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Flashcards in Session 6 Deck (16):
0

What happens in early OA?

Swelling of the cartilage usually occurs because of the increased synthesis of proteoglycans; this reflects an effort by the chondrocytes to repair cartilage damage.

This stage may last for years or decades and is characterised by hypertrophic repair of the articular cartilage.

1

What happens as OA progresses?

The level of proteoglycans eventually drop very low, causing the cartilage to soften and lose elasticity and thereby further compromising joint surface integrity.

Microscopically flaking and fibrillations (vertical clefts) develop along the normally smooth articular cartilage on the surface of an osteoarthritic joint.

Over time, the loss of cartilage results in loss of joint space.

2

What change in the normal metabolic balance occurs in OA?

There is an increase in the catabolic processes relative to the rate of synthesis of matrix components.

The end result is that the rate of repair is insufficient to maintain the normal integrity of the matrix,

When the changes in the cartilage structure have progressed to the point of affecting its physical characteristics, such as causing a decrease in cartilage resilience, then joint loads lead to further damage to the cartilage.

At this stage, biomechanics factors become the most prominent cause of further damage.

3

Describe the 3 stages of the evolution of the OA disease process

1) abnormally excessive proteolytic breakdown of the cartilage matrix,

2) fibrillation and erosions of cartilage liberates these breakdown products into the synovial fluid.

3) synovial cells take up these cartilage breakdown products, causing a chronic synovial inflammatory reaction and the ongoing production of proinflammatory cytokines. These cytokines then diffuse back to the cartilage to negatively impact the chondrocyte. By this stage, the chondrocyte has become increasingly sensitised to these pro inflammatory cytokines because of an increased number of cytokine cell receptors,

4

What are the clinical features of OA?

Pain

Stiffness

Deformity

Loss of function

Crepitus (a grating sound or sensation produced by friction between bone and cartilage or the fractured parts of a bone)

5

What are the radio graphic features of OA?

Loss of joint space

Osteocytes

Subchondral sclerosis

Subchondral cysts

Deformity

A image thumb
6

What is the effect of the erosion of the damaged cartilage in an OA joint?

Erosion progresses until the underlying bone is exposed.

Bone denuded of its protective cartilage continues to articulate with the opposing surface.

Eventually the increasing stresses exceed the bio mechanical yield strength of the bone.

The subchondral bone responds with vascular invasion and increased cellularity, becoming thickened and dense (a process known as eburnation) at areas of pressure.

The traumatised subchondral bone may also undergo cystic degeneration which is attributable either to Osseous necrosis secondary to chronic impaction or to the intrusion of synovial fluids.

Osteoarthritic cysts are also referred to as subchondral cysts, pseudo cysts or geodes and may range from 2 to 20mm in diameter.

At areas along the articular margin, vascularization of subchondral marrow, Osseous metaplasia of synovial connective tissue and ossifying cartilaginous protrusions lead to irregular outgrowth of new bone (osteophytes).

Fragmentation of these osteophytes or of the articular cartilage itself results in the presence of intra-articular loose bodies,

7

What might osteoarthritis lead to as well as joint damage?

Pathophysiological changes in associated ligaments and the neuromuscular apparatus.

For example, lateral collateral ligament complex abnormalities are common in knee osteoarthritis.

8

What are the treatment options for OA?

Conservative:

analgesics/NSAIDs

physiotherapy

joint injections glucosamine

 

Surgery: joint replacement, fusion, excision

9

What is Rheumatoid Arthritis?

A chronic systemic inflammatory disease of unknown cause.

An external trigger e.g. Cigarette smoking, infection or trauma that triggers an autoimmune destruction which leads to synovial hypertrophy and chronic joint inflammation, along with the potential for extra-articular manifestations, is theorised to occur in generally susceptible individuals.

10

Describe the Pathophysiology of RA

Complicated and not yet fully understood.

Synovial cell hyperplasia and endothelial cell activation are early events in the pathological process that progresses to uncontrolled inflammation and exuberant proliferation of the synovium (pannus formation) and consequent cartilage and bone destruction.

Genetic factors and immune system abnormalities contribute to disease propagation.

11

What molecules are important in RA?

CD4 T cells, mononuclear phagocytes, fibroblasts, osteoclasts and neutrophils play major cellular roles in the pathophysiology of RA, whereas B cells produce autoantibodies.

Abnormal production of numerous cytokines, chemokines and other inflammatory mediators e.g. TNF-alpha, IL-1 and PDGF have been demonstrated in patients with RA.

12

What are the radiological features of RA?

Joint space narrowing

Peri-articular erosions

Diffuse osteopenia

Deformity

A image thumb
13

What is the Clinical Examination of RA?

Stiffness

Tenderness

Pain on motion

Swelling

Deformity

Limitation of motion

Extra-articular manifestations

Rheumatoid nodules

14

What types of deformities are seen in RA?

Z Thumb

Subluxation MCPJ

Radial deviation wrist

Ulnar deviation MCPJ

Boutonnière deformity: PIP is permanently bent towards the palm and DIP is permanently bent away.

Swan neck: DIP hyperflexion and PIP hyperextension.

15

What is the treatment for RA?

Non operative: Analgesics/NSAIDs, DMARDS (disease modifying anti- rheumatic drugs), Immunotherapy, Steroids, Splints, Injections

Operative: Fusion, tendon transfers, joint replacement, excision

Goal of treatment: relieve pain, maintain function.