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Flashcards in Cartilage Aging Deck (26):

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
> 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?



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?