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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
Most patients will develop the advanced lesion and it is often present in all sites. True or false
false only 10-15% of patients will develop an advanced lesion and it is not present at all sites
26
The development of periodontitis is dependent on what factors?
risk factors host factors (response of the immune system)
27
What is a histological hallmark of the early lesion?
rete pegs formation
28
What are rete pegs ?
rete pegs form due to proliferation of SE and JE into collagen depleted areas
29
What is the common hallmarks of established and advanced lesions
* apical proliferation; conversion into pocket epithelium (pocket formation)
30
What are the 2 types of responses in the immune system ?
Innate response adaptive/acquired response
31
What are the mechanisms of the innate immune response?
* epithelial barriers * fluid with antibacterial factors e.g. saliva, GCF * complement cascade * vasoactive peptides e.g. histamine * adhesion molecules * neutrophils (PMNL) and macrophages
32
What occurs to the epithelial barriers (JE) in periodontitis/gingivitis ?
junctional epithelium becomes more permeable in disease it becomes permeable to bacterial products, GCF and neutrophils
33
What is the first line defence against periodontal bacterial infection?
junctional epithelium
34
How is the saliva able to provide an immune response?
* washes and dilutes * provides a medium for swallowing bacteria * contains antibacteria factors, lysozyme- **IgA**, IgG
35
How is the GCF able to provide an immune response?
composed of serum and locally generated materials carries components of serum such as complement proteins and immunoglobulins (IgG)
36
What causes oedema observed in gingivitis/periodontitis ?
increased GCF flow
37
What is the function of cytokine molecules?
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
What is the function of chemokine molecules?
attract other cells to the site of infection
39
What cytokine is heavily implicated in bone resorption? What kind of cytokine is it?
IL-1- proinflammatory molecule
40
What are the effects of IL-1?
* activation of osteoclasts * increases PMNL margination * increases PGE2 production * increase TNFa production * causes bone resorption
41
What are the effects of IL-6?
increases bone resorption
42
What are the effects of IL-8?
PMNL chemotaxis
43
What are the effects of IL-10?
cytokine suppression potent anti-inflammatory properties (produced by T and B lymphocytes)
44
What is the effect of TGF-B?
stimulates collagen synthesis implicated in the pathogenesis of fibrosis
45
What is the effect of TNF-a ?
* increased IL-1 production * increased PGE2 production
46
What is the effect of PGE2 molecules?
stimulates bone resorption
47
What is the main vasoactive peptide of interest in periodontal disease? What cells release this vasoactive peptide ?
Histamine mast cells and basophils
48
What complement proteins are responsible for the release of histamine?
C3a and C5a
49
What complement protein induces the release of histamine from mast cells?
C5a
50
What is the effect of histamine on the pathogenesis of periodontal disease?
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
List important adhesion molecules involved in the innate immune system
* ICAM- I * ICAM- II * ELAM-I * LFA-I
52
The expression of adhesion molecules on vasculature is controlled by …
cytokines
53
Leukocyte extravasation is mediated by …
signalling molecules and adhesion molecules
54
What are the steps of leukocyte extravasation in inflammation?
* rolling- make or break contacts * margination-stronger receptor binding * diapedesis - squeezing through blood cells * chemotaxis
55
What are the components of the PMNL?
* receptor - pathogen recognition, opsonisation * cytoskeleton- permits movement * lysosomes- contain lysozymes to destroy bacterial structures * oxygen radicals- superoxides to destroy bacterial structures
56
What is opsonisation?
use of opsonins to tag foreign pathogens for elimination by phagocytes (PMNL, macrophages)
57
Give examples of opsonins
IgG, C3b
58
Briefly describe the intracellular killing of bacteria in PMNL cells
* PMNL phagocytes bacteria * internal degranulation of PMNL * digestion of microbe * expels remnants of microbe * PMNLthe undergoes apoptosis * host cell damage may occur
59
What method of killing bacteria increases the risk of collateral damage?
extracellular killing of bacteria
60
Macrophages developed from …
circulating monocytes in the blood
61
What is the role of macrophages in inflammation?
* phagocytosis * secrete tissue degrading enzymes * secrete compement components * secrete mediators - IL-1, TNFa, prostaglandins
62
What is the role of macrophages in immunity?
* process and present antigens (B and T cells) * secrete IL-1
63
Macrophages have a dual- role, what is their other function?
Aside from phagocytosis they are antigen presenting cells
64
What do macrophages contain that allows recognition between host and foreign tissue? Where else are they present?
MHC-II also found on other APCs, dendritic cells and B cells
65
When is the complement cascade activated?
inflammatory response
66
What form do complement proteins circulate in?
inactive form
67
What is the main role of complement activation?
* recruit phagocytes * aid phagocytosis- opsonisation * kill bacteria by forming a membrane attack complex (MAC)
68
What are the 2 complement pathways?
Classical and alternative
69
What do both complement pathways lead to?
activation of C3 (C3a, C3b)
70
What is the larger cleaved molecule of activated C3 protein? What is the function of this protein?
C3b opsonisation
71
What is the function of the C3a molecule?
activation of C5
72
What is the effect of the C3a molecule?
chemotaxis of phagocytes
73
What is the effect of the C3b molecule?
cytokine production secreted from macrophages opsonisation
74
What is the effect of the C5a molecule?
* leucocytes stick to vessel walls * neutrophils release enzyme amd O2 radicals
75
What is the effect of the C3a and C5a molecule?
increased vascular permeability due to histamine release from mast cells
76
What is the effect of the C3b and C5a molecule?
production of oxygen radicals
77
What is the effect of the C5a and C567 complex?
leucocyte chemotaxis
78
What is the effect of C5b, C6, C7, C8 and C9?
bacterial cell lysis MAC
79
What cells are involved in the acquired immune response?
T and B lymphocytes
80
What are the classes of immunoglobulin?
IgM IgG IgA IgE IgD
81
What are the most important immunoglobulins periodontal disease and where are they found?
IgG- GCF; originates from blood plasma IgA- exists as a dimer; from the saliva
82
What lymphocytes cells are present in the initial and early lesions?
T lymphocytes
83
Briefly outline the role of T lymphocytes in the pathogenesis of periodontal disease (activation of T lymphocytes)
* 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
How are B lymphocyes are activated?
* 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
Where does the antibody-antigen complex bind on PMNL cells?
the Fc receptors on PMNL
86
What are the features of the innate immune response?
* constantly in function * rapid response * usually involved in gingival inflammation * T cells> B cells
87
What are the features of the adaptive immune response?
* specific cell-cell interactions * slower response * ususally in advanced gingivitis and periodontitis * B cells >T cells
88
What stage of periodontal disease is the adaptive immune response involved in?
advanced gingivitis periodontits
89
What stage of periodontal disease is the innate immune response involved in?
early gingival inflammation
90
What are the bacterial factors of periodontitis?
* increased numbers * specific pathogens * direct tissue * invasion
91
What are the host factors of periodontitis?
* reduced effectiveness of host defences * increased damage in response to microbial changes
92
What is the most important aspect of treatment of periodontitis?
mechanical removal of causative bacteria

Clinical Knowledge 2 (40 decks)

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