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MSS > MSS03 Introduction To Degenerative Joint Disorders > Flashcards

MSS03 Introduction To Degenerative Joint Disorders Flashcards

1
Q

Osteoarthritis

A
  • Progressive loss of articular cartilage (hyaline cartilage)
  1. Attempted repair of the cartilage
  2. Remodelling and sclerosis of subchondral bone
  3. Subchondral bone cyst formation
  4. Marginal osteophyte
  • Common, Age-related, Heterogeneous group of disorders characterised pathologically by
    —> focal areas of **Loss of articular cartilage in synovial joints
    associated with:
    —> **    Synovitis
    —> **Subchondral bone change
    —> **    Osteophyte formation
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2
Q

Articular cartilage

A
  • Avascular (obtain nutrient by diffusion from bone)
  • Aneural
  • Alymphatic
  • No capacity to repair structural damage due to injury / disease
Content:
1. Chondrocytes (1%)
2. ***Water (70%)
3. ECM (structural macromolecules)
- ***Type II collagen (60%)
- ***Proteoglycan
—> Protein core + ***Glycosaminoglycan e.g. hyaluronic acid, chondroitin sulfate, keratan sulfate, dermatan sulfate) chains
- ***Glycoproteins and Non-collagenous proteins
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3
Q

Chondrocyte-matrix interactions

A

Chondrocytes:
—> degrade and synthesize **matrix macromolecules
—> synthesize and release **cytokines

Matrix:
—> **protects chondrocyte from mechanical damage
—> transduce and **transmits signals with loading

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4
Q

Articular cartilage: Aging vs OA

A
  1. Structural changes
    Aging: Stable
    OA: Progressive
  2. Water content
    Aging: ↓
    ***OA: ↑ (swelling)
  3. Collagen
    Aging: ↑ cross-linking
    ***OA: Disruption of macromolecular organisation
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5
Q

OA articular cartilage changes

A
  • ***↑ water content
  • slow progressive ***loss of proteoglycans
  • change in arrangement and size of ***collagen fibres
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6
Q

Primary OA

A

Joint overload —> surface damage

  1. ***Hips and knees
  2. ***DIP joint of hand (Heberden’s nodes)
  3. Other synovial joints
    - CMC joint of **thumb
    - MTP joint of **    great toe
    - facet joints of spine
    - elbows
    - shoulders
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7
Q

What cause OA

A

Mixture of:

  1. Systemic factors —> predispose to disease
  2. Local mechanical factors —> distribution and severity
  3. Genetic foci: minor contributions
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8
Q

Systemic factors

A
  1. Age
  2. Sex (female more common)
  3. Ethnicity
  4. ***Hormonal status
  5. Bone density
  6. ***Nutritional and metabolic factors
    - DM
    - obesity
    - hypertension
    - sarcopenia (muscle loss)
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9
Q

Local mechanical factors

A
  1. ***Joint deformity / malalignment
  2. ***Obesity
  3. Joint injury
  4. Occupational factors
  5. Sports
  6. Muscle weakness
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10
Q

Lower limb alignment

A

Normally:
Centre of Hip, Knee, Ankle —> straight line —> knee 微向內曲

Malalignment (Eccentric loading):

  • ***Genu valgum (knock knee)
  • ***Genu varum (bow leg)
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11
Q

Prevalence of OA hip and knee

A

OA hip: more prevalent in whites

OA knee: more prevalent in Chinese

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12
Q

Diagnosis of OA

A 
EULAR (European League Against Rheumatism)
3 signs
- Crepitus
- Restricted ROM
- Bony enlargement

3 symptoms

  • Persistent pain
  • Limited morning stiffness
  • Reduced function

ACR (American College of Rheumatology)

  • > 50
  • <30 mins morning stiffness
  • Crepitus
  • Bony tenderness
  • No enlargement
  • No palpable warmth
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13
Q

***Clinical features of OA

A
  1. ***Triphasic mechanical pain:
    - With activities
    —> ↑ when start to walk
    —> ↓ after a while
    —> ↑ again with long walk
    - Severity
    —> at rest
    —> at night
    —> need of pain killers
    —> walking distance and walking aids
    —> effect on daily activities, occupation, hobbies
  2. ***Stiffness
    - Gelling
    —> after wake up
    —> after prolonged immobility
    - Effect on daily activities
    —> hip: cannot put on socks
    —> knee: cannot squat
    - Physical examination
    —> limitations of passive ROM
  3. ***Crepitus
    - on movement (palpable, due to loss of cartilage and chondral bone)
  4. Bony enlargement
  5. Deformity
  6. Limping
    - abnormal gait patterns
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14
Q

