Osteoarthritis Flashcards
What are the pathobiological hallmarks of OA?
- Reduction in joint space
- Breakdown of articular catrilage
- Synovitis - Synovium (membrane) becomes inflammed
- Thickend joint capsule
- Osteophyte formation - bony projections
- Subchondral bone cyst formation - fluid-filled sac (dark regions on X-ray)
- Sclerosis - an unusual hardening or thickening of your bone/increasing bone density (white intensities - X-ray)
Is OA simply wear and tear?
No - Wear, flare and repair
Better to view it as a low-grade chronic inflammatory condition
Is OA the most common form of arthritis? What is the most common symptom?
Yes, OA is the most common form of arthritis and its prevalence is increasing
Pain is the most common symptom (related to activity)
Leads to impaired quality of life and disability
What are the risk factors for OA?
- Age - increased risk with age
- Female
- Genetics
- Heritable component 50%, polygenic
- BMI - Obesity and metabolic syndrome
- Diet
- Physical inactivity and muscle weakness
- Occupations with repetitive joint use
- Some sports – in the individuals that are genetically predisposed
- Joint injury-trauma
Risk factors in bold - potentially modifiable
What joints are typically effected by OA?
Characteristic distribution
1. Hips
2. Knees
3. PIP and DIP joints of the hands
4. Facet joints (Apophyseal) of lower cervical (neck) and lumbar spine (lower back)
- PIP = proximal interphalangeal joint – between the first (proximal) and second (intermediate) phalanges
- DIP = distal inter-phalangeal – joints closest to the tips of tops, fingers and thumbs (synovial joints where the middle and distal phalanges meet)
X-ray images of OA in hands, knee and hips.
Small little thing for hand OA…
- Different nodes that appear in the hand
a) Heberden’s nodes – closest to the fingertips
b) Bouchard node- middle joints (joint down from the top
What is something to keep in mind when thinking about the impact of OA on an individual’s life?
Not a simple relationship between pathology and symptoms - symptoms do not correlate with pathological changes
Experience of OA is affected by:
1. Biology
2. Physiology
3. Social factors
4. Cultural factors
5. Psychological factors
6. Individual subjectivity
Hence, we need to examine to what extent OA is impacting daily living (self-care, walking, eating etc.) and participation restriction (employment, social and leisure, etc.)
A biopsychosocial model helps us to understand the level of biographical disruption OA is causing.
How is OA diagnosed?
Clinical diagnosis - basically means that a diagnosis is made based on the symptoms experienced by the patient - no investigation or test is required.
However…
1. X-ray – can be used to examine the extent of disease
2. Erythrocyte sedimentation rate (ESR) – can be used as a non-specific marker of inflammation
What are the goals of OA management?
- Reduce pain
- Improve function
- Improve quality of life
What is the first line/most important treatment for OA?
- Patient education - explain nature of condition, permanent nature and prognosis
- Weight control - especially helpful for lower limbs
- Exercise - strengthening & aerobic excercise + balance
- Social support
Are there any drugs that can be perscribed for OA?
Drugs mainly used for OA-Pain control
- Oral Paracetamol
- Topical non-steroidal anti-inflammatory drugs (NSAIDs)
- Oral NSAIDs - problems – peptic ulcer/gastric ulcers
- Intra-articular injection of glucocorticoids for swollen acutely painful joint
Note - There are no disease modifying agents for OA
Is surgery an option if OA is very severe?
Yes, joint replacement is a possibility - Hip and knee most common - very effective surgeries - arthoplasty
Indicated for patients who have failed treatment and who have significant impairment in their quality of life
Given the replaced joint has limited life - you don’t want to do it too early as this means that it wil have to be replaced sooner
Summary of OA treatment/management?
- Education
- Lifestyle - e.g weight loss
- Support systems
- Analgesia for pain - paracetamol/topical NSAIDs - followed by escalation if necessary
- Last option - surgery
What do we know about OA pathogenesis?
We know that there is both environmental and genetic factors at play
Wide range of factors that are associated, just a couple examples…
1. Structural abnormalities/previous trauma - SUFE, DDH and limb deformities - are at increased risk of OA
2. Occupations/sports - farmers (hip OA), miners (knee OA) and elite or professional athletes (knee and ankle OA) - increased biomechanical loading on joint
3. People with ACL injuries have increased risk
4. Obesity - increased stress + pro-inflammatory cytokine environment
5. Oestrogen appears to play a role; lower rates of OA have been observed in women who use hormone replacement therapy (HRT)
What are the main presenting symptoms of OA?
Main presenting symptoms - pain and functional restriction
Pain
a) Insidious (gradual) onset over months/years
b) Variable or intermittent nature over time
c) Mainly related to movement/weight-bearing – relieved on rest
d) Only brief (<15 mins) morning stiffness and brief (<5 mins) “gelling” after rest
e) Usually one or a few joints painful
