Joints, Articular cartilage and Synovial fluid L2: Hyaline cartilage & synovial joint pathology Flashcards
Hyaline cartilage is vascular/avascular
Avascular
When is hyaline cartilage highly vulnerable?
Excessive, impulsive high loading
Hyaline cartilage health depends on ______.
Loading patterns.

Alterated loading patterns (for hyaline cartilage) such as ____, _____ and _____ can lead to altered compositional properties.
Excessive, Prolonged and Absence
The _______ contributes directly to interstitial fluid pressurization –> attract H2O and offer______ resistance to interstitial fluid flow.
proteoglycan network strong
Most curved surfaces compressed by ____ forces (eg. compression)
external

What 2 types of loading alter chondrocytes metabolism?
- Increased intermittent hydrostatic pressure
- Shear stress
How does increased intermittent hydrostatic pressure alter chondrocytes metabolism?
- Aggrecan
- Type II collagen
- macromolecule
How does shear stress alter chondrocytes metabolism?
- increased the release of the proinflammatory mediator,
- decreased aggrecan and Type II collagen expression, and
- induced molecular changes associated with apoptosis (self-destruction, pre-programmed cell-death)
What are the 5 changes that occur in ECM during ageing?
- hypertrophic changes in chondrocytes
- chondrocytes hypertrophy before they die- aging chondrocytes hypertrophy
- 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
- Tide mark = the line marking the border between the calcified cartilage and the non-calcified cartilage
What are the 4 causes of hyaline cartilage patholgy?
- Acute trauma
- Impulsive high rate of application
- Altered kinematics
- Prolonged overloading
- Obesity ( body weight)
- Prolonged immobilization
- Lack of stimulus
How are ACL ruptures associated with primary cartilage damage & development of OA?
- Mechanism = simultaneously valgus + rotation = dynamic loading in multiple planes
- Often associated with
- Meniscal damage (non-contact, rapid deceleration, valgus force rapid change of direction)
- Primary or secondary
- Medial meniscus (most common injury)
- Meniscal damage (non-contact, rapid deceleration, valgus force rapid change of direction)
- Direct articular cartilage lesion
- Usually femoral condyles (split, impact lesion on femoral condyle = change in ECM)
- Collateral ligament tears (MCL)
- Bone marrow lesion (change in stiffness)
- Haemarthosis
- Bleeding, rapid swelling –> 2nd reaction –> irritation of inflammatory mediators (eg. synovial)
What are the 2 changes (in proteogylcans) that occur in hyaline cartilage during immobilisation?
- • Significant ↓ Proteoglycans ipsilateral side
- Significant ↑ Proteoglycans contralateral side
- Increase in loading of contralateral side
- Even after 50 weeks, ipsilateral side did not fully recover
What are the 4 reasons why hyaline cartilage is unable to spontaneously repair?
*not normal post-inflammatory response
- avascular & aneural
- low cellular density
- less cells to maintain
- low metabolic activity
- inability to migrate to the site of injury (chondrocytes can’t move around)
Why is OA a ‘whole joint disease’?
It affects:
- Cartilage
- Bone
- Intra-articular & periarticular structures
What causes OA?
A result of excessive mechanical stress applied in the context of systemic susceptibility
What are 6 factors that can increase the risk of OA?
- Age
- Thinning of cartilage
- Poor proteoglycan
- Changes in synovial fluid
- Obesity
- Previous injury
- Female gender
- hormonal, biomechanics- pelvis, strength
- Genetic inheritance
- Nutritional factors
What are 4 various theories of pathological changes due to previous injury or disease (sequelae)/
- Mechanical wear &tear
- Bearing surface failure under repeated high loads
- Altered lubrication
- Change in quality of synovial fluid
- Loss of fluid film between articular surface
- Alteration in chondrocyte activity
- Alteration in ECM
- Altered subchondral bone stiffness
What is the chondrocytes theory?
There are 2 types of hyaline cartilage:Temporary and permanent
How does the chondrocytes theory affect endochondral ossification (default pathway)?
- Mesenchymal cells differentiate into chondrocytes
- Chondrocytes undergo terminal differentiation
- Hypertrophy & apoptosis
- Cartilage –> bone
How does the chondrocytes theory affect the normal articular hyaline cartilage?
the terminal differentiation of chondrocytes is halted
What are the 2 types of inflammatory theories?
- Local
- Systemic
What is the local inflammatory theory?
- 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
What is the systemic inflammatory theory?
- Metabolic syndrome
- Age