week 5 Flashcards
1
Q
What colour is gram positive and why?
A
Purple because there is lots of peptidoglycan in the cell wall
2
Q
What is an example of a gram positive bacteria?
A
Lipotechnoic acid
3
Q
What colour is gram negative and why?
A
Pink, thin layer of peptidoglycan
4
Q
What is an example of gram negative?
A
Lipopolysaccharide
5
Q
What is saccharolytic metabolism?
A
resides in supragingivial plaque and sugars promote acid production.
6
Q
What does it mean that saccharolytic metabolism forms fructans
A
its food storage for biofilm bacteria and it aids in bacterial attachment.
7
Q
What is Asaccharolytic metabolism?
A
breaks down proteins into amino acids and nitrogen in periodontal pockets
8
Q
What are obligate anaerobes?
A
O2 is toxic because they lack the enzymes to break it down. Eg P Gingivalis
9
Q
What are facultative anaerobes
A
grow in or without oxygen, supragingival species such as streptococcus mutans
10
Q
what are microaerophilic bacterias?
A
require little O2 for growth
11
Q
Capnophilic bacteria
A
requires CO2
12
Q
Is the development of the oral biofilm in toddlers influenced by the eruption of teeth?
A
Yes
13
Q
At what age does the oral microbiome become complex?
A
3 yrs
14
Q
Does the oral microbiome continue to develop in complexity over time?
A
Yes
15
Q
Is an edentulous patient’s oral microbiome as complex as that of a fully dentate adult?
A
No
16
Q
List three main components of the oral microbiome:
A
Shedding surfaces, non-shedding surfaces, secretions
17
Q
Can plaque biofilms form on shedding surfaces?
A
Yes
18
Q
Are shedding surfaces self-cleansing?
A
Yes
19
Q
What are aerobic shedding surfaces?
A
gum tissues, soft and hard palate
20
Q
What are anaerobic shedding surfaces?
A
Interproximal areas, subgingival areas, back of tongue
21
Q
Give 4 examples of non-shedding surfaces in the oral cavity
A
Hard surfaces such as restorations, dentures, ortho, implants, and teeth. supra and subgingival
22
Q
What is the source of saliva?
A
salivary glands
23
Q
What is the source of gingival crevicular fluid (GCF)
A
blood plasma
24
Q
What is the habitat provision for saliva and GCF?
A
Moist, aqueous, nutrient-rich environment beneficial for biofilms. Flushing action eliminates planktonic bacteria and poorly adhered cells
25
What are the nutrients in saliva?
Water, carbs, protein, vitamin
26
What are the nutrients in GCF
protein, Haem containing nutrients, erythrocytes
27
What are the antibacterial properties of saliva?
flushing action, antibodies, mucins, agglutinins
28
What are the antibacterial properties of GCF
Cytokines, antibodies, Compliment neutrophils
29
What are the habitat and growth requirements of bacteria
oxygen, pH, temp, nutrients, food webs, carb metabolism, protein metabolism
30
What is the normal pH of the gingival sulcus in health?
6.75-7.25
31
what change in pH occurs in gingival plaque during periodontal disease?
increase
32
What effect does an increase in pH in gingival sulcus have on the growth of periodontal pathogens?
improves it
33
what is the normal temp of gingival sulcus in health?
36.8 degrees
34
What change in temperature occurs in active periodontal pockets?
increase
35
What effect does an increase in temp have on enzyme activity and gene expression (eg protease production by P. gingivalis
increase
36
Why are bacterial adhesion to the pellicle and coaggregation important bacterial interactions in biofilms?
oral bacteria can get washed away quickly by saliva
37
What cell surface features facilitate surface binding by early colonising bacteria?
pili, flagella, receptors
38
What is a foodweb?
interdependent relationships between different bacteria occur when the metabolic byproducts of one bacteria can be used for another species
39
Give an example of a food web
streptococci produce bacteria which is used by veillonella spp
40
List the three innate host defenses present in the periodontal tissues.
saliva - lubricates, digests, nutrition, antibodies
Junctional and Sulcular Epithelial Barriers - attachment to tooth, antimicrobial defense, GCF flow
41
Does the junctional epithelium have an active role in host defense
yes
42
List the elements of the non-specific plaque hypothesis
all plaque is equally pathogenic, it is the bulk that causes the disease
43
what is the supporting evidence for the NSPT
plaque growth resulted in gingival inflammation within 10-20 days, after reinstituting oral hygiene it resolved back to health
44
What were the deficiencies or limitations of the NSPT?
not all patients progressed from gingivitis to periodontitis
45
of those patients with gingivitis who progressed to periodontitis, what happened
there was a spectrum of disease progression, some patients had rapid attachment loss with little plaque, not all sites within the patient behaved the same way
46
During the 1950's and 1960's, the progression of periodontitis was thought to be slow, linear and continuous.
Given contemporary knowledge, are the linear pathogenesis and continuous disease progression models valid?
