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What is the 'arthritis cycle'?

The 'arthritis cycle' represents the continual degradation and imbalance of metabolic processes within the joint once the osteoarthritic disease cycle is established. OA can be initiated by a range of external factors, such as joint injury and trauma. Once the arthritis process is initiated there are multiple processes that undergo a deteriorating cycle. Three of these cycles are discussed below and shown in the diagram following.

 

Cycle 1 – Vascular Occlusions

Cartilage derived antigens released into synovial fluid can activate blood leucocytes to express pro-coagulant and cytokine activities.

This may result in deposition of lipid and fibrin clots in synovial tissues and in the small blood vessels supplying the subchondral bone (Arnoldi, 1996).

When blood flow and nutrition to bone and synovial cells is compromised by these occlusions the result is ischaemia, cell necrosis and joint pain (Ghosh and Cheras, 2001).

In response to the cellular necrosis and trauma, there is remodelling and thickening of subchondral bone altering its mechanical compliance.

These changes increase the load-bearing stresses carried by the overlying articular cartilage, thereby subjecting it to excessive mechanical stresses. These mechanical factors all contribute to cartilage failure and further antigen release.

 

Cycle 2 – Synovial Degradation

The cartilage fragments and matrix degradation products (e.g. from proteoglycans and Type II collagen) released from the damaged articular cartilage are antigenic and when they localise in the synovial membrane, they can provoke an inflammatory response (synovitis).

Once the synovitis becomes established in the joint, the synovial lining cells together with leucocytes recruited from the blood, release a host of noxious substances which can perpetuate the OA processes (Hamerman, 1993).

These noxious substances include proteinases, prostaglandins, cytokines (IL-1, TNF-α) and free radicals, all of which can directly and indirectly degrade cartilage, bone and the hyaluronic acid of synovial fluid.

Subsequently, synoviocyte metabolism is abnormal producing a poor quality, low molecular weight hyaluronic acid (Francis et al., 1993) perpetuating greater joint friction and further degradation of the articular cartilage.

 

Cycle 3 – Proteolytic Enzymes

Abnormal joint structure from cartilage failure elevates mechanical stresses and inflammatory feedback.

The stresses result in abnormal chondrocyte metabolism elevating the production of catabolic metalloproteinases (e.g.collagenase) that breakdown the cartilage matrix (Hamerman, 1993).

Chondrocytes produce tissue inhibitor of metalloproteinase (TIMP) to counteract the enzyme release but not in sufficient quantities to reduce the destructive processes.

Further cartilage degradation results in further joint abnormalities and progress of the disease process.

Below is a graphical representation of the arthritis cycle. It shows the healthy joint at the top, with a range of external factors influencing the joint, from hereditary and genetic problems to injuries and trauma. The external factors help initiate the arthritis cycle. Once initiated there are various pathways of the disease that continually deteriorate if not provided proper treatment and care.

Arthritis Cycle

 

REFERENCES

Arnoldi CC (1996) Development from osteoarthritis and nontraumatic osteonecrosis to osteoarthrosis. ARCO Newsletter 8(1):4-27

Francis DJ, Hutadilok N, Kongtawelert P, Ghosh P (1993) Pentosan polysulphate and glycosaminoglycan polysulphate stimulate the synthesis of hyaluronan in vivo. Rheumatol Int 13:61-64

Gardner DL (1983) The nature and causes of osteoarthrosis. Br Med J 286:418-424

Ghosh P and Cheras PA (2001) Vascular mechanisms in osteoarthritis. Best Prac and Res Clin Rheum 15(5):693-710

Hamerman D (1993) Aging and osteoarthritis: Basic mechanisms. J Am Geriatr Soc 41(7):760-770