Osteoarthritis Flashcards
arthritic conditions
inflammatory- characterised by inflammation of joints and other tissues, degenerative, OA- multifunctional disease
causes of serious joint pain
malignancy or infection ,inflammatory arthritis, metastatic disease, septic arthritis
OA risk factors
genetics, joint mobility, age- increased age, BMI- obesity, muscle, gender- female, race, pain perception, joint morphology
hip OA
loss of joint space, degenerative joint disease that may be caused by progressive damage to articular cartilage, and other structures- 11% of people affected
hip OA- changes
osteophyte formation- extra bony growth§, subchondral sclerosis- shows up on MRI, subchondral cysts, deformity
knee OA
OA affects 8.5 million in UK, 4th largest cause of disability, 4.7 million sought out medical treatment for painful knee OA, projected that it will double due to increasing age population and life choices
what is cartilage composed of
extracellular matrix that is produce by chondrocytes. it consists of 80% of water and collagen fibres, proteoglycans, glycosaminoglycans, and some non collagenous proteins. no blood vessels/ nerves/ lymphatics- receive nutrients via diffusion of molecules through extracellular matrix
different zones in articular cartilage
zone 1/2/3 separated from zone 4 that contains calcified cartilage, which lies superficial to subchondral zone, there is a tide mark that highlights separation- indication of where cartilage starts to calcify
articular cartilage- collagen fibres
the collagen fibres within articular hyaline cartilage showing strength under tension and the ability to withstand compression. type 2 collagen is most prominent in articular cartilage (90%)- composed of compact topological collagen molecules= strength
proteoglycans
proteins that are responsible for majority of water content in tissue- provide strength, consist of linear protein, attached to proteoglycan aggregate= elastic properties and mechanical strength
normal cartilage homeostasis in joint
maintained by delicate balance between synthesis and degradation of extracellular matrix by chondrocytes. MMP- key in degradation of type 2 collagen- activity is increased by IL-1 and TNF, is inhibited by- TIMP
articular cartilage in OA
increase in water content and progressive breakdown in collagen network due to breakdown of type 2 collagen. IL-1 stimulation of chondrocytes causes these cells to produce plethora- activates which increases amount of plasmin- leads to breakdown of cartilage by activation of matrix MPS and collagenase in MM3, breakdown of structure
the normal subchondral bone- boundary
boundary between calcified cartilage and noncalcified is tide mark- the region for CC to bone marrow in subchondral bone, primary cells are osteoblasts, which produce bone matrix, and osteoclasts that are responsible for bone reabsorption and breakdown of matrix=remodeling
tidemark in OA knee
the tide mark is breached and the articular cartilage extends through the tide mark into the subchondral plate and blood vessels from SC bone- leads to vascularization of cartilage- this is accompanied by the growth of nerves- leads to signals of pain being sent- these structures are now painful tissues
where does OA pain come from
ligaments, muscle, joint capsule, AC and synovial osteophytes
bony changes in OA
progressive cartilage degeneration- joint space narrowing, increased bone absorbing sclerosis, osteophytes- bony outgrowth- attempt to stabilize joint
the kellgren- Lawrence OA classification- grade- 0, I, II
0- normal, I- doubtful narrowing of joint space, possible osteophyte development, II- define osteophytes, absent or questionable narrowing of joint space
the kellgren- Lawrence OA classification- grade- III, IV
III- moderate osteophytes, definite narrowing, some sclerosis, and possible joint deformity
IV- large osteophytes, marked narrowing, severe sclerosis and joint deformity
progression of BML
associated with pain in patients with OA, highlighted in progressive OA on MRI. they are a result of synovial fluid penetrating through defects in articular cartilage and entering the subchondral bone leading to microfracture and oedema
BMLs and pain
associated with pain, cartilage nutrition, bone nutrition, meniscal pathology. can have structural changes with disability, OA split into- pain, disability and structural changes
clinical symptoms of knee OA
pain on most days of the last month, inactivity stiffness lasting no longer than 30 mins- if longer= inflammatory arthritis crepitus on moving joint, bony tenderness, limitations of movement, no palpable warmth, bony enlargement with osteophytic lipping,
when are symptoms of OA greatest
individuals greater than 5- years of age
summary of OA
OA is well conserved active/ reparative process, most OA is clinically occult, subchondral bone remodelling, vascularization of the NCC and CC, multiple risk factors, attribute risk varies between sites, risk factors may be intact, biomechanical risk factors appear dominant