No
47
The advent of which two microbiological techniques greatly expanded our knowledge of periodontal
microbiology?
postulates for "putative periodontopathogens" and DNA-DNA hybridisation
48
in health, there is little
bacterial load, and saccharolytic plaque.
49
In health, there is predominantly
aerobic gram positive organisms
50
In health, the species are
cocci
51
In gingivitis the species are
gram positive rods
52
In periodontitis there is high
bacterial load and subgingival plaque, asaccharolytic bacteria, motile rods
53
In periodontitis the species are
gram negative rods
54
What is the Specific Plaque Theory?
A few specific pathogens within the biofilm that causes periodontisis. The remaining microbiome doesn't influence the disease process
55
If the SPT explained the aetiology of periodontitis, how does this knowledge shift the approach to periodontal
treatment?
continued use of antibiotics resulted in antibiotic resistance and sensitivity. putative periodontopathogens returned after sessation of antibiotic use
56
The aetiology of which two periodontal conditions are explained by the SPT? List the applicable bacteria.
periodontitis - opportunistic endogenous bacteria
gingivitis - treporema denticola and fusiforms
57
List the main limitations of the SPT.
disease is caused by resident microflora, the bacteria associated with active periodontitis are found in low proportions of the dental plaque in health and gingivitis states
58
List four significant contributions Haffajee and Socransky made to periodontal microbiology.
identified purative periodontal pathogen
used DNA to study complex microbial ecosystems
associated red complex bacteria with periodontal disease parameters such as probing depth
59
List the five postulates or conditions a bacterium must achieve before being described as a "putative
periodontopathogen"
association, elimination, host response, animal studies, virulence factors
60
describe "association" as a requirement for something being putative periodontopathogen
in higher numbers in disease
61
describe "elimination" as a requirement for something being putative periodontopathogen
reduced numbers in health
62
describe "Host Response" as a requirement for something being putative periodontopathogen
higher antibody levels against the putative periodontal pathogen in periodontitis patients
63
describe "animal studies" as a requirement for something being putative periodontopathogen
the putative pathogen isolated from periodontal pockets must cause periodontitis in animals
64
describe "virulence factors" as a requirement for something being putative periodontopathogen
the putative pathogen must demonstrate virulence factors that cause periodontal disease
65
Name the three bacteria that make up the red complex
P gingivalis, T forsythia, T Denticola
66
What is the cell morphology of P gingivalis, T Forsythia, T Denticola
Red Complex
67
What are the characteristics of P Gingivalis
non-motile, gram-negative, requires haemin for growth
68
What are the characteristics of T Forsythia
gram negative, difficult to culture, grows on blood agarplate
69
what are the characteristics of T Denticola
gram negative, difficult to culture only possible through DNA analysis
70
what are the virulence factors of P Gingivalis
Trypsin-like proteases, gingipains, invade epithelial cells
71
What are the virulence factors of T Forsythia
trypsin like proteases, invades epithelial cells
72
What are the virulence factors for T Denticola
adherence, motility, trypsin, invades epithelial cells
73
Summarise the conclusions from Socransky, Haffajee, Goodson, Lindhe's (1984) Random burst theory paper.
Sites enter a state of disease activity for short periods of time followed by longer periods of remission and no activity
74
Does periodontitis progress on a site-level or at a patient (or dentition) level?
site level
75
What is a biofilm?
an arranged community of microorganisms that are 3-D, located in an aqueous environment, embedded in a protective slime/sticky matrix called extracellular polymeric substance
76
Are conditions the same throughout a biofilm?
no
77
Are conditions the same throughout a biofilm?
no
78
Does this property of biofilms increase or decrease the biodiversity of plaque?
increase
79
What is "extracellular polymeric substance" (EPS)?
consists or organic and inorganic material derived from bacteria, saliva, and GCF
80
List three main functions of EPS.
1. helps bacteria stay together
2. protects against phagocytosis
3. provides a source of energy and nutrients to bacteria
81
What is the purpose of "fluid channels" in a biofilm"?
allows movement of nutrients and O2 for bacteria and removes waste products and enzymes. communicates with other genetic materials and increases metabolic diversity.
82
what are the main stages of biofilm formation
1. formation of pellicle
2. passive transport of salivary microorganisms
3. reversible attachment of bacteria to pellicle
4. irreversible attachment of early colonisers
5. secondary colonisers bind, maturation, detachment
83
describe pellicle formation
adsorption of salivary proteins onto a tooth surface. electrostatic attachment with hydroxyapatite onto enamel
84
describe irreversible attachment of early colonisers
adhesins to pellicle receptors (streptococci) attach to glycoproteins by their fimbriae/pilli
85
describe secondary colonisers bind
co-aggregation - receptor binding driven by bacterial cells, aerobic bacyeria consume oxygen, inflammation
86
describe maturation of biofilm formation
stable, mature plaque, diverse ecology, motiles covered by EPS
87
what is the purpose of detachment in biofilm formation?
allows colonization elsewhere
88
which bacteria are early colonising species?
blue, purple, green, yellow
89
which bacteria are orange
secondary colonisers
90
which bacteria are red
late/tertiary colonisers
91
Does saliva influence the binding of the biofilm layers and constituents?
