chronic inflammation

Question 1

acute inflammmation vs chronic inflammation

Answer 1

acute - occurs rapidly (days), complete restoration of tissues, mostly neutophils in inflammatory response
chronic - persistent and can occur over months / years / forever. greater destruction, inflammatory infiltrate mainly macrophages and lymphocytes

Question 2

what are the 3 main classes of chronic inflammation

Answer 2

non specific chronic inflammation
specific (primary) chronic inflammation
chronic granulomatous inflammation

Question 3

non - specific chronic inflammation

Answer 3

failure to resolve acute inflammation e.g gingivitis to periodontitis 
excesseive suppuration (pus formation)

Question 4

specific (primary) chronic inflammation

Answer 4

arises with no warning e.g autoimmune diseases such as rheumatoid arthritis

Question 5

chronic granulomatous inflammation

Answer 5

subset of specific chronic inflammation
characterised by the formation of granulomas
OFG is an example

Question 6

what is specific chronic inflammation characterised by

Answer 6

excessively activated macrophages

Question 7

what are non immunological agents that can cause specific chronic inflammation

Answer 7

foreign body reaction e.g grit/ dirt in wound

inhaled - e.g asbestos, silica

Question 8

what are immunological agents that can cause specific chronic inflammation

Answer 8

autoimmune reactions
hypersensitivity
infection by fungi/ parasites

Question 9

commensal bacteria

Answer 9

healthy bacteria that dont cause disease

Question 10

what does the sustained immune response seen in chronic inflammation result in

Answer 10

generation of cells and molecules that destroy tissues

Question 11

epitheloid macrophages

Answer 11

modified macrophages, multi-nucleated , fused together forming giant cells
the predominant cell type of chronic granulomatous inflammation

Question 12

what agents induce chronic granulomatous inflammation

Answer 12

same as specific chronic inflammation

Question 13

do M1 macrophages result in tissue injury or tissue repair

Answer 13

tissue injury as they are pro inflammatory

M2 macrophages produce cytokines that aid tissue repair

Question 14

describe how epitheloid macrophages are formed

Answer 14

macrophages present antigen to lymphocytes
lymphocytes (t cells) produce cytokines (IL-12, IL-2 , IFN-gamma)
these cytokines induce the formation of epitheloid macrophages which contribute to giant cell formation

Question 15

what is the phenotype of OFG

Answer 15

swelling of oral tissues

Question 16

if intestinal crohns is present what is OFG termed

Answer 16

oral crohns

Question 17

what is periodontiti. characterised by

Answer 17

resorption of the alveolar bone

Question 18

is it only hard tissue that is destroyed in periodontitis ?

Answer 18

no , destruction of both soft and hard tissues

Question 19

functions of MMP’s (matrix metalloproteinases)

Answer 19

remodel and degrade ECM to allow immune cell migration 
drive angiogenesis (formation of new bv's)
cause soft tissue destruction

Question 20

what cells produce MMP’s

Answer 20

immune cells such as macophages, dendritic cells, lymphocytes

Question 21

osteoclastogenesis

Answer 21

resorption (degradation) of bone that is mediated by osteoclasts

Question 22

how are osteoclasts activated

Answer 22

activated when RANKL, produced by osteoblasts, activates their RANK receptor. (RANKL production is heavily controlled so bone resorption is very limited)

Question 23

osteoblastogenesis

Answer 23

leads to bone formation and is mediated by osteoblasts

Question 24

what is the function of OPG (osteoprotogerin) secreted by osteoblasts

Answer 24

OPG inhibits RANKL therefore controls bone resorption

Question 25

how does an excessive immune response affect the RANKL /. OPG ratio

Answer 25

sees an increase in RANKL/ OPG ratio meaning an increase in bone resorption
this is seen in periodontitis