Incidence-national and international Osteoarthritis (OA)
There are over half a million New Zealanders with OA .
It is the most common form of joint disease in
Australasia (Brown & Edwards 2012).
It is more prevalent in NZ women than men. Maori men have an increased prevalence compared to Pakeha men. Pacific women and Asian men and women have a significantly lower incidence than European / other women (MoH, 2008)
In the USA, most people over the age of 65 years have radiological evidence of OA, even if asymptomatic
(Ebersole et al., 2008).
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Aetiology including risk factors OA is no longer considered part of the normal aging process but aging is one risk factor for the development of the disease. Other risk factors include nutritional deficits, obesity, menopause (reduction in oestrogen levels, genetic factors and sporting or employment activities which exacerbate joint wear and tear (Brown & Edwards 2012).
OA may be idiopathic (occurs spontaneously or from unknown causes) or may occur secondary to a known event which causes damage to the joint structure (Brown &
Edwards 2012).
Cartilage provides the cushioning between the bones of the joints.
Over time, collagen and proteins are lost from smooth cartilage, causing it to retain more water. This results in the cartilage which is normally smooth and translucent to becoming thinner, yellow and granular which is softer, less flexible and less able to withstand damage due to heavy use. Repair of the cartilage does not keep pace with the destruction occurring leading to the articular surfaces of the joint bones to rub together, causing destruction of the joint and overgrowth of bone at the joint margins. The joint range of movement decreases and the joint enlarges. Common sites for OA are knees, hips, cervical & lumbar
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spine, finger & thumbs (Lemone et al, 2011, Brown
& Edwards
2012).
Pathophysiology
Illness
Trajectory
Progressive condition. As joint damage progresses, an inflammatory reaction can occur as small pieces of cartilage break off and lodge between the articulating surfaces. The pain increases & the person’s activity levels decrease, leading to other problems e.g. increased risk of obesity leading to increased stress on weight-bearing joints, & further pain. Can cause significant changes to lifestyle activities depending on affected joint (e.g. walking, bending, use of hands for writing, ability to participate in usual hobbies may be curtailed). Cessation of leisure activities may impact on socialisation, leading to isolation & depression.
Joint replacement surgery may be required if hips or knees affected .
Risk of falls which may lead to fractures increases with age and level of disability(Hunter 2012, Brown & Edwards 2012).
Signs and
Symptoms
relate to pathophysiolo gy
Stiffness with inactivity & pain with activity, relieved by rest. Swelling of the affected joint with hard bony protuberances and limitation of range of movement (Jarvis 2008). Changes in gait e.g. length of stride and standing stance due to reduced range of movement and pain. As the disease progresses there may be increased pain at rest and pain associated with minimal activity if more joints become affected. Sleep can become affected by joint discomfort and changes in barometric pressure
(weather patterns) can impact on pain and levels of function. The person may experience difficulty in lowering to sit and rising to stand if weight bearing joints are affected (Brown & Edwards 2012 )
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Two commonly used medications and expected treatment effect
Non-steroidal anti inflammatory drugs (NSAID) e.g. Ibuprofen
Goals are to reduce inflammation and pain and limit joint deformity/destruction which results from chronic inflammation.
Ibuprofen inhibits the action of the inflammatory response. High doses and prolonged use may affect platelet aggregation (ability to form clumps) and result in GI bleeding (Adams & Koch 2010).
Paracetamol -non
