Osteoarthritis Flashcards
2 types of arthritis
> Inflammatory
- Rheumatoid
- Ankylosing Spondylitis
- Juvenile Idiopathic Arthritis
- Lupus
> Degenerative
- Osteoarthritis = 4th largest cause of population due to obesity and sedentary lifestyles (progressive damage to articular cartilage + surrounding structures)
Normal Cartilage Makeup
> Extracellular matrix - produced by chondrocytes in lacuna of matrix (no lymph/ nerve/ blood vessels - nutrition is via diffusion of synovial fluid)
- 80% water
- Collagen fibres
- Proteoglycans
- Glycosaminoglycans
- non-collagenous proteins
Normal Cartilage Structure
> Zone 1 = superficial - few cells + collagen fibres > Zone 2 = Intermediate - collagen > Zone 3 = Deep - vertical collagen > Zone 4 = calcified cartilage > Subchondral bone
- Between Zone 3 and 4 = tidemark where calcified cartilage starts
Collagen network
> Mostly type 2 collagen (90%)
Each fibre = 3 helical collagen molecules = interwoven peptide chains
- this gives cartilage its strength under tension + ability to withstand compression
Proteoglycans
> Proteins within matrix (with glycosaminoglycan side chains)
Bind water - responsible for water content of cartilage
- provides elastic properties and compressive strength
Normal homeostasis
> Matrix metalloproteinases (MMP’s) - responsible for degradation of type 2 collagen
MMP activity is increased by interleukin 1 (IL-1) and tumour necrosing factor alpha (TNF-a)
MMP activity is inhibited by tissue inhibitor of MMP (TIMP)
Early OA changes
> IL-1 stimulates chondrocytes to produce plasminogen activators
levels of plasmin increase
activates MMP’s to breakdown triple helix structure of collagen
- results in increased water content and progressive breakdown of collagen network (denaturation of type 2 collagen)
Normal Subchondral bone
> Lies under calcified cartilage (separated by osteochondral junction)
Primary cells = osteoblasts which produce collagen and bone matrix + osteoclasts which are responsible for bone resorption
Subchondral bone in OA
> Fissures break osteochondral junction
allows blood vessels to grow into calcified and non-calcified cartilage (accompanied nerve cell in growth = pain signals)
Bony changes in OA
> osteophytes - bony outgrowths covered in fibrocartilage (produced to try and resolve mechanical instability or abnormal repair of a stress fracture within the subchondral bone)
Sclerosis - bone under cartilage becomes harder + more dense
Reduced joint space - measure of cartilage degradation
Kellgren Lawrence scale
> 0 = normal
1 = doubtful narrowing of joint space - likely softening and formation of small fissures in cartilage
= possible osteophyte formation
2 = definite osteophyte formation
= questionable narrowing of joint space (ie might be might not)
3 = moderate osteophyte
= definite narrowing + possible joint deformity
= some sclerosis
4 = Large osteophytes
= marked narrowing + joint deformity
= severe sclerosis
Bone marrow lesions
> Associated with developing OA if patient is healthy or if patient has OA - associated with pain
Many theories but main one is that it is due to synovial fluid infiltrating subchondral bone via fissures creating microfractures and oedema
associate with:
- pain
- disability
- structural change (cartilage + bone attrition as well as meniscal pathology in knee)
*Patient may not have all 3 symptoms but likely will have 1
Summary of OA
> OA is impaired repair process (may not progress but most likely to at hip)
Characterised by subchondral bone remodelling, neovascularisation of synovium and calcification of cartilage
Many risk factors (change depending on joint site)
- biomechanical factors seem to be most important
Risk factors for both onset and progression of OA
> Genomics > Joint mobility > Muscle > BMI > Age > Gender (female>male) > Race > Pain (perception) > Joint morphology (abnormal wearing/loading)
Hip OA
> characterised by:
- loss of joint space
- osteophyte formation
- subchondral sclerosis
- subchondral cysts (fluid filled space forms in bone)
- deformity of femoral head
