Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

ODDR > Biochemistry/ Microbiology > Flashcards

Biochemistry/ Microbiology Flashcards

1
Q

what is the origin of the connective tissue of the PDL?

A

mesendermal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what cells are found in the connective tissues in the PDL?

A
  • fibroblasts
  • cementoblasts
  • osteoblasts.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is the extracellular matrix made up of in the connective tissue of the PDL?

A
  • fibres

- ground substance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what do elastic fibres in the PDL mature from oxytalan to?

A
  • elaunin.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

why do elastin fibres in the PDL never mature to elastin?

A

so they are always embryonic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what type of fibres make up the majority of the PDL?

A

Collagen Type 1.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is the base structure of type 1 collagen?

A
  • triple helical of 3 polypeptide alph chains.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the main amino acid in the polypeptide chain of type 1 collagen?

A

Glycine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are the 3 amino acids that make up type 1 collagen?

A
  • Glycine
  • Proline
  • Hydroproline.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what amino acid in type 1 collagen forms hydrogen bonds between the 3 chains?

A

Glycine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what type of bond is formed between the 3 polypeptide bonds in type 1 collagen to give it the helical structure?

A

hydrogen bonds.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what % of the collagen in the PDL is Type 1?

A

80%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what % of the collagen in the PDL is type 3?

A

20%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

where in the body can type 1 collagen be found?

A
  • Bone
  • Dentine
  • Tendon
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what can cause % of type 3 collagen variations between people?

A

age.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what has to be expressed for type 3 collagen to be expressed?

A

Type 1 collagen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

why is hydroxyproline important in the structure of type 1 collagen?

A

for the stability of the collagen triple helix

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what does hydroxyproline need to work in the body?

A

Vitamin C.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are the effects of not having enough vitamin C?

A

Skirvy - without vit C hydroxyproline will not be stable causing a breakdown of collagen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is the enzyme that hydrolates proline?

A

prolyl hydroxylase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is prolyl hydroxylase dependent on?

A

vitamin C.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

at what terminal is collagen assembled?

A

Carboxyl.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

why once the helix of collagen is formed does the carboxyl terminal chains come together in globular form?

A

to prevent the 3 helix chain from unfolding.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is Pro-collagen?

A

central helical domain with 2 non-helical globular extentions at the amino and carboxyl terminals.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

how does pro-collagen become tropocollagen?

A

once pro-collagen is secreted into the extracellular matrix, propeptidase cleaves off the globular extensions becoming tropocollagen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

how are fibrils in the PDL stabilised?

A

via covalent cross links formed from modified lysine and hydroxylysine residues.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what does Lysyl oxidase convert R groups of lysine and hydroxysine to?

A

Allysine and Hydroxyallysine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what is Lysyl oxidase dependent on?

A

copper.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what are non-reducible cross links? and are they found in the PDL?

A

they are stable non-reducible cross-links formed spontaneously with age. This doesn’t happen in the PDL.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what does it mean for the PDL when they do not form non-reducible cross-links? and why dont they have any?

A

forever young.

dont have any due to the fast turnover rate of protein within the PDL tissue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Is procollage intracellular or extracellular?

A

intracellular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Is tropocollage intracellular or extracellular?

A

extracellular.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what is the function of collagenase?

A

break down collagen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what is collagenase produced by?

A
  • fibroblasts
  • polymorphonuclepcytes
  • macrophages
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what is collagenase inhibited by?

A

TIMP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How does collagenase break down collagen?

A

Cleaves collagen to 3/4 and 1/4 fragments.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what enzyme breaks down collagen further after collagenase?

A

gelatinase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

why does collagen have a very high turnover rate?

A

because it never matures.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what makes up ground substance?

A
  • non-collagenous proteins (NCPs)
  • Hyaluronic acid (GAG)
  • Protoglycans (PGs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what are glycoproteins?

A
  • protein plus -O- and -N- linked sugars.

- protease resistant.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what is the basic structure of a protecglycans?

A

protein core and GAGs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

In the PDL what are the 2 small leucine-rick proteoglycans?

A
  • Decorin

- Biglycan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what are the main functions of PGs and GAGs in connective tissue?

A
  • collagen fibril orientation/ diameter.
  • control of mineralisation
  • generation of the eruptive force.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

How do PGs and GAGs control collagen fibril orientation/ diameter?

A
  • PGs bind to collagen fibrils enabling them to control fibrillogenesis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

If there is a higher GAG concentration in the PDL what can we assume about the collagen fibrils?

A

smaller.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

If there is a higher decorin concentration in the PDL what can we assume about the collagen fibrils?

A

larger diameter fibrils.

