2. Osteoarthritis Flashcards Preview

M2 Musculoskeletal > 2. Osteoarthritis > Flashcards

Flashcards in 2. Osteoarthritis Deck (48):

Osteoarthritis: number of joints affected? inflammatory vs non? timing? distribution?

-could be mono, oligo, or polyarticular




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osteoarthritis: general features? (progression, cause, age of patients, morning stiffness, appearance of joints?)

slowly progressive, disintegration of cartilage. cause unknown. generally age >50, morning stiffness < 30 min, crepitus, no inflammation, bony enlargement/tenderness can cause secondary damage to surrounding structures

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primary osteoarthritis - prevalence?

very common. most people get this as they age.


secondary osteoarthritis - what is the cause?

degenerative process that was preceded by RA, mechanical or metabolic problem (excessive Fe, ACL tear)


OA: what is seen on labs? (ESR, RF titer, fluid aspiration)

ESR < 40

RF Titer < 1:40

non-inflammatory synovial fluid


OA: what is seen on imaging?


-joint space narrowing

-subchondral cysts and sclerosis

-malalignment of joints

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RA is a disease of what part of the joint?

the synovium. synovium proliferates (almost tumor-like)

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psoriatic arthritis is a disease of what part of the joint?

synovium and enthesis (tendon)

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gout, pseudogout, septic arthritis are diseases where what is occuring?

infection and the presence of things in the joint that don't belong there (urate crystals, bacteria, CPPD- which are another kind of crystals)

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OA is a disease of what part of the joint?

cartilage. wears away over time

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Two features of the joint seen in early stage of OA?

-degeneration of cartilage

-reactive new subchondral bone

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Three features of the joint seen in later stage of disease?

-cartilage particles in joint space

-loss of cartilage -> bone on bone

-bone hypertrophy

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Articular/hyaline cartilage: what is the main purpose? general qualities? what is it made of?

-shock absorber of diarthroidial joints

-high H20 content, stiffness: like a gel-pack, fluid under pressure

-well-organized arcs of collagen fibers, with proteoglycans in matrix

-chondrocytes interespersed throughout

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what lies directly beneath articular/hyaline cartilage?

subchondral bone


what happens to cartilage in early OA? (grossly)

-increased water content --> soggy

-more pliable

-deformation with loading


what happens to cartilage in early OA, at the histological level?

-small tangential clefts on surface

-deeper vertical clefts

-splitting/fibrillation (shagginess)

-chondrocytes clump together

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Later in OA progression: what happens to cartilage? bone? infiltrates? other structures?

-cartilage -> progressive fibrillation and loss/erosion

-bone: osteophytes and subchondral sclerosis

-some inflammatory infiltrates in synovium

-ligaments -> lax

-weak surrounding muscles

-Bone on bone

(pic: partial erosion of cartilage, condensation of subchondral bone, osteophyte)

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general qualities of chondrocytes? (metabolic activity? vascular supply? what do they do? regeneration?)

-only cell type in adult cartilage matrix

-low metabolic activity; no vascular supply

-maintains structure/function of cartilage matrix

-little ability to regenerate

-maintains low turnover rate of ECM proteins


OA: what cell type is the main problem?



generally, how do chondrocytes contribute to OA?

normally they are quiescent cells, but in response to stress/injury they will activate --> promote matrix degradation and downreg repair.

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what are the specific processes by which chondrocytes contribute to OA?

chondrocyte stress leads to proliferation and stress response such as growth factors, cytokines, cartilage-degrading proteinases, other inflammatory mediators -> matrix degradation

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matrix degradation leads to what?

matrix degradation products feedback and upregulate the chondrocyte stress response -> vicious cycle. may also release anabolic factors -> osteophyte formation

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which joints does OA most commonly affect?

hands, hips, knees


Hand involvement with OA: distribution by gender? which joints most affected?

-Females 4x more likely to have hand involvement than men (more freq found post-menopause). especially basilar thumb joint (first carpometacarpal - CMC).

