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Osteoarthritis

Osteoarthritis (OA)

Otherwise known as Degenerative joint disease. The hyaline cartilage in the joints degenerates and the articular surfaces of the bones approximate. This can cause hypertrophy of the bone and subsequent production of osteophytes.
Arthritis is the major cause of disability and chronic pain in Australia, with 3.85million Australians affected at a cost to our economy of more than $23.9 billion each year in medical care and indirect costs such as loss of earnings and lost production1. 2.4 million of those people are of working age (not a disease of the aging. (http://www.arthritisaustralia.com.au/index.php/arthritis-information/what-is-arthritis.html.Accessed 23.03.2013.)
It is the most common condition of the joints and most people have degenerative changes by the time they turn 40 (usually asymptomatic). Usually affects the weight bearing joints such as the hips and knees but is also common in other joints;
Fingers
Vertebrae (cervical and lumbar spine)
Big toe
Hips
Knees

Pathophysiology
Quite a complicated process so I shall try to break it down as much as possible.
• Triggered by a change in the internal environment whereby the chondrocytes (cells of the cartilage) start to divide and there is an increase in the synthesis of proteoglycans and type II collagen.
• This stimulates the production of bone by the subcondral osteoblasts. Cellular activity is increased.
• The increase of bone formation in the subchondral area alters the physical properties in the region.
• The bone becomes stiffer and microfractures can occur, followed by callus formation, more stiffness, more microfractures and so on.
• The cellular changes of the peripheral synovial cells results in the periarticular formation of osteophytes.
• Pseudocytes (bony cysts) form in the marrow in the subchondral bone. This is quite an advanced stage and occurs because of the extrusion of the joint fluid through clefts in the hyaline cartilage.

In gross pathology there is roughening, pitting and irregularities of the hyaline cartilage surface and areas of the joint surface where there is complete loss of the cartilage.

Why do people get OA?

Fundamentally the cartilage is avascular, aneural and alymphatic. It is 95% water and extracellular cartilage matrix and only 5% chondrocytes. These cells have the longest cell cycle in the body. The health of the cartilage depends on the compression and release of the joint capsule to nourish it. Compression will pump fluid from the cartilage and into the joint space and into the capillaries and venules. Release allows the cartilage re-expand, re-hydrate and absorb the necessary nutrients.

Sedentary lifestyle-use it or lose it. Reduced mobility is the biggest cause of OA.
Poor nutrition
Obesity

Secondary OA can occur whereby the internal environment of the joints is altered due to disease (RA, congenital abnormalities, infections, metabolic, endocrine and neuropathic diseases), past trauma, repetitive use of the joints.
Signs and Symptoms
• Gradual onset involving usually 1 joint but can be more.
• Pain aggravated by exercise and relieved by rest.
• Morning stiffness easing after 15-30 mins when moving.
• Reduced range of motion in the joints
• Crepitus.
• Flexion contractures
• Joint enlargement (proliferation of soft tissue structures and joint effusion).
• Heat
OA in particular joints also has its own set of signs and symptoms;
Hips-groin pain and limping.
Spine-neurological symptoms.
Knees-locking, instability.

Diagnosis
Based on signs and symptoms
X-ray-shows narrowing of the joint space, increased density of subchondral bone, formation of osteopathytes and pseudocytes.
ESR-normal
Blood tests-help to rule out secondary causes of OA (RA, gout)
Synovial fluid analysis-clear and viscous

Treatment
Focuses on pain relief and prevention of further deterioration.
Important to educate clients about exercise and weight loss.
Stretches and muscle strengthening
Supplements
Analgesia if required
Steroid injections popular at the moment

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