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Basic dental care yr 2 > host responce in PDD/aetiolgy in PDD > Flashcards

host responce in PDD/aetiolgy in PDD Flashcards

1
Q

what do rete ridges do

A

prevent mobiltiy

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2
Q

junctional epitheliumis suceptible to

A

bacterial infection

bacterial produces can get access inaide tissue

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3
Q

why is junctional epithelium permeable

A

we need to secrete out into the OC

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4
Q

flattened cells

A

contain hemidesmosomes (contact BM)

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5
Q

pathologu of periodontal disease

A

saliva
epithelium
inflammatory responce

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6
Q

which antibody is found in saliva

A

secrety IgA

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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

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8
Q

what does IgA do to bacteria

A

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

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9
Q

what does bacteria need to grow

A

iron

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10
Q

lactofrrin

A

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

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11
Q

salivary thiocynate

A

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

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12
Q

types of antimicrobial proteisn

A

Defensins
Catholicidin peptides
Cathepsi C

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13
Q

Defensins

A
  • Highly cationic membranes that insert into the bacterial membrane to create pores and bacterial cell lysis
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14
Q

catholicidin peptides

A
  • punches holes in bacteria membranes in particular lipoprotein membranes(gram -)
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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
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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

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17
Q

what is secreted from JE

A

gingival crevicular fluid

18
Q

gingival crevicual fluid contains

A

C1-9

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
Q

how do neutrophils leave the blood stream

A

via extravasion and migrate towards site

attracted by chemokines

26
Q

functions of neutrophils

A

phagocytosis
bind to complement receptors (opsonisation)
(if macrophage present will use MHC class II)

27
Q

neutrophil function in PDD

A

production of Neutrophil extracellular traps

kill microbes by antimicrobial peptides

28
Q

how do NETs work

A
  • 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
Q

how do neutrophils attempt to remove biofilm

A
  • secrete enzymes and NETS
  • Kill bacteria and solublise plaque
  • Washed out by GCF
30
Q

chemokines funciton

A
  • 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
Q

tissue macrophages

A

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
Q

what can macrophages do

A
  • phagocytose
  • antigen presenting
  • secrete factors
  • secrte factors which increase inflame repsonce
33
Q

adaptive immune repsonce

A

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
Q

what happens to bacteria which has been swallowed

A
  • 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
Q

roles of antibodies in defence

A
  • acts an opsonin
  • activates neutrophil enzyme secretion (neutrophil degranulation)
  • prevents bacterial attachment
  • activates complement
36
Q

antibodies and soluble factors

A
  • neutralises toxins by binding to the active site

- inhibits enzymes (by binding to its active site)

37
Q

chronic marginal gingivitus and characteristics

A

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
Q

destructive periodonttis

A

Complete breakdown

  • alveolar bone broken down
  • not reversible
39
Q

periodontal pocket

A
  • pathologically deepened gingiva sulcus that may occur by coronal movement of the gingiva margin apical displacement of gingiva attachment or both
40
Q

cause of tissue damage and bone loss in periodotnal disease

A

bacteria products

host products

41
Q

bacteria products which damage bone and tissue

A

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
Q

host products which cuase tissue and bone loss

A

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

Basic dental care yr 2 (36 decks)

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