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Health 31 > Osteoarthritis > Flashcards

Osteoarthritis Flashcards

1
Q

LO
- To know the pathological features of OA
- To understand the key pathways and cell types that mediate OA joint pathology
- To understand why obesity is a risk factor for OA
- To understand the relationship between OA joint inflammation and joint pain

A
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2
Q

What are common osteoarthritis sites?

A
  • knee
  • hip
  • neck
  • spine
  • hand
  • big toe
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3
Q

What can be seen on the x-ray of an osteoarthritic patient?
(3 clincial features of OA)

A
  • loss of cartilage
  • narrowing of joint space
  • bony spurs (osteophytes)
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4
Q

px with OA usually present to GP with ….

A

pain + loss of mobility in joints

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5
Q

whats an Osteophyte?

A

bony spurs visible in Xray

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6
Q

what would you expect to see in the hands of someone with OA?

A

bony nodules

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7
Q

What are the risk factors for osteoarthritis?

A
  • older age
  • women (menopause + estrogen levels)
  • obesity
  • smoking
  • hypermobility (sports/traumatic injury)
  • osteoporosis
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8
Q

What parts of the joint does osteoarthritis affect? 4

A
  • cartilage
  • subchondral bone
  • synovium
  • skeletal muscle

whole joint, not just cartilage

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9
Q

How does osteoarthritis affect the cartilage within the joint?

A

causes fibrillation and degradation

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10
Q

How does osteoarthritis affect the skeletal muscle on a joint?

A

causes muscle weakness and atrophy

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11
Q

How does osteoarthritis affect the subchondral bone within the joint?

A

causes:

  • trabecular thickening
  • under-mineralisation
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12
Q

How does osteoarthritis affect the synovium within the joint?

A

causes thickening and inflammation

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13
Q

What is the function of articular cartilage?

A

absorb load on the joint

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14
Q

Where is the articular cartilage located within the knee and what are they called?

A
  • end of femur: femoral condyle cartilage
  • end of tibia: tibial plataeu cartilage
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15
Q

What is the names of the cartilage located in the hip joint?

A
  • femoral head cartilage
  • hip socket cartilage
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16
Q

how does cartilage look in normal joint?

A

white, glossy

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17
Q

what are the cells of the articular cartilage?

A

chrondocytes

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18
Q

what do chondrocytes produce?

A

proteins that form an extracellular matrix.

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19
Q

outline the extracellular matrix formed by chondrocytes

A

network of type 2 collagen fibres
proteoglycans with GAG side chains
- bottle brush appearance
- trap water which gives load absorbing properties
- non collangenous proteins such as fibronectin

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20
Q

60-80% of cartilage is made up of what?

A

water

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21
Q

articular cartilage structure typically acellular and doesnt have…

A

blood supply/ nerves/ lymphatic system

not well vascularised

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22
Q

explain what happens to the articular cartilage when its absorbs a load?

A

load applied to joint
cartilage compressed water
repulsive forces from proteoglycans within ECM balance applied load, load removed,
load removed
proteoglycans rehydrate and restore cartilage shape

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23
Q

what proteoglycan in particular is important in the absorbance of load, by cartilage?

A

aggrecan in ECM maintaining compressive + repulasive force

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24
Q

what does cartilage protect bone from?

A

shock impact

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25
Q

cartilage proteoglycan histological stains used?

A

H&E
safranin O (red)
Toluidine Blue

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26
Q

upon inflammatory stimuli chrondocytes proliferate and undergo what?

A

hypertrophy

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27
Q

upon inflammatory stimuli chrondocytes undergo hypertrophy. What happens to cartilage when RUNX2 and hedgehog (TFs) are induced?

A

promote more hypertrophy,
- reduced matrix synthesis due to reduced type 2 collagen and aggrecan proteoglycan
- increased matrix proteases MMPs and ADAMTS

28
Q

role of TFs RUNX2 and Hedgehog?

A

regulatory TFs, push chondrocytes to become more hypertrophic + pro-inflamm and start excreting matrix proteases

29
Q

name 2 matrix catabolic proteases excreted in process of chondrocyte hypertrophy
(cartilage degradation) + their role

A

MMPs degrade type 2 collagen fibres
ADAMTS4 and ADAMTS5 degrade aggrecan proteoglycans

30
Q

chondrocytes normally inactive + maintain tissue homeostasis. what happens in OA?

A

get big in inflammation + proliferate more

31
Q

what is OA subchondral bone described as ? and what does it look like?

A

sclerotic
thickened struc (but undermineralised), seen in Micro CT scans

32
Q

what is the Goldner stain used to observe in OA?

A

un-mineralised bone (subchondral)

yellow= cartilage
and none= lack of it. OA

33
Q

how is presence of abnormal type1/ alpha 1 collagen linked to brittle bone?

A

increased alpha1 collagen expression -> HOMOtrimer (normal type1 collagen = hetrotrimer) formn -> kinking in struc = brittle bone

34
Q

synovitis is an early feature of OA? What is this?

