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
