Lecture 4 - finished Flashcards
Define osteoarthritis
OA is a heterogenous group of conditions with a final common pathway that results in common histopathologic and radiologic changes. They are characterised pathologically by focal areas of loss of articular cartilage in synovial joints associated with varying degrees of osteophyte formation, subchondral bone change and synovitis.
Joints involved
Weight bearing joints
DIP’s of fingers (Heberdens nodes)
What are the 3 patterns of OA?
Pattern 1:
- begins with inflammatory phase
- affects many joints
- is the most common pattern
- often occurs in the middle aged or older women
Pattern 2:
- OA affects a single joint
- this pattern often occurs in young adults
- usually related to an injury or congenital joint abnormality
Pattern 3:
- OA affects a few large weight-bearing joints of the leg
- Often occurs in middle-aged people
What are the classifications of OA?
Primary (idiopathic)
Secondary (eg congenital dysplasia)
Epidemiology of OA
Most common arthritis Females more than males Usually after 45yoa Present in 10% of adults Present in 50% of adults over 60 20% of adults over 70 have SEVERE OA
Aetiology of OA
Idiopathic.
Occurs in previously intact joints and with no apparent initiating factors.
Abnormalities have been found in articular cartilage’s:
- ground substance
- collagen
- increased activity of matrix-degrading enzymes (eg collagenase)
- H20 content
Pathogenesis of OA
A number of factors (ie mechanical stress, genetic predisposition, inflammation etc) cause chondrocyte dysregulation. Instead of maintaining cartilage, the chondrocytes break down the cartilage. They also release chemotactic proteins, release proinflammatory cytokines and release matrix degrading enzymes which cause further inflammation in the joint and reduce proteoglycan and collagen synthesis in the joint. A lack of proteoglycan causes a lack of type 2 cartilage, and therefore the joint cartilage matrix is abnormal.
As the cartilage breaks down and thins away, repair processes are initiated. The body interprets this as something that needs to be fixed.
To do this the body releases growth factors, which encourage reactive cartilage growth, reactive bone growth and new capillary growth.
This all causes more damage as we have more bone, more cartilage, more blood in the joint than we’re supposed to. The new blood vessels in the cartilage increase oxygen supply to the cartilage, which causes the cartilage to calcify.
2 important pathological processes describe this:
- Initial biochemical changes in the synovial joint articular cartilage resulting in catabolism and accelerated wear of the cartilage.
- Subsequent reparative processes including low grade inflammation, neovascularisation and fibrosis.
Which parts of the joint are affected in OA?
Articular cartilage
Subchondral bone
Synovium
List some factors believed to be involved in OA pathogenesis
Genetic predisposition Metabolic influences on cartilage Hormonal influences on cartilage Pre-existing joint disposition Patterns/magnitude of joint usage Damage to cartilage WB stress Failure to repair repeated minor trauma
What are the early changes of OA
Biochemical changes appear in the articular cartilage:
- increased water content of cartilage matrix
- proteoglycans = decreased molecular size and increased rate of synthesis.
The altered cartilage wears away more quickly. Chondrocytes compensate by:
- increased metabolic activity
- increased cellular turnover resulting in the release of proteolytic enzymes with cause further damage
Cartilage loss exceeds cartilage replacement. Abnormalities gradually appear in the articular cartilage of the joints, esp WB joints.
- slight surface irregularity
- irregular fragmentation (fibrillation) of cartilage
Can see:
- discrete areas of full thickness cartilage loss
- continued thinning and degeneration of articular cartilage
- exposed subchondral bone appears as shiny foci on the articular surface (eburnation)
- areas of reactive cartilage growth.
Intermediate changes in OA?
Bare exposed bone (eburnation)
Patchy loss of cartilage
Calcification of cartilage margins (osteophytes)
Late changes of OA
Formation of lips (osteophytes) around joint margins
Sclerosis of subchondral bone plate
- stimulation of reactive proliferation of the plate (ie bone is stronger, denser and thicker - sclerotic
Extensive loss of cartilage
Cystic degeneration of underlying bone - loss of normal trabecular structure and deformation of the articular cartilage
Fibrosis of the joint
What are the clinical features of OA?
Pain:
- usually presenting symptom
- insidious onset
- local or referred
- worse on exertion and end range
- better at rest
- relief less complete over time
- pain worse at night
- local tenderness
Stiffness:
- post inactivity
- in time, becomes constant and aggressive
Swelling:
- intermittent = eg effusion of unknown cause
- continuous = eg capsular thickening and osteophytic growths
Deformity:
- capsular contraction
- joint instability
- osteophytes (heberben’s nodes)
- pre-existing deformity which results in OA
Loss of function:
- maybe due to joint damage, pain, muscle wasting
Crepitus:
- may be because of loose bodies in joint
OA CF P S S D L C
Clinical course of OA
Presents in middle age with slow progression
Intermittent course: alternating periods of varying length, characterised by low level/absent ssx and periods of exaccerbation
Only a few joints symptomatic at a time
Joint instability may occur
Pain reduces over time, but stiffness and loss of function remain.
What are the 4 key radiographic signs of OA?
Loss of joint space
Osteophytes
Subchondral sclerosis
Subchondral cysts
