B6.007 Prework 2 Osteoarthritis

Question 1

what parts of a joint can osteoarthritis affect?

Answer 1

articular cartilage, bone, synovium, and soft tissue

Question 2

clinical presentation of OA

Answer 2

gradual onset (years)
morning stiffness < 30 min
geling phenomenon (stiffness from sitting to standing)
crepitus with movement

Question 3

most common locations of OA involvement

Answer 3

knee
hip
hands (PIPs, DIPS, CMC)
spine (neck, lumbar)

Question 4

epidemiology of OA

Answer 4

most common joint disorder

leading cause of disability related to pain and reduced function

Question 5

person level risk factors for OA

Answer 5

age
female gender
joint biomechanics
inflammation
adiposity
genetics

Question 6

joint level risk factors for OA

Answer 6

joint injury
repetitive use
malalignment / developmental changes

Question 7

classifications of OA

Answer 7

primary (no comorbidities driving pathology)

secondary (atypical joints, young age, comorbidities present)

Question 8

etiologies of secondary OA

Answer 8

trauma (athletes)
genetics - Stickler’s (collagen mutation)
metabolic (hemochromatosis, hyperparathyroidism, acromegaly, amyloidosis)
neuropathic/Charcot’s
hemophilia induced
hypermobility (Ehlers Danlos)

Question 9

components of articular cartilage

Answer 9

70% water
organic compounds: type 2 collagen, aggrecan
number of other collagens, proteoglycans, and non collagenous proteins

Question 10

what creates the tensile strength of articular cartilage

Answer 10

collagen networks

Question 11

what creates compressive resilience in articular cartilage

Answer 11

charged proteoglycans entrap water through their hydrophilic glycosaminoglycan side chains

Question 12

pathological findings of articular cartilage in OA

Answer 12

surface fibrillation/fissuring
chondrocyte proliferation
chondrocyte hypertrophy
tidemark duplication
subchondral bone thickening
vascular invasion of subchondral bone

Question 13

impact of increased mechanical load on joints

Answer 13

mechanical load decreases production of sclerostin
decreased sclerostin leads to increased osteoblast bone formation
increased osteoblast bone formation leads to increased bone mass

Question 14

what is sclerostin

Answer 14

inhibitor of Wnt pathway

regulates osteoblast mediated differentiation

Question 15

decreased sclerostin

Answer 15

increased osteoblast production

Question 16

impact of unloading on joints

Answer 16

increased RANKL production
increased RANKL stimulates osteoclast precursors to differentiate into osteoclasts
increased bone resorption

Question 17

xray features of osteoarthritis

Answer 17

asymmetric joint space narrowing (altered biomechanics)
subchondral sclerosis (bright white)
subchondral cysts
osteophyte formation (bone spurs)

Question 18

MRI findings of OA

Answer 18

not routine
subchondral bone marrow lesions lead to ill defined areas of hyperintensity
reflection of increased loading

Question 19

nonpharm treatments for RA

Answer 19

exercise including water based therapy
weight loss
braces (CMC, knee)
insoles

Question 20

do any OA treatments address root cause?

Answer 20

no, mainly symptomatic ttx

Question 21

side effects of NSAIDs

Answer 21

peptic ulcer (bleeding)
hypertension
worsening renal failure

Question 22

mechanism of duloxetine

Answer 22

FDA approved for OA

potent inhibitor of serotonin and NE reuptake, weak inhibitor of dopamine reuptake

Question 23

procedure based therapies for OA

Answer 23

intraarticular injections (steroids, hyaluronic acid)
joint replacements

Question 24

discuss the effectiveness of hyaluronic acid injections

Answer 24

multiple available

not demonstrated to have benefit over placebo

Question 25

mechanism behind hyaluronic acid injections

Answer 25

charged proteoglycans provide compressive resilience by entrapping water

Question 26

additional OA treatment strategies that may be individualized

Answer 26

topical therapies
supplements (glucosamine-chondroitin)
acupuncture
tai chi
mindfulness