host response/perio/biomed sciences

Question 1

what is the non specific immune system?

Answer 1

skin and mucous membranes provide first line of defence

Question 2

what are types of local defence in the body?

Answer 2

saliva
fatty acids in skin
tears
low pH of stomach

Question 3

what cells are present in non specific immune reactions?

Answer 3

macrophages - clear intruder

neutrophils

Question 4

what is the complement system?

Answer 4

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

Question 5

what are cytokines?

Answer 5

immune response mediators

Question 6

what is the specific immune system?

Answer 6

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

Question 7

what are the cells of the specific immune system?

Answer 7

lymphocytes

Question 8

what are b lymphs?

Answer 8

produced in bone marrow

form antibodies

Question 9

what are t lymphs?

Answer 9

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

Question 10

what is the job of helper t cells?

Answer 10

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

Question 11

how are b cells activated?

Answer 11

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

Question 12

what is acute inflammation?

Answer 12

bacteria in tissue confronted with macrophages trying to phagocytose it

Question 13

what is present during acute inflammation?

Answer 13

complement
specific antibodies
macrophages

Question 14

what is the action of macrophages during acute inflammation?

Answer 14

releases IL1 and TNF

• neutrophils adhere to endothelium
• vasodilation
• increased endothelium permeability

Question 15

what are the 5 signs of acute inflammation?

Answer 15

rubor
calor
dolor
tumor
function lasea

Question 16

what is chronic inflammation?

Answer 16

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

Question 17

what cells are present in chronic inflammation?

Answer 17

neutrophils

chronic infiltrate

Question 18

what is primary intention wound healing?

Answer 18

healing of a clean wound with closely opposed edges

Question 19

how does primary intention healing work?

Answer 19

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

Question 20

what is healing by secondary intention?

Answer 20

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

Question 21

how does socket healing happen?

Answer 21

secondary intention

mucosa heals before bone

Question 22

what is necrosis

Answer 22

death of tissue because inadequate blood supply

• radiation/bisphosphonates
• spontaneous or trauma

Question 23

what are the 3 phases of acute inflammation?

Answer 23

• vascular phase
• increased vessel permeability and fluid exudate
• cellular phase

Question 24

what is the initial vascular phase?

Answer 24

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

Question 25

what is the vessel permeability and fluid exudate phase?

Answer 25

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

Question 26

what is the cellular phase?

Answer 26

Ig's fibrinogen and neutrophils come to wound area | chemotaxis : complement and leukotrienes produced by neutrophils

Question 27

what do inflammatory mediators cause?

Answer 27

vasodilation neutrophil migration chemotaxis and vessel permeability

Question 28

what is the action of complement?

Answer 28

helps antibodies or phagocytic cells | triggered by gram negatice endotoxins

Question 29

sequalae of acute inflammation?

Answer 29

resolution suppuration organisation chronic inflammation

Question 30

what cells are present during chronic inflammtion?

Answer 30

macrophages lymphoytes fibroblasts

Question 31

what is chronic inflammation the balance of?

Answer 31

balance between destruction and healing/repair

Question 32

what is the job of the host response?

Answer 32

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

Question 33

why is the host response not entirely beneficial?

Answer 33

causes tissue damage seen in gingivitis and periodontitis

Question 34

what are clinically healthy gingivae like?

Answer 34

still some infiltrate in the CT and plaque in crevice | cells contirnue to migrate through JE to combat microorganisms

Question 35

what is present in gcf?

Answer 35

``` various plasma proteins defence cells pmn's antibodies complement ```

Question 36

what is plaque confronted by?

Answer 36

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

Question 37

describe the initial lesion?

Answer 37

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

Question 38

describe the early lesion?

Answer 38

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.

Question 39

describe the established lesion?

Answer 39

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.

Question 40

describe the advanced lesion?

Answer 40

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.

Question 41

how is alveolar bone resorpbed?

Answer 41

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