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
2
Q
what are allochthonous microbiota
A
transiently present at the site
do not thrive at site but may colonise transiently
3
Q
what are the resident oral microbiota
A
archaea, viruses, fungi, bacteria
4
Q
what are archaea and when are they commonly detected
A
part of prokaryotes, separate from bacteria
detected in periodontal disease
5
Q
what is the most common virus
A
herpes simplex type 1 (HSV-1)
6
Q
how can HIV and Hept B be carried
A
symptomatically
7
Q
what infects bacteria and is the most common virus in the mouth
A
bacteriophage viruses
8
Q
what is the most common fungi in the mouth
A
candida spp
9
Q
what are the most abundant bacteria in the mouth
A
oral streptococci
10
Q
what oral diseases are streptococci responsible for
A
caries, periodontitis, abscesses
11
Q
what haemolysis does oral streptococci cause
A
a-haemolysis
12
Q
what occurs in alpha haemolysis
A
H202 is produced which bleaches the haemoglobin - greenish brown appearance
13
Q
what occurs in beta haemolysis
A
complete clearing of the agar
14
Q
what haemolysis does staphylococcus cause
A
gamma haemolysis
15
Q
what occurs is gamma haemolysis
A
no haemolysis
16
Q
why might there be a greenish tinge on the kiss plate
A
viridan (oral) streptococci
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
18
Q
what bacteria live on the tongue
A
streptococcus (salivarius/mitis group) veillonella actinomyces haemophilus prevotella
19
Q
what bacteria live on the cheek
A
streptococcus (mitis group)
haemophilus
simonsiella
20
Q
what bacteria form supragingival plaque
A
streptococcus
actinomyes
haemphilus
21
Q
what bacteria form subgingival plaque
A
streptococcus actinomyces peptostreptococcus fusobacterium porphyromonas aggregatibacter
22
Q
what bacteria are almost exclusively found in dental plaque
A
streptococcus gordonii
streptococcus sanguinis
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
24
Q
what can cause halitosis
A
anoxic bacteria and the bottom of the mouth
25
what are the microbial habitats in the mouth
lips, cheeks, palate
tongue
teeth
26
what are the characteristics of the lips, cheeks and palate
epithelial cells, continually shed (desquamation)
27
what are the characteristics of the tongue
highly papillated
reservoir for obligate anaerobes (perio.pathogens)
tonsils may also harbour perio pathogens
28
what are the characteristics of teeth
non-shedding
many different surfaces with different microbial populations
covered with acquired enamel pellicle
29
how can the pellicle be removed
by acid
30
what does the pellicle do
covers enamel
| prevents enamel dissolution but can also help bacteria
31
how can you culture the microflora
isolate bacteria
- understand basic physiology/biochem
- link organism to disease
- identify pathogenesis mechanisms
- test antibiotics
32
how can you count the no of different species of bacteria in a clinical sample
culturing and count colonies
33
what is the problem with the technique of culturing bacteria to estimate species
- 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
34
what is culture independent microbial analysis
based on the comparison of DNA sequences from different bacteria
35
what are the 2 ways culture independent microbial analysis works
sequencing of the 16S to work out the species present or sequences the whole DNA to work out gene functions
36
does culture independent microbial analysis require isolation of the organism
no
37
what does PCR do
looks at all bacteria, may find 'new' species
38
what does hybridisation do
quantifies sequences already discovered
39
what does next generation sequencing do and how
identifies all DNA present
| - target (16S rRNA 'microbiome' analysis) OR Full sequence ('metagenomics')
40
does saliva have bacteria in when secreted
no, its sterile when secreted and accumulates bacteria after
41
are there more bacteria attached to epithelial cells or free in saliva
3 times more attached to epithelial cells
42
how are bacteria removed from oral surfaces
```
sloughing of epithelial cells
mechanical debridement
active release (possibly)
```
43
what are the limitation of sampling saliva as a reflection of the overall oral microbiome
- proportions of microbial species are different from plaque/soft tissue biofilms
- care is required when sampling to 'standardise'
44
what microbiome is present in almost everyone
core microbiome of 13 phyla
45
what microbiome is present in some and not others
peripheral microbiome
46
what are clusters of the microbiomes
associated with differences in metabolome
47
what is the main source of the enamel pellicle
saliva
48
what is the difference between saliva and enamel pellicle
they have the same organisms but in different proportions
49
how can salivary compounds help to control plaque accumulation
through:
- aggregating bacteria which are then swallowed
- antimicrobial effects
50
why is saliva important for bacteria
its a key nutrient for them
51
what are the antimicrobial components of saliva
```
cystatins
VEGh
Lactoperoxidase
Lysozyme
Chitinase
Histatins
Defensins
Lactoferrin
Calprotectin
```
52
what are the microbial adhesion components of saliva
```
Gp340
Mucins
PRPs
Amylase
Statherin
S-lgA
```
53
what are the surface protection and maintenance components of saliva
```
mucins
ca2+
phosphate
bicarbonate
PRPs
statherin
```
54
what are some salivary molecules(proteins) that bind to bacteria
MG2 (muc7)
Salivary Agglutinin (gp340), PRPs
Statherin
55
what do the salivary molecules do
bind to bacteria and teeth
agglutinate or inhibit bacteria
promote or inhibit microbial colonisation
56
how have bacteria adapted to survive in the mouth
by sticking to the salivary pellicle
57
when does aggregation/agglutination occur and what does it result in
in the liquid phase
| results in large clumps which adhere poorly and are swallowed
58
how do bacteria adhere
due to proteins in the saliva pellicle and adhesion of bacterial cells to teeth
59
what are immunoglobulins and what do they do
a key feature of the immune system and are present in saliva, they agglutinate bacteria
60
what is the rate of secretory IgA at rest and stimulated flow
33mg/100mL resting flow
| 6mg/100mL stimulated
61
what are the immunoglobulins present in gingival fluid and what do they do
IgG, IgM
| they activate complement/opsonisation
62
what are the three modes of gp340 recognition
aggregation and adherence
aggregation << adherence
aggregation >> adherence
63
what are proline-rich proteins (PRPs)
host receptors which are acidic/basic/glycosylated proteins
64
where are PRPs found
high conc in parotid and submandibular saliva
65
what is the main function of PRPs
calcium phosphate stabilisation
66
what is the c-term for PRPS
a cryptitope- becomes an epitope after change in structure allowing antibodies to bind
67
what does the N-term in PRPs bind
hydroxyapatite
68
what does the C-term in PRPs bind
- Actinomyces spp.
