Osteoarthritis Flashcards
What is it
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
Clinical presentation
Joint pain exacerbated by exercise Joint stiffness after rest (transient in the Mornings) Reduced functionality Bony swellings and deformity Crepitus
In hand where are bony swellings of osteoarthritis - what are nodules called at these joints?
Distal interphalangeal - Heberden’s
Proximal Interphalangeal - Bouchard’s
Pathophysiology
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)
Aetiology
Usually primary
Sometimes secondary to particular joints that have been damaged/frequently used
General wear and tear
Risk factors
Females Family Hx Obesity Smoking Increased age Trauma to joint Conditions like haemochromatosis and Ehlers-Danlos syndrome
Epidemiology
Prevalence increases with age
More common in women
Most common form of arthritis
Diagnostic tests
Examination:
Diagnose in >45 years, actively related joint pain, with either no morning related stiffness or <30 mins of it
X-ray
What would you see on an X-ray of osteoarthritis
Loss of joint space
Osteophytes
Subarticular sclerosis
Subchondral cysts
Treatment of osteoarthritis
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)
Complications
Increased risk of gout
Chondrocalcinosis
What analgesia can be given in treatment
Regular paracetamol with or without topical NSAIDs
What can be given if 1st line analgesia isineffective
Codeine or short-term oral NSAID (+PPI)
Example of weak opioid that can be used alongside paracetamol
Dihydrocodeine
Main pathological features of OA
Loss of cartilage
Disordered bone repair
Mechanisms for pathogenesis
- 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
Features of cartilage (in joints)
Matrix of collagen fibres, enclosing a mixture of proteoglycans and water; it has a smooth surface and is shock-absorbing
Pathophysiology in more detail
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
What are the most commonly affected joints
• 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
Name of nodes at DIP joints and PIP (proximal interphalangeal) joints
DIP joints - Heberdens nodes
PIP joints - Bouchards nodes
(B comes before/proximal to H)
Differential diagnosis (differentiate from rheumatoid)
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.
Conservative treatment
Patient education
Encourage exercise and weight loss
Medical treatment
Analgesia e.g. paracetamol or non-steroidal anti-inflammatory drugs
Gels such as capsaicin may be useful
Steroid injections
Surgical treatment
Arthroplasty
