Cartilage Aging Flashcards
What is O?
- progressive and permenant degeneration of the articular cartilage
How does OA differ from rheumatoid arthritis?
> OA - lacks most common classical signs of inflam - serology negative for IgM rheumatoid factor - fibrillation and softening of cartilage surface on arthroscopy - narrowed joint space - osteophyte formation - sunchondral bone sclerosis -crepitus > rheumatoid - more d/t inflamed synovium - more cytokines inovled - not common in animals
Which cytokines are especially involved in cartilage degradation?
- IL1b
- TNFa
> enhance production of enzymes -> cartilage degradation
What forms of OA is most common in animals cf. humans?
animals 2* to trauma
- idiopathic in humans
What type of joints are ^ risk for OA?
- high mobility eg. MCP
What type of dogs are ^ risk OA?
- older
- greyhounds
- large breeds
- lumbosacral disk degeneration ^ freq in GSDs
What other species get OA?
Cats - esp older and in appendicular joints
- pigs get OCD
Is OA always preceded by OCD?
NO
What are the 4 main theories of aging?
> evolutionary theories
- disposable soma/antagonistic pleiotropy/mutation accumulation
molecular thoeries
- error catastrophe/somatic mutation/gener regulation/expression
cellular theories
- senescence/apoptosis/wear and tear/ free radicals
systems theories
- neuroendocrine/immunologic
What is disposable soma theory?
- repair mechanisms only maintained until the organism has reproduced
- balance repair and energy resources
WHat is the Stochastic theory of aging?
= error catastrophe
- randomevents at cellular/molecular level drive aging
- mutated proteins will be degraded but if the protein is itself needed for genetic components this will ^ risk of further muations
Functino of cartilage?
- template for bone growth (foetal)
- resists compression (weight-bearing)
- resilience
- support
- flexibility
- lubrication and movement at diarthrodial joints
What are the major components of hyaline cartilage ECM
- Collagen type 2
- proteoglycans (mostly aggrecan)
- water
- some chondrocytes (otherwise avascular, aneural, low cell density)
How does healthy cartilage behave under compressive loading and unloading?
- intstant deformation when loaded
- creep deformation and plateaux
- instant relaxation when unloded
- stress relaxtion
How does UNhealthy cartilage behave under compressive loading and unloading?
More deformation on loading
- either excessive rebound when unloaded (if slightly affected)
- or insufficient rebound when unloaded (with OA)
How do GAGs attract water?
Na and Cl attracted to balance charges, water by osmosis
What hydrostatic pressure is hyaline cartilage under?
-similar to car tyre pressure!!
What is mechanical behaviour determined by? How does OA affect this?
- water
- collagen
- PGs
> ^ collage ^ cartilage stiffness (tensile modulus)
> In OA disruption to collagen fibres decreases the strength of the solid matrix
What are the 2 theories of OA formation?
> wear and tear
- poor capacity of cartilage to repair itself
- no vasculature
biological process
- inblanace between anabolic (decreased) and catabolic (increased|) capabilities of cartilage cells - chondrocytes
What site is most common for dog OCD lesions?
Medial trochlear ridge
What drives OA formation?
Not classical inflam (few neutrophils, abscnece of systemic inflam)
- but activated B and T cells are ^, providing a source of IL-1b and TNF a
- 2* synovial involvement?
Risk factors for OA?
- age > cellularity v, calcification ^, proliferation of chondrocytes reduced, maybe thinning of cartilage? - genetic factors - sex - environment - mechanimcal trauma
Is thinning of cartilage predictive of DJD?
NO (study done, thicker cartilage not related to healthy tarsocrural joints)
How is weight distribution of cartilage defined?
Surface area, not thickness
- inverseverly proportional to the congruence of the joint (if it is evenly spread foce, the cartilage can be thinner and less deformation is required; if the joint is incongruent the thicker cartilage must be present to allow more deformation and ^ surface area this way )
How does “junk accumulation” affect joints?
- proteolytic mediated processing of PGs -> derease in fixed charge density d/t loss of PGs
- accumulation of junk degraded products
- altered activity of cells d/t junk ‘matrikine’ activity
Is OA an inevitable consequence of aging?
NO!!!
