Osteoarthritis

Question 1

Pathology

Answer 1

OA is the result of progressive breakdown of joint surfaces and can follow any insult to a joint (infection, direct/indirect trauma to articular cartilage and joint diseases)
Involves mainly large weight bearing joints
Primary OA includes several different conditions; the commonest being generalized nodal osteoarthritis. Onset can be sudden with hot, inflamed, distal IP joints.
Hip OA is more common in males, often unilateral with no other joint involvement and no with no obvious precipitating cause

Question 2

Secondary OA Causes

Answer 2

Obesity
Abnormal contour of articular surfaces, particularly mal-united #s
Mal-alignment of joints from deformity, #s or distortion of anatomy by previous surgery, particularly menisecetomy of knee
Joint instability due to trauma or generalised ligamentous laxity
Genetic/developmental abnormalities
Inflammatory diseases such as RA, gout and infection
Osteonecrosis
Neuropathies

Question 3

Development of OA.

Stage 1) Breakdown of Articular Surface

Answer 3

Normal smooth surface of articular cartilage is breached
The arcades of collagen fibres break and the surface becomes rough.
Friction against the rough surface generates particles of articular cartilage that are shed into the joint and absorbed by the synovium, where they cause an inflammatory response which the patient feels as stiffness or aching in joint after exercise rather than during.

Question 4

Development of OA.

Stage 2) Synovial Irritation

Answer 4

Irritation of synovium due to the release of intracellular enzymes, including lysosomes which produce hyperaemia and a cellular response in synovial layers.
Synovium can also produce enzymes and mediators which influence chondrocyte activity. Other potential causes of damage include free radicals and deposition of immune complexes.

Question 5

Development of OA.

Stage 3) Remodelling

Answer 5

Limited cartilage repair occurs. Superficial lesions of articular cartilage show little healing, but deep lesions that penetrate cortial bone allow the influx of marrow cells and formation of fibro cartilage. Subchondral bone is abnormally active in OA, which increases density of tissue and the number of cells. New bone forms (osteophytes) covered by fibro cartilage which restrict joint movement. A line of dense, hard bone forms below cartilage and remodels the joint, changing the shape and congruity. This alters the pattern of weight bearing, resulting in the load being taken by different areas of articular cartilage.

Question 6

Development of OA.

Stage 4) Eburnation of Bone and Cyst Formation

Answer 6

Repair process fails, articular surface is eroded, exposing subchondral bone, which becomes polished and eburnated.
Raw bone rubbing on raw bone causes pain, and eburnated bone is not as slippery as articular cartilage causing friction across joint and uneven weight transmission. Some parts of the joint therefore become overloaded causing micro fractures of cancellous bone.
Micro fractures heal with callus, increasing rigidity of bone, so bone becomes denser, more sclerotic and less resilient. This then causes more micro fractures and bone architecture is lost. Synovial fluid enters cancellous bone under pressure through cracks in articular surface, producing cavities seen on MRI. These cysts fill with fibrous tissue and become lined with a thin shell of cortical bone.

Question 7

Development of OA.

Stage 4) Disorganisation

Answer 7

Joint becomes progressively stiffer and deformed, osteophytes enlarge and bone surfaces are worn away. As bone is lost, ligaments become looser because bones they support become shorter.

Question 8

Radiological appearance of OA

Answer 8

Narrowed joint space
Sclerotic weight-bearing surface
Osteophytes around joint margins
Cysts in subchondral bone
Altered bone shape

Question 9

Clinical Presentation of OA

Answer 9

Pain
Loss of Movement
Altered Function

Question 10

Conservative Rx

Answer 10

Explanation of condition and reassurance.
Advice on lifestyle – keeping active, avoiding activities to avoid things that hurt or aggravate problem or overload joint.
Walking aids in the home.
Physiotherapy to maintain muscle bulk and joint ROM.
Heat treatment: ice, infrared lamps and short wave diathermy. Exercises to increase power of muscles around affected joint, to increase ROM and prevent contractures.
Drugs – intermittent analgesics and NSAIDs.
Steroid injections are helpful for extra-articular inflammation
Very occasional intra-articular steroid injections.