Osteoarthritis Flashcards
Describe the epidemiology of OA
Prevalence increases with age
Most people over 60 have some radiological evidence of it (although only a proportion of these have symptoms)
More common in women
What are the risk factors for OA?
Female sex Older age Family history Obesity Fracture through a joint Congenital joint dysplasia Pre-existing joint damage of any cause Occupation (e.g. OA of the hip in farmers and labourers) Repetitive use and injury associated with some sports
What is subchondral sclerosis?
Subchondral bone is the layer of bone just below the cartilage. With osteoarthritis, there is increased blood flow and other changes that develop in the subchondral layer . Subchondral sclerosis is defined as increased bone density or thickening in the subchondral layer. This often occurs with progressive osteoarthritis and shows up on x-rays as abnormally white (dense) bone along the joint line.
Describe the pathophysiology of OA?
OA is the result of active, sometimes inflammatory but potentially reparative processess, rather than the inevitable result of trauma and aging
It is characterised by progressive destruction and loss of articular cartilage with an accompanying periarticular bone response.
The exposed subchorndral bone becomes sclerotic with increased vascularity and cyst formation
Attempts at repair produce cartilaginous growths at the margins of the joint which later become calcified (osteophytes)
What mechanisms have been suggested for the pathogenesis of OA?
- Metalloproteinases e.g. stromelysin and collagenase, secreted by chondrocytes degrade collagen and proteoglycans
- IL-1 and TNF-α stimulate metalloproteinase production and inhibit collagen production
- Deficiency of growth factors e.g. insulin-like growth factor and transforming growth factor impairs matrix repair
- Genetic susceptibility (35-65% influence) from multiple genes rather than a single gene defect. Mutations in the gene for type II colagen hae been associated with early polyarticular OA
Most OA is primary with no obvious predisposing factor. Secondary OA occurs in joints that have been damage in some way or are congenitally abnormal
How does OA differ from inflammatory arthritis?
There is only transient (<30 minutes) morning stiffness
What is the main symptoms of OA?
Join pain, made worse by movement and relieved by rest
What are the joints most commonly involved in OA?
DIPJs Cartometacarpal joint of the hands First MTP joint of the foot Hips Knees Vertebrae
What joints are rarely affected by OA?
Elbows
Wrists
Ankles
What signs are seen on examination of a patient with OA?
Deformity and bony enlargement of the joints
Limited joint movement
Muscle wasting of surrounding muscle groups
Crepitus (due to disruption of normally smooth articulating surfaces)
Joint effusion
Heberden’s nodes
Bouchard’s nodes
Where do Heberden’s nodes occur?
DIP joints
Where do Bouchard’s nodes occur?
PIP joints
How is OA differentiated from RA?
Pattern of joint involvement
Absence of systemic features in OA
Absence of morning stiffness in OA
What are the main differentials for OA?
RA
“Pseudo-OA” (a chronic arthropathy seen in elderly women with severe chondrocalcinosis. Wrists and shoulder are usually involved and the hands are rarely involved.)
Chronic tophaceous gout
Psortiatic arthritis
What X-ray signs are seen in patients with OA?
X-rays are only abnormal in advance stages Show: - Narrowing of the joint space - Osteophytes - Subchondral sclerosis - Cyst formation
