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
75% of knee OA affects the ______ compartment.
Medial
How does the hip-knee-angle alignment affect OA/
- 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
What occurs in varus knee? Is there a higher or lower progression of OA?
- mechanical axis passes medial to the knee
- creates a moment arm
- further increases load on the medial compartment.
Higher tibiofemoral adduction moment –> OA progression
What is the role of muscles in knee OA?
To balance external adduction (varus) moment
Which muscles help to balance the external adduction (varus) moment of the knee?
- quadriceps *rectus femoris, (early stance)
- sartorius,
- long head biceps femoris,
- lateral gastrocnemius (late stance)
Decrease varus force = decreased progression of OA
What muscles control eccentric knee flexion @ HS to control loading rate?
Quadriceps
What muscles ensure pelvic control? Why is this important?
- 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 _______ eccentrically control the femur. Why is this important?
Adductors
- “lift” medial femoral condyle to resist varus
What are 4 possible 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
- Autologous chondrocyte implantation
How does the marrow stimulating techniques work in repairing cartilage?
- removing damaged cartilage – drilling holes in the underlying bone to cause bleeding
- natural replacement of hyaline cartilage with fibrocartilage
- quick recovery time
- effective articulating surface than hyaline cartilage
How does the osteochondral autografts and allografts work in repairing cartilage? What are the advantages and disadvantages?
- Remove injured cartilage and the underlying bone
- Replace with cartilage & bone from another site
- within the joint (autograft)
- 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
- gradually activity
- return to sport typically after 6-9 months
- 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
What is the advantage of using osteochondral autografts and allografts to repair cartilage?
the ability to replace both cartilage and bone with similar tissue.
What is the disadvantage of using osteochondral autografts and allografts to repair cartilage?
amount of tissue that can be taken from within a patient’s own joint
