Osteoarthritis is a degenerative disease, usually affecting people over the age of 45. The degenerative process can be hastened by injury to a special joint. It occurs due to failure of chondrocytes to repair damaged cartilage or when there is a disparity between the stress applied and the chondrocyte response, wear vs repair. Osteoarthritis affects the protective cartilage that covers the bones, causing it to break down, becoming rough and even torn in places. The response of the body is to try to increase the joint surface in response and this produces ridges or spurs also known as osteophytes. This exposes the bone, causing additional friction in the joint, which damages the cartilage and bone even further as they rub together. Osteoarthritis more often affects the weight-bearing joints, such as the knees and hips, as well as the spine.

The specific causes of osteoarthritis are not known and is considered a part of the ageing spectrum. Why some people develop it early in life while others donot suffer from it even in an advanced stage is not clearly known, what is known however is that several factors can increase the risk for developing it. These include age, obesity, and overuse due to sports or occupational stresses.Thus osteoarthritis could be:

• Primary - no obvious cause

• Secondary - occurs following certain predisposing factors (such as previous trauma, congenital deformity, infection or a metabolic disorder).

The changes that occur at molecular level in osteoarthritis are

1. Increased water content (in contrast to decreased water content in normal ageing) leading to weakening of type 2 collagen network.

2. Shorter chains and shifts in the concentration of proteoglycans. The chondroitin/keratin ratio is increased (opp. to ageing).

3. Disruption is caused by an increase in collagenase and proteoglycan-degrading enzyme (stromelysin & plasmin) concentration.

4. Rate of synthesis of DNA, collagen, and proteoglycans are increased

5. Increased levels of:

• Matrix Metalloproteinases (MMPs) (collagenase, gelatinase, and stromelysin).

• Cathepsins B and D

• IL1 - enhances enzyme synthesis & has a catabolic effect.

• IL6

• TNFa

• TGF beta

• GAGs and polysulfuric acid

Complications of Osteoarthritis: They could be -

1. Deformities

2. Subluxation

3. Ankylosis

4. Loose bodies leading to repeated locking and further progression

Treatment of Osteoarthritis:

Depending on the severity of your osteoarthritis, your doctor may try one or a combination of several different courses of treatment. Because pain is the major complaint in osteoarthritis, treatment will focus on reducing that pain. Following are various modalities that may be used:

• Protection of affected joints from overloading

o weight loss

o use of walking stick

• Exercise of supporting muscles around joints to avoid wasting

• Supportive measures such as pain relief by analgesics or NSAIDs

• Hyaluronic acid injections

• Glucosamine & chondroitin

• Surgical treatment - is indicated for patients with persistent symptoms and pain and ranges from arthroscopy to arthroplasty.

o Realignment osteotomies may be done in younger patients to redistribute weight bearing load at the knee to prevent further damage.

o In the most severe cases of osteoarthritis, joint replacement may be an appropriate treatment. Total joint replacement is also called `arthroplasty.' In a joint arthroplasty, the ends of the affected bones are resurfaced and replaced with a combination of plastic and metal components. These are more commonly performed on the hip and knee.

• New & Experimental Treatments:

1. Soft tissue grafts - periosteal / perichondral

2. Chondrocyte transplantation

3. Mosaicplasty (See Maitrise Orthopedique)

4. Artificial matrix - carbon fibre, collagen, polylactic acid

5. Fresh osteochondral grafts

6. Doxycycline - In animal studies, doxycycline inhibits cartilage collagenase activity and reduces the severity of osteoarthritis. (Although doxycycline is an antibiotic, it should not be thought that osteoarthritis is an infectious process)

7. Transforming growth factor beta (TGF beta) - packaged in liposomes can repair partial thickness articular cartilage lesions in animal models.

8. Metalloproteinase inhibitors - drugs that inhibit enzymes responsible for cartilage matrix destruction and block cytokines (proteins involved in the destruction).

9. Gene therapy - Genes that have either anti-arthritic or synthetic properties can be delivered into the joint via non-replicating viral vectors. Two human trials are presently underway in which a retrovirus is used to transfer human IL-1ra cDNA to the synovial lining of metacarpo-phalangeal joints of patients with rheumatoid arthritis. Although exciting and full of promise, the field of gene therapy still needs careful work and caution. In animal studies, for example, the transfer by gene therapy of TGF beta and BMP-7 to synovium and chrondroprogenitor cells resulted in death of the animals, possibly through overproduction of the proteins generated

• The potential long-term treatment or cure of osteoarthritis really lies in the development of agents that reverse the balance between degradative and synthetic processes of the chondrocyte.

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