host responce in PDD/aetiolgy in PDD Flashcards

(42 cards)

1
Q

what do rete ridges do

A

prevent mobiltiy

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

junctional epitheliumis suceptible to

A

bacterial infection

bacterial produces can get access inaide tissue

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

why is junctional epithelium permeable

A

we need to secrete out into the OC

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

flattened cells

A

contain hemidesmosomes (contact BM)

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

pathologu of periodontal disease

A

saliva
epithelium
inflammatory responce

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

which antibody is found in saliva

A

secrety IgA

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

IgA

A

secreted as a dimer into OC through epithelial cells

- when being secreted a J chain attatches to it which links th emonomers together to form a dimer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what does IgA do to bacteria

A

bind to bacteria or products to stop its function
4 potential contact points
aggregates bactera

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

what does bacteria need to grow

A

iron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

lactofrrin

A

compeititve inhbitor
binds to and sequesters free ion
binds LPS leading to formation of perioxide, increases bacterial membrane permeability

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

salivary thiocynate

A

enzyme
NADPH converted to hydrogen perioxoide, converted to HOSCN
is then coverted to hypothiocyanous acid in low amounts

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

types of antimicrobial proteisn

A

Defensins
Catholicidin peptides
Cathepsi C

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

Defensins

A
  • Highly cationic membranes that insert into the bacterial membrane to create pores and bacterial cell lysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

catholicidin peptides

A
  • punches holes in bacteria membranes in particular lipoprotein membranes(gram -)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

cathepsin C roles

A
  • serine protease released mainly by neutrophils
  • degrades the outer membrane protein of bacteria
  • activates other proteases via cleavage
  • cleaves ECM components
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

role of eptihelum

A

desquamation means any bacteria is shed
permability barrier
junctional epithelium more permeable, sulcus bactera trapped
epithelum can stimulate immune responce and release cytokines

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

what is secreted from JE

A

gingival crevicular fluid

18
Q

gingival crevicual fluid contains

19
Q

role of c3b

A
  • inserts itself into the membranes of the bacteria

- leukocytes phagocytose it

20
Q

C5-9

A
  • membrane attack complex
  • destroys microorganisms
  • forms a channel pore to lyse the bacteria
21
Q

C3a-C5a

A
  • attract neutprhils and macrophages to the area(if complement is activated)
  • vascular changes (increase permeability by the histamine)
  • stimulate histamine release
  • promote formation of leukotrienes and prostaglandins (pro inflammatory molecules)
  • attract phagocytes by chemotaxis and aid phagocytosis via opsonisation
22
Q

clotting cascade purpose

A

prevent spread to blood

fibrin forms a barrier to spread of infection

23
Q

kininogens

A
  • converted to kinins by proteases eg brady kinin
  • acts very similar to histamine, promotes inflammatory respnce
  • more serum and leukocytes into the OC due to vasodialtion
24
Q

gingival crevicualr fluid limiatiosn

A
  • bacteria in plaque can metabolise some components

- complement, immunoglobulin and other components partly consumed and degraded in crevice

25
how do neutrophils leave the blood stream
via extravasion and migrate towards site | attracted by chemokines
26
functions of neutrophils
phagocytosis bind to complement receptors (opsonisation) (if macrophage present will use MHC class II)
27
neutrophil function in PDD
production of Neutrophil extracellular traps | kill microbes by antimicrobial peptides
28
how do NETs work
- neutrophil will pick up and phagocytose as many bacteria as it can - as they die (eaten as many bacteraia as possibke)they throw DNA strands, this will capture bacteria on the outside - bacteria caught in the DNA strands - macrophage can recognise and eat it
29
how do neutrophils attempt to remove biofilm
- secrete enzymes and NETS - Kill bacteria and solublise plaque - Washed out by GCF
30
chemokines funciton
- stimulate immune response - release cytokines (drives inflammatory reponnsce) - phagocytose - stimulate healing (helps epithelium) if there is no permanet damage at this stage/no periodontits
31
tissue macrophages
Surveillance macrophages - once the microbial load is too great they’ll respond - secrete factors that recruit monocytes (blood) to the tissue - then turn into macrophages into the tissue
32
what can macrophages do
- phagocytose - antigen presenting - secrete factors - secrte factors which increase inflame repsonce
33
adaptive immune repsonce
1) Humoral immunity - B cells - Production of antibody by plasma cells 2) Cell mediated immunity - T cells - immune regulation and cytotoxic T cell killing of virally infected and neoplastic cells
34
what happens to bacteria which has been swallowed
- can be then associated with mucosal associated Lymphoid tissue - Degraded in the stomach - if not, in the intestines there are immune patches that have lymphoid tissue - bacteria antigens can get taken up by the MALT^ - presented by dendritic cells/macrophages - can then get B cell production of antibodies - antibodies enter the serum and come out of the JE as the blood vessels there are very leaky
35
roles of antibodies in defence
- acts an opsonin - activates neutrophil enzyme secretion (neutrophil degranulation) - prevents bacterial attachment - activates complement
36
antibodies and soluble factors
- neutralises toxins by binding to the active site | - inhibits enzymes (by binding to its active site)
37
chronic marginal gingivitus and characteristics
caused by expansion of the biofilm Some of the enzymes attack the biofilm so much the tissue begins to be damaged) Bleeding on probing (due to fragile tissue) False pocketing - due to swollen gingiva but functional epithelium still attached Junctional epithelium still attached - Gingivitis is reversible - alveolar bone is still intact
38
destructive periodonttis
Complete breakdown - alveolar bone broken down - not reversible
39
periodontal pocket
- pathologically deepened gingiva sulcus that may occur by coronal movement of the gingiva margin apical displacement of gingiva attachment or both
40
cause of tissue damage and bone loss in periodotnal disease
bacteria products | host products
41
bacteria products which damage bone and tissue
1) Endotoxins - may damage epithelium - fibroblasts 2) Bacterial enzymes - collagenase - hyaluronidase - gingipains break down the connective tissue 3) Lipopolysaccharide, capsular material, peptidoglcans,muramyl dipeptide, proteases may cause bone resorption
42
host products which cuase tissue and bone loss
1) Release of enzymes from neutrophils - damaging cell tissues - negative feedback tissues on our own issues 2) complement 3) production of IL-1, IL-6 by macrophages - stimulates bone resorption and epithelial proliferation - tries to drive an inflammatory responce 4) Inflammatory mediators - prostaglandins - other cytokines - leukotrienes also stimulates bone resorption