osteoarthritis

Question 1

summarise osteoarthritis *

Answer 1

condition of older people

chronic slowly progressive disorder due to failure of articular cartilage that affects the joints of the hand (particularly those in pinch grip), spine and weight bearing joints (hips and knees)

it is not an auto-immune disease - it is due to gradual degeneration of the joint

if overweight or have a job in construction - more at risk

Question 2

what joints does osteoarthritis usually effect *

Answer 2

joints of the hand - DIP, PIP, CMC (of thumb - this is a site of stress)

spine

weight baring joints of lower limbs - knees, hips, 1st MTP (a lot of weight goes through the big toe)

the bones swell at these joints - this is hard on palpation

the space where the cartilage is has gone - get bone on bone

osteophytes at the DIP joints are heberden’s nodes

osteophytes at PIP joints are bouchard’s nodes

Question 3

what is osteoarthritis associated with *

Answer 3

joint pain - worse with activity, better at rest (this is opposite in inflammatory arthritis) - element of morning stiffness but goes after 30mins

joint crepitus - creaking, cracking, grinding sound on moving affected joint (noise isnt associated with damage being done to the joint) when flex the knee you can feel the knee cap creaking because of bone rubbing on bone

joint instability - because pain causes atrophy of muscles supporting the joint

joint enlargement

joint stiffness after mobility - gelling

limitation of motion of joints - internal rotation is 1st movement to go

Question 4

radiological features of osteoarthritis *

Answer 4

joint space narrowing - lose cartilage

subchondral bony sclerosis - increased white

osteophytes - these are bony spurs

subchondral cysts - cysts in bone, look like circle on x-ray

Question 5

comparison of radiological features in RA and osteoarthritis *

Answer 5

joint space narrowing in both - in RA it is secondary to synovitis, in OA it is the primary abnormality

subchondral sclerosis only in OA

osteophytres in OA

osteopenia in RA - common in inflamm arthritis of any cause

bony erosions - in RA - occu initially at margins of the joint where the synovium is in direct contact with the bone

Question 6

describe difference between normal joint and osteoarthritic joint *

Answer 6

normally - smooth layer of cartilage that can distribute weight, synovial mem and fluid

in OA - break down of cartiliage, change to underlying bone = atrophy of muscles and bone spurs, sometimes cartilage break off into synovial fluid - cartilage fragments in fluid - can sometimes be seen on x-ray

Question 7

pathophysiology of osteoarthritis *

Answer 7

develops because of excessive loading ion joints and/or abnormal joint components

genetic and env componenets

osteoarth in hand is more common in women

trauma, dysplasia, obesity, misalignment, muscle weakness and loss of proprioception can cause abnormal stress

trauma - if fracture through joint is nt fused properly = OA

aging, inflamm, metabolic changes and endocrine factors can cause abnormal cartilage

there is chondrocyte apoptosis, loss of proteoglycans and collagen fibril damage

this causes cartilage fibrillation, osteocyte formation and subchondral bone sclerosis

Question 8

describe the features of articular cartilage *

Answer 8

avascular and aneural - therefore doesnt hurt8

aggrecan and collagen (mainly type 2) retain water - give cartilage strength for shock absorption

aggrecan has 100 chondroitin sulfate chains and 60 keratin sulfate chains

monomers of aggrecan are arranged into supramolecular aggregates consisting of central hyaluronic acid filament and non-covalently linked aggrecan

the negatively charged chamical groups of GAGs attract water

Question 9

what are proteoglycans *

Answer 9

they are glycoproteins containing 1/> sulphated glycosaminoglycan (GAG) chains

GAGs are repeating polymers of disaccharides

aggrecan is the main proteoglycan in articular cartilahe

hyaluronic acid is the only non-sulfated GAG and is the major component of synovial fluid - maintains teh viscosity

Question 10

describe the changes in cartilage in osteoarthritis *

Answer 10

reduced proteoglycan

reduced collagen

chondrocyte changes - eg apoptosis

Question 11

bone changes in OA *

Answer 11

changes in denuded sub-articular bone

• proliferation of superficial osteoblasts = sclerotic bone eg subchondral sclerosis
• focal stress on sclerotic bone can result in focal superficial necrosis

new formation at the joint margins - osteophytes - sometimes detectable clinically at bedside

question as to whether the bone is the detrimental feature of OA or if the bony changes are in response to OA in attempt to fix bone

Question 12

describe the management of OA *

Answer 12

education - reassure the pt not rheumatoid and that it is a benign prognosis - usually painful phase for 5yrs then goes away (perhaps pain is from bone remodelling)

physio and hydrotherapy - keep the muscle strong - prevent atrophy which causes instability and = viscuous circle

OT

weight loss where appropriate - hard when difficult to exercise

analgesia - paracetamiol, NSAIDS, intra-articular steroid injection to settle symptoms for short period but effect wears off after 6wks - repeated injection damages joint further

joint replacement - difficult to know when - too early and might have recovered or need another one, too late and the joint is too damaged = missed opportunity

Question 13

therapeutic approaches to OA not approved in UK *

Answer 13

glucosamine and chondroitin sulfate - diet supplement, controversy - idea is replace things lost in joint but question is if it actually leaves GI system ie bioavailability

intra-articular injection sof hyaluronic acid to increase lubrication (viscosupplementation), only in knee joint, not recommended by NICE

there are no disease modifying osteoarthritic drugs

possible future therapies might stop matrix break down, aggrecanase inhibitors, cytokine inhibitors, stimulate repair of matrix