-Male: wrists more common (possibly occupation-related)

-Both: DIP, PIP

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general gross appearance of hand joints in OA?

-bony enlargement in DIP and PIP joints. joints look swollen but feel like bone

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prevalence of OA in various compartments of the knees?

-75% medial (so usually yields a VARUS deformity: "knock-knees"

-48% patello-femoral

-25% lateral

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risk factors in OA?

age, sex, obesity, joint injury, status of ligaments (loose = bad), genetics (genetics impt)


women and OA: when is prevalence highest relative to men? possibly due to what? presentation of OA?

-After 50, women >> men in terms of OA prevalance -Possibly due to hormonal changes: HRT studies unclear -Women -> more generalized OA (involvement of hands, spine, knees, hips)


general points about obesity and OA?

-being 10 lbs overweight incr forces on knee by 30-60 lbs per step

-generally being overweight incr your risk of OA by quite a lot

-overweight people have higher rates of hand OA, suggesting circulating factor is involved (not just direct pressure on joints)


generally, what is the connection between injury and OA?

-injury predisposes to OA

-congenital dysplasias (esp hip)

-fractures through articular surfaces

-inj that leads to joint instability

--Essentially, if you fracture a joint, you are eventually going to get OA in that joint


generally, connection between genetic risk and OA?

in twin studies, genetics account for 50-70% risk in certain joints. BUT no single gene has been identified as responsible


OA of the MCPs, especially in a younger person --> what should I consider?


Pic: Hand x-ray of pt with hemochromatosis.

Note the extensive MCP (esp MCP 2, MCP 3) & wrist disease

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what are 3 causes of secondary OA?

(the three that he starred, from a list of many causes of secondary OA)

-inflammatory joint disease


-metabolic dz


OA: what is the good news/bad news?

-OA is less serious than RA (which is more systemic)

-We don't have good treatment for OA


Of all the various things we do to treat OA (treating mainly the pain) what has been shown to work?

weight loss, exercise, other non-pharm approaches, joint replacement (one study: diet + exercise improved mobility and pain by 50%)


how does exercise help OA?

pain directly correlates with degree of weakness, stronger muscles improve stability and lessen pain. Best is to train muscles of daily activity.


Treatment of OA when all else fails?

joint replacement.

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glucosamine/chondroitin sulfate: benefit to OA patients?

trial says no. measurement = pain score by patient assessment.


does arthroscopic surgery to clean out the debris in the knee joint help OA pain?


Results were not better than the control, which was a sham surgery!


does viscosupplementation (injection of HL Acid into joint) offer any help?

modest effect, helps some patients.


does Tanezumab (antibody to inhibit nerve growth factor) help OA?

nope. there was an effect but ultimately the patients on the drug had more knee replacements (incr use of a injured joint that was no longer painful due to meds)


in response to mechanical loading of articular cartilage, chondrocytes do all of the following except what?:

downregulate collagen



release MMP

produce anabolic factors

in response to mechanical loading of articular cartilage, chondrocytes do all of the following except what?: 

downregulate collagen



release MMP

produce anabolic factors

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what compartment of the knee is most commonly affected in OA?



average life expectancy of a prosthetic knee joint?

15-20 y, depends on patient


If MCPs are predominantly involved, there is ulnar deviation, and the DIPs are spared, should I think RA or OA?



if the DIPs are predominantly involved, and the MCPs are somewhat spared, should I think RA or OA?



What's going on?

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Top pic = normal.

Lower pic = Degenerative changes:

1.  Diffuse hypercellularity. More chondrocytes, lost a lot of the proteoglycans. Chondrocytes are both proliferating and hypertrophying.

2.  Extensive loss of acid mucopoly-saccharide from matrix with diminished red dye fixation. 

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What's going on here?

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As cartilage starts to give more under repeated loading, damage starts to occur, basically tearing & cracking

Early degenerative changes are now present in this articular cartilage:

1. Small tangential clefts on surface of already altered hyaline cartilage

2. Deeper vertical cleft

3. Splitting process , “fibrillation”

4. Clumping of chondrocytes

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