Osteoarthritis

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  • Created by: Hpgrice
  • Created on: 14-10-19 11:24

Osteoarthritis (OA) is a disease of articulating joints.

Joint composition:

  • Cartilage which is the thin tissue layer at the end of long bones which allows the joints to move friciton free.
  • Synovial fluid is the fluid inbetween bones which also helps to lubricate movement and provides nutrients to the carilage cells (chrondocytes)
  • Joint also has muscle, ligments and tendons to help hold it in place and fat, synovial fluid etc. provide nutrients

OA is characteristed but gradual loss of articular cartilage and bones that lose cartilage become sclerotic (thicken/ lose adaptability) = lots of pain. Joint space narrowing is a sign used in diagnosis.

OA doesnt have a major inflammatory repsonse in comparison to an autoimmune disease such as Rheumatoid Arthritis.

Primary OA affects 5 million people in UK.

Joints can have lesion such as from sports - badly jolt the joint can result in loss ofcartilage - can put chrondocytes into repair situation but inevitably will develop into severe secondary OA. Secondary because there is a cause.

Primary OA is usually older people where there is no obvious mechanical cause.

OA is bilateral so if in one hand will be in the other hand.

  • Cartilage made from one cell type: chrondocytes
  • They sit in isolation so limited communication to other cells.
  • Sit in pericellular matrix which together with the chronodcyte = chrondron
  • Then there is the extracellular matrix of collagen (rodlike structures) and proteoglycans.
  • Proteoglycans pull water into the tissue which makes the tissue expand and then the collagens resist - they form a network to stop the tissue expanding - ability to compress and then reform again 

When OA starts to develop there is a loss of surface of the cartilage (fibrillation), start to lose cells and extracellular matrix - doesnt take long for it to disappear and expose the underlying subchondral bone.

Primary OA observations:

  • subchondral sclerosis - thickening of the bone, new bone/cartilage develop on perifery of joint (think an attempt to stabilise the joint and known as osteophytes
  • can be slight inflammation of synovium (nothing compared to rheumatoid OA)
  • angulation of bone 
  • In general observations are cells that are trying to respond to the loss of cartilage (i.e no causing the loss. The main causal observation is the loss of cartilage

Patient symptoms:

  • joint pain, joint stiffness and reduced function (consequential loss of muscle mass due to less activity due to pain)
  • increased morbidity and mortality
  • maintaining movement is important for the disease but natural response is to do opposite and so people put on weight, lose muscle mass, and loss of muscle causes the joint to destabilise even further, and increases overall risk of cardiovascular disease

Treatment

  • no disease modifying drugs (rheumid OA drugs dont work for primary OA)
  • pain relief moderatively affective
  • surgery for large (hips and knees) and small (thumb) joints: replacement -  remove diseased tissue and insert implant, need to encourage exercise to stop loss of muscle (hip replacement x ray image showed other joint to have an irregular surface showing possible disease in that…

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