Osteoarthritis

Question 1

What is it

Answer 1

Degenerative arthritis affecting synovial joints and i characterised by cartilage degeneration, the associated response of the periarticular tissue and pain is typically worse at the end of the day.
Bone remodelling and inflammation

Question 2

Clinical presentation

Answer 2

Joint pain exacerbated by exercise
Joint stiffness after rest (transient in the Mornings)
Reduced functionality
Bony swellings and deformity
Crepitus

Question 3

In hand where are bony swellings of osteoarthritis - what are nodules called at these joints?

Answer 3

Distal interphalangeal - Heberden’s

Proximal Interphalangeal - Bouchard’s

Question 4

Pathophysiology

Answer 4

Progressive destruction of the articular cartilage (loss of articular space).
Exposed subchondral bone becomes sclerotic, increasing vasculairty and subchondral cyst formation -> repair produces cartilaginous growths that become calcified (osteophytes)

Question 5

Aetiology

Answer 5

Usually primary
Sometimes secondary to particular joints that have been damaged/frequently used
General wear and tear

Question 6

Risk factors

Answer 6

Females
Family Hx
Obesity
Smoking
Increased age
Trauma to joint
Conditions like haemochromatosis and Ehlers-Danlos syndrome

Question 7

Epidemiology

Answer 7

Prevalence increases with age
More common in women
Most common form of arthritis

Question 8

Diagnostic tests

Answer 8

Examination:
Diagnose in >45 years, actively related joint pain, with either no morning related stiffness or <30 mins of it
X-ray

Question 9

What would you see on an X-ray of osteoarthritis

Answer 9

Loss of joint space
Osteophytes
Subarticular sclerosis
Subchondral cysts

Question 10

Treatment of osteoarthritis

Answer 10

Core treatments: Exercise and general aerobic fitness improvement + Weight loss

Pharmacological: Analgesia e.g. paracetamol and can take weak opioid alongside (dihyrdocodeine)

Non-pharmacological: MDT approach (physiotherapists and occupational therapists), try heat or cold packs at the site of pain, walking aids etc

Surgery: Joint replacement (hips or knees)

Question 11

Complications

Answer 11

Increased risk of gout

Chondrocalcinosis

Question 12

What analgesia can be given in treatment

Answer 12

Regular paracetamol with or without topical NSAIDs

Question 13

What can be given if 1st line analgesia isineffective

Answer 13

Codeine or short-term oral NSAID (+PPI)

Question 14

Example of weak opioid that can be used alongside paracetamol

Answer 14

Dihydrocodeine

Question 15

Main pathological features of OA

Answer 15

Loss of cartilage

Disordered bone repair

Question 16

Mechanisms for pathogenesis

Answer 16

• Metalloproteinases (e.g. stomelysin and collagenase) secreted by chondrocytes, degrade the collagen and proteoglycan
• Interleukin 1 (IL-1) and tumour necrosis factor-alpha (TNF-alpha) stimulate metalloproteinase production and inhibit collagen production
• Deficiency of growth factors such as insulin-like growth factor and transforming growth factor impairs matrix repair
• Gene susceptibly (35-60% influence) from multiple genes rather than a single gene defect - mutations in the gene for type II collagen have been associated with early polyarticular OA

Question 17

Features of cartilage (in joints)

Answer 17

Matrix of collagen fibres, enclosing a mixture of proteoglycans and water; it has a smooth surface and is shock-absorbing

Question 18

Pathophysiology in more detail

Answer 18

Progressive destruction and loss of articular cartilage with an accompanying periarticular bone response
Cartilage has smooth surface and is shock absorbing
Balance between cartilage degradation by wear and its production by chondrocytes is lost in development of OA
Despite the increased synthesis of extracellular matrix the cartilage become oedematous
Subsequently focal erosion of cartilage develops and chondrocytes die. Repair is attempted by adjacent cartilage but the process is disordered, leading to a failure of synthesis of extracellular matrix. The surface becomes fibrillated and fissured
Cartilage ulceration exposes the underlying bone to increased stress, producing micro-fractures and cysts
The bone attempts repair but produces abnormal SCLEROTIC SUBCHONDRAL BONE and overgrowths at the joint margins which become calcified - known as OSTEOPHYTES
There is also some secondary inflammation
The exposed bone becomes sclerotic, with increased vascularity and cyst formation

Question 19

What are the most commonly affected joints

Answer 19

• Distal interphalangeal joints (DIPJs -
HEBERDEN’S NODES) and the first
carpometacarpal joints (base of thumb) of
the hands
• First metatarsophalangeal joint of the foot
• Weight-bearing joints - vertebra, hips and
knees

Question 20

Name of nodes at DIP joints and PIP (proximal interphalangeal) joints

Answer 20

DIP joints - Heberdens nodes
PIP joints - Bouchards nodes
(B comes before/proximal to H)

Question 21

Differential diagnosis (differentiate from rheumatoid)

Answer 21

Pattern of joint involvement and the absence of systemic features and marked early morning stiffness that occur in rheumatoid arthritis.
Chronic tophaceous gout and psoriatic arthritis affecting the DIPJs may mimic OA.

Question 22

Conservative treatment

Answer 22

Patient education

Encourage exercise and weight loss

Question 23

Medical treatment

Answer 23

Analgesia e.g. paracetamol or non-steroidal anti-inflammatory drugs
Gels such as capsaicin may be useful
Steroid injections

Question 24

Surgical treatment

Answer 24

Arthroplasty

Question 25

Signs and symptoms (mindmaps)

Answer 25

Pain and stiffness
Swelling around the joints involved
Crepitus
Heberden’s nodes at distal interphalangeal (DIP) joints (outer)
Bouchards nodes at proximal interphalangeal (PIP) joints

Question 26

Why would bloods be important to take

Answer 26

Not diagnostic usually but may be relevant when OA is related to another condition such as haemochromatosis