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
grade 4 OA
large osteophites
great JSN
severe OA
grade 0 OA
no OA
no osteophites
no jsn
OA imaging
Advanced Imaging Techniques
New promising imaging sequences that allow us to assess cartilage physiology before cartilage damage is evident
MRI T1rho: Associated proteoglycan content/concentration
MRI T2*: Associated with ECM orientation and free vs bound water
OA treatment
We currently have zero treatments that have been proven effective at reversing OA or stopping its progression
The treatments we do have:
Treat the symptoms (reduce pain)
Promote function
Prevent OA from happening in the first place
Injury prevention (Secondary OA)
Lifestyle (Primary OA)
Moderate Activity
Weight Management
OA medical management treatment for NSAIDS
Effective at reducing pain and targeting synovitis
Cheap
Cons: Some with comorbidities unable to use
Some have topical versions available
Con: Treats symptoms, no impact on disease
common NSAIDS OA treatment
Ibuprofen
Naproxen
Diclofenac
pharm interventions for OA
NSAIDs
Corticosteroids
Hyaluronic Acid
Biologics
surgery interventions for OA
Debridement
Cartilage Repair
Joint Replacement
corticosteroids treatment
common: cortisone injections (kenalog)
tx: Effective at reducing short-term pain and inflammation
Intended to be an adjunct
More localized treatment
Cons: Some with comorbidities unable to use
Con: Treats symptoms, no impact on disease
Con: Limited dosage schedule, infection risk
hyaluronic acid for OA
common: Viscosupplementation)
Synvisc
Hyalgen
Euflexxa
treatment:
Can improve symptoms and function in mild/moderate OA (high bias evidence)
“lubricates” the joint
Cons: Expensive (limited insurance coverage)
Con: Treats symptoms, no impact on disease
Con: Limited dosage schedule
biologics for OA tx
Common:
Stem Cell Therapy
Platelet Rich Plasma (PRP)
Treatment:
Promising basic science results
Some mixed results but mostly poor findings of effectiveness in vivo
No Standardization
Cons: Expensive (not covered by insurance)
Cons: Travel to special clinic
summary of medical management for OA
DMOADs do not exist yet
Corticosteroids have short-term symptomatic benefits and should be adjuncts
Placebo effect from injections (Bannuru 2015, Ayhan 2014)
Viscosupplementation studies that show benefit have high risk of bias
Recommendation: try it if the patient had little to no effect from steroid or can’t have steroid
Surgery:
Joint replacement is highly effective but still considered a salvage procedure
Reduces pain, reduces disability, improves QOL
rehab interventions: weight management
9-76% reduction in pain following gastric bypass (McGoey 1990)
Pain scores reduced, functional scores improve (Abu-Abeid 2005)
Improved joint space associated with weight loss (Abu-Abeid 2005)
Con: Poor adherence to interventions
Dose response exists (More weight loss more symptomatic improvement) Messier 2018
rehab interventions: exercise
Maintain and/or improve functional capacity
Supplement diet for weight loss
`No specific recommendations:
Moderate activity (ACSM)
No evidence to support a hierarchy of types of exercise
Whatever the patient likes to do will improve adherence
rehab program for exercise OA management
Decrease pain, improve function, improve QOL
Quad strength/power = Function
PT had better outcomes through 1 year follow up vs corticosteroid injection
bracing for management
Unloader braces have some symptomatic benefit
Other braces: Likely placebo/tactile
Braces are generally bulky, uncomfortable, and/or not aesthetically pleasing
the debate
dont unnecessarily load vs dont change activity pendulum
current opinoin
Not all OA is the same:
Primary vs secondary with phenotypes of each
It is unlikely there will be one blanket recommendation, each subset will need its own specific recommendations that is also adjusted to the individual patient
The most basic principle of treatment is the risk reward benefit to the patient
Primary OA: Should we promote physical activity (including that with high joint loading) despite the risk of promoting articular cartilage degeneration
Secondary OA: Does the risk reward benefit change given the different pathophysiology?
treattment principples summary
Promote physical activity for weight management, joint health maintenance, pain/mental health
Weigh the risk reward for whether higher loading activity is appropriate
Use irritability as a guide
Quad strength and power to maintain function
Combination of open and closed chain depending on joint irritability and compensations
Assistive device use for significant gait deviations
Self-management focus
Booster visits currently being explored, watch for evidence
the future
Harness mechanosensitivity of chondrocytes to promote regeneration
Can we identify specific loading inputs to optimize cartilage health after injury and surgery
Likely in combination with pharm
Use of biologics to regenerate damaged cartilage
Our current post-injury and post-op treatments are focused on short term goals of return to sport and function and have little focus on long-term joint health
inflammatory arthritis history
UNEXPLAINED joint pain with associated swelling (No MOI but inflammation). Joint(s) can look acutely injured or infected (warm, red, swollen, painful)
Frequently have relapsing remitting presentation
Joints can become damaged over time leading to changes similar to OA (chronic joint degradation)
Make sure you do a high quality systems review as many of these conditions have systemic effects impacting things other than MSK
rheumatoid arthritis
Fairly common: 0.3 – 1% in US (Alamanos 2006)
Chronic Systemic autoimmune disease that attacks the joints
Hands, wrists, shoulders, elbows, knees, ankles feet
General fatigue
How many joints and any structural deformity
Increased cardiovascular risk
Promote physical activity
psoriatic arthritis
Autoimmune disease in people with psoriasis that can impact joints
Nail and skin changes
1/3 of people with psoriasis
DIPs, wrists, ankles, knees
Can also impact enthesis (usually heel)
lupus
Arthritis/arthralgia is present in 95% of patients with SLE
-Mimics RA in 5-15%
lymes disease
Tends to occur in late stage infection
After systemic symptoms have resolved
Can have intermittent or persistent joint attacks
Lyme bacteria enters joint and can remain
Common in knee
Can have swelling without pain
gout
Inflamed joints due to urate crystal formation in synovial fluid.
3.9% in US
boutonniere
PIP flexed and DIP ext
swan neck
PIP extended, DIP flexed, MCP flexed
hitchhikers thumb
MCP flexion, IP extension
claw toe
MTP ext, PIP/DIP flexion
IA medical management - disease modifying antirheumatic drugs (DMARDS)
Many different DMARD protocols, used in virtually all inflammatory arthritis conditions
Typically have a maintenance dose that is then increased during flares
Trial and error to get maintenance and flare doses right (as little as gets the job done)
Can be combined with corticosteroids to minimize inflammation during flares
Common Pharm
Methotrexate
Leflunomide
Hydroxycholoroquine
Sulfasalazine
Because they inhibit immune response, increased risk of infection
IA PT Management
Identify when joints are “Hot”: Red, swollen, painful/irritable
During Flare:
Reduce pain and inflammation, promote ROM and maintain strength
Avoid high impact activity
During Remission:
Promote physical activity to limit systemic impacts
Promote moderate intensity exercise and maintenance of strength and ROM to avoid deformity and/or dysfunction
Always use your irritability principles to guide your treatment
Splinting for deformity (covered in Rehab Tech)
