Arthritis Flashcards
what is primary OA
idiopathic
what is secondary OA
post - traumatic
underlying cause or event or congenital malformation
prevalance of OA
302 mil world wide
1 in 4 people in US
leading cause of disability in older adults
spands decades of life
most commonly affects joints
hips
knees
hands
clinical features of OA
loss of articular cartilage
synovitis
boney changes
ligamentous changes
meniscal changes
patient impct of OA
Pain- -secondary affects contribute to the pain such as synovitis not necessarily loss of cartilage
Swelling – occur w synovitis
Stiffness – walking/moving on it less
Loss of Function
OA pathophysiology
degenerative process of the whole joint with different phenotypes emerging
risk factors for primary OA
age
obesity/metabolic disease
sex (60% female(
major components of normal cartilage
water
extracellular matrix (ECM) and proteoglycans
chondrocytes (responsible for both catabolism and anabolism)
function of cartilage
Withstand highly repetitive compressive and shear loads, maintain a near frictionless joint surface environment, allow force transmission between articulating bones
physiology and biomechanics of normal cartilage
Uses hydrodynamics- water flows out in response to compression
Proteoglycans are hydrophilic, attract water to flow back into cartilage following water loss
Combination of hydrodynamics and ECM structure allow compressive forces to be converted to shear at the calcified cartilage/bone interface
cartilage regeneration of normal cartilage
Chondrocytes repair ECM (very slow process) (Otero 2012, Eyre 2006) -> poor healing potential (Buckwalter 1998)
Chondrocytes are mechanosensitive, regenerative process is stimulated in response to loading (Gilbert 2018)
impairment of cartilage regeneration of OA
Regeneration is too slow to keep up with damage repair AND/OR regeneration pathway is altered
- Presence of inflammation impacts chondrocyte function
–Produce more pro-inflammatory markers and matrix degrading enzymes
–Early chondrocyte senescence (Liu-Bryan 2015) = death
Proteoglycan loss occurs first, followed by eventual ECM breakdown
-Loses ability to handle loads via hydrodynamics (less water), placing more stress on ECM
Articular Cartilage Breakdown
–This process is going on for YEARS/DECADES before we can see cartilage breakdown
–Translation: By the time we start to see cartilage breakdown its far too late
secondary OA due to an associated event could be
joint injury: PTOA
- knee injury 6x risk increases
abnormal alignment or geometry
- malalignment of the knee is on independent risk of OA progression
The normal joint structure and biomechanics are impacted resulting in both inflammatory environment and changes to loading environment
Slow cartilage metabolism does not adapt quickly enough to joint changes
PTOA
The major issue:
250k ACLR yearly (mostly impacting people under 25)
~50% will have radiographic OA within 10-20 yrs
Translation:
- Huge cohort of young individuals with old knees
–Lots of years left in the medical system
—Downstream healthcare impacts of physical inactivity and/or disability
–Joint arthroplasty only lasts~ 20 yrs
—These people may need multiple arthroplasties in their lifetime = $$$$$
summary of OA?
Much more complex than originally thought (not just wear and tear)
Cartilage regeneration is unable to keep up with microdamage
Impacted by biomechanics and/or inflammatory environment
Impacts the whole joint (not just articular cartilage)
We don’t fully understand what causes symptoms
Worse radiographic OA more likely to have symptoms
Primary OA: Intersection between aging, genetics, metabolic syndrome/obesity, lifestyle choices
Secondary OA: Intersection between joint biomechanics and inflammation
common imaging features
Loss of joint space width
Osteophyte formation
Sclerosis of subchondral bone
imaging modalities
radiographs (gold standard)
MRI
CT
grade 1 OA
possible osteophites
doubtful JSN
doubtful OA
grade 2
definite osteophites
possible JSN
mild OA
grade 3 OA
moderate osteophites
definite JSN
moderate OA