47
Q

If there is a higher CS rich PGs concentration in the PDL what can we assume about the collagen fibrils?

A

small fibres.

48
Q

why with age does the diameter of fibrils in the PDL increase?

A

due to GAG% decreasing and the decorin sulphate % increasing with age.

49
Q

How do PGs and GAGs control mineralisation in connective tissue?

A
  • GAGS can inhibit deposition of hydroxyapatite crystals in soft connective tissue - this prevents the PDL mineralising and becoming hard like bone.
50
Q

How do PGs and GAGs control the generation of the eruptive force?

A

GAGs attract water, swell up and push the tooth upwards.

51
Q

during disease of the PDL does GAG content increase or decrease?

A

increases,

52
Q

during disease of the PDL does dermatan sulphate content increase or decrease?

A

decreases

53
Q

during disease of the PDL does chondroitin sulphate content increase or decrease? and why?

A

increases - promotes the decrease in collagen size.

54
Q

what are the disease related changes in the PDL?

A
  • total sulphate GAG content increase
  • % decorin sulphate decreases and decorin decreases.
  • % CS increases and versican increases.
  • collagen content decreases
  • Gelatinase activity increases.
55
Q

what is a pathogen?

A

a microb capable of causing host damage/ disease

56
Q

what is a opportunistic pathogen?

A

an organism that is a member of the resident microbiota or normally inhabiting the external environment that causes infection under certain circumstances.

57
Q

what is a symbiont?

A

member of the resident microbiota that confers benefit to the host

58
Q

what is a pathobiont?

A

member of the resident microbiota that causes disease when loss of the normal balance between the host and resident microbiota occurs.

59
Q

what is pathognicity?

A

capacity of a microbe to cause damage in a host

60
Q

what is virulence?

A

relative capacity of an organism to cause damage in a host ‘degree of pathogenicity’

61
Q

what is a virulence determinant/factor?

A

component of pathogen that damages the host / allows pathogen to cause disease.

62
Q

what type of microbes are found in a healthy PDL?

A

Gram +ve facultative anaerobes predominate

63
Q

what type of microbes are found in gingivitis?

A

increase in obligately anaerobic population.

64
Q

what type of microbes are found in periodontitis?

A

Gram -ve anaerobes and spirochaetes predominate.

65
Q

what happens to the PDL during periodontal pocket formation?

A
  • increase inflammation
  • increase bleeding
  • increase temp
  • increase pH
  • decrease in O2
66
Q

what is the ecological plaque hypothesis?

A
  • increase plaque causes increase inflammation.
  • this then causes high GCF flow, bleeding, raises pH , raised temp and low O2.
  • This them encourages disease associated communities.
67
Q

why are their difficulties in defining aetiology for perio disease?

A
  • differences in definition of disease.
  • episodic / cyclic nature of the disease.
  • sampling and detection techniques .
68
Q

How much of the microbiota is non-culturable?

A

40%

69
Q

what are the 3 bacteria found in the complex cluster?

A
  • P. Gingivalis
  • T. Forsythia
  • T. Denticola.
70
Q

what are 2 tests that can be used in clinic to test for microbes?

A
  • parocheck

- my periopath.

71
Q

what causes diavetes-mellitus associated gingivitis?

A

increase proportions of capnocytophage.

72
Q

what innate defences are in GCF?

A
  • IgG
  • IgA
  • IgM
  • complement
  • lymphocytes
  • Polymorphes (neutrophils)
  • Defensins.
73
Q

how does epithelial defences produce an innate defence?

A

production of cylokine and chemokine following bacterial insult.

74
Q

how do neutrophils produce an innate defence?

A

regulate proportion of bacteria present/

75
Q

what is tissue damage in the PDL dependent on?

A

the survival of organisms via attachment to either other organisms or surfaces in the pocket/crevis.

76
Q

what is meant by accessory pathogens?

A

cells that cannot cause damage themselves just aid pathogens that can.

77
Q

what is the pathway for microbial pathogenesis?

A
  • entry
  • attachement
  • multiplication + consolidation
  • avoiding host defences.
  • tissue damage
  • release and spread.
78
Q

How can indirect damage be done to the PDL from bacteria?

A

host responses causing damage to host tissue due to being triggered by bacteria.

79
Q

what is the purpose of adhesin?

A

enable binding of bacteria

80
Q

what is the purpose of invasin?

A

enable invasion of bacteria

81
Q

what is the purpose of impedin?

A

enables avoidance of bacteria.

82
Q

what is the purpose of aggressin?

A

enables bacteria to cause direct damage to host.

83
Q

what is the purpose of modulin?

