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MSK/Derm > Osteoarthritis > Flashcards

Osteoarthritis Flashcards

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1
Q

What is osteoarthritis?

A

joint failure, a disease in which all structures of joint have undergone pathologic change, often in concert

hyaline articular cartilage loss, present in focal and, initially nonuniform manner

there are numerous pathways that lead to joint failure, but initial step is often joint injury in the setting of failure of protective mechanisms

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2
Q

pathological findings in osteoarthritis

A

main one is hyaline articular cartilage loss

thickening and sclerosis of subchondral bony plate, by outgrowth of osteophyes at joint margin

stretching of articular capsule

mild synovitis in many affected joints

weakness of muscles bridging joint

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3
Q

Why is the societal impact of osteoarthritis so large?

A

most common form of arthritis in humans

does not lead to disability ineveryone but is a common painful condition that increases with age

inadequacy of current treatment allows it to be the leading cause of chronic disability

risk of disability attributable to knee osteoarthritis in elderly

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4
Q

systemic risk factors for incident OA

A

age (all joint sites)

gender (all sites)

genetic factors (many sites, especially hand)

excess body weight (especially knee)

certain occupations

elite athletic activity

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5
Q

local risk factors for incident OA

A

major injury (all, even atypical sites)

meniscectomy (knee)

developmental abnormalities (especially hip)

varus alignment (knee)

meniscal tear, meniscal extrusion (knee)

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6
Q

What age-related changes contribute to development of OA?

A

decline in neuromuscular joint protective mechanisms (muscle function, proprioception, soft tissues sthat stabilize joints)

decline in biomechanical properties of cartilage matrix

reduced ability of joint to rebound from injury

reduced regenerative potential of joint tissue

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7
Q

How does excess body weight affect risk of getting OA?

A

increases risk of incident and progressive knee OA

weight in young adulthood/middle age predicts knee OA risk later in life

in overweight persons, weight reduction reduces risk of incident knee OA

increases risk of hip OA (less than for knee)

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8
Q

What are the structures that protect the joints?

A

joint capsule and ligaments - soft tissue restraint to excessive motion, mechanireceptors via sensory afferent nerves and spinal cord provide feedback for muscle activity

muscles and tendons - activity helps to decelerate joint before impact and to distribute load

synovial fluid - helps to reduce friction between articulating cartilage surfaces

failure of these joint protectors increases risk of joint injury and OA

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9
Q

What is the process of repair in response to join insult in OA?

A

destruction and repair of joints

attempt by all joint components to produce new tissue:

  • new bone (osteophytes)
  • synovial hyperplasia
  • capsular thickening
  • initial increase in chondrocyte number and activity
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10
Q

What is the natural history of OA?

A

site of initial insult may be any tissue of the joint

compensated OA - joint remodeling keeps pace with tissue loss

decompensated OA - severity/chronicity of insult outweighs repair process

natural history of one joint includes compensated and decompensated phases

not all joints with OA experience disease progression

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11
Q

What happens in compensated OA?

A

increased chondrocyte activity

new bone formation

capsular thickening sustains stability

mechanical forces redistributed across the compromised joint

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12
Q

What happens in decompensated OA?

A

disease progression

symptoms start occurring

disability results

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13
Q

What component of carilage provides most of its ability to sustain a load?

A

hydrostatic pressure in the interstitial water

water is absorbed because of the hydrophilic nature of the aggrecans

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14
Q

Whay happens to cartilage in OA?

A

gradual depletion of aggrecan

unfurling of tightly woven collagen matrix

loss of type II collagen

cartilage has greater water content due to destruction of collagen network and proteoglycan loss - impairs ability of cartilage to sustain load

without is compressive stiffness, cartilage becomes more vulnerable

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15
Q

What are the factors involved in balance of synthesis and catabolism in articular cartilage?

A

self-repair proteins (PDGF, IGF-1, TGF-beta)

cytokiens (IL1, TNFalpha)

lipid mediators (prostaglandins)

free radicals (NO)

matrix degradation products

synovial cells

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16
Q

What is the role of synovial cells in the balance of synthesis and catabolism in articular cartilage?

