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Periodontics > Unit 13 - Host Immune Response to Periodontal Pathogens > Flashcards

Unit 13 - Host Immune Response to Periodontal Pathogens Flashcards

1
Q

True or False: Research findings indicate that although bacteria are essential for disease to occur, the presence of suspected periodontal pathogens alone is insufficient to cause tissue destruction seen in periodontitis.

A

True

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2
Q

What is the cause of nearly all the destruction seen in periodontal disease?

A

The body’s response to the bacteria present in plaque biofilm.

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3
Q

What is the way that the body responds to peridontal pathogens known as?

A

Host response

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4
Q

What is the prime purpose of the human immune system?

A

To defend the life of the indiviudal / host

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5
Q

Are the body’s defences employed to preserve the tooth or its supportial periodontal tissues?

A

No. The body’s defences are employed to save the life of the host.

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6
Q

What are all the mechanisms that enable biofilm bacteria to colonize and damage tissues called?

A

Virulence factor

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7
Q

Viruluence factors may be either structural characteristics of bacteria or

A

Substances produced by bacteria

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8
Q

What are the factors enhancing microbial challenge?

A

Presence of lipolysaccharides
Ability to invade tissues
Ability to produce enzymes

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9
Q

What is the first line of defence against microbial invasion?

A

Acute inflammation

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10
Q

What is the return to homeostasis called?

A

Catabasis

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11
Q

What are the components of the immune system?

A

Polymorphonuculear leukocyte (PMN)
Macrophage
Plasma cell / B-lymphocyte
T-lymphocyte
Immunoglobulins

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12
Q

How does inflammation cause periodontal disease?

A

Proinflammatory mediators, like, PMNs, are recuited during the acute phase
Attracted to the bacteria process by chemotaxis
Overproduction of these mediators cause destruction of connective tissue matrix and resorption of bone
Proresolving lipid mediators are produced to terminate PMN recruitment

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13
Q

When does the inflammatory response become chronic?

A

If the acute inflammatory responses are not effective in controlling the invading microorganisms.

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14
Q

What is a long-lived, out of control inflammatory response that continues for more than a few weeks?

A

Chronic inflammation

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15
Q

What type of condition is chronic inflammation?

A

Pathological condition

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16
Q

Can chronic inflammation cause more damage than the original problem?

A

Yes

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17
Q

Are the classic warning signgs seen in acute inflammation usually present in chronic inflammation?

A

No

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18
Q

True or False: in chronic inflammation, pain is often absent.

A

True

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19
Q

Why does chronic inflammation occur?

A

Because the body is unable to rid itself of the invading organism

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20
Q

The invading microorganisms are persistent and stimulate an

A

Exaggerated immune response

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21
Q

Can chronic iflammation become so intense that it does permanent damage to the body tissues?

A

Yes

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22
Q

What are biochemical mediators?

A

Biologically active compounds secreted by the immune cells that activate the body’s inflammatory response

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23
Q

What are the inflammatory mediators of importance in periodontal disease?

A

Cytokines
Prostaglandins
Matrix metalloproteinases (MMPs)

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24
Q

What are cytokines?

A

Proteins released by host immune cells (cell protein)