- Streptococcus mutans
- Streptococcus sanguinis
69
what is statherin and its function
host receptor thought to be involved in calcium phosphate stabilisation (with PRPs)
70
what does statherin bind
hydroxyapatite, porphyromonas gingivalis and actinomyocytes spp.
71
when does statehrin not bind bacteria
when in the soluble state- only when its stuck to the surface
72
what are the important antibacterial enzymes in saliva that inhibit bacterial growth
lysozyme
lactoperoxidase
lactoferrin
73
what do lysozymes do
cleaves bacterial cell wall peptidoglycan, can cause non enzymatic cell degradation triggering autolysis when not active
74
what does lactoperoxidase do and what are reaction products
targets peroxide produced bacteria. producing hypothiocyanite plus some cyanosulphurous acid and cyanosulphuric acid
75
what is the acid base eqm in the thiocynate reactions
HOSCN->
76
what effect the does the pK for HOSCN/OSCN- being 5.3 have on the reaction and what does this do to bacteria
more acid favours HOSCN which penetrates bacterial cell envelopes
77
what produces lactoperoxidase
produced by host and bacteria
78
what does lactoferrin do
binds iron and makes it unavailable and some bacteria produce iron-binding proteins called siderophores to complete for host iron
79
which toothpastes contain components of saliva
those targeted to specialist markets
- dry mouth
- pets
- children
80
what dental product contains lysozyme, lactoperoxidase, and lactoferrin
BioXtra toothpaste
81
what dental product contains a dual enzyme system
Biotene toothpaste
82
what are the tooth surfaces available for colonisation
fissure
smooth surfaces
approximal
gingival crevice
83
what are the characteristics of supragingival plaque
present in health
mainly aerobic
fairly easily removed from smooth surfaces
84
what is the nutrient source for supragingival plaque
saliva
85
what are the characteristics of subgingival plaque
periodontal pockets become anaerobic
significant plaque associated with gingivitis/periodontitis
difficult to remove
86
what is the nutrient source for subgingival plaque
gingival crevicular fluid
87
what are the environmental factors affecting dental plaque accumulation
diet/smoking
88
what are the host factors affecting dental plaque accumulation
saliva amount/composition
89
what are the bacterial factors affecting dental plaque accumulation
adhesins that recognise pellicle/congregation
90
how fast does dental plaque start to accumulate and how
within mins of tooth cleaning, faster at day than night.
| pioneer colonisers attach to saliva pellicle
91
what binds to the pellicle
only selective organisms due to receptors on its surface
92
how to bacteria attach to teeth
primary colonising bacteria attach to the pellicle (the conditioning layer)
93
what are the characteristics of the enamel pellicle
1-3 micro metres thick (exceptionally 10)
may permeate the outer layer of enamel
not easily removed
deposit of saliva proteins
94
how does the pellicle form
precipitation of denatured salivary proteins
| selective adsorption of salivary proteins: molecules bind in proportion to their affinity for a substrate
95
where do additional components in the formation of the pellicle originate from
GCF
oral mucosa
microbial cells
96
what is the importance of the pellicle
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
97
what is the importance of the pellicle reducing the mobility of calcium and phosphate ions
diffusion barrier and binding to PRP
| reduces enamel demineralisation (erosion and caries)
98
what is the importance of the pellicle preventing inappropriate crystal growth
Statherin and PRP
| ensuring hydroxyapatite crystal doesn’t dissolve but also that we don’t want more on top
99
what active enzymes does the pellicle contain
```
amylase-receptor for bacteria
lysozyme
peroxidase
glucosyltransferase-produced by bacteria
carbonic anhydrase
```
100
what inhibits s.mutans biofilm formation
mucin MG1
101
what salivary proteins in the pellicle act as receptors for bacteria
```
MG1
amylase
PRP
Statherin
Gp340 (salivary agglutinin)
```
102
what are the 4 main types of human oral streptococci
mitis
anginosus
salivarius
mutans
103
what are mitis group streptococci
most numerous
104
what are anginosus group streptococci
generally commensal but are associated with abscesses
105
what are salivarius group streptococci
generally commensal (some investigated as probiotics)
106
what are mutans group streptococci
associated with dental caries
107
what is antigen I/II
large protein on the surface of many oral streptococci (binds bacteria)
108
what does antigen I/II do
binds to receptors in the pellicle
109
what does antigen I/II mediate
adhesion to salivary agglutinin gp340 in fluid phase or in pellicle
110
what are the multi domain proteins on antigen I/II
```
N-terminal domain
Alanine-rich repeats
Variable region
Proline-rich repeats
Carboxy-terminal domain, containing motif for wall anchoring
```
111
what is actinomyces spp.
gram positive pleimorphic rods
facultative anaerobes
mostly harmless, can cause disease
interact with streptococci and colonise surfaces
112
what are examples of actinomyces spp.
A. naeslundii, A. oris, A. israelii
113
what is veillonella spp.
gram negative cocci
strict anaerobes
feed on lactate streptococci produce .
elevated caries
114
what are examples of veillonella spp.