A

enalbles the bacteria to induce indirect damage by pertubing regulation of host defenses.

84
Q

How does the capsule around bacteria benefit it?

A
  • k-antigens
  • adhesion
  • resistance to phagocytosis and complement.
85
Q

how does the pili/fibrils around bacterial benefit it?

A
  • adhesion
  • gene transfer
  • receptors.
86
Q

how do extra-cellular products in the bacteria benefit it?

A
  • nutrition
  • host damage
  • interaction with host cells.
87
Q

how does the flagellum benefit the bacteria?

A
  • mobility
  • H antigens
  • inter-action with host cells.
88
Q

how can the peptidoglycan cell wall around bacteria benfit it?

A

induction of cytokines.

89
Q

what is part of the cell wall in bacteria that is only found in Gram +? and how does it help the bacteria in the host?

A

Lipoteichoic acids

  • adhesion
  • induction of cytokines
  • resistance to host defences.
90
Q

what is part of the cell wall in bacteria that is only found in Gram -? and how does it help the bacteria in the host?

A

Lipopolysaccharides.

  • o- antigen
  • induction of cytokines and inflammatory response
  • resistance to host defences
  • adhesion
  • mediation of bone resorption
  • killing of macrophages.
91
Q

where are toll-like receptors found?

A

on immune cells.

92
Q

what is the function of toll-like receptors?

A

detect microbial components and start cellular response.

93
Q

what is the purpose of protease?

A

break down host proteins.

94
Q

what are extracellular virulence factors?

A
  • enzymes (proteases, collagenase, fibrinolysine, IgA/IgG protease)
  • Leukotoxins
  • Cytotoxins
95
Q

what is the purpose of collagenase?

A

distruction og PDL

96
Q

what is the purpose of fibrinolydin/ hyaluronidase/ heparinase?

A

breakdwon of host proteins.

97
Q

what is the purpose of IgA and IgG protease?

A

breakdown of immunoglobulins.

98
Q

what is the purpose of leukotoxins?

A

kill polymorphs

99
Q

what is the purpose of cytotoxins?

A

specific toxins and metabolic products will cause host cell death.

100
Q

what is the main idea of the keystone pathogen concept?

A

that some organisms may have a disproportionate influence on the pathogenicity of the community.

101
Q

what are examples of keystone pathogens?

A

Porphyromonas gingivalis.

Aggregatibacter actinomycetemcomitans

102
Q

why is Porphyromonas gingivalis a keystone pathogen?

A
  • it manipulates host defences.
  • produces extracellular vesicles.
  • invasion of epithelial cells and local chemokine paralysis.
  • inhibits e-selectin up-regulation - affecting neutrophil migration and adhesion.
  • inhibition of complement activation
  • direct cytotoxicity
103
Q

what are the virulence factors for Porphyromonas gingivalis?

A
  • gingipain
  • PPAD
  • LPS
  • capsule
  • haemagglutinin
  • Fimbriae
  • extracellular vesicles.
104
Q

what type of pathogen is Porphyromonas gingivalis?

A

Gram - ve obligate anaerobe

105
Q

what type of pathogen is Aggregatibacter actinomycetemcomitans?

A

Gram -ve coccobaculus anaerobic

106
Q

what are the virulence factors for Aggregatibacter actinomycetemcomitans?

A
  • produces potent leukotoxins for neutrophils and over produced by serotype B.
  • cytolethal distending toxin - lymphocytes
  • Adhesins - epithelial cells, biofilm formation, coaggnegation
  • LPS - stimulates bone resorption
  • cell-associated material - induces bone resorption
  • collagenase
  • invasive-gingival connective tissue
107
Q

what are gingipains unique to?

A

p. gingivalis

108
Q

what are leukotoxins unique to?

A

Aggregatibacter actinomycetemcomitans

109
Q

what are the main function of gingipain?

A
  • cleave host defence peptides, complement, Ig.
  • cleave cell receptors eg CD14
  • degrade cytokines, chemokines, plasma protease inhibitors
  • Activation of protease activated receptors.
  • Activation of matrix metallo-proteinsases (MMPs) and degradation of tissue inhibitors of MMPs (TIMPS)
  • immune evasion
  • nutrition
110
Q

what is the function of stem cells in the PDL?

A

To differentiate into other cells - they aid in keeping the PDL young.

111
Q

is procollagen a procollagen peptidase?

A

no.

112
Q

what is ankylosis?

A

where the PDL is mineralised, meaning that the tooth is stuck in place and cannot be removed. XLa of a tooth like this could result in jaw fracture.

113
Q

where is decorin found?

A

around collagen fibres in the PDL - it decorates it.

ODDR (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions