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MY BONES > Osteoarthritis > Flashcards

Osteoarthritis Flashcards

1
Q

how do surgeons look at cartilage for ex in miniscus?

A

arthroscopy

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2
Q

what is the only cell in articular cartilage

A

chondrocytes

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3
Q

what are the three zones in cartilage

A

deep, intermediate superficial

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4
Q

why are the cartilage zones important to bear in mind?

A

have functional relevance, chondrocytes are stacked differently in each zone

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5
Q

structure of chondrocytes in deep zone?

A

stacked, bone like

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6
Q

what is below the three cartilage layers? (in order from out to in)

A

tide mark, calcified layer, bone

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7
Q

structure of chondrocytes in intermediate space

A

more round, widely spaced, sitting in lacuni

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8
Q

superficial layer chondrocyte structure

A

flatter

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9
Q

what are the three components of healthy extracellular matrix?

A

water, proteoglycan , type 2 colagen

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10
Q

role of type II colagen

A

high tensile strength

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11
Q

what is the most promenent/ dominant proteoglycan?

A

aggrecan

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12
Q

role of proteoglycan

A

they bind water molecules and so exert a swelling pressure and resist compression

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13
Q

Is the chondrocyte a big constituent of cartilage? what %

A

no, 5% but still very important

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14
Q

what does the chondrocyte do?

A

1) produces and degrades cartilage matrix (ECM)
2) (because of 1) and other stuff its generally very metabolically active)
3) has these protrusions- herakia- that protrude n matrix and interact with it a) growth factors b) are involved in mechano-transduction (transducing movement signal)

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15
Q

What special environment characteristic does the chondrocyte withstand in cartilage due to the nature of cartilage?

A

hypoxia

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16
Q

when do chondrocytes stop dividing?

A

asolesance

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17
Q

why is it bad that chondroyte stops dividing in adolesance?

A

bad at healing if we injure, we replace it with fibrilar cartilage which is much worse

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18
Q

what does a normal aggrecan molecule look like?

A

bottle brush

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19
Q

what are the two types of chains on aggrecan that hold onto water? (brush parto pf bottle brush structure)

A

chondroitin sulfate and keratin sulfate

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20
Q

what is the aggrecan molecule linked to on the other end (not brush end)

A

hyaluronan chain - glycoprotein

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21
Q

what are the two types of enzymes that can break down aggrecan?

A

matrix metalloproteinases e.g. MMP-3 and aggrecanases e.g. ADAMTS 4+5

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22
Q

when do we have these enzymes?

A

in health and disease

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23
Q

where do aggrecanases and mmps cleave aggrecan

A

in specific section between specific amino acids each time

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24
Q

what happens when these enzymes cleave aggrecan

A

aggrecan loses its brush part of the molecule, this part leaves cartilage, the one that binds water and it cant bind water anymore

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25
Q

two types of anti-catabolic factors for articular cartilage in the joint

A

intrinsic (from inside cartilage) and extrinsic (from out of cartilage)

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26
Q

examples of intrinsic anti- catabolic cartilage matrix factors

A

a) TIMPs TIssue Inhibitor of metalloproteinases: 4 of these

b) growth factors FGF-2, IGF, TGF-beta, activin A

27
Q

examples of EXTRINSIC anti- catabolic cartilage matrix factors

A

a) hormones (testosterone oestrogen)
b) some drugs eg. FGF-18

28
Q

2 mechanisms of matrix loss?

A

not enough anabolism, too much loss

29
Q

what is something that cartilage/ chondrocyte sneed to maintain cartilage thickness and turnover?

A

mechanical load

30
Q

what happens to cartilage when u dont move

A

cartilage atrophy

31
Q

how does the pressure put on your knees change for different movements?

A

Walking – 2-6 X body weight
Jumping – 7-9 X body weight
Running – 3-8 X body weight
Climbing stairs – 3-10 X body weight

32
Q

what happen if u increase your wight by 5 kg?

