Hyaline cartilage and synovial joint pathology

Question 1

hyaline cartilage health

Answer 1

Hyaline cartilage health is promoted by appropriate loading patterns.
Altered loading patterns (excessive, prolonged or absence - gives time for fluid to flow out and expose solid) may alter the compositional properties of hyaline cartilage.

Question 2

The proteoglycan network

Answer 2

contributes directly to the interstitial fluid pressurisation > the charged glycosaminoglycan chains attract H2O & offer strong resistance to interstitial fluid flow
* Hyaline vulnerable to shear stress

Question 3

Types of load alter chondrocyte metabolism

- Intermittent hydrostatic pressure increased

Answer 3

• Aggrecan
• Type II collagen
• macromolecule

Question 4

Types of load alter chondrocyte metabolism

- Shear stress

Answer 4

• increased the release of the proinflammatory mediator,
• decreased aggrecan and Type II collagen expression, and
• induced molecular changes associated with apoptosis

Question 5

Age relatation of the ECM

Answer 5

• hypertrophic changes in chondrocytes
• loss of glycosaminoglycans (associated with aging and OA)
• calcification of the ECM
• increased number of tidemarks > 60 years age
• movement of the tide mark to the cartilage surface = replacement
of the lower calcified cartilage by bone

Question 6

Tidemark

Answer 6

Tidemark = the line marking the border between the calcified cartilage and the non-calcified cartilage

Question 7

Causes of hyaline cartilage pathology

Answer 7

1. Acute trauma
2. Altered kinematics
3. Prolonged overloading
4. Prolonged immobilisation

Question 8

ACL ruptures associated with primary cartilage damage & development of OA

Answer 8

Mechanism = simultaneous valgus + rotation = dynamic loading in multiple planes
Often associated with:
• *Meniscal damage ~65-75% of ACL ruptures
• primary or secondary
• medial meniscus
• *Direct articular cartilage lesion ~50%
• usually femoral condyle
• Collateral ligament tears
• Bone marrow lesions
• Haemarthrosis - get rapid swelling

Question 9

ACL

Answer 9

usually non-contact valgus with rotation

• high load, impulsive
• occurs in change in direction

Question 10

Immobilisation

Answer 10

• Significant ↓ Proteoglycans ipsilateral side
• Significant ↑ Proteoglycans contralateral side
• Even after 50 weeks ipsilateral side did not fully recover
“The proteoglycan depletion was not reversed in all of the cartilage surface sites even after a 50 week remobilisation period.”

Question 11

Inability to spontaneously repair

Answer 11

1. avascular & aneural
2. low cellular density
3. low metabolic activity
4. inability to migrate to the site of injury

Question 12

Osteoarthritis is a ‘whole joint disease’

Answer 12

• Cartilage
• Bone
• Intra-articular&periarticular structures

Question 13

Multifactorial aetiology of osteoarthritis

Answer 13

A result of excessive mechanical stress applied in the context of systemic susceptibility Susceptibility to OA may be increased by:
• age (slow condrocytes, thinnong of cartilage, synovial fluid)
• obesity
• previous injury
• female gender
• genetic inheritance
• nutritional factors

Question 14

Various theories of pathological sequelae

Answer 14

Mechanical wear & tear
• Bearing surface failure under repeated high loads
• Altered lubrication
Alteration in chondrocyte activity Alteration in ECM
Altered subchondral bone stiffness

Question 15

Chondrocyte theory

Answer 15

2 types of hyaline cartilage: temporary and permanent

Question 16

Chondrocyte theory

- Endochondral ossification

Answer 16

• Mesenchymal cells differentiate into chondrocytes
• Chondrocytes undergo terminal differentiation
• > hypertrophy & apoptosis
• Cartilage>bone

