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Osteoarthritis is an age related degenerative condition that affects the synovial joints of the human body. Simplistically, synovial joints are comprised of two bones with very specialised tissue called articular cartilage lining their ends. Articular cartilage distinctive features include specialised proteins that act like a sponge to attract and squeeze out water molecules, thereby facilitating shock absorption and friction free movement. The joint is then enclosed by a joint capsule and a fluid rich membrane. Osteoarthritis is essentially a breakdown of this special cartilage leading to associated inflammation of the joint lining, pain, stiffness and loss of function. This differs from rheumatoid arthritis which is a genetic auto-immune disease, that leads to the same degenerative joint process, however can occur much earlier in life. Joints that are affected by osteoarthritis are primarily the weight bearing joints of the lower limb, knee and hip being most prominent.

Although the majority of the population eventually suffer some degree of osteoarthritis (OA) in their lifetime, the severity, distribution and onset of the disease depends on a multitude of factors:

Lifestyle choices including sports and occupation play a major role. A marathon runner who runs to the age of 65 is significantly more likely to suffer knee OA than a 65 year old couch potato, who may suffer co-morbidities such as heart disease. Sometimes it can be a juggling act to balance joint health with cardiovascular health. This is where low impact exercise can play a crucial role.

Biomechanical variations such as leg length discrepancies, bow legs, knock knees or foot over pronation can accelerate the degenerative process. In extreme cases these can be treated surgically, however majority of the time we can implement compensatory measures with a physiotherapeutic approach; stretch/release and strengthen. Foot orthoses can also play a crucial role here and your sports podiatrist can point you in the right direction.

Morphological changes include abnormalities in joint shape or size. This commonly occurs in the hip joint where an abnormally positioned or depth socket can lead to joint impingement and accelerated degeneration of articular cartilage. Similarly, the femoral head (ball of hip joint) can have some extra bone between the head and neck leading to impingement and degenerative change. The knee cap can also be abnormally shaped, or it’s groove shallow, leading to poor patella tracking and increased cartilage wear and tear.

Active joint control relates to the ability of the individuals muscle system to safely control the joint. Research over the past 20 years has identified that the majority of joints are supported by a specialised type of endurance muscle that has the primary role of stabilising the joint while other more global muscles provide movement. In cases of injury or deconditioning (ie. our lazy couch potato) these muscles may not provide the stabilising support leading to increased joint wear.

Previous injury can contribute to OA in two ways. It either causes painful inhibition of the deep stabilisers as mentioned above, or through direct trauma to articular cartilage. Bone fractures that occur close to a joint are generally of a poor prognosis if the fracture extends into the joint surface.

Unfortunately there is no cure for OA. Prevention is the most effective strategy, however this can be a challenge and requires recognition of the contributing factors. In some cases, such as joint trauma, prevention is impossible. The variables that are available to be manipulated such as lifestyle factors, biomechanical factors and joint control should be adjusted accordingly. This may include things like implementing a low impact exercise plan, retraining deep stabilising musculature or employing orthotic devices to correct foot pronation. New surgical techniques with hip arthroscopy to correct morphological changes are becoming routine in order to preserve joint health.

So what do we do when the arthritic process has begun? OA is generally thought of as an age related disease, however the number of younger 30-40 year old patients diagnosed with OA is growing. Conservative management of OA includes a low impact exercise regime, specific joint stabilisation / strength training, strengthening of shock absorber musculature and intermittent medication therapy. Short courses of Non steroidal anti-inflammatories can be effective at settling flare ups. The much publicised glucosamine can be effective in some patients, and although there is no strong scientific evidence in support for it, a 6 week trial should be undertaken of a glucosamine/chondroitin combination. Current medical management includes injection therapy of growth factors to stimulate healing, or viscous supplements to smooth roughened/worn cartilage Although we can only manage or attempt to prevent the disease, the future seems bright with a large focus on stem cell therapy. WATCH THIS SPACE!!
 

Shane O’Sullivan
Sports Physiotherapist
Prahran Sports Medicine Centre