Hyaline cartilage and synovial joint pathology Flashcards
hyaline cartilage health
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.
The proteoglycan network
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
Types of load alter chondrocyte metabolism
- Intermittent hydrostatic pressure increased
- Aggrecan
- Type II collagen
- macromolecule
Types of load alter chondrocyte metabolism
- Shear stress
- increased the release of the proinflammatory mediator,
- decreased aggrecan and Type II collagen expression, and
- induced molecular changes associated with apoptosis
Age relatation of the ECM
• 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
Tidemark
Tidemark = the line marking the border between the calcified cartilage and the non-calcified cartilage
Causes of hyaline cartilage pathology
- Acute trauma
- Altered kinematics
- Prolonged overloading
- Prolonged immobilisation
ACL ruptures associated with primary cartilage damage & development of OA
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
ACL
usually non-contact valgus with rotation
- high load, impulsive
- occurs in change in direction
Immobilisation
• 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.”
Inability to spontaneously repair
- avascular & aneural
- low cellular density
- low metabolic activity
- inability to migrate to the site of injury
Osteoarthritis is a ‘whole joint disease’
- Cartilage
- Bone
- Intra-articular&periarticular structures
Multifactorial aetiology of osteoarthritis
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
Various theories of pathological sequelae
Mechanical wear & tear
• Bearing surface failure under repeated high loads
• Altered lubrication
Alteration in chondrocyte activity Alteration in ECM
Altered subchondral bone stiffness
Chondrocyte theory
2 types of hyaline cartilage: temporary and permanent
Chondrocyte theory
- Endochondral ossification
- Mesenchymal cells differentiate into chondrocytes
- Chondrocytes undergo terminal differentiation
- > hypertrophy & apoptosis
- Cartilage>bone
Chondrocyte theory
-Normal articular hyaline cartilage
• the terminal differentiation of chondrocytes is halted
Chondrocyte theory
- Osteophyte formation
• Mesenchymal cells in periosteum differentiate into chondroblasts
• Cartilage at joint periphery
• Chondrocytes undergo terminal differentiation A/A
to decrease stress, increase csa
Inflammatory theories:
Local:
• 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
Inflammatory theories:
systemic
metabolic system
age
* twice as likely as in obese women
75% of knee OA affects the medial compartment
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
knee OA
increasing varus, increasing MA of mechanical load baring axis
- medical component undergoes OA
The role of muscles in knee OA
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
Articular cartilage repair procedures
- Arthroscopic lavage and debridement
- cleaning out and evening up the joint surface - short-term relief - Marrow stimulating techniques
- Osteochondral autografts and allografts 4. Autologous chondrocyte implantation
Cartilage repair - Marrow stimulating techniques
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
Cartilage repair - Osteochondral autografts and allografts
- 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
Cartilage repair - Osteochondral autografts and allografts
pros and cons
- 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
Cartilage repair - Autologous chondrocyte implantation
• 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
• Chondrocytes produce proteolytic enzymes (breaks down proteins)
> 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
