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Clinical Knowledge 2 > Pathogenesis of Periodontal Disease > Flashcards

Pathogenesis of Periodontal Disease Flashcards

1
Q

What is the first bacteria to colonise the tooth surface?

A

Streptococci- gram positive bacteria

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2
Q

How long does it take for gram negative bacteria to be present in the plaque biofilm subgingivally?

A

2 days if plaque is not removed withi 2 days

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3
Q

What are endotoxins?

A

membrane bound compounds on gram negative bacteria than elicit an immune response e.g. LPS

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4
Q

What are the histological stages of the immune response?

A
  • initial lesion
  • early lesion
  • established lesion
  • advanced lesion
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5
Q

When does the initial lesion develop?

A

2-4 days after plaquea accumulation

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6
Q

What is the main occurrence in the initial lesion?

A

vasculitis of blood cells below the JE occurs; inflammation
increased leucocyte migration to the JE

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7
Q

The initial lesion is clinically visible. True or false

A

false

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8
Q

The initial lesion is a ________ condition

A

stable

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9
Q

The early lesion is also known as ___________.

A

early gingivitis

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10
Q

When does the early lesion develop?

A

7-10 days after plaque accumulation

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11
Q

What bacteria dominate in the early lesion stage?

A

anaerobic filamentous bacteria

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12
Q

What bacteria dominate in the early lesion stage?

A

anaerobic filamentous bacteria

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13
Q

What are the hallmarks of the early lesion stage?

A
  • increased fluid exudate
  • increase in PMNL
  • oedema and erythema visible (reddening of the skin and mucosa)
  • proliferation of the basal cells at the junctional epithelium)
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14
Q

What is the junctional epithelium made up of?

A

internal basal lamina
external basal lamina

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15
Q

The internal basal lamina of the JE is attached to …

A

tooth surface

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16
Q

The external basal lamina of the JE is attached to …

A

connective tissue

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17
Q

What is a PMNL? What types of cells does it include?

A

Polymorphonuclear cells
granuloycytes- neutrophils, basophils, eosinophils

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18
Q

What is an erythema ?

A

increase blood flow which causes reddening of th skin or mucosa

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19
Q

The established lesion is also referred to as …

A

established gingivitis

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20
Q

When does the established lesion develop?

A

21-28 days

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21
Q

What types of cells dominate the established lesion?

A

T cells >B cells
increased neutrophils

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22
Q

What are the hallmarks of the established lesion?

A
  • further proliferation at the junctional epithelium
  • gingival crevice deepens
  • continuing loss of collagen
  • breakdown of connective tissue but no bone loss
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23
Q

What are the hallmarks of the advanced lesion?

A

*junctional epithelium migrates apically to form a periodontal pocket
* plaque and endotoxins are able to permeate the surface layer of the cementum
* loss of collagen and bone

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24
Q

What types of cells dominate the advanced lesion ?

A

B cells > T cells in the advanced lesion
plasma cells

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25
Q

Most patients will develop the advanced lesion and it is often present in all sites. True or false

A

false

only 10-15% of patients will develop an advanced lesion and it is not present at all sites

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26
Q

The development of periodontitis is dependent on what factors?

A

risk factors
host factors (response of the immune system)

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27
Q

What is a histological hallmark of the early lesion?

A

rete pegs formation

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28
Q

What are rete pegs ?

A

rete pegs form due to proliferation of SE and JE into collagen depleted areas

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29
Q

What is the common hallmarks of established and advanced lesions

A
  • apical proliferation; conversion into pocket epithelium (pocket formation)
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30
Q

What are the 2 types of responses in the immune system ?

A

Innate response
adaptive/acquired response

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31
Q

What are the mechanisms of the innate immune response?

A
  • epithelial barriers
  • fluid with antibacterial factors e.g. saliva, GCF
  • complement cascade
  • vasoactive peptides e.g. histamine
  • adhesion molecules
  • neutrophils (PMNL) and macrophages
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32
Q

What occurs to the epithelial barriers (JE) in periodontitis/gingivitis ?

