MSK 11: Osteoarthritis Flashcards
Clinical Course
- pre-OA: asymptomatic, but risk factors at work to induce OA present
- early OA: intermittent symptoms presentation (ie. mild joint pain)
- evident OA: constant symptom presentation (daily pain, stiffness, etc.)
- end stage: high levels of pain, intense stiffness, and functional disability
Describe the pathogenic changes to the cartilage, synovium, and subchondral bone that underlie OA.
- cartilage thins
- bone remodels due to loss of cartilage
- osteophytes (bone spurs) form
- synovium inflames (source of pain)
OA Molecular Endotypes – Cartilage-driven
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OA Molecular Endotypes – Synovitis-driven
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OA Molecular Endotypes – Subchondral Bone-driven
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Discuss the mechanisms that contribute to pain in OA.
- peripheral sensitization
- central sensitization – NMDA receptor activation
Discuss the concept of disease modifying OA drugs (DMOADs).
to develop drugs that block production of inflammatory cascade
- ability to impede or reverse advancement of structural deterioration in joint
examples:
- anakinra – IL-1b inhibitor (DMARD)
- adalimumab and infliximab – TNF-α inhibitors (DMARDs)
- tanezumab – NGF sequestering antibody
Describe the approach to treatment (treatment cascade/algorithm) commonly used to manage OA.
- non-pharmacologic
- add acetaminophen
- assess risk for GI events (see chart)
- full-dose NSAID + gastroprotection, supplement with duloxetine or local injections
- surgery
Topical NSAIDs
- 1st line for knee and hand OA
- NOT recommended for hip OA due to depth of joint
Drugs:
- diclofenac diethylamine (Voltaren Emulgel)
- diclofenac Na 1.5% (Pennsaid)
- compounded diclofenac 10%
Topical Capsaicin
- knee OA
- alternative to topical NSAIDs prior to oral therapies, or add-on
Acetaminophen
- mild-moderate OA pain
- may be used as adjunct treatment with topical NSAID
- interaction with alcohol and warfarin
Oral NSAIDs and COX-2 Inhibitors
- strongly recommended
- all NSAIDs equally effective
- similar benefit between COX-2 inhibitors and non-selective NSAIDs
Drugs:
- ibuprofen
- naproxen
- diclofenac
- celecoxib
Treatment to Reduce GI Risk
- add gastroprotective agent: PPI, misoprostol
- switch to COX-2 inhibitor: celecoxib
- switch to combo product: diclofenac/misoprostol, naproxen/esomeprazole
Duloxetine
- knee OA with comorbidities, or failed treatment
- central inhibition of pain
Corticosteroids
- hip and knee OA, conditionally hand oA
- option if CI with NSAIDs, not responding to other OA meds, adjunct treatment
- short-term (4-6 weeks)
- elevated BP and blood glucose, water retention, joint sepsis/infection (low risk)
- INTRA-ARTICULAR ONLY – NOT ORAL (SIGNIFICANT SIDE EFFECTS)
Drugs:
- methylprednisolone acetate
- triamcinolone acetonide
- betamethasone acetate
Tramadol
- weak analgesic
- unable to take oral NSAIDs, receive IA injections, or failed treatment
- may be used in conjunction with acetaminophen and/or NSAIDs
- requires dosage adjustment in kidney disease
- constipation, respiratory depression, seizures
Other Opioids
- LAST line for severe OA pain
- generally avoided
- inferior effects on pain/function with strong vs. weak opioids
- pruritus, falls, sedation, constipation
Drugs:
- oxycodone
- morphine
Hyaluronic Acid (Viscosupplementation)
- not routinely recommended due to limited efficacy, risk of AE/ADR, high cost
- may consider for knee OA when other options exhausted
- IA injection
Non-Pharm – Strong
- exercie/physical activity
- weight optimization
- assistive devices (ie. cane)
- self-efficacy and self-management programs
- tai chi
Non-Pharm – Conditional
- yoga, balance training
- heat/cold
- CBT
- acupuncture
- kinesiotaping
- paraffin
Pharm – Strong
- topical NSAIDs (knee)
- non-selective oral NSAIDs + celecoxib
- intra-articular corticosteroids (hip, knee)
Pharm – Conditional
- topical NSAIDs (hand)
- topical capsaicin (knee)
- acetaminophen
- duloxetine (knee)
- tramadol
- intra-articular corticosteroids (hand)
