Osteoarthritis pathology + management Flashcards
What is osteoarthritis?
→ A common form of arthritis typically with onset during middle or old age that is characterised by progressive degenerative changes in the articular hyaline cartilage of one or more joints.
→ Accompanied by thickening and overgrowth of adjacent bone.
→ Marked symptomatically by stiffness, swelling, pain, deformation of joints and loss of ROM.
What are the main pathological characteristics of OA?
→ progressive degradation breakdown of articular hyaline cartilage
→ synovitis (intermittent bouts > chronic)
→ soft tissue length changes (muscles tighten + become more lax)
→ formation at new bone at joint surface + edges (subchondral sclerosis + osteophytes)
→ cyst formation in subchondral bone + collapse of joint surfaces underneath cartilage
Pathological changes of OA may result in what symptoms?
- increasing pain (ache during + after WB + as day progresses
- joint swelling
- progressive loss of ROM (morning stiffness)
- muscle inhibition/atrophy
- joint deformity + bone enlargement
- functional limitations
- reduced quality of life
Joints commonly affected by OA?
Cervical spine
Acromioclavicular joint
1st carpometacarpal joint
Phalangeal joints
Lumbar spine
Hip
Knee
Ankle
Great toe
What is primary OA?
- No known cause
- Due to genetic factors?
- Chondrocyte dysfunction?
- Initiating factors in bone/synovium?
What is secondary OA?
KNOWN CAUSE:
- developmental
- inflammatory e.g. gout
- infective
- metabolic
- neuropathic
- endocrine
- traumatic e.g. fracture
- mechanical e.g. cam deformity, femero-acetabular impingement
POSITIVE ASSOCIATION WITH OBESITY + INCREASE AGE + FEMALE
Cells within articular hyaline cartilage?
Chondroblasts = immature cartilage cells
Chondrocytes = mature cartilage cells
- synthesise + maintain molecular framework of the matrix (collagen/proteoglycans, etc)
balanced system of production + degradation under normal circumstances
Ex. matrix within articular hyaline cartilage?
Water (60%) - ability to deal with stress
Proteoglycans - protein core
Collagen fibres - ‘collagen arcades’
What is the struture of proteoglycans?
Contain many long unbranched GAGs attached to a core protein.
Radiate out of the protein creating “bristle-brush” structure
Proteoglycans bind with water creating a molecular sponge (form hydrogen bonds with trapped water molecules).
Create cushioning or lubricating factors.
How is collagen organised?
Superficial zone - has horizontal collagen fibres parallel to the surface to prevent shearing forces
Middle zone - ‘collagen arcade’ - collagen fibres randomly orientated, providing structural support and elasticity.
Deep zone - vertical collagen fibres to anchor the cartilage to the underlying bone, and provides resistance to compressive forces
Functions of articular hyaline cartilage?
- provides low friction self-lubricating surface
- distribution of joint load = shock absorber
- protects subchondral bone
- durable, string + resilient structure, resistance to wear
A drawback of hyaline cartilage?
Lacks direct blood supply - nutrition provided by “sweep and squeeze” mechanism + subchondral bone
Why does cartilage degenerate?
Imbalance between synthesis + degradation of matric constituents due to biomechanical + biochemical changes in the joint
Cartilage attempts repair when necessary, but chondrocytes sparse + easily overwhelmed + cartilage avascular.
What are the early stages of OA pathology?
→ Cartilage matrix destruction
→ Cartilage fibrillation
What occurs in cartilage matrix destruction?
- Activation of degrading enzymes (produced by chondrocytes + synovial cells)
- Proteoglycans break up + water released giving ex. matrix high water content
- Decreased water content = softening of cartilage (less compressible)
- Collagen fibre breakdown - collagen arcade loosens + weakens cartilage framework
Cartilage begins to split + dry out.
What occurs during cartilage ‘fibrillation’ (wearing away)?
→ Tiny particles flake off joint surface + cause irritation of the synovial membrane
→ Inflammatory activity of synovial membrane and:
- inc. activity of synovial cells, creating mucin
- inc. volume + viscosity synovial fluid
What does intermittent bouts of inflammatory synovits cause?
Joint effusions + the increase of fluid in the joint leading to:
- inhibition of muscles crossing joint e.g. quads
- joint adopts loose pack position
Symptoms of cartilage fibrillation?
→Grating or crepitus - crunchy/clicking feeling
→Increased friction - joint stiffness
→Pain on WB
→ Sub-chondral bone exposed
What are the later stages of OA pathology?
- recurrent + chronic synovitis
- progressive + uneven loss of cartilage thickness
- fissuring in deep vertical collagen fibres
- subchondral sclerosis
- marginal osteophytes
- subchondral cysts
- flattening/collapse of joint surfaces
What does recurrent/chronic synovitis lead to?
The joint capsule becomes tighter + harder to move impacting ROM
What does progressive + uneven loss of cartilage thickness lead to?
- reduced joint movement
- contraction of hamstrings/lengthening of quads of surrounding soft tissues (knee)
- sclerosis of subchondral bone - bone thickens to protect itself
What does fissuring in deep vertical collagen fibres lead to?
May extend into bone creating sub-chondral micro-fractures
Weight-bearing subjects the knee to pressure
What does subchondral scleorosis lead to?
Increased bone density due to increased loading (visible on x-ray)
What are marginal osteophytes and what do they lead to?
At articular margins, the bone generates new bone.
Limits end of available joint range.