A

inflammation of the synovium

35
Q

how can synovitis be detected early on?

A

MRI,
ultrasound,
histochemical analysis of synovial tissue and increased amounts of pro inflammatory cytokines in joint fluid

36
Q

how would synovium appear in OA?

A

thicker, inflamed
and more pro inflamm cytokines picked up as bright white legions in MRI/ radiograph

37
Q

2 things that together drive both joint damage and joint pain?

A

synovitis and inappropriate activity of fibroblast cells

38
Q

synovial inflamm cytokines promote what?

A

cartilage degradation and further synovial inflammation

39
Q

how does synovitis + fibroblast cells drive joint pain?

A

synovial inflamm cytokines promote cartilage degradation and further synovial inflammation

inflamm OA synovial fluid cytokines sensitises joint nociceptors

sensitised nociceptors promote pain signalling -> dorsal horn

40
Q

drug class for the 1st line treatment of OA?

A

topical or oral NSAIDS

41
Q

name 2 drugs that would be appropriate for the 1st line treatment of OA OTC to provide short term pain relief?

A

aspirin and ibuprofen

42
Q

MoA of aspirin/ ibuprofen in the treatment of OA?

A

inhibit COX enzymes, reduce prostaglandins as PEG2 promotes pain in OA

43
Q

why are NSAIDs not appropriate for the long term treatment of OA?

A

non selective = GI issues, peforation, ulceration and bleeding, reduces protective prostanoids in GIT

44
Q

main component of ibuprofen/ nurofen?

A

arachidonic acid

45
Q

why might celecoxib and similar drugs be better than ibuprofen for pain management in OA?

A

cox 2 selective so reduced inflammation and more gastro protective

46
Q

why are cox 2 selective inhibitors not recommended for routine use except those at high risk of GI issues?

A

associated with increased CV risk.
caused by increase in balance between TXA2 and PGI2 -> vasoconstriction +platelet aggregation

47
Q

how do selective COX2 inhibitors –> CV events? SE

p364 pics!

A

PGs and TXA2 maintain vasoconstriction + dilation of BV, normally in a fine balance.

drugs tip scales so get:
↑ TXA2
↑ vasoconstriction
↑ platelet aggregation
↑ risk of CV events

48
Q

name an adjunct therapy that is appropriate for patients with knee OA?

A

glucocorticoid (GCC) intraarticular injections

49
Q

although GCC injections relieve pain, why are they short lived?

A

frequent injections accelerate cartilage damage

50
Q

outline how excess glucocorticoids can cause bone resorption and have the opposite desired effect?

A
  • ↑RANKL ↓OPG secretion from osteoblasts
    -> activation of osteoclasts
  • chronic ↑PTH and ↓BMP2
  • osteoblast proliferation ↓
  • osteocyte apoptosis ↑
  • ↓bone sensing + initiation of bone remodelling
51
Q

What does BMP2 do?

A

acts on osteoblasts to form bone

52
Q

how many more times at risk are obese people of developing osteoarthritis?

A

3-5

53
Q

what fruit shape is associated with excess fat around the belly region and which fruit shape is associated with excess fat around the hip and thighs?

A

apple and pear

54
Q

is a high WHR (>0.9) and a low WHR (<0.85) associated with increased risk of OA?

A

high whr

55
Q

outline some of the reasons why obesity a risk factor for OA?

A
  • traumatic loading can induce cartilage damage
  • degredation fragments like fibronectin promote more inflammation
  • high whr suggests metabolic syndrome related effect
  • adipose tissue is endocrine tissue and secretes adipokines
  • obese tissue secretes more pro inflammatory cytokines which affect the tissue joints
56
Q

is which areas is visfatin highly expressed and what does it promote?

A

areas of cartilage damage,

promotes induction of MMPs in cartilage

57
Q

___ ____ drives an abnormal Type 1 collagen a1/a2 bone phenotype change

A

adipokine resistin

58
Q

what type of fibroblasts are more inflamm + more proliferative?

A

obese

59
Q

whats been recently identified as central mediators of the inflamm repsonse?

A

LncRNAs
expression induced by obesity-associated pro-inflamm cytokines/adipokines

60
Q

what LncRNA mediates inflamm obese Synovial Fibroblast Phenotype ()

A

MALAT1

61
Q

what identifies distinct fibroblast cell subset populations (drivers of certain phenotypes) associated w joint pain?

A

single cell (RNA) sequencing

62
Q

name a gene present in fibroblasts at sites of joint pain that is also a promotor of nerve cell growth?

A

NRN1

63
Q

true or false: pain associated fibroblasts do not promote the survival and growth of neurones

A

false

64
Q

Summarise the treatment options for OA.

A

no disease modifying therapeutics, only symptom treating drugs:

  • NSAIDs, COX2 inhibitors
  • intra-articular glucocorticoid injections
65
Q

obesity + OA what 2 processes can adipokines drive?

A

cartilage damage
sclerotic bone formation

Health 31 (16 decks)

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