V.atypica, V.dispar
115
how does dental plaque form
```
adhesion to salivary pellicle
coaggregation -> growth
coadhesion
mature biofilm
dispersal
```
116
what are the characteristics of mature supragingival dental plaque
```
contains 10^11 microbial cells/gram
stratified appearance (gram-positive cocci and short rods at tooth surface; filaments towards outer layers)
```
117
what problems can mature supragingival dental plaque cause
caries follows a shift towards acidogenic/aciduric bacteria
| gingivitis occurs when plaque grows below the gum line
118
what happens when there is failure to control dental plaque
accumulation of plaque at gum margins directly irritates gum tissue, or form calculus which in turn irritates the gums
gingivitis -> periodontitis
119
roughly how many bacteria are in the subgingival crevice
relatively few
| 10^3 to 10^6 CFU/crevice
120
what bacteria are found in the subgingival crevice
```
anaerobic bacteria (found here or on dorsal surface of tongue)
asaccharolytic, proteolytic bacteria, but not the same as in perio disease
```
121
what are the characteristics of fusobacterium nucleatum
gram negative, proteolytic, anaerobic, long rod-shaped cells
Can be present in high numbers in subgingival plaque
122
what does fusobacterium nucleatum coaggregate with
early colonisers (e.g. Streptococcus spp.) and late colonisers (e.g. T.denticola)
123
what is dental calculus
mineralised plaque
124
what is supragingival calculus a deposit from
saliva
125
what is subgingival calculus is a deposit from
serum
126
what is subgingival calculus also known as
serumnal calculus
127
what do rough surfaces of calculus trigger
inflammation -> gingivitis -> periodontitis
128
what are the 2 types of calculus
gross, very gross
129
where does calculus form
preferentially near salivary duct openings
130
what is the epitactic agent in calculus formation
probably a bacterium
131
where do sialoliths form and how
in salivary ducts
Supersaturated calcium phosphate
High pH
132
what is an important bridging organism between early and late colonisers
F.nucleatum
133
what are the types of caries
```
anatomicals sites
primary vs recurrent caries
residual caries
cavitated vs non cavitated
active vs inactive
```
134
what are the anatomical sites of caries
pits and fissures, smooth surfaces (enamel caries or root caries, which starts on exposed cementum/dentin)
135
what is recurrent caries
occurs after treatment/restoration
136
what is residual caries
insufficient treatment
137
what appears in early non cavitated caries
white spot lesion
138
what is early childhood caries
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
139
what are the theories that caries is the result of microbial sugar fermentation
```
worms
chymical theory
parasitic theory
chemico-parasitic theory (most important)
proteolytic theory
proteolysis-chelation theory
```
140
what are the 2 stages of the chemico-parasitic theory (chemical and bacteria)
1- decalcification of enamel
| 2- dissolution of enamel
141
what is the chymical theory
food putrefaction released unidentifued chemical agent which dissolved teeth
142
what is the parasitic or septic theory
filamentous parasite in plaque responsible
143
what is the proteolytic theory
microbes invade enamel lamellae and initiate caries by proteolysis
144
what is the proteolysis-chelation theory
microbial proteolytic destruction of the organic matrix
145
what is the ecological plaque hypothesis
disease as an imbalance
146
what is the specific plaque hypothesis
caries aetiology
147
what are the bacteria commonly associated with caries
mutans streptococci
lactobacillus spp.
actinomyocenes spp.
bifidobacterium spp. and related
148
what are the virulence factors for bacteria linked to caries
```
acid production from sugars
acid tolerance
intracellular storage granules
extracellular polysaccharides
adhesins
```
149
what are the mutans streptococci found in humans
s. mutans
s. sobrinus
streptococci is broken down into 4 groups, one is the mutans streptococci
150
wha are the characteristics of the mutans streptococci
gram-positive, catalase-negative, saccharolytic, facultive anaerobes
151
which mutans streptococci is generally more acidogenic and adherent
s.sobrinus (less frequently carried)
152
what are non-mutans low-pH streptococci
a typical member of other species
153
why can koch's first postulate not be applied in the case of bacteria associated with dental caries
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
154
in a longitudinal study which cultured bacteria with early childhood caries, what were the bacteria most associated
s.mutans
scardovia wiggsiae
anaerobic, pleemorphic gram positive bacilli
155
what do sacchorytic bateria produce
acetic and lactic acid
156
what are the virulence factors of mutans streptococci
adhesins
acid production
acid resistance
157
what are the adhesins important in mutans streptococci important for colonisation
antigen I/II protein
glucosyltranferases (GTFs)
glucan binding proteins
158
what is involved in acid producing virulence factors in mutans streptococci
F-ATPase
159
what is involved in acid resistance (acidurity) in mutans streptococci
dna repair proteins
| protective membrane proteins
160
what are the health promoting factors of non-mutans streptococci
adhesins of commensal bacteria - antigen I/II protein (streptococci)
alkali production
161
how can carbohydrates be utilised by caries associated bacteria
acid production
| high energy bond in sucrose harnessed to produce polysaccharide
162
why is sucrose more cariogenic than glucose
only sucrose leads to the production of glucans therefore is more cariogenic
163
how do sugars get into bacterial cells e.g polysaccharides
transporters
polysaccharides can be digested
mon/disaccharides can be imported
164
why does xylitol import into cells lead to a futile cycle
its gets phosphorylated then dephosphorylated which can drain strep of energy and inhibit it
165
how is sugar uptake into cells regulated in high sugar
lactate is the major product and glycolysis is accelerated
| IPS are made
166
how is sugar uptake into cells regulated in low sugar
mixed acid fermentation- lactate hydrogenase is inhibited
| IPS are degraded
167
why is O2 an important regulator if fermentation
it inhibits pyruvate formate lyase
168
what is the importance of intracellular polysaccharides in bacterial cells
storage
glycogen-type glucan
broken down and used for glycolysis in starvation
(produced via glucose-1-phosphate when carbs in excess)
169
what is the importance of food webs in bacterial cells
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
170
what does preacidification result in
greater acid tolerance, particularly in bacteria that are relatively acid sensitive
171
what are the mechanisms of acid adaptation
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
172
what are the 2 ways we can make alkali in the mouth
arginine deaminase pathway
| urease pathway
173
when is salivary deaminase and urease higher
in caries free subjects
174
whats involved in the plaque biofilm matrix
macromolecules and smaller molecules that may be trapped within the matrix
175
what are the macromolecules in the plaque biofilm matrix
polysaccharides
proteins
nucleic acids
176
what are the small molecules in the plaque biofilm matrix
nutrients
