Osteoarthritis(OA), or degenerative joint disease, is characterized by deterioration of articular cartillage that results in formation of new bone at the surfaces of the joint. It differs from RA in that it is a noninflamatory disorder with symptoms typically limited to the joints where cartilage degeneration is occuring, which are most commonly the weight-bearing joints.
Osteoarthritis can be categorized as either primary or secondary.
Primary OA is idiopathic in nature (i.e., no predisposing factor is known for the cartilage failure).
Secondary OA results from underlying trauma, another joint disorder, or a systemic metabolic or endocrine disorder.
Risk factors for OA include:
1) Age
2) History of trauma to the joints
3) History of fracture or infection
4) Obesity and stress from the patient's occupation or sports are controversial; the relationship of these risk factors with OA has not been clearly defined.
The signs and symptoms of OA are listed below:
Signs are:
1) Radiographic evidence of joint degeneration
2) Visible deformities of fingers
Symptoms are:
1) Pain
2) Morning stiffness
3) Limited range of motion
4) Crepitus
5) Instability
6) Joint tenderness
7) Muscle atrophy
Analgesics and anti-inflammatories are the foundations for OA; however, this treatment is only symptomatic.
As in RA, analgesic and anti-inflammatory agents donot alter the progression of OA. Scheduled acetaminophen upto 4 gms per shows benefit in many patients who do not require anti-inflammatory effects, and should be considered initially.
Caution against excessive use or use in patients with liver disease is necessary, however, because of the risk of hepatoxicity associated with acetaminophen.
If simple analgesics fail or toxic effects or inflammation are present, NSAID therapy should be initiated. Either conventional NSAID or COX-2 inhibitor therapies are generally the next therapeutic option for patients not responding to acetaminophen.
Although the COX-2 inhibitor may offer benefit over conventional NSAID products to patients who are at high risks of gastrointestinal side effects, it is important to be aware of the possibility of gastrointestinal, cardiovascular, renal, or hepatic toxicity with any of these agents.
Evidence of benefit in treating OA with the over-the-counter (OTC) dietry supplements glucosamine and/or chondroitin is being seen as well. For OA of the knee, injection of hyaluronic acid derivatives directly into the joint offer another option. Such injections may be used in combinations with oral therapies.
If all other options are unsuccessful, narcotic analgesics may offer some pain relief to the patients. Narcotic treatment is considered as a final option.
Like in RA, nondrug therapies are also important in OA. Overweight patients are counseled regarding weight loss to decrease stress on the weight bearing joints. Physical therapy, including exercise and appropriate use of heat and cold, may help to maintain joint function and to relieve pain. Patients with severe, debilitating disease may be candidates for surgical intervention.