***Pathoanatomy of OA (記)

A
  1. Articular cartilage damage (narrowing joint space)
    - grade 0-IV
  2. ***Osteophyte formation (bone spur —> body try to ↑ SA to ↓ pressure on joint)
  3. ***Subchondral sclerosis
    - thickening of subchondral bone plate —> white area instead of white line
    - bone become denser —> sclerotic
    - stronger but more brittle under higher stress
    - cracks —> synovial fluid sips through cracks —> subchondral cysts
  4. ***Subchondral cyst
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15
Q

OA articular cartilage damage grading

A

Grade 0: Normal cartilage

Grade I: Cartilage becomes ***soft and swells (↑ water content: change in consistency)

Grade II: Partial-thickness defect with **fibrillation (shredded appearance) / **fissures (depressions)

Grade III: Increased amount of damage to the level of ***subchondral bone / fissures extend to subchondral bone

Grade IV: Exposed subchondral bone - ***Eburnation (bare bone)

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16
Q

Biomechanics of OA

A
  1. Single-legged stance during walking
    —> 3x body weight
    —> weight of body part + force created by muscle contraction
  2. Knee joint surface loads
    —> 3x body weight during level ground walking
    —> 4x body weight with stair walking
    —> medial knee / tibia (60-70% stress)
    —> ↑ varus malalignment (medial knee even bigger stress)
    —> ↑ knee adduction moment
  3. Patellofemoral joint surface loads
    —> 2-3x body weight while descending stairs
    —> ↑ deep knee bend
    —> ↑ abnormal patellar height
    —> ↑ abnormal tracking (knee cap shifting out of place)
17
Q

***Investigations of OA

A
  1. Plain radiographs (Kellgren Lawrence classification)
    - **narrowing of joint space
    - **    marginal osteophyte
    - **subchondral sclerosis
    - **    subchondral cyst
    - body contour change / defect
  2. MRI
    - Meniscal tear (cannot be seen on X-ray)
    —> traumatic
    —> degenerative
    - **Loose bodies
    - **    Cysts
    —> Baker’s cyst / Popliteal cyst
  3. Blood tests
    - **normal white cell count
    - **    normal ESR (↑ ESR / CRP —> inflammatory rather than degenerative causes)
    - normal bone profiles (Ca, PO4, alkaline phosphatase)
  4. Joint aspiration
    - clear straw colour
    - total cell count <1000 / mm3
    - **gram smear -ve, culture -ve
    - **    crystals -ve
    —> urate crystal (Gouty arthritis)
18
Q

Management of OA

A
  1. Education and modify risk factors
    - lifestyle modification (must walk more to strengthen cartilage, NOT advise to rest)
    - ***weight loss
    - walking aids
    - understanding of disease
  2. Physical
    - ***muscle strengthening
    —> core muscles
    —> knee muscles
    - ROM exercise
    - muscle stretching
    - aerobic exercises
    - knee brace, shoe insoles
  3. Pharmacological
    - Acetaminophen
    - NSAID
    —> Non-selective
    —> COX-2 specific inhibitor
    - Topical agents
    - Others
    —> Narcotic analgesic
    —> Anticonvulsants (Neuralgia)
    —> Antidepressants
  4. Cartilage supplements
    - Glucosamine
    —> substrate for synthesis of proteoglycans
    - lack level I evidence
    - placebo effect
  5. Intra-articular injections
    - Hyaluronate
    —> Glycosaminoglycan
    —> Visco-supplementation
    ——> supplement viscosity of joint fluid —> lubrication and cushioning
    ——> pain relief (incomplete, not always, lasts 6-9 months)
  • Steroid (reserved for inflammatory causes)
    —> anti-inflammatory
    —> short term benefit
    —> no >4 times in single joint within 1 year
    —> side effects
  • Platelet-rich plasma (PRP)
    —> anti-inflammatory effect
    —> lack level I evidence
  • Stem cells
    —> lack level I evidence
  1. Surgical
    - Arthroscopy
    —> loose bodies, meniscal tear with locking symptoms in the knee
    —> arthroscopic lavage / debridement
    ——> washout debris, synovial fluid and remove damaged cartilage / bone
    ——> ineffective / surgical placebo
  • ***Realignment osteotomy
    —> redistribute stress to normal part of the joint
  • ***Joint replacement

MSS (32 decks)

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