Pathology of OA Flashcards
Name the 6 progressive characteristics of OA?
- Progressive degradation of articular cartilage
- Synovitis (begins as intermittent bouts –> becomes chronic)
- Soft tissue length changes (capsular fibrosis)
o Ligaments
o Tendons
o Fibrocartilaginous joint capsule - Formation of new bone at the joint surface and edges (subchondral sclerosis and osteophyte formation)
- Cyst formation in the subchondral bone
- Collapse of the joint surfaces
What is the clinical presentation of OA?
Increased pain Joint swelling Progressive loss of ROM Muscle inhibition/insufficiency/atrophy Joint deformity and body enlargement Functional limitations
What is primary OA?
No known cause
Contribution of genetic factors, chondrocyte dysfunction and initiating factors from the bone/synovium
What makes up the cellular components of cartilage?
Immature chondroblasts
Mature chondrocytes
What makes up the extracellular matrix of cartilage?
water (60%)
Proteoglycans
Collagen
What is the role of chondrocytes?
synthesis and maintain the ECM - normal turnover occurs
What is the role of proteoglycans?
brush like structure acts as a molecular sponge - to bind water
Protien core with side chains of chondroitin sulphate and keratin sulphate
What is the role and organisation of collagen in cartilage?
Hold the ECM and cells in place
Superficial horizontal collagen fibres
Intermediate collagen arcade
Deep vertical collagen fibres
What are the 4 functions fo the hyaline cartilage?
- Low friction self-lubricating surface for joint movement
- Distribution of load – acts as a shock absorber
- Protects the subchondral bone
- Durable, strong and resilient – resistant to wear
How is nutrition supplied to cartilage?
Avasular - nutrition via the sweep and squeeze mechanism and the underlying subchondral bone
What is are the two phases of early OA?
Cartilage matrix dysfunction and cartilage fibrilation
What occurs during cartilage matrix dysfunction?
o Degrading enzymes - produced by chondrocytes and synovial cells
o Cause the break down in structure of proteoglycans –> water is released
o Decreased water content –> softening of the cartilage –> decreased tissue stiffness –> Cartilage becomes less resilient to normal stresses
o Breakdown of collagen fibres –> loosens the collagen arcade –> weakens the cartilage framework
o Cartilage begins to split up
What occurs during the fibrillation phase?
o Drying out of the cartilage causes it to be more fragile – breaking off of small parts of collagen
o Tiny particles of cartilage which have broken off cause synovial irritation
o Leads to inflammatory response by synovial membrane –> Increase in synovial cell activity
• Increased amounts of mucin & increased volume and viscosity of the fluid
o Intermittent bouts of this ‘inflammatory synovitis’ causes joint effusion
Why might a patient feel grating or crepitus?
Due to fibrillation - as disease progresses there is a change from fine grating to coarse grating
What are the 7 stages of late OA?
- recurrent and chronic synovitis
- progressive and uneven loss of cartilage thickness
- fissuring in deep vertical collagen fibres
- Increased sclerosis of subchondral bone
- Marginal osteophytes
- Subchondral cysts
- Flattening and collapse of joint surfaces