metals
signalling molecules
water channels
177
what are the 2 basic exopolysaccharides and what are they made by
glucans- glucosyltransferase
| fructans- fructosyltransferase
178
what are expopolysaccharides made from
sucrose outside the cell
179
what are expopolysaccharides responsible for on sucrose containing agar
crystalline colony appearance
180
why is sucrose the substrate for expopolysaccharides
high energy in the glycosidic bond between the disaccharide
181
what can the energy released from glycosidic bonds be used for
to synthesis polymers
182
what do anomeric carbons give rise to
isomers
183
what are the types of fructan polymers
inulins (beta-2,1 bond type)- 96%
| levans (beta-2,6 bond type)- 5%
184
what are fructan polymers (inulins) synthesised by
strep.mutans and some strains of strep.salivarius
185
what are fructan polymers (levans) made by
strep. sanguinis
strep. salivarius
actinomycesnaeslundii
some strep sobrinus
186
what are fructan polymers (levans) not made by
strep mutans
187
what are the two basic types of glucan polymers
```
water insoluble (mutan)- alpha 1,3 linked
water soluble (dextran)- alpha 1,6 linked
```
188
what is water insoluble (mutan) formed from
strep sobrinus
189
what are water soluble (dextran) formed from
strep salivarius
190
what is the variation of dextran formed from
strep sobrinus
191
how can dextran be identified
rotates polarised light to the right
192
what is the structure of the variant of dextran
numerous side chains of a-1,3 linked glucose (short) , every 15 backbone residues
193
what are similar dextran-like polymers produced by
other strains e.g. strep mutans
194
what is the structure of similar dextran-like polymers
side chains twice as numerous but shorter
| comprises of single glucose residue linked alpha-1.3 to the branch residue
195
what can form polymers comprising of both both α-1,3 and α-1,6 bonds
GTF enzyme of S. gordonii
effect on the local enviro
do not need primer
196
how does exogenous glucan accelerate the reaction of polymer formation of both α-1,3 and α-1,6 bonds
- binds to a site remote from catalytic site
| - conformational change
197
how do GTFs affect the environment
extracellular- secreted into complex enviro
198
what can glucans act on for unrelated GTFs
acceptors
| semi-processive reaction
199
what is in the glucan soup
GTF
200
what are other enzymes except those in the glucan soup
proteases -may modify GTF
| dextranases
201
what do GTFs and FTFs do
cleave sucrose or add glucose/fructose to an existing chain
202
what do GTF-S produce
produce water soluble dextran-like glucans with an α-1,6 linked backbone
203
what do GTF-I produce
an insoluble α-1,3 backbone polymer
204
what do GTF-SI produce
a partially soluble α-1,3 backbone polymer
205
what is the primer independent GTF called
GTFSi
206
where are GTF-I, GFT-SI & GFT-S are enzymes found
s.mutans
207
what is gtfA
- sucrose phosphorylase (transfers glucose from sucrose to a phosphate)
- bears little resemblance structurally to the GTFs
208
what two types of FTFs have been found
one that synthesises an insulin like polymer and one a levan
209
what bacteria is FTF absent from
strep.sobrinus
210
what is essential for s.mutans biofilms
mutan
211
how do biofilms grown in glucose and sucrose vary
glucose- thin with little or no matrix
sucrose- thicker (mutanase reduced biofilm)
Knockout mutants lacking gtfBor gtfC form thin biofilms
212
what pH are mutan-rich microcolonies at
low pH
213
what are glucan binding proteins (GBP)
proteins that bind glucans and mediate aggregation
214
what are the types of GBP
some are bacterial surface proteins and some are secreted
215
how do GBPs differ
```
in size, strength of bond formed with glucan
function i.e. adhesion/aggregation
```
216
what do GBPA deficient mutans produce
flatter but more even biofilms
217
what do GBPC deficient mutans of strep mutans produce
thicker biofilms than the parent strain
218
what is the caries aetiology of FTFs
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
the total amount of fructan in plaque low, what does this suggest
fructans are overturned rapidly
220
how is fructan degradation achieved
by the enzyme fructanase
221
what is the caries aetiolgy of GTFs
mutan streps cannot adhere well to teeth and glucans help them stick
222
how are soluble dextrans involved in GTFs interactions
mediate cell to cell interaction (aggregation)
223
how are insoluble dextrans involved in GTF interactions
mediate cell-surface interactions (adherence)
224
what do glucan bridges allow for
other bacteria to adhere to s.mutans
225
what interspecies interactions will cell-cell adhesion enhance in plaque biofilms
Metabolite cycling
Competition
Signalling
226
what are functional amyloids
proteins in the biofilm matrix that form robust fibrils with with β-strands running perpendicular to the length of the fibril.
227
what is the role of functional amyloids
biofilm stabilisation
melanin formation
initiation of innate antiviral immune response
228
what produces large amounts of extracellular DNA and how can the biofilm be distrupted
P.aeruginosa
DNase I
229
what are the functions of extracellular DNA
bacteria exchange genes (transformation)
| source of nutrients
230
where is eDNA present
subgingival plaque
231
how DNase enzyme be used NucB
inhibits plaque formation
| reduced colonisation by periodontal pathogens
232
what is plaque fluid
fluid which fills the spaces between bacteria in dental plaque
233
what is the composition of plaque fluid
saliva (modified)
bacterial metabolites/waste
material leeched from the tooth
gingival fluid
234
what are the functions of plaque fluid
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
what are dental abscesses
Collection of pus, which is walled off by a barrier of inflammatory reaction (contained)
236
what is the pathogenesis of abscesses
Abscesses can develop in any confined space to which bacteria can gain access and multiply
237
what is the difference between a periodontal abscess and dentoalveolar
the tooth of periodontal abscess has a vital pulp
238
what are the signs and symptoms of periodontal abscesses
swelling and erythema
| pus likely to discharge from gingival margin
239
what it the microbiology of periodontal abscesses
Associated with
Porphyromonas species
Prevotella species
Fusobacterium species
haemolytic streptococci
Actinomyces species and spirochaetes
240
how can periodontal abscesses be managed
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
what are the routes of infection for dental alveolar abscesses and periapical abscesses
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
where may you get swelling in a dentoalveolar abscess / periapical abscess
swelling in the sulcus adjacent to the tooth affected
243
what is the most common endodontic infection
Infected pulp
244
what does root canal treatment involve
cleaning out canals and sealing to prevent bacterial access - disinfect and sterilise the pulp
245
what is commonly used to kill residual bacteria in endodontic infections
Sodium hypochlorite, chlorhexidine, calcium hydroxide and iodine
246
what are the microbial species in abscess formation
facultative and strict anaerobes
247
what are the facultative anaerobes in abscess formation
Oral (viridans) streptococci
Streptococcus anginosus group
Staphylococcus spp.