A

junctional epithelium becomes more permeable in disease

it becomes permeable to bacterial products, GCF and neutrophils

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33
Q

What is the first line defence against periodontal bacterial infection?

A

junctional epithelium

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34
Q

How is the saliva able to provide an immune response?

A
  • washes and dilutes
  • provides a medium for swallowing bacteria
  • contains antibacteria factors, lysozyme- IgA, IgG
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35
Q

How is the GCF able to provide an immune response?

A

composed of serum and locally generated materials
carries components of serum such as complement proteins and immunoglobulins (IgG)

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36
Q

What causes oedema observed in gingivitis/periodontitis ?

A

increased GCF flow

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37
Q

What is the function of cytokine molecules?

A

molecule that stimulate cells to perform other functions

they can cause cells to release other molecules

cytokines and lymphokines cause cells to perform other functions

38
Q

What is the function of chemokine molecules?

A

attract other cells to the site of infection

39
Q

What cytokine is heavily implicated in bone resorption? What kind of cytokine is it?

A

IL-1- proinflammatory molecule

40
Q

What are the effects of IL-1?

A
  • activation of osteoclasts
  • increases PMNL margination
  • increases PGE2 production
  • increase TNFa production
  • causes bone resorption
41
Q

What are the effects of IL-6?

A

increases bone resorption

42
Q

What are the effects of IL-8?

A

PMNL chemotaxis

43
Q

What are the effects of IL-10?

A

cytokine suppression
potent anti-inflammatory properties

(produced by T and B lymphocytes)

44
Q

What is the effect of TGF-B?

A

stimulates collagen synthesis
implicated in the pathogenesis of fibrosis

45
Q

What is the effect of TNF-a ?

A
  • increased IL-1 production
  • increased PGE2 production
46
Q

What is the effect of PGE2 molecules?

A

stimulates bone resorption

47
Q

What is the main vasoactive peptide of interest in periodontal disease? What cells release this vasoactive peptide ?

A

Histamine
mast cells and basophils

48
Q

What complement proteins are responsible for the release of histamine?

A

C3a and C5a

49
Q

What complement protein induces the release of histamine from mast cells?

A

C5a

50
Q

What is the effect of histamine on the pathogenesis of periodontal disease?

A

they are vasoactive- have an effect on blood vessells
they cause vasodilation- this slows the blood flow allowing margination of PMNL

also increase permeabiluty of blood vessels

51
Q

List important adhesion molecules involved in the innate immune system

A
  • ICAM- I
  • ICAM- II
  • ELAM-I
  • LFA-I
52
Q

The expression of adhesion molecules on vasculature is controlled by …

A

cytokines

53
Q

Leukocyte extravasation is mediated by …

A

signalling molecules and adhesion molecules

54
Q

What are the steps of leukocyte extravasation in inflammation?

A
  • rolling- make or break contacts
  • margination-stronger receptor binding
  • diapedesis - squeezing through blood cells
  • chemotaxis
55
Q

What are the components of the PMNL?

A
  • receptor - pathogen recognition, opsonisation
  • cytoskeleton- permits movement
  • lysosomes- contain lysozymes to destroy bacterial structures
  • oxygen radicals- superoxides to destroy bacterial structures
56
Q

What is opsonisation?

A

use of opsonins to tag foreign pathogens for elimination by phagocytes (PMNL, macrophages)

57
Q

Give examples of opsonins

A

IgG, C3b

58
Q

Briefly describe the intracellular killing of bacteria in PMNL cells

A
  • PMNL phagocytes bacteria
  • internal degranulation of PMNL
  • digestion of microbe
  • expels remnants of microbe
  • PMNLthe undergoes apoptosis
  • host cell damage may occur
59
Q

What method of killing bacteria increases the risk of collateral damage?

A

extracellular killing of bacteria

60
Q

Macrophages developed from …

A

circulating monocytes in the blood

61
Q

What is the role of macrophages in inflammation?

A
  • phagocytosis
  • secrete tissue degrading enzymes
  • secrete compement components
  • secrete mediators - IL-1, TNFa, prostaglandins
62
Q

What is the role of macrophages in immunity?

