periodontal pathogenesis Flashcards

1
Q

describe the pathogenesis of human periodontitis

A

microbes release LPS’s & Ag’s which causes the body to launch immuno inflammatory response( antibodies, cytokines, prostanoids MMPs) this affects connective tissue and bone metabolism which causes the clinical signs of the disease and progression.

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2
Q

what do environmental risk ( smoking)factors affect?

A

host immunoinflammatory response and connective tissue and bone metabolism

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3
Q

Whats the non-specific plaque hypothesis?

A

its the high number of bacteria that cause the problems

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4
Q

whats the specific plaque hypothesis?

A

its the quality of bacteria that causes problems

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5
Q

whats the ecological plaque hypothesis?

A

environment shifts from aerobic to anerobic

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6
Q

What are some bacterial virulence factors associated with plaque?

A

exotoxins and endotoxins

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7
Q

Innate immunity factors in defense

A

1st line of defense, present at birth, not enhanced by prior exposure, lacks memory, fast but lacks specificity

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8
Q

examples of innate immunity

A

saliva, GCF, epithelium, commensal microflora

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9
Q

explain why innate immunity can cause damage?

A

its not specific,

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10
Q

Epitheliums role

A

barrier( tight jxns), high turnover rate,

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11
Q

Salivas role

A

prevents bacterial attachment, contains IgA, IgM, IgG

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12
Q

charecteristics of adaptive immunity

A

specific, memory, diverse, recognition of self cells, humoral( antibodies), cell mediated( immune cells)

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13
Q

inflammatory mediators purpose is…

A

to initiate, perpetuate, and terminate an inflammatory response.

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14
Q

what are the pro-inflammatory cytokines?

A

interleukins, chemokines, interferins

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15
Q

Interleukin 1-

A

major mediator of periodontitis

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16
Q

Which cells does IL1 target?

A

T-cells, epithelial cells ,endothelial cells, fibroblasts

17
Q

IL1 induces what?

A

proinflammatory proteins, hematopoesis, differentiation of Th17 cells

18
Q

IL 2-5 are all what?

A

lymphocyte signaling cytokines

19
Q

IL2 is produced by what?

A

CD4, CD8, and activated T lymphocytes

20
Q

what does IL4 do?

A

regulated immunoglobilin production, suppresses activated macrophages and causes their apoptosis

21
Q

TNF-a is produced by what and does what?

A

macrophages, works like IL1 and mediates inflammatory response and connective tissue destruction

22
Q

what are the 2 key mediators of chronic inflammatory diseases?

A

TNFa, IL-1

23
Q

what does IL6 do?

A

causes fusion of monocytes to form osteoclasts

24
Q

what does IL8 do?

A

induces directional migration of PMNs, monocytes, Tcells to accumulat at inflammation sites

25
Q

what does IL10 do?

A

suppresses immune and inflammatory response,

26
Q

what does transforming growth factor B do?

A

its a chemoattractant for monocytes and suppreses their activation

27
Q

prostaglandins are ________ derivatives?

A

arachidonic, important inflammation mediators

28
Q

matrix metalloproteinases do what?

A

tissue remodeling and degradation of ECM. Their regulated by hormones, growth factors and cytokines

29
Q

Bone loss in response to inflammation depends on ….

A

concentration of inflammatory mediators in gingival tissues.

30
Q

what are the proinflammatory cytokines that lead to bone resorption?

A

IL1, 6, 11, 17, TNFα, Oncostatin M, Leukemia inhibitory factor, Bradykinin, Kallidin and Chemokines

31
Q

what are antiinflammatory cytokines that inhibit bone resorption?

A

IL4, 10, 12, 13, 18, IFN-β, IFN-γ

32
Q

whats RANKL

A

receptor activator of nuclear factor kappa B ligand, its expressed by osteoblasts, fibroblasts, tcells, bcells

33
Q

RANK

A

the receptor for RANKL and is on osteoclasts

34
Q

OPG

A

osteoprotegerin, expressed by osteoblasts, it binds to RANKL to prevent it from activating osteoclasts

35
Q

RANKL, RANK, OPG and bone resorption

A

elevated RANKL / =OPG or =RANKL / lowerOPG

36
Q

RANKL, RANK, OPG and bone formation

A

lowered RANKL / =OPG or =RANKL / elevated OPG