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finals - extra > host response/perio/biomed sciences > Flashcards

host response/perio/biomed sciences Flashcards

1
Q

what is the non specific immune system?

A

skin and mucous membranes provide first line of defence

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2
Q

what are types of local defence in the body?

A

saliva
fatty acids in skin
tears
low pH of stomach

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3
Q

what cells are present in non specific immune reactions?

A

macrophages - clear intruder

neutrophils

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4
Q

what is the complement system?

A
  • classical pathway - immune complexes
  • alternate - cell wall structure sets off
  • attract neutrophils
  • cell lysis
  • phagocytosis
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5
Q

what are cytokines?

A

immune response mediators

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6
Q

what is the specific immune system?

A

defense against a specific target
antigens cause a reaction
immunological memory produced

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7
Q

what are the cells of the specific immune system?

A

lymphocytes

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8
Q

what are b lymphs?

A

produced in bone marrow

form antibodies

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9
Q

what are t lymphs?

A

form in b marrow and mature in thymus - helper and killer t cells

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10
Q

what is the job of helper t cells?

A

helper t cell contacwts antigen and releases IL2 which encourages t cells to divide and help killer t cells or help b antibodies produce antibodies

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11
Q

how are b cells activated?

A

b cell recognises antigen and with assistance from t cell produced immune response
2nd - memory cells = faster reaction

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12
Q

what is acute inflammation?

A

bacteria in tissue confronted with macrophages trying to phagocytose it

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13
Q

what is present during acute inflammation?

A

complement
specific antibodies
macrophages

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14
Q

what is the action of macrophages during acute inflammation?

A

releases IL1 and TNF

  • neutrophils adhere to endothelium
  • vasodilation
  • increased endothelium permeability
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15
Q

what are the 5 signs of acute inflammation?

A 
rubor
calor
dolor
tumor
function lasea
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16
Q

what is chronic inflammation?

A

inflammatory agents are pesristing/ bacteria are virulent and cant be broken down, deficient immune system

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17
Q

what cells are present in chronic inflammation?

A

neutrophils

chronic infiltrate

18
Q

what is primary intention wound healing?

A

healing of a clean wound with closely opposed edges

19
Q

how does primary intention healing work?

A

blood vessels cut = platelet aggregation and fibrin mesh produced
macrophages attratc cytokines and fibroblasts released
meshwork of fibrin guides cells to grow into clot and granulation tissue is produced
replaced slowly with collagen and scar forms

20
Q

what is healing by secondary intention?

A

substantial loss of tissue
larger clot formation and more granulation tissue
shortening of myofibroblasts and collagen = wound contraction and irreg scarring

21
Q

how does socket healing happen?

A

secondary intention

mucosa heals before bone

22
Q

what is necrosis

A

death of tissue because inadequate blood supply

  • radiation/bisphosphonates
  • spontaneous or trauma
23
Q

what are the 3 phases of acute inflammation?

A
  • vascular phase
  • increased vessel permeability and fluid exudate
  • cellular phase
24
Q

what is the initial vascular phase?

A 
triple response of lewis 
- flush - cap dilation
- flare - chem mediators/dilation
- wheal - tissue exudate 
vessel walls are more permeable and immune cells adhere to wall
25
Q

what is the vessel permeability and fluid exudate phase?

A

necrosis of endothelium or chemical mediators cause intercellular gaps to widen
1. immediate response - histamine
2. delayed - neutrophils/bradykinin/complement
3. immediate but prolonged - necrosis
Fluid exudate dilutes damaging cells and waste material and brings nutrients for inflammatory cells

26
Q

what is the cellular phase?

A

Ig’s fibrinogen and neutrophils come to wound area

chemotaxis : complement and leukotrienes produced by neutrophils

27
Q

what do inflammatory mediators cause?

A

vasodilation
neutrophil migration
chemotaxis and vessel permeability

28
Q

what is the action of complement?

A

helps antibodies or phagocytic cells

triggered by gram negatice endotoxins

29
Q

sequalae of acute inflammation?

A

resolution
suppuration
organisation
chronic inflammation

30
Q

what cells are present during chronic inflammtion?

A

macrophages
lymphoytes
fibroblasts

31
Q

what is chronic inflammation the balance of?

A

balance between destruction and healing/repair

32
Q

what is the job of the host response?

A

response to plaque biofilm - protection of host against local microbial attack = prevent spread of micro organisms

33
Q

why is the host response not entirely beneficial?

A

causes tissue damage seen in gingivitis and periodontitis

34
Q

what are clinically healthy gingivae like?

A

still some infiltrate in the CT and plaque in crevice

cells contirnue to migrate through JE to combat microorganisms

35
Q

what is present in gcf?

A 
various plasma proteins 
defence cells
pmn's 
antibodies
complement
36
Q

what is plaque confronted by?

A

gcf flow
microorganisms killed by inflammatory and immune cells
organsisms shed during desquamation
destruction by complement and Ig cells

37
Q

describe the initial lesion?

A

occurs 24-48 hours after plaque accumulation, plaque present in gingival crevice are aerobic, gram positive and saccharolytic. An immune response is stimulated by release of bacterial factors and an inflammatory exudate builds up in the CT. There is increased gcf, pmn’s and vasodilation with minimal tissue damage

38
Q

describe the early lesion?

A

occurs 1 week after plaque accumulates, plaque is becoming predominently gram negative and anaerobic. More inflammatory exudate fills the CT and Ig’s and cytokine production is stimulated. Swelling occurs from the CT build up and along with loss of collagen and fibroblasts a deeper crevice forms with a false pseudopocket.

39
Q

describe the established lesion?

A

inflammatory exudate fills most of the Ct and fibrosis is seen. The JE becomes ulcerated and rete peg growth is seen. The gingical crevice deepens further and there are more Ig’s and complement present. Bacteria cause direct damage by enzymes and indirect damage because of the host response.

40
Q

describe the advanced lesion?

A

Fibrosis is occuring in the CT as exudate increases. The JE is ulcerated further and begins to migrate apically down the crown because of PDL fibre breakdown. Bone loss is also seen.

41
Q

how is alveolar bone resorpbed?

A

osteoclastic activity
host response releases cytokines prostaglandins and leukotrienes
periodontitis produces IL-1 and prostaglandins

finals - extra (9 decks)

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