A
  • process and present antigens (B and T cells)
  • secrete IL-1
63
Q

Macrophages have a dual- role, what is their other function?

A

Aside from phagocytosis
they are antigen presenting cells

64
Q

What do macrophages contain that allows recognition between host and foreign tissue? Where else are they present?

A

MHC-II

also found on other APCs, dendritic cells and B cells

65
Q

When is the complement cascade activated?

A

inflammatory response

66
Q

What form do complement proteins circulate in?

A

inactive form

67
Q

What is the main role of complement activation?

A
  • recruit phagocytes
  • aid phagocytosis- opsonisation
  • kill bacteria by forming a membrane attack complex (MAC)
68
Q

What are the 2 complement pathways?

A

Classical and alternative

69
Q

What do both complement pathways lead to?

A

activation of C3 (C3a, C3b)

70
Q

What is the larger cleaved molecule of activated C3 protein? What is the function of this protein?

A

C3b
opsonisation

71
Q

What is the function of the C3a molecule?

A

activation of C5

72
Q

What is the effect of the C3a molecule?

A

chemotaxis of phagocytes

73
Q

What is the effect of the C3b molecule?

A

cytokine production
secreted from macrophages
opsonisation

74
Q

What is the effect of the C5a molecule?

A
  • leucocytes stick to vessel walls
  • neutrophils release enzyme amd O2 radicals
75
Q

What is the effect of the C3a and C5a molecule?

A

increased vascular permeability due to histamine release from mast cells

76
Q

What is the effect of the C3b and C5a molecule?

A

production of oxygen radicals

77
Q

What is the effect of the C5a and C567 complex?

A

leucocyte chemotaxis

78
Q

What is the effect of C5b, C6, C7, C8 and C9?

A

bacterial cell lysis
MAC

79
Q

What cells are involved in the acquired immune response?

A

T and B lymphocytes

80
Q

What are the classes of immunoglobulin?

A

IgM
IgG
IgA
IgE
IgD

81
Q

What are the most important immunoglobulins periodontal disease and where are they found?

A

IgG- GCF; originates from blood plasma
IgA- exists as a dimer; from the saliva

82
Q

What lymphocytes cells are present in the initial and early lesions?

A

T lymphocytes

83
Q

Briefly outline the role of T lymphocytes in the pathogenesis of periodontal disease (activation of T lymphocytes)

A
  • antigen presented to T cells by APC
  • undifferentiated T cells express IL-2 receptor and bind to the IL-2 produced by the T-helper cells
  • undifferentiated T cells differentiate into effector T cells as a result of IL-2 binding
  • cytotoxic T cells reach tissue and lyse bacteria
  • memory T cells remain in lymph tissue
84
Q

How are B lymphocyes are activated?

A
  • Th2 cells necessary for anti-body production in B cells
  • endotoxin causes activation of independent T cells
  • native/independent T cells release IL-2 and causes proliferation of B cells which head to the tissue
  • this causes tissue enlargement and production of immunoglobulins
  • foreign antigens bind to B cells via Ig receptors
85
Q

Where does the antibody-antigen complex bind on PMNL cells?

A

the Fc receptors on PMNL

86
Q

What are the features of the innate immune response?

A
  • constantly in function
  • rapid response
  • usually involved in gingival inflammation
  • T cells> B cells
87
Q

What are the features of the adaptive immune response?

A
  • specific cell-cell interactions
  • slower response
  • ususally in advanced gingivitis and periodontitis
  • B cells >T cells
88
Q

What stage of periodontal disease is the adaptive immune response involved in?

A

advanced gingivitis
periodontits

89
Q

What stage of periodontal disease is the innate immune response involved in?

A

early gingival inflammation

90
Q

What are the bacterial factors of periodontitis?

A
  • increased numbers
  • specific pathogens
  • direct tissue
  • invasion
91
Q

What are the host factors of periodontitis?

A
  • reduced effectiveness of host defences
  • increased damage in response to microbial changes
92
Q

What is the most important aspect of treatment of periodontitis?

A

mechanical removal of causative bacteria

Clinical Knowledge 2 (40 decks)

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