Management of OA Flashcards
Osteoarthrosis other names
“OA”, osteoarthrosis, Degenerative Joint Disease, DJD,
* (Arthritis, Osteoarthritis)
OA definition
Non-inflammatory degenerative joint disease leading to Progressive, IRREVERSIBLE, degeneration of articular cartilage
OA can leaad to what type of inflammation
- Low-grade non-suppurative inflammation
<><> - But remember that OA is a non-inflammatory process overall
what anatomic structures does OA affect?
Affects the ENTIRE joint +other systems
* Cartilage degradation
* Osteophyte formation
* Subchondral bone remodeling
* Periarticular tissue changes (i.e., fibrosis)
* Neural sensitization…
primary OA etiology, prevalence, risk factors…
PRIMARY
* Infrequent: Prevalence unknown
* Genetic predisposition, age , obesity…
secondary OA prevalence, etiology, cause, anatomic locations
SECONDARY
* MOST COMMON IN SMALL ANIMALS
* Caused by another disease affecting the joint
* Fracture, elbow dysplasia, hip dysplasia etc…
ALWAYS LOOK FOR THE CAUSE!
secondary OA pathogenesis
- Normal stresses + abnormal joints
OR - Abnormal stresses + normal joints
=> Production of inflammatory mediators and enzymes by chondrocytes and synoviocytes (I)
> prostaglandins
> collagenases
> proteinases
> interleukin
> etc…
=> all leads to cartilage degradation, which causes more inflammatory mediators… etc…. in a feedback loop
OA morphologic changes
- low grade synovitis
- Cartilage loss and subchondral bone sclerosis
- Marginal Osteophytes
OA joint flulid changes
- Inflammation increases the protein content of synovial fluid and changes permeability of synovial barrier
<><><><>
Degradation of proteoglycans - Decreases viscosity and quality
- Alters oncotic/osmotic balance
> ** Joint Effusion**
OA diagnosis - history
- Slowly progressive, initially low grade lameness
- Intermittent to permanent
- Worse after period of rest or over-exercise
- Respond well to NSAIDS
OA diagnosis - physical exam
- Joint pain / lameness (mild–moderate)
- Effusion
- Joint capsule thickening
- Crepitus
- Decreased range of motion
purpose of ancilliary tests for OA?
what tests can we do? what are their characteristics?
- Rule out other disease processes
- Identify cause
- Assess overall health of patient
<><><> - Radiographs: Poorly sensitive but SPECIFIC
> Effusion, osteophytosis (>2 weeks), sclerosis - CT: More sensitive than radiographs
- Arthrocentesis
- Arthroscopy: Direct visualization
- (Blood work)
arthrocentesis results for OA
- volume
- viscosity
- appearance
- cell count
- cell type
- volume: inc. + to ++
- viscosity: decreased > normal is viscous, inflamed or septic is watery
- appearance: clear-turbid > normal is clear, inflamed or septic is more turbid
- cell count: <5000/mcl > normal is <3000, inflamed or septic is more marked increase
- cell type: Mono, PMN <12% > normal is Mono, PMN <12%, inflamed or septic is just PMN >12%
Management of Osteoarthrosis
- aims? what can we do?
- specific plans?
- No cure
- Alleviate pain and discomfort
- Reduce and control inflammation
- Minimize further cartilage degeneration
- Improves joint mobility
- Increase activity level
- IMPROVE QUALITY OF LIFE
<><><><> - Identify and correct primary cause
- Clinical signs are highly variable
<><><><> - Weight Management!
- 5 to 8% weight loss significantly improve
lameness scores
<><><><>
Lifestyle modification and physical rehabilitation - Rest if flare-up
- Moderate but regular exercises
- Avoid intense activity
- Avoid unnecessary concussive activity
how much weight should we lose to improve lameness scores with OA?
5 to 8% weight loss significantly improve
lameness scores
Lifestyle modification and physical rehabilitation strategies for OA
- Rest if flare-up
- Moderate but regular exercises
- Avoid intense activity
- Avoid unnecessary concussive activity
rehabilitation for OA - does it have benefits? like what?
Benefits mostly extrapolated from human but evidence is growing…
* Treating pain
* Maintain joint mobility
* Maintain muscle mass
* Improves well-being
*…
Management of Osteoarthrosis - what drugs do we give? what is our first choice? how much do we give?
Anti-inflammatory drugs
* NSAIDs (generally first choice)
> As required with rest (during flare-ups, after/before activity…)
> Lowest dose effective
> Safety!…they are generally safe but not benign…
=> Blood work, exam, UA, beware of “off label” use …
Management of Osteoarthrosis: NSAIDS
- which should we use?
No clear winner…if one does not work, try another
* Meloxicam (No limit in dog, Max 5 days cats…)
* Robenacoxib (No limit in dog, Max 6 days cats…)
* Deracoxib (Not cats)
* Carprofen (Not cats)
* Gapriprant – Prostaglandin receptor antagonist (Not cats)
non-NSAID drugs we can use for management of OA?
- Amantadine > NMDA receptor agonist, used to treat neurogenic pain… 1 study in dogs
- Gabapentin > GABA agonist used to treat neurogenic pain… no studies in dogs or cats
- Amitryptiline > antidepressant
- Tramadol synthetic Mu agonist
> Most recent study show no efficacy compared to placebo in dogs
<><><><> - Intra-articular Corticosteroids
> Limit their use, strict rest.
> Generally when other therapies have failed
Disease Modifying Agents (DMOAs) that have been used for OA?
how do we administer? use / efficacy?
- Polysulfated glycosaminoglycans (Adequan) (bovine tracheal cartilage)
- Pentosan Polysulfate (Cartrophen) (from hemicellulose, structure similar to heparin)
<><><> - Injectable
- Mechanism of action unknown
- Moderate level of comfort recommending usage
- Efficacy? (anecdotal)
Nutritional Management for OA - how useful?
Glucosamine sulfate
* Influence on chondrocyte metabolism?
* Not enough evidence to support use?
<><><><>
Chondroitin sulfate
* Anti-inflammatory effect?
* Not enough evidence to support use?
<><><><>
* Omega 3 fatty acids
omega 3 fatty acids - use for OA? mechinism?
- Probably the highest level of comfort
- “Hijacks” the inflammatory cascade by replacing omega 6FA
<><><><>
Joint diets: - Hill’s J/D
- Royal Canin Mobility
- Purina JM
Mesenchymal stem cell therapy for OA
- what is the goal? does it work?
- Regenerative therapy?
- Mostly stromal cells, few stem cells…
- Immunomodulation through paracrine effect or
soluble factors released in the solution? - Evidence not strong!
Platelet Rich Plasma (PRP) for OA - does it work?
- Large variability in preparation technique
- Same mechanism of action as stromal cells?
- Not enough evidence
Hyaluronic Acid (HA) for OA - goal? efficacy?
- Restore viscosity of synovial fluid
- Evidence not strong
OA Take Home Message
- mostly primary or secondary in dogs and cats?
- what does it lead to?
- Dx?
- Tx goals and strategies?
- OA is generally SECONDARY in dogs and cats
- Irreversible changes in cartilage but also entire
joint - Radiographs are specific but not sensitive
- Treatment is mostly symptomatic and aims at minimizing progression and improving quality of life
- A combination of lifestyle changes and treatments are often required