248
what are the obligate anaerobes in abscess formation
- Fusobacterium species
- Prevotella species
- Porphyromonas
- Tannerella forsythia
- Treponema denticola
- Clostridium
- Actinomyces
249
what are the Factors affecting bacterial population in abscesses
Oxygen tension (selects for anaerobes)
Availability of nutrients (selects for proteolytic bacteria)
Bacterial interactions (selects for mutual co-operation)
250
what are the POSSIBLE EXPLANATIONS FOR SELECTING A BACTERIAL POPULATION OF 3-4
SPECIES:
Multiple infection but only certain species survive
One species infects and prepares the way for appropriate others
251
what can coaggregation between different bacteria lead to
Coinvasion of epithelial cells
| Coinvasion of dentine tubules
252
how does infection spread in periodontal abscesses (locally)
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
how can infection spread further in PA
```
Into adjacent fascial spaces
If progresses into deeper layers (osteomyelitis)
Into maxillary sinus
Indirect spread:
- Lymphatic routes
- Haematogenous routes
```
254
what is osteomyelitis
Inflammation of the medullary bone within the maxilla or mandible with posterior extension into the adjacent cortical bone and overlying periosteum
255
when is osteomyelitis more common and what species are involved
if reduced vascularity
When infection present typical isolates include obligate anaerobes and Actinomyces species
256
how is Osteomyelitis treated
based on local debridement, topical antiseptic on exposed areas, antibiotics as required
257
when is there a risk of sepsis associated with PA
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
how does infection spread from a lower molar tooth infection
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
how does infection spread from a upper molar tooth infection
infections can track up the maxillary sinuses
260
what tissue spaces can dental infections spread into
* Pterygomandibular space
* Lateral pharyngeal space
* Retropharyngeal space
* Submasseteric space
* Buccal space
* Vestibular space
* Sublingual space
* Submandibular space
* Submental space
261
where do abscesses from mandibular premolars spread and why
into the sublingual space because the root apices lie below the mylohyoid line
262
where do abscesses from mandibular molars spread
to submandibular space
263
where do abscesses from mandibular wisdom teeth spread
infection in the lateral pharyngeal space
264
where do abscesses from maxillary teeth spread
into the buccal space
265
what are steps in the management of dental abscesses
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
what are local measures taken to treat dental abscesses
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
when is antibiotic prescription indicated
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
what are the warning signs for abscesses
* 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
what occurs in ludwigs agina
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
what are the species involved in the microbiology of ludwigs angina
* Prevotella species
* Porphyromonas species
* Fusobacterium species
* Anaerobic streptococci
271
what is periocoronitis
superficial infection of operculum
infection in the space between the tooth and overlying soft tissue
pain and swelling
associated with wisdom teeth issue
272
what bacteria is pericoronitis associated with
- P. intermedia
- Anaerobic streptococci
- Fusobacterium species- greater abundance in patients with clinical symptoms
- T. forsythia
- A. actinomycemcomitans
273
how can pericoronitis be managed
Local measures – mouthwash etc
Irrigation
(extraction- not local)
274
what bacteria does metronidazole target
anaerobes
275
what antibiotic is prescribed for pericoronitis if there is spreading infection and systemic involvement
metronidazole
276
what causes cervicofacial actinomycosis
Opportunistic infection caused by members of the Actinomyces genus
- A. israelii (90% of cases)
- A. bovis
- A. naeslundii
277
what symptoms does cervicofacial actinomycosis present superficially
submandibular swelling
| swelling at angle of mandible
278
what is likely to precipitate infection in cervicofacial actinomycosis and why
Tooth extraction or trauma with bacterial species reaching deeper tissues
279
as swelling develops in cervicofacial actinomycosis what can occur
multiple sinuses develop which are painful and slow growing
associated with thick yellow pus ('sulphur granules')
pus can persistently spread through tissue space
280
what can cause acute necrotising ulcerative gingivitis (ANUG)
Poor oral hygiene, poor plaque control
Often immunocompromised
Poor diet and poor general health, stress
Smokers
281
what are the signs of (ANUG)
Ulceration of the gingivae
Necrotising inflammation of the papillae between the teeth
Pain and halitosis
Superficial infection of the gingival margins
282
what bacteria is ANUG associated with
fuso-spirochaetal bacteria
others:
- Treponema species
- Prevotella intermedia
283
what are the local treatment measures of ANUG
• OHI and improvement in oral hygiene
• Removal of supra and subgingival deposits, scaling / ultrasonic debridement
Risk factor identification
284
if there is spreading infection associated with ANUG, what drug should be prescribed
metronidazole
285
what are some fungal soft tissue infections (secondary forms of oral candidosis)
Angular cheilitis (fungal and bacteria)
Median Rhomboid Glossitis
Chronic Mucocutaneous Candidosis
286
what is angular cheilitis
inflammation of one or both corners of the mouth.
287
what causes angular cheilitis
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
how can angular cheilitis be treated in patients with dentures
antifungal cream e.g. miconazole
289
what is the reservoir for infection for angular cheilitis in
1. denture patients
2. non denture patients
1. likely caused by candida so reservoir is the mouth
| 2. likely staphylococcus so anterior part of the nose
290
how can angular cheilitis be treated in patients where its likely bacterial in origin
Sodium fusidate (fusidic acid) ointment
291
what is Median Rhomboid Glossitis
Chronic infection (asymptomatic) Symmetrical-shaped area in the midline of the dorsum of the tongue
292
what causes Median Rhomboid Glossitis
Atrophy of the filiform papillae
293
what is Median Rhomboid Glossitis infection strongly associated with
smoking and Use of inhaled steroids
294
what is Chronic Mucocutaneous Candidosis
immune disorder of T cells, it is characterized by chronic infections with Candida that are limited to mucosal surfaces, skin, and nails
295
what is Chronic Mucocutaneous Candidosis associated with and what is a predisposing factor
rare congenital disorders
impaired cellular immunity against Candida
296
what are the Treatment of Oral Candidosis
Rectify any local factors e.g unclean/ poor fitted denture, steroid inhaler
If locals fail - Antifungal medication (topical and systemic)
297
what do polyenes (nystatin, amphotericin) do
disrupt fungal cell membrane (topical)
298
what do azoles (fluconazole, clotrimazole, miconazole, ketocanazole, itraconazole) do
inhibits ergosterol biosynthesis (interfere with lanosterol demethylase)
topical or systemic
299
what is periodontology
area of dentistry that deals with pd (supporting structures of the teeth as well as the diseases that affect them )
300
what is the periodontnum
the supporting tissues of the teeth: gingivae, alveolar bone, cementum and pdl
301
what is pd
Spectrum of conditions that are polymicrobial in origin (can be irreversible/ reversible) affecting the supporting structures of the teeth
302
what are the types of PD
reversible- gingivitis
irreversible- periodontitis
necrotising (NUG, NUP, NUS(stomatitis))
periodotal abscesses
303
what are 3 division of pd in the new 2017 classification
periodontal health, gingival diseases and conditions
periodontitis
other conditions affecting the periodontium
304
what is the disease process for PD
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
how do pd pockets form
bone has shrunk the back- tooth is not supported
microorganisms in the crevice, inflammatory response
306
what is looked at in a clinical examination of PD
clinical attachment loss
| interproximal loss
307
what are the details of periodontal pocket chart
```
deep pockets >5mm around the teeth
recession
loss of periodontal bone support
mobility
tooth loss
```
308
once calculus is on the root surface what occurs
bacteria have a surface which they can colonise
inflammatory cells recruited
attachment loss and formation of pockets
309
the development of pd is caused by a change in environmental conditions, what does this cause
it disrupts microbial homeostasis causing an altered microbial population- this causes an exaggerated inflammatory response damaging the supporting tissues of the teeth
310
what are the environmental changes that occur in the periodontal pockets during the disease process
```
flow of gingival crevicular fluid
nutrition
temperature
pH
oxygen and oxidation
aerobic to anaerobic
```
311
what is the function of the GCF
- 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
what are the problems that GCF can cause
it also provides proteins and glycoproteins which can serve as substrates for bacterial metabolism- the conditions in the niche favour bacteria for disease
313
how does the GCF act as a substrate for bacteria
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
how does the temp change in pd pockets during the disease process
increases due to inflammation
315
how does the pH change in pd pockets during the disease process
proteolysis leads to pH going from neutral to slightly alkali
316
how does the oxygen and oxidation potential change in pd pockets during the disease process
anaerobic enviro selecting for anaerobic bacteria
317
what is the subgingival biofilm colonised by
gram negative bacteria
- early colonisers (streptococcus and actinomyocenes)
- bridging organisms like fusobacterium
- periodontal pathogens attach by coaggregation /coadhesion
318
what are the 3 component that contribute to the disease process in PD
microbial dysbiosis
individual patient
hyper-inflammatory host response
319
what is the concept of microbial dysbiosis
change in biofilm which promotes changes towards the disease.