A

phagocytize cartilage fragments released into joint

synovial inflammation

synovial cells release matrix metalloproteinases and cytokines which further alter extracellular matrix and activate chondrocytes

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17
Q

What is the role of matrix metalloproteinases in cartilage degradation?

A

main proteinases involed in cartilage destruction of OA

made by chondrocytes and synoviocytes under influence of cytokines

activities controlled by TIMPs (tissue inhibitors of metalloproteinases)

major proteinases involved in tissue destruction - collagenase-3 (MMP13) and aggrecanase-1 (ADAMSTS4)

these enzymes are a potential target for drug development to try to modify disease course

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18
Q

What is the pathology of OA?

A

cartilage - initial surface fibrillation and irregularity, then full thickness defect (extending down to bone), then larger area of cartilage damaged and/or lost, leaving bare bone

bone - thickening and stiffness of subchondral plate, osteophytes form at joint margins

synovium - can become edematous and inflamed

capsule - edema, and later fibrosis

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19
Q

OA phase 1

A

edema of extracellular matrix

microcracks appear on cartilage surface

focal loss of chondrocytes, alternating with areas of chondrocyte proliferation

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20
Q

OA phase 2

A

microcracks deepen

vertical clefts form in cartilage

clusters of chondrocytes appear around these clefts and at surface

21
Q

OA phase 3

A

fissures cause cartilage fragments to break off (osteocartilaginous loose bodies

subchondral bone uncovered

subchondral cysts

mild synovial inflammation (more focal and milder than RA)

subchondral bone sclerosis

22
Q

What are the common sites affected by primary OA?

A

hands - distal interphalangial (DIP), proximal interphalangeal (PIP), first metacarpal (CMC)

cervical and lumbar spine

feet - especially 1st metarsophalangeal (MTP)

knees - medial or lateral compartment (not both), patellofemoral involvement may accompany tibiofemoral or be present alone

hips - superolateral or inferomedial narrowing

23
Q

What are the joints commonly affected in secondary OA?

A

MCP, wrist, elbow, shoulder, ankle

often premature onset

24
Q

generalized OA

A

defined as OA in hands and at least one large joint:

  • familial predisposition
  • more common in women, onset middle age
  • multiple Heberden’s nodes
  • polyarticular finger interphalangeal joint OA
  • symptoms persist for years, but settle down
  • later predisposition to OA at other common OA sites especially knee and medial//patellofemoral
25
Q

What are the patterns of joint involvement in OA?

A

mono-, oligo-, or poly-articular

26
Q

What are the common symptoms of OA?

A

pain

morning stiffness

stiffness after inactivity

swelling

knee - pain/difficult with stairs, sit-to-stand, feeling that knee may give way

hip - pain in growin or deep posterolateral, pain/difficult with getting in/out of car, putting on shoes and socks

spine - pain in region of involvement, radicular symptoms if nerve roots compressed by osteophytes

27
Q

What are the characteristics of pain associated with OA?

A

aching pain

early OA - increases with joint use, relieved by rest, relieved by simple analgesics

advanced OA - pain at rest as well as with use, night pain, not relieved easily, sleep interference impacts well-being and worsens pain experience

pain/structure change closest relationship at hip, weakest at hand and spinal apophyseal joints

28
Q

What are the physical exam findings indicating OA?

