week 4: osteoarthritis

Question 1

define osteoarthritis

Answer 1

• progressive collection of pathological changes in a synovial joint
• often associated with wieght bearing/overused joints

Question 2

obvious signs of OA

Answer 2

loss of articular cartiliage, pain, loss of ROM, and soft tissue defects, deformity

Question 3

when is the peak onset of OA?

Answer 3

• peak onset is 50-60
• 9.3 % of the poulation have it

Question 4

clinical signs of OA

Answer 4

• pain in affected joint
• stiffness after inactiivty
• joint enlargment
• limitied ROM
• muscle inhibition
• joint instability
• deformities

Question 5

pathological signs of OA?

Answer 5

cartiliage loss
subchondral sclerosis
subchrondral cysts
synovitis and inflammation
osteophytes (excess bone growth)
local muscle weaknes and impairment

Question 6

what are the 3 areas we see OA degradation?

Answer 6

cartiliage
bone
joint capsule and ligaments

Question 7

how is cartiliage degraded?

Answer 7

• excess forces or normal forces applied to an inadequatly controlled joint leads to cartiliage loss
• leads to abnormal turnover and chrondocyte activity
• chrondocytes release cytokines that release damaging enzymes (MMP’s), leading to further degradation
  -cartiliage leads to being composed of more water, degraded materials and less cells to maintain the tissue
• can increase apoptosis, increased phagocytosis and cell mediators

end result:
- cartiliage softening
- crackling
- fibrilation
- pieces sloughing off
- bone starts to become articulating surface (eburntion)

Question 8

how is bone affected

Answer 8

subchondral scelrosis (scarring)
- bone starts to become articulating surface
- causes microfractures in subchrondal bone (bone underneath cartiliage)

subchrondral cysts:
- synovial fluid goes into fractures causing synovial cysts

synovitis and inflammation:
- angeogenitis + fibroplasia (granulation tissue) invades synovium

development of osteophytes (excess bone growth)
- inflammatory stimmulation fo bone growth
- osteoblast actiivty is a side effect of enzymes
- can limit ROM and increase pain

tracbecular bone distibution of loading is affected

Question 9

how ar joint capsule and ligaments affected?

Answer 9

• loss of caritilage decreases size of joint capsule
• ligaments become slack making joint unstable, and decreased control of joint
• can also lead to further abnormal forces being applied ot the joint

Question 10

risk factors of OA

Answer 10

wieght:
- increases chance of OA
- eg. by 4x in knee if BMI is 30-35

obesity:
- changes in mechanical stress across joint
- joint alignment influences distribution of load
- on articular cartiliage
- on other tissues of wieght bearing joints
- leading to OA

Question 11

ateology (casues)

Answer 11

primary:
- not known
- ageing

secondary:
- trauma
- anotomical
- inflammatoy
- nueropathic
- hameophillia
- heredity (collagen predisposition)

Question 12

why do ppl experience nociception with OA

Answer 12

experience becuase of
- alteration in shape
- ostephytic growth
- joint instability
- loss of ROM
- mechanically sensitised nociceptors

nociception in their bone:
- high interosseous pressure in subchondral bone
- impaoired venous system

nociception due to inflammation/synovitis:
- chemical meidators sensitise nociceptive fibres in mild situations
- can be ongoin due to angiogenesis

Question 13

where does swelling occur with OA

Answer 13

• bony swelling occurs at joint margin, due to cartiliage and bone outgrowths at joint margin
• may be synovitis (inflammation)

Question 14

what is crepitis

Answer 14

• course crepitations
• due to roughening of joint surfaces, bone growth
• it is when the joint does not have smooth movement

Question 14

treatments?
- pharma
- physio

Answer 14

pharma: paracetamol
physio: movement and excercise, surrounding joints by strong muscles