320
what is the polymicrobial synergy and dysbiosis (PSD) model of PD
synergistic interactions among contributing bacteria, give rise to a dysbiotic community able to flourish
321
how can you determine the subgingival microflora
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
what is checkboard hybridisation used for and how is it done
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
what are the microbial changes that occur in subgingival plaque
tooth surface colonised by streptococcus
fusobacterium nucleatum act as bridging organisms and stick to streptococcal cells
red complex organisms bind
324
what is fusobacterium nucleatum
gram negative, proteolytic, anaerobic, long rod-shaped cells
coaggregate with early colonisers (strep) and late colonisers (t.denticola)
325
what are the characteristics of ALL red complex bacteria
fastidious gram-negative, proteolytic anaerobes
the can adhere to strep with no bridging organisms
326
what are the 3 red complex bacteria
Porphyromonas gingivalis
Tannerella forsythia (Bacteroides forsythus)
Treponema denticola
327
what are the characteristics of Porphyromonas gingivalis
- Short rods.
- Produces black and brown porphyrin (haem- containing) pigments.
- Highly proteolytic.
- Adheres to certain oral streptococci.
328
what are the characteristics of Tannerella forsythia
- 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
what are the characteristics of Treponema denticola, which PD is it a major cause of
- 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
why doesn't kochs postulates apply to PD
more than one organism
| organism may not be isolated in pure culture
331
what is TM7 phylum
large group of bacterial species frequently detected in subgingival dental plaque (Elevated in mild periodontitis )
332
what is used to track TM7
Axenic culture obtained using Fluorescence in situ hybridization (FISH)
333
what happens when TM7 is co cultured
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
what is the genome of TM7
Small genome (<1 Mbp), may reflect a dependence on other bacteria for growth
335
what are the virulence factors of P. gingivalis (gram negative)
- 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
what are the P. gingivalis proteases
Cysteine proteases :
- Arg-Xaa specific protease (RGP)
-Lys-Xaa specific protease (KGP)
These are major antigens in infections.
337
what is the role of P. gingivalis proteases
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
what is Aggregatibacter actinomyctemcomitans (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
what are the virulence factors of A.a
```
Adhesins/invasins- fimbriae and gene products
LPS
Leukotoxin- targets immune cells
Cytolethal distending toxin
Proteases (trypsin-like)
```
340
what isActinomycetemcomitans JP2
one particular clone- Derived from West Africa
strongly haemolytic
strong leukotoxin activity.
Rapid progressive form of PD in adolescence
341
how is pd linked to systemic disease
• 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
how are subgingival bacteria and proinflammatory molecules able to enter circulatory system and potentially affect sites and systems elsewhere in the body
• Periodontium is highly vascular
343
what are the diseases Linked with PD
```
cvs- atherosclerosis
respiratory system- pneumonia
endocrine- diabetes
muscular- rheumatoid arthritis
GI- cancers, oral, pancreatic, colonic
reproductive system- adverse pregnancy outcomes
```
344
how is pd linked to adverse pregnancy outcomes
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
how is pd Associated with diabetes mellitus
- 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
how is pd Associated with cvs
- Increased infectious/inflammatory burden and maybe cardiovascular events
- Association with atherosclerosis
- P. gingivalis, F. nucleatum and A. actinomycetemcomitans detected within atheromatous plaques
347
how is pd Associated with rheumatoid arthritis
Both conditions show some similarities in that they are associated with a similar host-mediated chronic inflammatory response
348
what are fungi, outline their structure
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
what are the 2 phylums of fungi
Basidiomycota and Ascomycota
350
what are basidomycetes (refer to spore production) and what is an ex of one that can cause disease in humans
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
what are ascomycetes (refer to spore production) and what is an example
form ascospores in sacs called asci INTERNALLY during sexual reproduction
Example: Candida
352
what are fungal cells
```
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
what is the structure of fungal cells
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
why is the cell wall in fungal cells important
in terms of antigenicity and adherence to host cells
355
what is the most common fungi in the mouth
candida species specifically candida albicans
356
which candida species is more resistant to antifungals
candida globrata
357
what is the genus of candida
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
what form of candida albicans are most oral infections associated with
hyphal form of candida albicans
359
outline the candida species associated with oral infections
c. albicans
c. glabrata
c. krusei
c. tropicalis
c. guilliermondii
c. dubliniensis
360
why is the genus candida referred to as an 'opportunistic infection'
infection is dependant on some underlying predisposition ('disease of diseased')
361
outline how a candida infection can become pathogenic
harmless commensals
change in environmental or systemic conditions
conditions favour candida proliferation
pathogenic disease causing infection
362
outline candida morphology
can exist as yeast form or hyphae
| pseudohypahae
363
what occurs when candida transitions from yeast to hyphae
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
what is the morphotype switching under the control of
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
how is candida affected when in a mixed species biofilm
hyphae long structures associated with rods
serum trigger hyphal production
oral bacteria trigger hyphae due to peptidoglycan
366
which protein Promotes C. albicans Hyphae Formation
S. gordonii Antigen I/II
367
what protein Inhibits C. albicans Hyphae Formation
S. mutans Competence Stimulating Peptide
368
overall, do oral streptococci appear to benefit Candida spp
yes
369
how do Lactobacillus spp. affect Candida spp.
they tend to inhibit Candida spp.