A

your knees support 15-30 kg more pressure on walking

33
Q

other tissues affected in OA other than art cart

A

soft tissue, subchondral bone, sinovium,

34
Q

3 processes in joint important in OA

A

inflammation, pain, repair and remodelling

35
Q

collagen is also cleaved by what enzymes

A

collagenases (basically 3 different metalloproteinases: mmp-1, 8, 13)

36
Q

where is collagen cleaved

A

3/4 of way from N to C terminal

37
Q

Molecular changes precede structural changes in cartilage in osteoarthritis

A

Proteoglycan (fragmented by aggrecanases)
Collagen (broken down by collagenases)
Water (initial swelling of matrix, then lost)

38
Q

what are the early changes seen in OA

A

1) loss of proteoglycan on the surface zone of cartilage \
2) fibrillation on the surgace- loss of articulate cartilage integrity

39
Q

what is the pathology of established OA/ what can be seen

A

1) fissuring
2) partial or full cartilage thickness loss, bone cysts, synovial inflammation, osteophytes (as it goes on more structures involved)

40
Q

what can OA lead to in the joint?

A

joint failure

41
Q

what are some risk factors of OA

A

age, obesity, injury (and other mechanical factors) , single gene defects, secondary, conditions: haemochromatosis, secondary OA (from rheumatoid)

42
Q

how many varients rn associated with OA risk?

A

about 100, most very low ( one ex: ITGF beta )

43
Q

what ercentage of oa is post- traumatic oa?

A

50%

44
Q

what percentage of people with injury develop oa and how many years after

A

50% in 5-10 years

45
Q

why does trauma increase risk of OA

A

theres ans inflammatory responce seen in the joint in responce to trauma: mmp-3, IL-6 in synovial fluid

46
Q

what kind of general mechanisms underly oa?

A

not only wear and tear, its an active process (think enzymes bla bla)

47
Q

what are the two main risk factor paths leading to OA

A

INCREASED Load, normal joint/ normal load abnormal joint-> mechanical tissue injury <-> tissue damage/ inadequate repair -> if this equilibrium not achieved then you have symptomatic OA

48
Q

WHY IS (medial joint of) knee mostly affected

A

more weigth falls on it

49
Q

does all OA progress?

A

no

50
Q

why is OA increasing?

A

obesity and age increasing

51
Q

how is it diagnosed

A

clinical, syndrome diagnosis thing, pain, stifness<30 mins, loss of function, crepitus, bony deformity, loss of normal range, inflammation - effusion -warm

52
Q

how is it diagnosed

A

clinical, syndrome diagnosis thing, pain, stifness<30 mins, loss of function, crepitus, bony deformity, loss of normal range, inflammation - effusion -warm

53
Q

why are x rays used

A

staging and treatment plan

54
Q

what can you see in x ray of oa joint

A

loss of space, osteophytes, subchondral sclerosis, bone cysts

55
Q

routine blood tests?

A

not routine, maybe some CRP bc of infl bit much lower than rheumatoid, mainly excluding other factors

56
Q

MOST COMMON JOINT FOR OA which gender

A

knee women

57
Q

what other common joint

A

DIP, PIP, base of thumb, multiple joint disease

58
Q

when in women common in fingers?

A

around menopause

59
Q

core interventions with all people with OA

A

exercise, weight management, information (misconception, not inevitable to prevent, there are things w ecan do, anesthaets steroids, anestelgia ect)

60
Q

surgery done for knee and hip OA

A

joint replacement: arthroplasty

61
Q

base of thumb surgery

A

trapeziectomy

62
Q

what do we aim for in future

A

pain relief. improve function. preventionnn, complex relation bwtween pain and structural changes: doing both is challenging

63
Q

what needs to be imporved

A

1) right drug targets, weve talked a lot about these enzymes, making sure drugs are safe and effective
2) spotting the subgroups of higher risk better: to get better outcomes
3) finding better ways to emasure outcomes (ex. xrays are pretty insensitive way used rn…)

MY BONES (2 decks)

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