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2.5 BRS Musculoskeletal & Rheumatology > Cartilage and OA > Flashcards

Cartilage and OA Flashcards

1
Q

What is osteoarthritis?

A

Loss of articular cartilage at a joint —> bones rub

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2
Q

What is articular cartilage?

A

Hyaline cartilage surrounding the ends of bones

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3
Q

What are the 5 layers of articular cartilage?

A
  1. Superficial
  2. Transitional/intermediate
  3. Deep/radial
  4. Tide mark —> separates cartilage and bone
    (becomes calcified)
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4
Q

What are the 3 components of articular cartilage?

A
  1. Proteoglycan (aggrecan)
  2. Type II Collagen
  3. Water
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5
Q

What are chondrocytes?

A

Producer and degrader of cartilage matrix
- only cells found in cartilage (<5% cartilage tissue)
- highly active —> always in hypoxia
- stop dividing after adolescence —> no more bone
growth (just there for repair)

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6
Q

What are MMPs?

A

Metalloproteinases —> enzymes that breakdown matrix molecules

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7
Q

What is the structure of type II collagen?

A

Triple helix of 3 α strands

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8
Q

Which enzymes breakdown collagen? (2)

A

MMPs
- 1, 3 (stromelysin), 8, 13
- collagenases - specific
- non-specific (cathepsin K)

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9
Q

What is the structure of aggrecan?

A
  1. Hyaluronan backbone
  2. Branches of keratin or chondroitin sulfate
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10
Q

Which enzymes breakdown aggrecan? (2)

A
  1. MMPs
  2. Aggrecanases - ADAMTS-4 & 5
    - cut near where branch meets
    hyaluronan —> lose most of branch
    —> aggrecan loses function
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11
Q

Which 4 non-enzymatic factors contribute to articular cartilage production/breakdown?

A

Intrinsic
1. TIMPs = Tissue Inhibitor of Metalloproteinases
- 1, 2, 3, 4
2. Growth factors - FGF-2, IGF, TGF-β, activin A

Extrinsic
3. Hormones - testosterone (deficicency —> atrophy)
- oestrogen (women OA)
4. Drugs

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12
Q

Which 4 tissues are involved in OA development?

A
  1. Articular cartilage
  2. Synovium
  3. Subchondral bone
  4. Surrounding ligaments and soft tissue
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13
Q

What happens to articular cartilage in OA? (3)

A

Degrades:
1. Proteoglycans fragmented by aggrecanases
2. Collagen broken down by collagenases
3. Water loss (initially swelling)

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14
Q

What are the 3 main symptoms of OA?

A
  1. Pain
  2. Inflammation
  3. Repair remodelling —> shape changes
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15
Q

What can be seen in scans of joints with OA?

A
  1. Cartilage loss —> thinner/none
  2. Fibrillation —> bits breaking off
  3. Loss of proteoglycan
  4. Fissuring
  5. Synovial inflammation
  6. Bone —> osteophytes, cysts
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16
Q

What are the risk factors for OA? (9)

A
  1. Age
  2. Obesity
  3. Female
  4. Family history
  5. Mechanical factors (injury, malalignment)
  6. Chondrodysplasias = collage II defects
    - eg. Stickler Syndrome
  7. Co-morbidities - eg. haemochromatosis
  8. Inflammatory arthropathies —> secondary damage
  9. Genetics
17
Q

How can trauma lead to OA in later life?

A

Joint injury —> inflammatory response to trauma (see MMP-3 and IL-6 in synovial fluid) —> develops into OA over years
- commonly —> meniscal tear
—> cruciate ligament tear

18
Q

What is the process of developing OA? (5)

A
  1. Normal joint with abnormal load
    Abnormal joint with normal load
  2. Mechanical tissue injury
  3. Tissue damage
  4. Inadequate repair
  5. Repeated cycle of 2-5
19
Q

How is OA diagnosed?

A
  1. Clinically
    • Pain with activity
    • Stiffness (<30 mins)
    • Loss of function
    • Examination —> crepitus (crackling noise)
      —> bony deformity
      —> joint line tenderness
      —> loss of range (movement)
      —> warmth
      —> effusion (swollen)

Not necessary:
2. X-rays —> staging, treatment planning, progress
3. Blood test —> not rheumatoid arthritis
—> secondary causes (iron, calcium,
PTH, glucose)

20
Q

Which joints are most commonly affected by OA?

A
  1. Knee (more common in women)
  2. Hand - distal interphalangeal —> Heberden’s nodes
    proximal interphalangeal —> Bouchard’s
    base of thumb
    - menopause —> settle 2-5 years later
21
Q

How is OA managed?

A
  1. Lifestyle - exercise
    - weight management
    - suppport (life activities)
  2. Drugs
  3. Surgery - arthroplasty —> full joint replacement
    - knee —> uni-compartmental replacement
    - thumb base —> trapeziectomy
22
Q

Which 2 types of drugs for OA are being developed?

A
  1. SyMOAD = symptom modifying
    —> treat pain + improve function
  2. DMOAD = disease modifying
    —> slow progression/prevent OA

2.5 BRS Musculoskeletal & Rheumatology (7 decks)

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