370
how can candida be grown and identified
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
how can multiple candida species from the same infection be determined
CHROMagar Candida
Biochemical tests are also useful, especially carbohydrate utilisation 9API strips)
molecular methods ( Sequencing of ribosomal RNA, PCR )
372
how does adherence acts as a virulence factor in c.albicans
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
how does morphology acts as a virulence factor in c.albicans
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
how does Phenotypic switching acts as a virulence factor in c.albicans
Ability to rapidly change cell morphology
Responsive to environmental stimuli
```
Associated with altered gene expression affecting
Antigenicity
Adhesion
Phagocyte resistance
Drug susceptibility
```
375
how does Aspartyl Proteinases acts as a virulence factor in c.albicans
- 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
how do Phospolipases Proteinases acts as a virulence factor in c.albicans
Hydrolyse phospholipids (membranes)
Damage host cells - Host cell membrane damage, promoting cell lysis or exposure of receptors to facilitate adherence
377
what is candidalysin
Virulence Factor protein that break up into peptides
it helps candida albicans penetrate epithelial cells
378
what is the host response to oropharyngeal candidiasis
c.albicans hyphal penetration and secretion of proteolytic enzymes, the host responds with Th1 and Th17 adaptive immune response
379
what is the host response to denture stomatitis
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
what is the host response to hematogenously disseminated candidiasis
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
what is the host response to gastro-intestinal candidiasis
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
what is the host response to intra-abdominal candidiasis
onset of infection triggered by a c.albicans invasion of abdominal organs resulting in the formation of abscesses
383
what is the host response to vulvovaginal candidiassis
c.albicans hyphal transition and invasion of vaginal mucosa, triggering innate immune response. damage propagated by host response , predominantly neutrophils
384
what oral candidosis
oral thrush
Not a single infection
Could be a marker for an underlying systemic condition e.g, immune level testing, diabetes
385
what local factors may contribute to oral candidosis
Denture wearing
Inhaled corticosteroids e.g. asthmatic patients
Reduced salivary flow
Carbohydrate-rich diet
386
what medications are associated with oral candidosis and who is more likely to be affected ?
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
serious systemic disease associated with reduced immunity are associated with oral candidosis?
Blood dyscrasias o Leukaemia
Malignancy
HIV
388
how is Oral Candidosis diagnosed
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
what are the 4 primary forms of Oral Candidosis?
Acute pseudomembranous candidosis
Acute erythematous Candidosis
Chronic erythematous Candidosis
Chronic hyperplastic Candidosis
390
which oral candidosis is the most common (produces pseudomembrnae – the white layer) and which one is the most common associated with dentures
Acute pseudomembranous candidosis
Chronic erythematous Candidosis (dentures)
391
what is Acute pseudomembranous Candidosis and what is it associated with
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
what is Acute erythematous Candidosis and what is it associated with
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
what is Chronic erythematous Candidosis and what is it associated with
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
how can denture stomatitis be managed
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
what is Chronic hyperplastic Candidosis and what is it associated with
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
in which candida infection can the white patches be scraped off
Acute pseudomembranous Candidosis
397
how can Chronic hyperplastic Candidosis (Candidal leukoplakia) be diagnosed
need biopsy to diagnose
| Hyphae invading epithelial cells
398
what are Other Secondary Forms of Oral Candidosis
Angular Cheilitis
Median Rhomboid Glossitis
Chronic Mucocutaneous Candidosis
399
what is Angular Cheilitis caused by and what is used as a treatment
infection with:
- Candida
- Streptococcus or Staphylococcus
Treatment (Consider the cause)
- Miconazole cream
- Sodium fusidate ointment
400
what is Median Rhomboid Glossitis and what is it associated with
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
what is Chronic Mucocutaneous Candidosis and what is it associated with
affects Skin, mucous membranes and nails
Associated with rare congenital disorders
Key predisposing factor impaired cellular immunity against Candida
402
what are antifungal mediations
Topical antifungal medications
-Suspension, gel, lozenges
Systemic antifungal medications
-Tablets
403
what is the main source of halitosis and what % is it
oral
| 85-90%
404
what are the sources of halitosis (give the %)
oral 85-90%
5-10% nose (sinusitis)
3% tonsils (putrefaction)
1% other- bronchial and lung infections, kidney failure, carcinomas, stomach, protein rich diet
405
what are the oral sources of halitosis
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
what are the Intra-oral spaces where halitosis originates
Bacterial niches
- Posterior tongue dorsum
- Periodontal tissue sites
- E.g. ANUG, ANUP, abscesses
Oral Candidosis
Oral tumours
407
why are tongue dorsum thought to be major source of halitosis
Tongue coating
Numerous depression
Deep fissures
Anaerobic environment in tongue fissures - thickened tongue coating
408
what are the Gram negative anaerobes in halitosis
Treponema denticola
Porphyromonas gingivalis
Bacteriodes forsythus (Tannerella forsythia)
Fusobacterium
Veillonella
Haemophilus
409
what are the Gram positive anaerobes in halitosis
Stomatococcus mucilaginous
410
what are the most active bacteria in halitosis
Porphyromonas gingivalis
Treponema denticola
Tannerella forsythia
These are the ones correlated with PD
411
what is Halitosis primarily caused by
microbial degradation of both sulphur-containing and non-sulphur containing amino acids(cystine) derived from proteins
412
what is the source of proteins degraded in halitosis
exfoliated human epithelial cells and white blood cell debris, or present in plaque, saliva, blood and tongue coatings
413
which substances produce volatile sulphur compounds (VSC)
- Bacteriodes melaninogenicus
- T. denticola
- P. gingivalis
- P. intermedia
- Bacteriodes loescheii
- B. forsythus (T. forsythia)
- Centipeda periodontii
- Eikenella corrodens
- Fusobacterium peridonticum
414
what are the VSC associated with halitosis
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
how are sulphur compounds released
due to proteolysis of amino acids
416
how is skatole produced
Tryptophan metabolism
417
how is Cadaverine produced
Protein breakdown
418
how is Putrescine produced
Protein breakdown
419
how is Isovaleric acid produced
Metabolite
420
how can halitosis be diagnosed by Nasal appraisal
Self-assessment
- Wrist licking
- Smelling expectorated saliva
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Subjective organoleptic analysis by confidant (SOAC) smelling another person’s breath
Assess the smell of
o Breath
o Floss
o Tongue scrape