Question 17

Chondrocyte theory

-Normal articular hyaline cartilage

Answer 17

• the terminal differentiation of chondrocytes is halted

Question 18

Chondrocyte theory

- Osteophyte formation

Answer 18

• Mesenchymal cells in periosteum differentiate into chondroblasts
• Cartilage at joint periphery
• Chondrocytes undergo terminal differentiation A/A
to decrease stress, increase csa

Question 19

Inflammatory theories:

Local:

Answer 19

• Synovium irritated by cartilage fragments
> inflammatory response
> Inflammatory markers in synovial fluid
> activate superficial chondrocytes
>Proteases > Cartilage breakdown
• Abnormal mechanical stress / increase in shear stress
> mechanotransduction
> synthesis of inflammatory mediators by chondrocytes & subchondral osteocytes

Question 20

Inflammatory theories:

systemic

Answer 20

metabolic system
age
* twice as likely as in obese women

Question 21

75% of knee OA affects the medial compartment

Answer 21

Hip-knee-ankle alignment
contributes to the load distribution across the knee articular surface proportionately divides load between the medial and lateral compartments
* The load-bearing mechanical axis
= a line from the centre of femoral head to the center of the talus
In a varus knee
> mechanical axis passes medial to the knee
> creates a moment arm
> further increases load on the medial
compartment.
Higher tibiofemoral adduction moment increases OA progression

Question 22

knee OA

Answer 22

increasing varus, increasing MA of mechanical load baring axis
- medical component undergoes OA

Question 23

The role of muscles in knee OA

Answer 23

To balance external adduction () moment:
• quadriceps, rectus femoris, (early stance), sartorius,long head biceps femoris, lateral gastrocnemius (late stance)

To control eccentric knee flexion @ HS to control loading rate
• Quadriceps

Pelvic control
• Contralateral hip abductors - gluteus medius & minimus
• Contralateral hip drop moves CoM toward swing limb i.e. further from
centre of stance knee > increases moment arm of ground reaction force

Stance limb hip adductors eccentric control of femur
• “lift” medial femoral condyle to resist valgus

Question 24

Articular cartilage repair procedures

Answer 24

1. Arthroscopic lavage and debridement
   - cleaning out and evening up the joint surface - short-term relief
2. Marrow stimulating techniques
3. Osteochondral autografts and allografts 4. Autologous chondrocyte implantation

Question 25

Cartilage repair - Marrow stimulating techniques

Answer 25

removing damaged cartilage – drilling holes in the underlying bone to cause bleeding
> encourages the natural replacement of hyaline cartilage with fibrocartilage
- quick recovery time
- but, less effective articulating surface than hyaline cartilage

Question 26

Cartilage repair - Osteochondral autografts and allografts

Answer 26

• Remove injured cartilage and the underlying bone
• Replace with cartilage & bone from another site
• within the joint (autograft) or
• a tissue donor (allograft)
• The replacement core is gently tapped into place until it lines up with the surrounding tissue. No screws or other devices are typically needed to hold the replacement core in place since it fits tightly.
• start to weight-bear within 4-6 weeks of surgery
• activity gradually increased
• return to sport typically after 6-9 months

Question 27

Cartilage repair - Osteochondral autografts and allografts

pros and cons

Answer 27

• advantage = the ability to replace both cartilage and bone with similar tissue.
• limitation = amount of tissue that can be taken from within a patient’s own joint

Question 28

Cartilage repair - Autologous chondrocyte implantation

Answer 28

• 250mg cartilage from low-load region
• Extract chondrocytes and grow for 6 weeks
• Applied in arthrotomy
• Scaffold matrix
• Covered with periosteal flap
or other membrane
• 77% success rate at 2- & 5-years

Question 29

• Chondrocytes produce proteolytic enzymes (breaks down proteins)

Answer 29

> degrade proteoglycans & collagen type II 
> altered biomechanics:
• lower modulus
 • increased permeability 
- Greater & more rapid deformation
> exposes the solid component to stress 
> exposes chondrocytes to shear stresses 
> cartilage breakdown
> surface fibrillation
> increased frictional forces