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25
What do cytokines do in regards to inflammation?
Signal to the immune system to send more phagocytes to the site of infection Increase vascular permeability that increases movement of immune cells into the tissues Can initiate tissue destruction and bone loss in chronic infections
26
What cells produce cytokines?
PMNs Macrophages B lympthocytes Epithelial cells Gingival fibroblasts Osteoblasts
27
Cytokines important in periodontal diseae include
IL-1 IL-6 IL-8
28
What are prostaglandins?
Powerful inflammatory mediators derived from fatty acids that play a role in bone drestruction in periodontitis
29
What series of prostaglandins play a role in periodontitis?
D E F G H I
30
What do prostaglandins do in regards to inflammation?
Dilation of blood vessels - increase permeability and dilation of blood vessels to promote increased movement of immune cells and complement to the infection site Trigger osteoclasts to destroy the alveolar bone
31
What are matrix metalloproteinases (MMPs)?
Family of at least 12 different enzymes that are produced by various cells of the body (PMNs, macrophages, fibroblasts, JE cell) and they break down the connective tissue matrix
32
What are major sources of MMPs in periodontitis?
PMNs Gingival fibers
33
What is the function of MMPs in periodontal health?
MMPs facilitate normal turnover of the periodontal connective tissue matrix
34
What does an increased MMP level cause in the periodontium?
Extensive collagen destruction in perdiontal tissues
35
What happens to tissues of the gingiva, periodontal ligament, and support alveolar bone without collagen?
They degrade resulting in recession, pocket formation, and tooth mobility
36
What recruits PMNs and macrophages to the infection site?
Cytokines
37
What increases vascular permeability allowing immune cells and complement to move to the infection site?
Prostaglandins
38
What facilitates normal turnover of the connective tissue matrix?
MMPs
39
What intiates tissue destrution and bone loss?
Cytokines
40
What triggers osetoclasts to destroy alveolar bone?
Prostaglandins
41
What deals with collagen destruction?
MMPs
42
What are the factors affecting the host immune response?
Genetic Environmental Acquired
43
What is the current theory of pathogenesis?
Pathogenesis of health to gingivitis to periodontitis is complex and multilayered. - microbial infection activates host response - genetic and environmental factors modify the inflammatory response - mediators are produced by cells of the inflammatory response
44
What type of lesion is the early bacterial accumulation phase?
Initial lesion
45
What type of lesion is the early gingivitis plaque overgrowth phase?
Early lesion
46
What type of lesion is the established gingivitis sibgingival plaque phase?
Established lesion
47
What type of lesion is the periodontitis tissue destruction phase?
Advanced lesion
48
In the initial lesion or early bacterial accumulation phase, bacterial colonization is near the
Gingival margin
49
In the initial lesion or early bacterial accumulation phase, immune response from the presence of gram-________ bacteria
Negative
50
In the initial lesion or early bacterial accumulation phase, PMNs released pass from the blood vessels into the
Gingival connective tissue
51
In the initial lesion or early bacterial accumulation phase, cytokines are released, PMNs migrate to the gingival sulcus, and the _______ system is activated
Complement
52
In the initial lesion or early bacterial accumulation phase, what are the clinical features?
Gingiva looks healthy
53
Inital lesion develops ____ days following plaque accumulation
2 - 4 days
54
What is the outcome of the hose response in the initial lesion or early bacterial accumulation phase
Successful if bacteria destrored. If not controlled, early gingivitis develops
55
What happens during early gingivitis or plaque overgrowth phase?
Bacterial toxins penetrate into the JE Large # of PMNs move into CT Lymphocytes are evident SE and CT are the most affected Collagen loss of 60-60% and SE starts forming epithelial ridges
56
What are the clinical features of early gingivitis or plaque overgrowth phase?
Edema and redness
57
Early lesion develops from ____ days following biofilm accumulation
4 - 7 days
58
What is the outcome of the host response in early gingivitis or plaque overgrowth phase?
PMN may control bacterial pathogens Good OH disrupts plaque biofilm If not distrupted, bacterial pathogens will cause initial lesion to become establish gingivitis
59
What happens during the established gingivitis or subgingival plaque phase?
Plaque biofilm extends subgingivally and distrupts the attachment of the coronal-most portion of the JE from the tooth surface Antibodies produced Eptihelial ridges extend deeper in CT JE loosens its attachment to root surface Pocket epithelium is thinner and more permeable
60
What are the clinical features of established gingivitis or subgingival plaque phase?
All of the usual clinical features of gingivitis are evident
61
Established gingivitis is generally observed ____ days following plaque biofilm accumulation
21 days
62
What is the outcome of the host response in established gingivitis or subgingival plaque phase?
Some is adequate to contain bacterial challenge Controlled by instrumentation and OH If not controlled established gingivitis progresses to periodontitis
63
What happens during periodontitis or tissue destruction phase?
Plaque biofilm grows laterally and apically along the root surface Perio pocket provides an indeal environment for growth of subgingival bacteria Chronic host challenge Intense immune response begings to harm periodontium Cytokines cause CT and PDL destruction and bone loss
64
What are the clinical features of periodontitis or tissue destruction phase?
Advanced lesion Periodontal pocket formation BOP Alveolar bone loss Furcation involvement Tooth mobility
65
What is the outcome of host response in periodontitis or tissue destruction phase?
Outcome is affected by abnormal PMN function, virulent bacteria in biofilm, acquired and environmental factors such as smoking and stress, systemic factors such as diabetes or genetic factors
66
What are the four distinct phases of microscopic changes in the periodontium?
Early bacterial accumulation phase Early gingivitis - plaque overgrowth phase Establish gingivitis - subgingival plaque phase Periodontitis - tissue destrcution phase
67
What is bone remodeling?
The breakdown of old bone and subsequent deposition of new bone
68
True or False bone is in a constant state of remodeling.
True
69
What breaks down the existing bone matrix?
Osteoclasts
70
What synthesizes collagen and other bone proteins?
Osetoblasts
71
What is the bone remodeling cycle?
Resorption phase Reversal phase Formation phase Resting phase
72
What happens during the resorption phase of the bone remodeling cycle?
Osteoclasts create erosion cavities in bone
73
What happens during the reversal phase of the bone remodeling cycle?
Osteogenic signals stimulate osteoclasts to cease action. Mononuclear cells adhere to eorsion cavities and send signals to attract osteoblasts
74
What happens during the formation phase of the bone remodeling cycle?
Osteoblasts line erosion cavities and form matrix to replace resorbed bone
75
What happens during the resting phase of the bone remodeling cycle?
Interval between cessation of bone resorption and bone remodeling
76
What is the RANKL/RANK/OPG pathway?
A signlaing mechanism that occurs between the osteoclastic precursor and osteoblasts
77
What is RANKL?
Cell membrane bound protein on the surface of an osteoblast
78
What is RANK?
Cell surface receptor expressed on osteroclastic precursors
79
What is OPG?
Soluble secreted protein released by the osteoblast
80
How does the RANKL/RANK/OPG pathway work?
RANKL binds to RANK to signal fusion of osteroclastic precursors to differentiate into bone-resorving osteroclasts The cumulative effect of the RANKL/RANK interaction is bone resorption OPG blocks the binding of RANKL to RANK to protect the bone The ratio of OPG to RANKL produced by osteroblasts determines the extent of bone resorption
81
What happens if RANKL bines to OPG?
Bone is protected
82
What happens is RANKL binds to RANK?
Bone is resorbed
83
The body attempts to maintain the balance of OPG to RANKL in
Homeostasis
84
There is increased expression of RANKL from osteoblasts in
Periodontal disease

Periodontics (15 decks)

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