Osteroarthritis (OA) Flashcards
Define osteoarthritis in simple terms.
Often described as “wear and tear” in the joints.
= NON-INFLAMMATORY DEGENERATIVE ARTHRITIS!
It is not an inflammatory condition like rheumatoid arthritis.
The –itis ending is misleading.
Is osteoarthritis an inflammatory condition?
NO!
Define osteoarthritis.
A non-inflammatory degenerative disorder of moveable joints characterised by the deterioration of articular cartilage and the formation of new bone.
Describe the epidemiology of OA.
- Most common type of arthritis
- Most common cause of disability in the Western world in older adults
- Prevalence increases with age - uncommon before the age of 50
Describe the usual onset of OA.
> 50yrs, slow and gradual
Give the key points in the pathophysiology of OA.
General wear and tear -> a chronic degenerative disease.
Loss of articular cartilage - exposed bone becomes sclerotic.
Attempts at repair produces osteophytes (nodules).
Describe the disease process behind OA in detail (pathophysiology).
- Normal physiology - there is a dynamic balance between cartilage degradation by wear and its production by
chondrocytes. - In OA: initial imbalance in cartilage homeostasis
- Leads to cartilage degradation, remodelling of the bone + associated inflammation of the joint
- Over time, continuous ‘wear’/trauma to the joint
= local inflammation
= stimulates chondrocytes
= they release degradative enzymes
= enzymes break down collagen + proteoglycan
= lead to the destruction of the articular cartilage - Over time, cartilage thins a lot:
= exposes the underlying subchondral bone
= causes subchondral sclerosis
= continuous remodelling of subchondral bone
= this forms subchondral cysts and osteophytes.
= this eventually leads to a progressive loss of joint space.
What are the most important cells responsible for OA?
Chrondrocytes.
What are the 2 key pathological features of OA?
Main pathological features:
* Loss of cartilage
* Disordered bone repair
Which tissues gets most affected in OA?
Articular cartilage
What disease lowers your risk of developing osteoarthritis?
Osteoporosis
Give 5 risk factors for developing OA.
- Genetic predisposition.
- Local Trauma.
- Abnormal biomechanics e.g. joint hypermobility.
- Occupation e.g. manual labour.
- Obesity; pro-inflammatory state.
- Increasing age.
- Being female.
- Inflammatory arthritis e.g. RA.
OA risk factor: Occupation - what joints can manual labour be associated with?
The small joints of the hand
OA risk factor: Occupation - what joints can being a farmer be associated with?
OA of the hips
OA risk factor: Occupation - what joints can being a footballer be associated with?
OA of the knees
Why does the prevalence of OA increase with age?
Due to the cumulative effect of trauma and a decrease in neuromuscular function.
What joints might be affected in osteoarthritis? Give 5.
BASICALLY - Those that are used a lot!
Weight-bearing joints:
- Hips
- Knees
- Sacro-iliac joints in the cervical spine
- Veterbra
- Distal-interphalangeal joints in the hands (DIPs - Heberden’s nodes)
- The 1st carpometacarpal joints at the base of the thumb of the hands
- Wrist
Which surface of the knee is most commonly affected by OA?
The medial surface.
Name 3 joints of the hand that are commonly affected in osteoarthritis.
- Distal interphalangeal joint (DIP).
- Proximal interphalangeal joint (PIP).
- Carpal metacarpal joint (CMC).
Nodal osteoarthritis can affect the DIP and PIP joints. What are the two terms used for nodes on these joints?
- PIP - Bouchard’s nodes.
- DIP - Herbeden’s nodes.
Remember: since B is before H, so Bouchard’s are more proximal than Heberden’s.
What are Herbeden’s and Bouchard’s nodes?
Soft tissue swellings on the fingers
Seen in the early stages of OA
Herbedens = DIP
Bouchards = PIP
(HD AND BP)
Give 5 symptoms of OA.
- Morning stiffness (<30 minutes).
- Pain - aggravated by activity.
- Tenderness (tender to palpation).
- Walking and ADLs affected (activities of daily living).
- Joint effusion (too much fluid builds up around a joint) and bony enlargement.
- Deformities.
- Crepitus (a popping, clicking or crackling sound in a joint).
Describe the character of the pain from OA.
Increases with movement, worse at the end of the day.
How is the pain different in osteroarthritis vs inflammatory arthritis?
Osteoarthritis:
- Morning stiffness only lasting up to 15 mins, generally worsens throughout day
Inflammatory arthritis:
- Stiff for 30+ mins, better with use
Describe the pattern of joint involvement of OA.
Asymmetrical:
- Arthritis that occurs in just 1 joint or a joint on only 1 side of your body.
Finger joints, thumbs + weight bearing joints (hip/knee/big toe)
What systemic features are present in osteoarthritis?
NONE
A patient complains of ‘locking’, what is the most likely cause of this?
This is probably due to a loose body e.g. a bone or cartilage fragment.
Investigations: What would the lab findings be in OA?
- Rheumatoid factor = RhF -ve
- Antinuclear antibodies = ANA -ve
- Normal ESR/CRP typically normal
What is the primary investigation used to make a diagnosis of OA?
X-ray.
Investigations: What would be the radiological findings in osteoarthritis?
X-ray - LOSS:
Loss of joint space.
Osteophytes.
Subchondral cysts.
Subchondral Sclerosis.
What is an osteophyte?
An area of bone which has been reactively laid down in the wrong place.
What is sclerosis in relation to arthritis?
Thickening and widening of the bone at the joint.
How do you end up with bony changes in OA?
- Mechanical forces –> cartilege lost.
- Cartilage loss = cytokines - TNFa, IL-1, NO.
- Cytokines = cartilage cannot repair properly.
- Loss of cartilage = bone rubbing on bone.
- Reactive changes in bone, it is not designed to rub on bone.
Describe features of the non-medical management for OA.
- Education.
- Exercise.
- Weight loss.
- Physiotherapy.
- Occupational therapy.
- Walking aids.
Describe the pharmacological management for OA.
Step-wise use of analgesia to control symptoms:
1st line: topical NSAIDs
2nd line: oral paracetamol + topical NSAIDs
(consider adding a PPI to protect their stomach)
3rd line: short-term NSAIDs (+PPI) + paracetamol + topical capsaicin
4th line: weak opioid (e.g. dihydrocodeine), NSAIDs (+PPI) + paracetamol + topical capsaicin
- Intra-articular corticosteroid injections
- DMARDs if there is an inflammatory component
Describe the surgical management for OA.
- Arthroscopy for loose bodies.
- Scope inserted into joint to assess damage + remove loose
bodies - Osteotomy (cut bone to change bone length/shape).
- Arthroplasty (joint replacement - knee or hip).
- Arthrodesis - Fusion (usually ankle and foot - to prevent painful grinding of the bones).
What is the indication for arthroscopy in OA?
Loose bodies e.g. bone or cartilage fragment that cause ‘knee lock’
Give 3 indications for surgery - joint replacement in OA.
- Significant limitation of function.
- Uncontrolled pain (particularly at night).
- Waking at night from pain.
What is the disadvantage of having a joint replacement and getting a prosthetic joint?
Prosthetic joint has lifespan of 10-15 years and will need
replacement.
In a young person, this could be as much as 3 times.
What is the treatment for loose bodies?
Arthroscopy.
What main features would you use to differentiate between rheumatoid arthritis and osteoarthritis
(inflammatory VS degenerative)?
- Pattern + distribution of joint involvement.
- Absence of systemic features of OA.
- RA has marked early morning stiffness lasting >60mins.