A

bony enlargement

limitation of motion - limited flexion, inability to achieve full extension

peri-articular muscle weakness

crepitus

malalignment

mild inflammation, warmth, effusion (if moderate or severe, consider joint infection or acute crystal process)

29
Q

synovitis as a warning sign of OA

A

acute or subacute - flares are common in OA and may show mild joint inflammation

more marked synovitis warrants urgent investigation for another cause (crystal, septic arthritis - damaged joints are predisposed, coexisting CPPD and septic arthritis)

30
Q

general clinical characteristics of OA

A

onset tends to be gradual

usually only one/few joints problematic at any given time

evolution of symptoms and structure change tends to be slow

strong age association (men 40s and older, women peri-menopause and older)

31
Q

laboratory findings in OA

A

blood and urine tests have no role

synovial fluid analysis reveals non-inflammatory fluid characteristics:

  • low turbidity
  • low white blood cell count (<2000)
  • may show CPPD (calcium pyrophosphate dihydrate) crystals
32
Q

radiographic findings in OA

A

focal joint space narrowing

marginal and central osteophytes

subchondral sclerosis and cysts

osteochondral bodies

bony attrition

33
Q

role of x-ray in OA

A

help confirm diagnosis (and rule out other suspected conditions)

assess OA severity, which helps develop pland and treat as well as understand prognosis and expected course

34
Q

role of MRI in OA

A

MRI plays a large role in research, but a small role in OA patient care

35
Q

When is MRI useful for OA?

A

if the patient is considering referral for arthroscopy

patient in whom avascular necrosis is a possibility

patient with unusual features of pattern or course

36
Q

causes of secondary OA

A

any other arthritis

injury

developmental abnormalities (acetabular dysplasi)

osteonecrosis

CPPD, apatite crystal deposition disease

Paget’s disease

hemochromatosis

onchronosis

hyperparathyroidism

Wilson’s disease

acromegaly

37
Q

What are the outcomes of OA?

A

disease progression - structural changes at the joint level

symptoms - pain and stiffness

physical function decline - decline in performance of discrete actions

disability - limitation in performance of socially defined tasks expected of an individual within a typical environment

38
Q

What is the prognosis for individuals with OA?

A

prognosis is variable from one person to the next and from one joint to the next

some have disease progression but not functional decline or disability

others have functional decline or disability but no disease progression

worsening is not inevitable

39
Q

factors associated with disease progression in knee OA

A

excess body weight

varus alignment

valgus alignment

meniscal damage

40
Q

factors associated with functional decline in knee OA

A

pain severity

excess body weight

inactivity

muscle weakness

joint laxity

low self-efficacy

depression/anxiety

poor social support

other medical conditions

41
Q

treatment goals in OA

A

relieve symptoms

maintain or improve function

limit disability

avoid drug toxicity

modify disease course - no drug available as yet that achieves this goal

42
Q

non-pharmacologic treatment for OA

A

mild or intermittent symptoms - may only need reassurance or non-pharm treatment

patient education - self management and social support

physical and occupational therapy:

  • exercise to preserve range of motion, strength, aerobic capacity
  • assistive devices

improve ambulation and ADLs

weight loss (if overweight)

43
Q

What are the available systemic pharmacologic treatments for OA?

A

non-narcotic analgesic (ex. ecetaminophen)

anti-inflammatory (NSAIDS and selective cyclooxygenase-2 inhibitors)

narcotic analgesics (for advanced OA)

44
Q

What are the local pharmacologic treatments for OA?

A

intra-articular corticosteroid treatment

hyaluronic acid - no evidence

45
Q

When should NSAIDs be used for OA? What types are there?

A

consider first with severe pain and signs of inflammation

2 forms - COX-1 expresse din many tissues and COX-2 in normal tissue in response to physiological stress

selected COX-2 inhibitors have improved benefit-to-GI risk rario, but offer little advantage in terms of other toxicities - may have greater CV risk

46
Q

glucosamine and chondroitin for OA

A

efficacy is not certain

recent trials suggest borderline to no disease modifying effect

47
Q

What are some future treatments for OA?

A

tissue engineering - chondrogenic precursor cell populations or chondrocytes combined with scaffold and growth factors

48
Q

surgical therapy for OA

A

in advanced OA, can do total joint replacement

in mild/moderate OA without response to conservative therapy, the role of surgical options is much less clear

arthroscopy may play a role if mechanical symptoms are present, but improvements in outcome are uncertain

MSK/Derm (54 decks)

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