yes
92
Do biofilms protect resident bacteria from antimicrobial agents?
yes
93
Can biofilms become resistant to antimicrobials through horizontal gene transfer?
yes
94
Give two examples of bacterial communication throughout a biofilm.
when an antibody dies, they lyse and eDNA is released and easily transferred to another bacterium. Horizontal gene transfer, free uptake of DNA
95
Can bacteria actively suppress neighbouring species?
yes
96
where does supragingival plaque form?
interproximal surfaces, enamel pits and fissures
97
where does subgingival plaque form?
epithelium, tooth and root surfaces in a periodontal pocket
98
what are the oxygen conditions of supragingival plaque
aerobic and anaerobic
99
what are the oxygen conditions of subgingival plaque?
anaerobic
100
what is the nutrient source for supragingival plaque?
Saliva
101
what is the nutrient source for subgingival plaque?
GFC
102
what are the typical bacteria properties of supragingival plaque
sacchorolytic gram positive
103
what are the typical bacterial properties of subgingival plaque
motile, gram negative
104
what is an example of a supragingival bacteria
streptococcus mutans
105
what is an example of a subgingival bacteria
spirochaetes
106
How does calculus form?
by mineralising plaque, precipitation of phosphate salts within
107
what are the differences in colour between supra and subgingival plaque?
sub is darker because it is stained with haemin from blood
108
Bacteria are required to trigger and propagate the host response in periodontitis. True or False
True
109
Is the host response responsible for most of the tissue damage in periodontitis?
Yes
110
What innate host defenses are present in the periodontium?
Resident flora, secretions, epithelial barriers, inflammation, compliment proteins
111
What triggers gingival inflammation?
plaque bacteria and plaque antigens
112
What is the speed of inflammatory response to plaque bacteria?
rapid
113
What is the speed of immune response to plaque antigens?
slow
114
what is involved in inflammatory response to plaque bacteria?
epithelial barrier, compliment cascade, cytokines, adhesion molecules
115
what is involved in immune response to plaque antigens?
Helper Ts, cytotoxics, B cells, antibodies, macrophages, compliment cascade
116
which response to plaque bacteria triggers chronic inflammation?
immune response
117
what happens when inflammatory response and immune response happen together?
chronic stimulation because plaque is not removed by host responses
118
Why are neutrophils the "first line of defense" against the plaque front?
phagocytose foreign bacteria, create extracellular nets, degranulate lysosomal enzymes
119
How do activated cytotoxic T cells cause tissue damage in periodontitis?
compliment system forming membrane attack complex, stimulates B cells, creates pores that disrupts bacterial cell wall integrity and cell lysis occurs.
120
How does antibody release by plasma cells cause tissue destruction in
periodontitis?
targets soluble antigens in extracellular material leading to tissue destruction
121
What is bystander damage?
host destruction of its own tissue. Involves alveolar reabsorption, connective tissue breakdown and apoptosis of epithelial cells
122
How does periodontal tissue destruction of collagen occur?
14-21 days of plaque formation, anoxia in capillaries causing RBC to escape breaking down collagen
123
How does periodontal tissue destruction of bone occur?
extensive number of T cells and plasma cells
124
For "Initial lesion" of biofilm induced gingivitis how many days has the plaque been there and what it is the state of the gingiva?
2-4 days, healthy
125
For "Early Lesion" of biofilm induced gingivitis how many days has the plaque been there and what it is the state of the gingiva and what immune cell type is working?
1 week, supragingival plaque, gram positive microbes, some destroyed collagen fibres, T cells and macrophages activated
126
For "Established Lesion"/chronic of biofilm induced gingivitis how many days has the plaque been there and what it is the state of the gingiva and what immune cell type is working?
1-2 weeks, pocket formation, chronic gingivitis, damaged fibroblasts and collagen fibres, plasma cells derived from B
127
For "Advanced Lesion" of biofilm induced gingivitis how many days has the plaque been there and what it is the state of the gingiva and what immune cell type is working?
over 2 weeks, periodontitis, coronal detachment, damaged fibroblasts collagen fibres and alveolar bone reabsorption, plasma cells
128
Do all established lesions progress to advanced lesions?
No
129
The red complex bacteria are implicated in periodontal tissue breakdown,
however the host response to these bacteria (i.e. inflammation and immune
responses) is responsible for how much of the tissue destruction in
periodontitis?
80%
130
what are the main concepts of symbiosis
a mutual relationship of oral flora and host. nutrient competition, barrier function, protection
131
what are the main concepts of dysbiosis
the shift from gram positive to gram negative, altered pH or diet, smoking causing a pathogen enriched microflora
132
summarize ecological plaque theory
both the quantity and quality of bacteria can trigger the dease condition and the host risk factors contribute to the severity and extent of the resulting gingivitis and periodontitis
133
summarize keystone pathogen theory
host defenses can't effectively clear the pathogen
134
summarize the IMPEDE Model
no RX - dysbiosis and tissue damage can be exacerbated
