrinus and mutans are resistant to it so they can be selected for using it