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Gas chromatography
421
how can halitosis be diagnosed by Instrumental sniffers
Very sensitive to H2S
Low sensitivity to mercaptan
Benzoyl Arginine Naphthylamide (BANA)
422
how is Benzoyl Arginine Naphthylamide (BANA) used to detect halitosis
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
what are the arguments for Relationship between halitosis and periodontal disease
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
what are the arguments against Relationship between halitosis and periodontal disease
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
what is halitosis caused by
microorganisms that complete metabolic degradation of sulphur-containing amino acids
426
what can Treatment strategies for halitosis include
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
what Improvements in oral hygiene can be used to manage halitosis and what are the issues with this
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
what are other way halitosis can be managed
Avoidance of dry mouth
Gum chewing- larger saliva volumes
Oxidation of VSCs (volatile sulphur compounds
Mouthrinses
429
what is the Systematic review conclusion of the efficacy of mouthrinses in reducing halitosis
Mouthrinses containing antibacterial agents (chlorhexidine and cetylpyridinium chloride) or those containing chlorine dioxide and zinc can reduce halitosis to some extent
430
what is the Critical summary assessment. of the efficacy of mouthrinses in reducing halitosis
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
what do parasites act as
eukaryotic pathogens
| pathogenic symbionts, infectious agents- includes viruses, bacteria and eukaryotes
432
what are Parasitic protozoa
pathogenic microbial eukaryotes – protists
433
what are exavata
Euglenozoa: Leishmania spp. Parabasalia: Trichomonas tenax
434
what are Amoebozoa
Archamoebae: Entamoeba gingivalis
435
what are Amoebozoa
Archamoebae: Entamoeba gingivalis
436
what is symbiosis
the association between organisms from different species – different types of association can be defined, briefly there are three major categories: Mutualism, Commensalism, Parasitism
437
what is mutualism
both partners benefit from the interaction and they are co-dependent for thriving
438
what is Parasitism
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
what is Parasitism
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
what are facultative pathogens
they don’t cause disease all the time – blurring the distinction between parasites ,commensals and mutualists (Some parasites)
441
what are facultative pathogens
they don’t cause disease all the time – blurring the distinction between parasites ,commensals and mutualists (Some parasites)
442
what are Opportunistic pathogens
those that cause pathologies when the host is compromised – e.g. due to immunodeficiency (as in AIDS, due to malnutrition or chemotherapies)
443
how do parasites interact with their host
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
what are the 2 key contradictory functions Mucosal surfaces must mediate simultaneously
Protect the individual from microbial, chemical and physical insults
Facilitate exchanges between outside and inside our body
445
where are the members of the mucosal microbiota are intimately associated with both of these functions
respiratory, digestive and urogenital tracts
446
what is eubiosis
Microbiota taxonomic and functional structures that lead to homeostasis/health
447
what is dysbiosis
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
what are pathobionts
members of the microbiota that have the potential to cause damage/pathologies
Some mucosal microbial parasites could be considered as pathobionts
449
what are monoxenous parasites
Parasite requiring a single host for completing their life cycle
450
what are heteroxenous parasites
Parasite requiring two or more hosts for completing their life cycle
451
what are promiscuous parasites
they are capable of infecting a broad range of hosts (e.g. Trichomonas tenax, Leishmanis spp.) -common in cats and dogs
452
what are zoonoses
Human diseases caused by animal parasites, the animal hosts represent reservoirs for the human pathogens
453
what are the resident oral microbiota
Archaea- Methanobrevibacter oralis
Bacteria-responsible for oral diseases
Microbialeukaryotes
- fungi- Protozoa-Microbial parasites
- protists- Protozoa-Microbial parasites
Viruses
454
what are Autochthonous microbiota
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
what are Two common oral • Autochthonous microbial eukaryotes associated with periodontitis
Trichomonastenax
Entamoeba gingivalis
456
what are Allochthonous microbiota
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
what is the most common Allochthonous microbiota
Leishmania species: most commonly (i) cutaneous can become (ii) systemic or (iii) mucocutaneous (including the oral-skin interface)
458
what is the Leishmania species a member of
Euglenozoa, Excavata
Not possible to have Leishmania without sand flies
459
where are the most common places for infection with the Leishmania species
on the arm, face etc. not in the oral cavity e.g. mucutaneous Leishmaiasis
460
what are the effects of Trichomonas vaginalis
Infect Humans
Genitourinary tract
Associated with HIV, bacterial vaginosis, Pelvic Inflammatory Disease and low birth weight
461
what are the effects of Trichomonas gallinae
Infect birds
Common among pigeons/columbiform
Can causes epidemics and high mortality rates
462
what are the effects of Trichomonas tenax
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
what is Trichomonas vaginalis pathobiology
Interactions between bacteria and viruses affects mucosal surface
Damage and facilitates HIV
464
what are the Different way the Trichomonas vaginalis parasite contributes
Inflammation
Dysbiosis - profiling of microbiota changes, becomes more complex
Epithelial cells -damage them
This combination contributes to more fragile susceptible mucosa to infections
465
What is the molecular basis of Trichomonas spp. mucosal life style and pathobiology?
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
what are the characteristics of Trichomonas spp.
Cell surface proteins involved in parasite-microbiota/host
| interactions, (ii) metabolic enzymes and (iii) enzymes targeting other microbes
467
which enzymes does Trichomonas spp. candidate peptidoglycan (PG) target and what is the role of the enzymes
NlpC/P60, GH19 and GH25
These enzyme play a key role in trigminomas bacteria interactions
468
what is Entamoeba a member of
Amoabozoa
469
what is The Entamoeba gingivalis (and E. histolytica) transmission like
Classical oral transmission that uses a cyst form
470
what is the Entamoeba histolytica pathobiology
Most asymptomatic parasite is able to get through mucus layer and modify microbiota composition
471
How could Trichomonas tenax and Entamoeba gingivalis contribute to periodontitis?
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
how can Trichomonas tenax and Entameoba gingivalis Contribute to dysbiosis
they feed on bacteria and change the inflammatory tone of the tissue
excessive diversity
pathobiont expansion
loss of mutualists
reduced diversity
473
what else can Trichomonas tenax and Entamoeba gingivalis contribute to
Likely contribute directly and indirectly to the inflammation characteristic of periodontitis
Contribute at boosting local neutrophil population
